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Bibliography studies are no longer recommended for suspected small-bowel Bibliography bleeding given their poor diagnostic yield (3%-6%). Disorders of the Esophagus Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated international con- Hemodynamically Unstable Patients sensus diagnostic criteria for eosinophilic esophagitis: proceedings of the AGREE conference. Gastroenterology. 2018;155:1022-1033.e10. [PMID: As in LGIB, CT angiography is the diagnostic test of choice for 30009819] doi:10.1053 /j.gastro.2018.07.009 hemodynamically unstable patients or for those with brisk small- Hirano I, Chan ES, Rank MA, et al; AGA Institute Clinical Guidelines bowel bleeding. It is widely available, provides rapid testing, and Committee. AGA Institute and the Joint Task Force on Allergy-Immunology Practice Parameters clinical guidelines for the management of eosinophilic has good diagnostic accuracy (sensitivity, 89%; specificity, 85%). esophagitis. Gastroenterology. 2020;158:1776-1786. [PMID: 32359562] In patients with contraindications to CT, technetium-99m-— doi:10.1053/j.gastro.2020.02.038 Katzka DA. Eosinophilic esophagitis. Ann Intern Med. 2020:172:ITC65-ITC80. labeled red blood cell or sulfur colloid nuclear scanning may be [PMID: 32365374] doi:10.7326/AITC202005050 considered. The primary weakness of radioisotope-labeled scan- Klavan H, Russell MB, Macklin J, et al. Barrett’s esophagus: A comprehensive ning is the propensity to poorly localize the bleeding site. review for the internist. Dis Mon. 2018:64:471-487. [PMID: 29880269] doi:10.1016/j.disamonth.2018.04.001

Katzka DA. Eosinophilic esophagitis. Ann Intern Med. 2020:172:ITC65-ITC80. labeled red blood cell or sulfur colloid nuclear scanning may be [PMID: 32365374] doi:10.7326/AITC202005050 considered. The primary weakness of radioisotope-labeled scan- Klavan H, Russell MB, Macklin J, et al. Barrett’s esophagus: A comprehensive ning is the propensity to poorly localize the bleeding site. review for the internist. Dis Mon. 2018:64:471-487. [PMID: 29880269] doi:10.1016/j.disamonth.2018.04.001 Moayyedi P, Eikelboom JW, Bosch J, et al: COMPASS Investigators. Safety of Management proton pump inhibitors based on a large, multi-year, randomized trial of After hemodynamic stabilization, therapy is guided by the patients receiving rivaroxaban or aspirin. Gastroenterology. 2019;157:682- 691.e2. [PMID: 31152740] doi:10.1053 j-gastro.2019.05.056 source and location of bleeding. For active bleeding identified Pauwels A, Boecxstaens V, Andrews CN, et al. How to select patients for antire- by CT angiography or red blood cell scanning, angiography with flux surgery? The ICARUS guidelines (international consensus regarding preoperative examinations and clinical characteristics assessment to select embolization should be performed. When a bleeding source is adult patients for antireflux surgery). Gut. 2019;68:1928-1941. [PMID: identified on video capsule endoscopy or CT angiography, 31375601] doi:10.1136 gutjnl-2019-318260 device-assisted enteroscopy (single-balloon system, double- Rohof WOA, Bredenoord AJ. Chicago classification of esophageal motility disorders: lessons learned. Curr Gastroenterol Rep. 2017;19:37. [PMID: balloon system, or spiral enteroscopy) or push enteroscopy 28730503] doi:10.1007/s11894-017-0576-7 should be performed with one or more endoscopic methods of Sandhu DS, Fass R. Current trends in the management of gastroesophageal reflux hemostasis. Intraoperative endoscopy during laparotomy/ disease. Gut Liver. 2018;12:7-16. [PMID: 28427116] doi:10.5009 gnll6615

Moayyedi P, Eikelboom JW, Bosch J, et al: COMPASS Investigators. Safety of Management proton pump inhibitors based on a large, multi-year, randomized trial of After hemodynamic stabilization, therapy is guided by the patients receiving rivaroxaban or aspirin. Gastroenterology. 2019;157:682- 691.e2. [PMID: 31152740] doi:10.1053 j-gastro.2019.05.056 source and location of bleeding. For active bleeding identified Pauwels A, Boecxstaens V, Andrews CN, et al. How to select patients for antire- by CT angiography or red blood cell scanning, angiography with flux surgery? The ICARUS guidelines (international consensus regarding preoperative examinations and clinical characteristics assessment to select embolization should be performed. When a bleeding source is adult patients for antireflux surgery). Gut. 2019;68:1928-1941. [PMID: identified on video capsule endoscopy or CT angiography, 31375601] doi:10.1136 gutjnl-2019-318260 device-assisted enteroscopy (single-balloon system, double- Rohof WOA, Bredenoord AJ. Chicago classification of esophageal motility disorders: lessons learned. Curr Gastroenterol Rep. 2017;19:37. [PMID: balloon system, or spiral enteroscopy) or push enteroscopy 28730503] doi:10.1007/s11894-017-0576-7 should be performed with one or more endoscopic methods of Sandhu DS, Fass R. Current trends in the management of gastroesophageal reflux hemostasis. Intraoperative endoscopy during laparotomy/ disease. Gut Liver. 2018;12:7-16. [PMID: 28427116] doi:10.5009 gnll6615 laparoscopy is the most invasive modality and is a last resort. Sharma P, Shaheen NJ, Katzka D, et al. AGA clinical practice update on endo- scopic treatment of Barrett's esophagus with dysplasia and/or early cancer: Pharmacologic therapy is possible for some underlying expert review. Gastroenterology. 2020;158:760-769. [PMID: 31730766]

E wn Item 1 On physical examination, vital signs are normal. The ~n <6) abdomen is nontender and mildly distended, with normal wn A74-year-old woman is evaluated in the emergency depart- wn bowel sounds. ment for yellow skin, dark urine, and light stools of 10 days’ id Serum creatinine level is 1.1 mg/dL (97.2 pmol/L). = duration. Q Random urine protein-creatinine ratio is 16 mg/g. rn On physical examination, vital signs are normal. Jaun dice and icteric sclerae are noted. Which of the following is the most appropriate additional Laboratory studies: treatment? Alkaline phosphatase 175 U/L Alanine aminotransferase 57 U/L (A) Discontinue atorvastatin Aspartate aminotransferase 49 U/L (B) Discontinue lisinopril Total bilirubin 6.0 mg/dL (102.6 mol/L) (C) Initiate lactulose Direct bilirubin 4.6 mg/dL (78.7 pmol/L) (D) Initiate low-protein diet CT reveals retroperitoneal fibrosis and a “sausage-shaped” pancreas with a narrowed pancreatic duct. Endoscopic ultra sound with fine-needle aspiration is negative for malignancy Item 4 but shows more than 10 IgG4-positive cells/hpf. A 30-year-old woman is evaluated at a new-patient visit. She was born in Somalia and immigrated to the United Which of the following is the most appropriate States 2 years ago. management? On physical examination, vital signs and other findings are normal. (A) Azathioprine Laboratory studies: (B) Endoscopic retrograde cholangiopancreatography Alanine aminotransferase 24 U/L with biliary stent placement Hepatitis B virus DNA Undetected (C) Prednisone Hepatitis B core antigen IgG antibody Positive (D) Total pancreatectomy Hepatitis B surface antibody Negative Hepatitis B surface antigen Positive Hepatitis E antigen Negative Item 2 Hepatitis E IgG antibody Positive A 45-year-old woman is evaluated at follow-up for abnor- Which of the following best describes this patient’s phase mal alkaline phosphatase levels on three previous blood of hepatitis B virus infection? tests. She has mild pruritus. She has no family history of liver disease. She has no other medical concerns and does (A) Immune active not take any medications. (B) Immune control Vital signs and other physical examination findings are (C) Immune tolerant normal. Her complete blood count and alanine aminotrans- (D) Reactivation ferase, aspartate aminotransferase, serum albumin, serum total bilirubin, and total protein are within normal limits. Item 5 The alkaline phosphatase level is 212 U/L. A 52-year-old man is evaluated in the emergency depart ment because of a 6-day history of fatigue, malaise, fever, Which of the following is the most appropriate diagnostic and abdominal pain. He has not recently traveled. Five test to perform next? weeks ago, he had a 1-week episode of low-grade fever and (A) Antimitochondrial antibody left-lower-quadrant abdominal pain that resolved sponta (B) Anti-smooth muscle antibody neously. On physical examination, temperature is 38.2 °C (100.9 °F), (C) Liver biopsy blood pressure is 110/80 mm Hg, pulse rate is 92/min, and (D) Serum IgG4 respiration rate is 16/min. The right upper quadrant of the abdomen is tender to palpation. The remainder of the exam ination is normal. Item 3 Laboratory studies: A 50-year-old man is evaluated for newly developed asci- Leukocyte count 17,000/uL (17 x 10°/L) tes. He has cirrhosis due to nonalcoholic steatohepatitis. Alkaline phosphatase 220 U/L Paracentesis confirms cirrhosis as a cause of the ascites Alanine aminotransferase 65 U/L and excludes infection, and a low-sodium diet is imple- Aspartate aminotransferase 55 U/L mented. Medical history includes type 2 diabetes mellitus, hypertension, and dyslipidemia. Current medications are Ultrasound demonstrates a 3.5-cm hypoechoic, metformin, lisinopril, and atorvastatin. fluid-filled mass in the right side of the liver.

ferase, aspartate aminotransferase, serum albumin, serum total bilirubin, and total protein are within normal limits. Item 5 The alkaline phosphatase level is 212 U/L. A 52-year-old man is evaluated in the emergency depart ment because of a 6-day history of fatigue, malaise, fever, Which of the following is the most appropriate diagnostic and abdominal pain. He has not recently traveled. Five test to perform next? weeks ago, he had a 1-week episode of low-grade fever and (A) Antimitochondrial antibody left-lower-quadrant abdominal pain that resolved sponta (B) Anti-smooth muscle antibody neously. On physical examination, temperature is 38.2 °C (100.9 °F), (C) Liver biopsy blood pressure is 110/80 mm Hg, pulse rate is 92/min, and (D) Serum IgG4 respiration rate is 16/min. The right upper quadrant of the abdomen is tender to palpation. The remainder of the exam ination is normal. Item 3 Laboratory studies: A 50-year-old man is evaluated for newly developed asci- Leukocyte count 17,000/uL (17 x 10°/L) tes. He has cirrhosis due to nonalcoholic steatohepatitis. Alkaline phosphatase 220 U/L Paracentesis confirms cirrhosis as a cause of the ascites Alanine aminotransferase 65 U/L and excludes infection, and a low-sodium diet is imple- Aspartate aminotransferase 55 U/L mented. Medical history includes type 2 diabetes mellitus, hypertension, and dyslipidemia. Current medications are Ultrasound demonstrates a 3.5-cm hypoechoic, metformin, lisinopril, and atorvastatin. fluid-filled mass in the right side of the liver. 87

rn od = Empiric treatment with ceftriaxone plus metronidazole Ultrasound of the right upper quadrant shows hepato- > is initiated. megaly, minimal ascites, liver echogenicity, and no biliary wn 72) CONT. stones or ductal dilation. @ wn n Which of the following is the most appropriate additional = treatment? Which of the following is the most appropriate i) = management? or (A) Needle aspiration > 2) (B) Percutaneous drain (A) Cefepime - Surgical resection (B) Liver biopsy (C) (D) No additional treatment is necessary (C) Pentoxifylline (D) Prednisolone Item 6 Item 8 A 65-year-old woman is evaluated in the emergency depart ment for a 2-day history of left-lower-quadrant abdominal A 60-year-old woman is evaluated for follow-up after pain and constipation. She reports having had nausea for screening colonoscopy. Colonoscopy revealed a 7-mm ses- 1 day but no vomiting. She has hypertension and type 2 dia- sile serrated polyp, which was completely removed. Three betes mellitus and underwent renal transplantation 2 years 2-mm hyperplastic polyps were removed from the rectum. ago. Current medications are prednisone, mycophenolate She is asymptomatic and has no other medical conditions. Family history is negative for colon cancer. She takes no mofetil, enalapril, and insulin. On physical examination, temperature is 37.8 °C (100.1 °F); medications.

ago. Current medications are prednisone, mycophenolate She is asymptomatic and has no other medical conditions. Family history is negative for colon cancer. She takes no mofetil, enalapril, and insulin. On physical examination, temperature is 37.8 °C (100.1 °F); medications. other vital signs are normal. Abdominal examination reveals left-lower-quadrant tenderness, with no guarding or mass. Which of the following is the most appropriate surveillance approach? Laboratory studies: Hemoglobin 13 g/dL (130 g/L) (A) Colonoscopy in 1 year Leukocyte count 11,000/uL (11 x 10°/L), with 70% (B) Colonoscopy in 5 to 10 years polymorphonuclear cells (C) Fecal DNA-based testing in 3 years Blood urea nitrogen 22 mg/dL (7.9 mmol/L) Creatinine 1.2 mg/dL (106.1 umol/L) (D) Fecal occult blood testing annually

other vital signs are normal. Abdominal examination reveals left-lower-quadrant tenderness, with no guarding or mass. Which of the following is the most appropriate surveillance approach? Laboratory studies: Hemoglobin 13 g/dL (130 g/L) (A) Colonoscopy in 1 year Leukocyte count 11,000/uL (11 x 10°/L), with 70% (B) Colonoscopy in 5 to 10 years polymorphonuclear cells (C) Fecal DNA-based testing in 3 years Blood urea nitrogen 22 mg/dL (7.9 mmol/L) Creatinine 1.2 mg/dL (106.1 umol/L) (D) Fecal occult blood testing annually Contrast-enhanced CT scans of the abdomen and pel vis show diverticula in the sigmoid colon with bowel wall Item 9 thickening and pericolonic mesenteric fat stranding. There A 44-year-old woman is evaluated for a 3-month history is no abscess, obstruction, or fistula. of irregular bowel habits, characterized by four or five epi- sodes of watery, nonbloody watery diarrhea daily for 2 to Which of the following is the most appropriate 3 days every 3 to 4 weeks. She has lost 2.3 kg (5.1 Ib) during management? the past 3 months. She also has osteoporosis treated with

Contrast-enhanced CT scans of the abdomen and pel vis show diverticula in the sigmoid colon with bowel wall Item 9 thickening and pericolonic mesenteric fat stranding. There A 44-year-old woman is evaluated for a 3-month history is no abscess, obstruction, or fistula. of irregular bowel habits, characterized by four or five epi- sodes of watery, nonbloody watery diarrhea daily for 2 to Which of the following is the most appropriate 3 days every 3 to 4 weeks. She has lost 2.3 kg (5.1 Ib) during management? the past 3 months. She also has osteoporosis treated with (A) Colonoscopy now calcium, vitamin D, and alendronate. Her sister has celiac disease. (B) Discharge to home with oral antibiotics On physical examination, vital signs and other findings (C) Hospitalization for intravenous antibiotics are normal. BMI is 21. (D) Surgery Laboratory evaluation reveals a total IgA level less than 500 mg/dL (5 g/L), tissue transglutaminase IgA level of 0 U/mL (normal, 0-3 U/mL), and IgG level of 800 mg/dL Item 7 (8 g/L). A 43-year-old woman is evaluated in the emergency depart- ment for confusion and a 1-week history of yellow skin. She Which of the following is the most appropriate consumes 12 beers daily. management? On physical examination, temperature is 38.5 °C (101.3 °F): (A) Anti-deamidated gliadin peptide IgG antibody blood pressure is 120/50 mm Hg, pulse rate is 100/min, and measurement respiration rate is 24/min. Her sclerae are icteric and skin is (B) Anti-gliadin IgA and IgG antibody measurement jaundiced. Tender hepatomegaly is present. She has asterixis and is oriented to person only. No source of infection has been (C) Gluten-free diet identified. Maddrey discriminant function score is 35. (D) HLA-DQ2and HLA-DQ8 testing

(A) Colonoscopy now calcium, vitamin D, and alendronate. Her sister has celiac disease. (B) Discharge to home with oral antibiotics On physical examination, vital signs and other findings (C) Hospitalization for intravenous antibiotics are normal. BMI is 21. (D) Surgery Laboratory evaluation reveals a total IgA level less than 500 mg/dL (5 g/L), tissue transglutaminase IgA level of 0 U/mL (normal, 0-3 U/mL), and IgG level of 800 mg/dL Item 7 (8 g/L). A 43-year-old woman is evaluated in the emergency depart- ment for confusion and a 1-week history of yellow skin. She Which of the following is the most appropriate consumes 12 beers daily. management? On physical examination, temperature is 38.5 °C (101.3 °F): (A) Anti-deamidated gliadin peptide IgG antibody blood pressure is 120/50 mm Hg, pulse rate is 100/min, and measurement respiration rate is 24/min. Her sclerae are icteric and skin is (B) Anti-gliadin IgA and IgG antibody measurement jaundiced. Tender hepatomegaly is present. She has asterixis and is oriented to person only. No source of infection has been (C) Gluten-free diet identified. Maddrey discriminant function score is 35. (D) HLA-DQ2and HLA-DQ8 testing Laboratory studies: Leukocyte count 14,000/uL (14 x 10°/L) Prothrombin time 14.0 s (control, 10.0 s) Item 10 Alkaline phosphatase 200 U/L A 36-year-old woman is evaluated for a 3-day history of Alanine aminotransferase 30 U/L constant right-upper-quadrant abdominal discomfort and Aspartate aminotransferase 62 U/L abdominal distention. She has no significant medical history. Total bilirubin 17.0 mg/dL (290.7 pmol/L) Her only medication is a combined oral contraceptive pill.

Laboratory studies: Leukocyte count 14,000/uL (14 x 10°/L) Prothrombin time 14.0 s (control, 10.0 s) Item 10 Alkaline phosphatase 200 U/L A 36-year-old woman is evaluated for a 3-day history of Alanine aminotransferase 30 U/L constant right-upper-quadrant abdominal discomfort and Aspartate aminotransferase 62 U/L abdominal distention. She has no significant medical history. Total bilirubin 17.0 mg/dL (290.7 pmol/L) Her only medication is a combined oral contraceptive pill. 88

ot On physical examination, vital signs are normal. Pal- ® Item 13 = pation reveals a tender, enlarged liver. Ascites is present. Ged A 22-year-old woman is evaluated in the emergency depart- i=

On physical examination, vital signs are normal. Pal- ® Item 13 = pation reveals a tender, enlarged liver. Ascites is present. Ged A 22-year-old woman is evaluated in the emergency depart- i= = Bowel sounds are normal. ment for an episode of confusion, diaphoresis, and tremu- Laboratory evaluation shows an alanine aminotrans- 2) lousness. Similar symptoms have been present for 6 months wn ferase level of 152 U/L and aspartate aminotransferase level r<0) but are becoming more frequent and severe. wn of 138 U/L. wn Fingerstick blood glucose level is 30 mg/dL (1.7 mmol/L). << Her symptoms resolve with administration of glucose. Sub- a Which of the following is the most appropriate diagnostic oy sequent evaluation reveals an elevated C-peptide level, a rn test to perform next? plasma glucose level of 45 mg/dL (2.5 mmol/L), and an ele- (A) Abdominal Doppler ultrasonography vated fasting insulin level. A contrast-enhanced multidetector CT scan shows a (B) Abdominal radiography highly vascular mass consistent in appearance with a pan (C) Hepatobiliary iminodiacetic acid scintigraphy creatic neuroendocrine tumor. (D) Noncontrast abdominal CT Genetic testing for which of the following should be included in this patient’s evaluation? Item 11 (A) Multiple endocrine neoplasia type 1 A 22-year-old man is evaluated in the office for hepatitis A virus (HAV) exposure that occurred 5 days ago. The (B) Multiple endocrine neoplasia type 2 source of exposure is the patient’s college roommate, (C) Neurofibromatosis type 1 who is now at home recovering from the illness. The (D) Tuberous sclerosis patient’s mother has confirmed he has never been vacci- nated against HAV. On physical examination, vital signs and other findings Item 14 are normal. A 52-year-old man is evaluated for a 6-month history of constipation. He has bowel movements once every 5 days, Which of the following is the most appropriate preventive low back pain after 2 days without a bowel movement, and measure? straining during defecation. He reports no abdominal pain. Colon cancer screening was performed 2 years ago with (A) Hepatitis A virus vaccine fecal immunochemical testing. (B) HAV immune globulin On physical examination, vital signs are normal. (C) HAV vaccine and HAV immune globulin Abdominal examination reveals palpable stool in the left (D) No preventive measures lower quadrant without tenderness. Result of digital ano- rectal examination is normal. Laboratory studies show a hematocrit of 44%.

= Bowel sounds are normal. ment for an episode of confusion, diaphoresis, and tremu- Laboratory evaluation shows an alanine aminotrans- 2) lousness. Similar symptoms have been present for 6 months wn ferase level of 152 U/L and aspartate aminotransferase level r<0) but are becoming more frequent and severe. wn of 138 U/L. wn Fingerstick blood glucose level is 30 mg/dL (1.7 mmol/L). << Her symptoms resolve with administration of glucose. Sub- a Which of the following is the most appropriate diagnostic oy sequent evaluation reveals an elevated C-peptide level, a rn test to perform next? plasma glucose level of 45 mg/dL (2.5 mmol/L), and an ele- (A) Abdominal Doppler ultrasonography vated fasting insulin level. A contrast-enhanced multidetector CT scan shows a (B) Abdominal radiography highly vascular mass consistent in appearance with a pan (C) Hepatobiliary iminodiacetic acid scintigraphy creatic neuroendocrine tumor. (D) Noncontrast abdominal CT Genetic testing for which of the following should be included in this patient’s evaluation? Item 11 (A) Multiple endocrine neoplasia type 1 A 22-year-old man is evaluated in the office for hepatitis A virus (HAV) exposure that occurred 5 days ago. The (B) Multiple endocrine neoplasia type 2 source of exposure is the patient’s college roommate, (C) Neurofibromatosis type 1 who is now at home recovering from the illness. The (D) Tuberous sclerosis patient’s mother has confirmed he has never been vacci- nated against HAV. On physical examination, vital signs and other findings Item 14 are normal. A 52-year-old man is evaluated for a 6-month history of constipation. He has bowel movements once every 5 days, Which of the following is the most appropriate preventive low back pain after 2 days without a bowel movement, and measure? straining during defecation. He reports no abdominal pain. Colon cancer screening was performed 2 years ago with (A) Hepatitis A virus vaccine fecal immunochemical testing. (B) HAV immune globulin On physical examination, vital signs are normal. (C) HAV vaccine and HAV immune globulin Abdominal examination reveals palpable stool in the left (D) No preventive measures lower quadrant without tenderness. Result of digital ano- rectal examination is normal. Laboratory studies show a hematocrit of 44%. Item 12 Which of the following is the most appropriate management? A 40-year-old man is evaluated in the emergency depart- ment for severe epigastric abdominal pain radiating to the (A) Colonoscopy back that has worsened in the past 12 hours. (B) Prucalopride On physical examination, temperature is 39.4 °C (C) Psyllium (102.9 °F), blood pressure is 100/60 mm Hg, pulse rate is 110/min, and respiration rate is 28/min. Palpation of (D) Radiopaque marker study abdomen elicits epigastric pain without guarding.

Item 12 Which of the following is the most appropriate management? A 40-year-old man is evaluated in the emergency depart- ment for severe epigastric abdominal pain radiating to the (A) Colonoscopy back that has worsened in the past 12 hours. (B) Prucalopride On physical examination, temperature is 39.4 °C (C) Psyllium (102.9 °F), blood pressure is 100/60 mm Hg, pulse rate is 110/min, and respiration rate is 28/min. Palpation of (D) Radiopaque marker study abdomen elicits epigastric pain without guarding. Laboratory studies: Item 15 Leukocyte count 18,000/pL (18 x 109/L) A 34-year-old woman is evaluated at routine follow-up Alanine aminotransferase 178 U/L after diagnosis of primary sclerosing cholangitis (PSC) ear- Aspartate aminotransferase 145 U/L lier this month. The diagnosis of PSC was confirmed with Total bilirubin 1.1 mg/dL (18.8 umol/L) magnetic resonance cholangiopancreatography showing Lipase 100 U/L multifocal intra- and extrahepatic bile duct strictures with- Blood and urine cultures are pending. out evidence of a dominant stricture or mass. A carbohy- Fluid resuscitation with lactated Ringer solution is drate antigen 19-9 measurement was normal. She has no initiated. other medical conditions and takes no medications. Which of the following is the most appropriate initial Which of the following is the most appropriate management? management at this time?

Laboratory studies: Item 15 Leukocyte count 18,000/pL (18 x 109/L) A 34-year-old woman is evaluated at routine follow-up Alanine aminotransferase 178 U/L after diagnosis of primary sclerosing cholangitis (PSC) ear- Aspartate aminotransferase 145 U/L lier this month. The diagnosis of PSC was confirmed with Total bilirubin 1.1 mg/dL (18.8 umol/L) magnetic resonance cholangiopancreatography showing Lipase 100 U/L multifocal intra- and extrahepatic bile duct strictures with- Blood and urine cultures are pending. out evidence of a dominant stricture or mass. A carbohy- Fluid resuscitation with lactated Ringer solution is drate antigen 19-9 measurement was normal. She has no initiated. other medical conditions and takes no medications. Which of the following is the most appropriate initial Which of the following is the most appropriate management? management at this time? (A) Contrast-enhanced CT (A) Colonoscopy (B) Empiric antibiotics (B) Endoscopic retrograde cholangiopancreatography (C) Endoscopic ultrasonography (C) Liver biopsy (D) Triglyceride measurement (D) Liver transplantation 89

Self-Assessment Test 2) © a Item 16 Item 19 b= wn A 65-year-old woman is hospitalized for acute pancreatitis A 68-year-old woman is evaluated in the emergency m) @o due to alcohol use. During hospitalization, she receives department for sudden-onset, crampy, left-lower w nw lactated Ringer solution overnight and is taking nothing by quadrant abdominal pain followed several hours later by = mouth. passage of bright red blood per rectum. She has hyperten- oO = On physical examination the morning after admis sion and hyperlipidemia. Current medications are lisinopril = sion, the patient reports improved pain. Vital signs are nor and simvastatin. o WH Cad mal. She has mild epigastric pain without guarding. Bowel On physical examination, vital signs are normal. Abdo- sounds are present. men is soft and nondistended, with left-lower-quadrant After fluid resuscitation, hematocrit decreases from tenderness and no rebound or guarding. Anorectal exam 45% at admission to 38% 12 hours later. ination shows scant bright red blood in the rectal vault. Laboratory testing shows a leukocyte count of 12,000/uL Which of the following is the most appropriate (12 x 10°/L) and a blood urea nitrogen level of 24 mg/dL management? (8.5 mmol/L); other routine laboratory results are normal. Abdominal and pelvic CT scan shows only segmental ( A) Initiate enteral tube feeding thickening of the descending and sigmoid colon. ( B) Initiate oral feeding ( C) Maintain nothing-by-mouth status Which of the following is the most likely diagnosis?

sion, the patient reports improved pain. Vital signs are nor and simvastatin. o WH Cad mal. She has mild epigastric pain without guarding. Bowel On physical examination, vital signs are normal. Abdo- sounds are present. men is soft and nondistended, with left-lower-quadrant After fluid resuscitation, hematocrit decreases from tenderness and no rebound or guarding. Anorectal exam 45% at admission to 38% 12 hours later. ination shows scant bright red blood in the rectal vault. Laboratory testing shows a leukocyte count of 12,000/uL Which of the following is the most appropriate (12 x 10°/L) and a blood urea nitrogen level of 24 mg/dL management? (8.5 mmol/L); other routine laboratory results are normal. Abdominal and pelvic CT scan shows only segmental ( A) Initiate enteral tube feeding thickening of the descending and sigmoid colon. ( B) Initiate oral feeding ( C) Maintain nothing-by-mouth status Which of the following is the most likely diagnosis? ( D) Transfuse 2 units of packed red blood cells A) Acute diverticulitis B) Clostridioides difficile infection C) Colonic ischemia Item 17 D) Ulcerative colitis A 55-year-old man is evaluated for gastroesophageal reflux disease (GERD). He has a 20-year history of GERD, which is well controlled with medication. He is an active cigarette Item 20 smoker with a 30-pack-year history. He does not drink alcohol. A chest radiograph obtained 2 years ago for the A 20-year-old woman is evaluated for loose, bloody stools

( D) Transfuse 2 units of packed red blood cells A) Acute diverticulitis B) Clostridioides difficile infection C) Colonic ischemia Item 17 D) Ulcerative colitis A 55-year-old man is evaluated for gastroesophageal reflux disease (GERD). He has a 20-year history of GERD, which is well controlled with medication. He is an active cigarette Item 20 smoker with a 30-pack-year history. He does not drink alcohol. A chest radiograph obtained 2 years ago for the A 20-year-old woman is evaluated for loose, bloody stools evaluation of fever and cough revealed a hiatal hernia. His up to three times daily with prominent fecal urgency. She has no other symptoms. only medication is omeprazole. On physical examination, all vital signs are normal. On physical examination, vital signs are normal. BMI is 37. Other than abdominal obesity, the physical examination Abdominal examination is normal. Anorectal examination elicits mild discomfort. is normal. Laboratory evaluation shows a normal complete blood count and liver chemistries. Results of testing for Clostridi- Which of the following is the most appropriate initial oides difficile toxin are negative. management? Colonoscopy shows moderate inflammatory muco- (A) Bariatric surgery sal changes involving the rectum in a diffuse, continuous

evaluation of fever and cough revealed a hiatal hernia. His up to three times daily with prominent fecal urgency. She has no other symptoms. only medication is omeprazole. On physical examination, all vital signs are normal. On physical examination, vital signs are normal. BMI is 37. Other than abdominal obesity, the physical examination Abdominal examination is normal. Anorectal examination elicits mild discomfort. is normal. Laboratory evaluation shows a normal complete blood count and liver chemistries. Results of testing for Clostridi- Which of the following is the most appropriate initial oides difficile toxin are negative. management? Colonoscopy shows moderate inflammatory muco- (A) Bariatric surgery sal changes involving the rectum in a diffuse, continuous (B) Esophageal motility study fashion, characterized by edema, erythema, and erosions. Abrupt transition to normal-appearing mucosa in the upper (C) Fundoplication rectum is evident, and the remaining colonic mucosa above (D) Upper endoscopy the rectum is normal. Biopsy specimens from the rectum reveal moderate chronic colitis with crypt architectural distortion. Item 18 A 47-year-old woman is evaluated at a follow-up appoint- Which of the following is the most appropriate treatment? ment. Autoimmune hepatitis was diagnosed 1 year ago (A) 5-Aminosalicylate suppository when she developed jaundice. Current medications are prednisone and azathioprine. Her liver enzyme levels (B) Glucocorticoid suppository have been normal for 9 months, and her jaundice has (C) Oral 5-aminosalicylate resolved. (D) Oral glucocorticoid Vital signs and other physical examination findings are normal. Item 21 Which of the following is the most appropriate A 42-year-old man is evaluated after screening labo- management? ratory tests obtained before initiation of statin therapy revealed isolated elevated aminotransferase levels. He is (A) Continue immunosuppressant therapy asymptomatic. His only active medical condition is type 2 (B) Perform liver biopsy now diabetes mellitus. Medications are metformin and moderate- (C) Stop azathioprine and taper prednisone intensity atorvastatin. (D) Stop azathioprine, taper prednisone, and perform On physical examination, vital signs and other findings liver biopsy are normal. Waist circumference is normal. BMI is 23.

(B) Esophageal motility study fashion, characterized by edema, erythema, and erosions. Abrupt transition to normal-appearing mucosa in the upper (C) Fundoplication rectum is evident, and the remaining colonic mucosa above (D) Upper endoscopy the rectum is normal. Biopsy specimens from the rectum reveal moderate chronic colitis with crypt architectural distortion. Item 18 A 47-year-old woman is evaluated at a follow-up appoint- Which of the following is the most appropriate treatment? ment. Autoimmune hepatitis was diagnosed 1 year ago (A) 5-Aminosalicylate suppository when she developed jaundice. Current medications are prednisone and azathioprine. Her liver enzyme levels (B) Glucocorticoid suppository have been normal for 9 months, and her jaundice has (C) Oral 5-aminosalicylate resolved. (D) Oral glucocorticoid Vital signs and other physical examination findings are normal. Item 21 Which of the following is the most appropriate A 42-year-old man is evaluated after screening labo- management? ratory tests obtained before initiation of statin therapy revealed isolated elevated aminotransferase levels. He is (A) Continue immunosuppressant therapy asymptomatic. His only active medical condition is type 2 (B) Perform liver biopsy now diabetes mellitus. Medications are metformin and moderate- (C) Stop azathioprine and taper prednisone intensity atorvastatin. (D) Stop azathioprine, taper prednisone, and perform On physical examination, vital signs and other findings liver biopsy are normal. Waist circumference is normal. BMI is 23. 90

Self-Assessment Test tek Laboratory studies: od Item 24 — =) Hemoglobin 18 g/dL (180 g/L) =< A 62-year-old man is admitted to the ICU for hematemesis. Alanine aminotransferase Aspartate aminotransferase 43 U/L 56 U/L He has a history of cirrhosis due to alcohol use. He under- SI 2) goes hemodynamic stabilization and initiation of octreotide wo Ferritin 1200 ng/mL (1200 ug/L) Y and antibiotics. Other current medications are propranolol, wn Ww spironolactone, and furosemide. Which of the following is the most appropriate diagnostic = On physical examination, blood pressure is 104/58 mm a test to perform next? a Hg, pulse rate is 62/min, and respiration rate is 16/min. nr (A) o,-Antitrypsin antibody measurement Ascites is present. Bowel sounds are normal, and abdomen (B) Liver biopsy is not tender. Endoscopy reveals large varices isolated to the gastric (C) Transferrin saturation measurement fundus, along the greater curvature of the stomach, that (D) Urine porphyrin measurement have stigmata of recent bleeding.

Laboratory studies: od Item 24 — =) Hemoglobin 18 g/dL (180 g/L) =< A 62-year-old man is admitted to the ICU for hematemesis. Alanine aminotransferase Aspartate aminotransferase 43 U/L 56 U/L He has a history of cirrhosis due to alcohol use. He under- SI 2) goes hemodynamic stabilization and initiation of octreotide wo Ferritin 1200 ng/mL (1200 ug/L) Y and antibiotics. Other current medications are propranolol, wn Ww spironolactone, and furosemide. Which of the following is the most appropriate diagnostic = On physical examination, blood pressure is 104/58 mm a test to perform next? a Hg, pulse rate is 62/min, and respiration rate is 16/min. nr (A) o,-Antitrypsin antibody measurement Ascites is present. Bowel sounds are normal, and abdomen (B) Liver biopsy is not tender. Endoscopy reveals large varices isolated to the gastric (C) Transferrin saturation measurement fundus, along the greater curvature of the stomach, that (D) Urine porphyrin measurement have stigmata of recent bleeding. Item 22 Which of the following is the most appropriate next step in management? A 25-year-old woman is evaluated for watery, nonbloody diarrhea of 9 months’ duration, occurring four times daily but (A) Abdominal CT with contrast not nocturnally. It is usually accompanied by abdominal pain (B) Abdominal ultrasonography in the periumbilical area or left lower quadrant. Pain usually (C) Balloon tamponade diminishes after a bowel movement. She has had no weight loss. (D) Band ligation of varices On physical examination, vital signs are normal. BMI is 22. Abdominal examination reveals minimal tenderness in the left lower quadrant. Item 25 Laboratory studies show normal fecal calprotectin, A 21-year-old woman is evaluated at follow-up after thyroid-stimulating hormone, hematocrit, tissue trans- upper endoscopy and colonoscopy, which were per- glutaminase IgA, and liver chemistries. The test result for formed because of iron deficiency anemia unresponsive to Clostridioides difficile is negative. oral iron therapy. Upper endoscopy revealed fundic gland polyps carpeting the stomach and multiple small adeno- Which of the following is the most appropriate diagnostic test? matous polyps in the duodenum. Colonoscopy demon-

Item 22 Which of the following is the most appropriate next step in management? A 25-year-old woman is evaluated for watery, nonbloody diarrhea of 9 months’ duration, occurring four times daily but (A) Abdominal CT with contrast not nocturnally. It is usually accompanied by abdominal pain (B) Abdominal ultrasonography in the periumbilical area or left lower quadrant. Pain usually (C) Balloon tamponade diminishes after a bowel movement. She has had no weight loss. (D) Band ligation of varices On physical examination, vital signs are normal. BMI is 22. Abdominal examination reveals minimal tenderness in the left lower quadrant. Item 25 Laboratory studies show normal fecal calprotectin, A 21-year-old woman is evaluated at follow-up after thyroid-stimulating hormone, hematocrit, tissue trans- upper endoscopy and colonoscopy, which were per- glutaminase IgA, and liver chemistries. The test result for formed because of iron deficiency anemia unresponsive to Clostridioides difficile is negative. oral iron therapy. Upper endoscopy revealed fundic gland polyps carpeting the stomach and multiple small adeno- Which of the following is the most appropriate diagnostic test? matous polyps in the duodenum. Colonoscopy demon- (A) Abdominal ultrasonography strated more than 100 polyps throughout the colon, with 2 polyps in the rectum. Biopsy of a 3-cm polyp in the (B) Colonoscopy with biopsy of right and left colon sigmoid colon revealed moderately differentiated adeno- (C) Stool testing for Escherichia coli O157:H7 carcinoma. The patient has no family history of colorectal (D) Stool testing for Giardia cancer.

(A) Abdominal ultrasonography strated more than 100 polyps throughout the colon, with 2 polyps in the rectum. Biopsy of a 3-cm polyp in the (B) Colonoscopy with biopsy of right and left colon sigmoid colon revealed moderately differentiated adeno- (C) Stool testing for Escherichia coli O157:H7 carcinoma. The patient has no family history of colorectal (D) Stool testing for Giardia cancer. Which of the following is the most appropriate treatment? Item 23 A 70-year-old man is hospitalized for a 12-hour history (A) Colectomy of painless intermittent maroon stools (four episodes). (B) Endoscopic removal of the adenocarcinoma One hour ago he evacuated a large maroon stool. He (C) Left hemicolectomy has hypertension, coronary artery disease, and osteoar (D) Sulindac thritis. Current medications are metoprolol, atorvasta- tin, aspirin, acetaminophen, naproxen as needed, and omeprazole. On physical examination, blood pressure is 90/50 mm Item 26 Hg and pulse rate is 100/min. The abdomen is soft and non A 50-year-old man is evaluated at a routine follow-up tender. Maroon stool is present around anus. appointment. He has a history of cirrhosis due to hepatitis C Hemoglobin level is 11 g/dL (110 g/L). virus (HCV) infection. He previously underwent successful After a 500-mL infusion of 0.9% saline, blood pressure antiviral therapy for HCV infection. He has never had symp- is 96/65 mm Hg and pulse rate is 105/min. toms referable to liver disease and feels well. He is not taking Bilious return is noted on gastric lavage after placement any medications. of a nasogastric tube. On physical examination, vital signs are normal and other findings are unremarkable. Which of the following is the most appropriate next Laboratory studies: diagnostic test? Platelet count 155,000/uL (155 x 10°/L) INR 1.0 (A) Angiography Albumin 3.4 g/dL (34 g/L) (B) Colonoscopy Alanine aminotransferase 25 U/L (C) CT angiography Aspartate aminotransferase 34 U/L (D) Upper endoscopy Total bilirubin 1.2 mg/dL (20.5 umol/L)

Which of the following is the most appropriate treatment? Item 23 A 70-year-old man is hospitalized for a 12-hour history (A) Colectomy of painless intermittent maroon stools (four episodes). (B) Endoscopic removal of the adenocarcinoma One hour ago he evacuated a large maroon stool. He (C) Left hemicolectomy has hypertension, coronary artery disease, and osteoar (D) Sulindac thritis. Current medications are metoprolol, atorvasta- tin, aspirin, acetaminophen, naproxen as needed, and omeprazole. On physical examination, blood pressure is 90/50 mm Item 26 Hg and pulse rate is 100/min. The abdomen is soft and non A 50-year-old man is evaluated at a routine follow-up tender. Maroon stool is present around anus. appointment. He has a history of cirrhosis due to hepatitis C Hemoglobin level is 11 g/dL (110 g/L). virus (HCV) infection. He previously underwent successful After a 500-mL infusion of 0.9% saline, blood pressure antiviral therapy for HCV infection. He has never had symp- is 96/65 mm Hg and pulse rate is 105/min. toms referable to liver disease and feels well. He is not taking Bilious return is noted on gastric lavage after placement any medications. of a nasogastric tube. On physical examination, vital signs are normal and other findings are unremarkable. Which of the following is the most appropriate next Laboratory studies: diagnostic test? Platelet count 155,000/uL (155 x 10°/L) INR 1.0 (A) Angiography Albumin 3.4 g/dL (34 g/L) (B) Colonoscopy Alanine aminotransferase 25 U/L (C) CT angiography Aspartate aminotransferase 34 U/L (D) Upper endoscopy Total bilirubin 1.2 mg/dL (20.5 umol/L) 91

Self-Assessment Test nr a = Routine abdominal ultrasound screening and follow- past 2 hours. Symptoms began while he was eating chicken, > 7) up MRI show a 1.5-cm lesion in the left liver consistent with when he felt that the bolus did not move all the way down v2) f3°) hepatocellular cancer. There is no evidence of metastatic his esophagus. During evaluation, he begins to sense that wo wn disease. he can swallow again. He has had several previous but less 3 severe episodes of dysphagia. His other medical conditions @o = Which of the following is the most appropriate management? include asthma, seasonal allergies, and episodes of eczema. - oi Current medications are budesonide-formoterol inhaler © (A) Liver transplantation wn and loratadine as needed. (B) Surgical resection Coal On physical examination, vital signs and other findings (C) Transarterial chemoembolization are normal. (D) Ongoing surveillance Upper endoscopy is scheduled. Which of the following is the most likely diagnosis? Item 27 (A) Barrett esophagus A 34-year-old man is evaluated at follow-up for abnormal (B) Eosinophilic esophagitis liver chemistry test results. The abnormal results were oe detected 2 weeks ago, on the day of hospital admission for — C) Esophageal cancer an ulcerative colitis flare. During hospitalization, he was D) Peptic stricture treated with intravenous glucocorticoids. At the time of dis- E) Systemic sclerosis charge, acute prostatitis was diagnosed and a 4-week course of levofloxacin was initiated.

detected 2 weeks ago, on the day of hospital admission for — C) Esophageal cancer an ulcerative colitis flare. During hospitalization, he was D) Peptic stricture treated with intravenous glucocorticoids. At the time of dis- E) Systemic sclerosis charge, acute prostatitis was diagnosed and a 4-week course of levofloxacin was initiated. Follow-up laboratory studies: Item 30 Alkaline phosphatase 258 U/L A 62-year-old man with compensated cirrhosis is evaluated Alanine aminotransferase 39 U/L at a follow-up visit. Six months ago, he was diagnosed with Aspartate aminotransferase 42 U/L hepatitis C virus infection and treated with direct-acting Total bilirubin 1.0 mg/dL (17.1 umol/L) antiviral agents. He experienced sustained viral response. Magnetic resonance cholangiopancreatography shows Current liver ultrasound shows a small nodular liver com- normal bile ducts and gallbladder, with no gallbladder stones. patible with cirrhosis and no masses. On physical examination, vital signs and other findings are normal. Which of the following is the most appropriate next step in management? Which of the following is the most appropriate biannual (A) Discontinuation of levofloxacin surveillance modality? (B) Endoscopic retrograde cholangiopancreatography (A) Abdominal MRI (C) Liver biopsy (B) Contrast-enhanced CT (D) Liver ultrasonography (C) Ultrasonography of liver (D) No surveillance

normal bile ducts and gallbladder, with no gallbladder stones. patible with cirrhosis and no masses. On physical examination, vital signs and other findings are normal. Which of the following is the most appropriate next step in management? Which of the following is the most appropriate biannual (A) Discontinuation of levofloxacin surveillance modality? (B) Endoscopic retrograde cholangiopancreatography (A) Abdominal MRI (C) Liver biopsy (B) Contrast-enhanced CT (D) Liver ultrasonography (C) Ultrasonography of liver (D) No surveillance Item 28 A 33-year-old woman is evaluated during her annual follow- Item 31 up visit. She is asymptomatic. She has a 2-year history of left-sided ulcerative colitis, now in remission. Current med- A 57-year-old woman is evaluated in the emergency ications are an oral 5-aminosalicylate and azathioprine. All department for a 9-month history of increasing abdominal immunizations are up to date, and depression and anxiety pain that has worsened in the past week. After a total screening results are negative. Skin cancer screening was knee replacement 9 months ago, postoperative pain was performed 6 months ago. Her last cervical cancer screening managed with oxycodone. During this time she developed

Item 28 A 33-year-old woman is evaluated during her annual follow- Item 31 up visit. She is asymptomatic. She has a 2-year history of left-sided ulcerative colitis, now in remission. Current med- A 57-year-old woman is evaluated in the emergency ications are an oral 5-aminosalicylate and azathioprine. All department for a 9-month history of increasing abdominal immunizations are up to date, and depression and anxiety pain that has worsened in the past week. After a total screening results are negative. Skin cancer screening was knee replacement 9 months ago, postoperative pain was performed 6 months ago. Her last cervical cancer screening managed with oxycodone. During this time she developed was | year ago. bilateral lower abdominal pain and constipation. Her con- stipation has improved with polyethylene glycol, but the abdominal pain continued to increase and is now diffuse and Which of the following is the most appropriate health near-constant. Three days ago, she increased the frequency maintenance screening test to perform? of oxycodone from three times daily to four times daily, and (A) Anal cancer screening the abdominal pain intensified in frequency and severity. (B) Cervical cancer screening Despite this current level of pain, the patient is adamant that

was | year ago. bilateral lower abdominal pain and constipation. Her con- stipation has improved with polyethylene glycol, but the abdominal pain continued to increase and is now diffuse and Which of the following is the most appropriate health near-constant. Three days ago, she increased the frequency maintenance screening test to perform? of oxycodone from three times daily to four times daily, and (A) Anal cancer screening the abdominal pain intensified in frequency and severity. (B) Cervical cancer screening Despite this current level of pain, the patient is adamant that (C) the only thing that helps her pain is oxycodone. Colonoscopy On physical examination, vital signs are normal. Dif- (D) Dual-energy x-ray absorptiometry fuse abdominal tenderness without guarding is noted. Bowel sounds are hypoactive. Findings on colonoscopy 6 months ago were normal. Item 29 ACT scan obtained in the emergency department with oral A 27-year-old man is evaluated in the emergency depart- and intravenous contrast shows moderate stool throughout ment for inability to eat, drink, or swallow his saliva for the the colon but no other abnormalities. 92

Self-Assessment Test ant cH Which of the following is the most appropriate Which of the following is the most appropriate diagnostic fee shot management? test to perform next? < CONT. ao (A) Add lubiprostone (A) Colonoscopy with biopsy E wa (B) Add methadone (B) CT angiography w & wn (C) Colonoscopy with biopsy (C) Doppler ultrasonography wn (D) Opioid discontinuation (D) Magnetic resonance angiography = re t) ”

(D) Opioid discontinuation (D) Magnetic resonance angiography = re t) ” Item 32 Item 34 A 55-year-old man is evaluated at a follow-up visit. Two A 60-year-old man is evaluated for a 4-month history of months ago he was admitted to the ICU for severe acute four to five loose bowel movements daily with antecedent pancreatitis from alcohol use. CT during hospitalization abdominal cramps. He does not have nocturnal diarrhea, revealed an edematous pancreas with fat stranding and and the diarrhea has no relationship to eating. He also has peripancreatic fluid collections. He was discharged after a 1-year history of type 2 diabetes mellitus, treated with 12 days. Two weeks before follow-up he had abdominal lifestyle interventions until 4 months ago, and hypothy- pain, and contrast-enhanced pancreas-protocol CT was per- roidism, diagnosed 10 years ago. He completed a course of formed. The scan demonstrated several hypodense lesions amoxicillin for pneumonia 6 months ago. Current medica- throughout the pancreas, including a 12-cm hypodense tions are metformin and levothyroxine. structure with a well-defined wall and no solid debris. The On physical examination, vital signs are normal and pancreatic duct was normal and no mass was identified. other findings are unremarkable. His abdomen is soft, Today the patient reports feeling well; he has abstained nontender, and nondistended; active bowel sounds are from alcohol since hospitalization. normal. On physical examination today, vital signs and other Erythrocyte sedimentation rate is 15 mm/h, leukocyte findings are normal. count is 4900/uL (4.9 x 10°/L), and hematocrit is 44%.

Item 32 Item 34 A 55-year-old man is evaluated at a follow-up visit. Two A 60-year-old man is evaluated for a 4-month history of months ago he was admitted to the ICU for severe acute four to five loose bowel movements daily with antecedent pancreatitis from alcohol use. CT during hospitalization abdominal cramps. He does not have nocturnal diarrhea, revealed an edematous pancreas with fat stranding and and the diarrhea has no relationship to eating. He also has peripancreatic fluid collections. He was discharged after a 1-year history of type 2 diabetes mellitus, treated with 12 days. Two weeks before follow-up he had abdominal lifestyle interventions until 4 months ago, and hypothy- pain, and contrast-enhanced pancreas-protocol CT was per- roidism, diagnosed 10 years ago. He completed a course of formed. The scan demonstrated several hypodense lesions amoxicillin for pneumonia 6 months ago. Current medica- throughout the pancreas, including a 12-cm hypodense tions are metformin and levothyroxine. structure with a well-defined wall and no solid debris. The On physical examination, vital signs are normal and pancreatic duct was normal and no mass was identified. other findings are unremarkable. His abdomen is soft, Today the patient reports feeling well; he has abstained nontender, and nondistended; active bowel sounds are from alcohol since hospitalization. normal. On physical examination today, vital signs and other Erythrocyte sedimentation rate is 15 mm/h, leukocyte findings are normal. count is 4900/uL (4.9 x 10°/L), and hematocrit is 44%. Which of the following is the most appropriate Which of the following is the most likely cause of the management? patient’s diarrhea?

Item 32 Item 34 A 55-year-old man is evaluated at a follow-up visit. Two A 60-year-old man is evaluated for a 4-month history of months ago he was admitted to the ICU for severe acute four to five loose bowel movements daily with antecedent pancreatitis from alcohol use. CT during hospitalization abdominal cramps. He does not have nocturnal diarrhea, revealed an edematous pancreas with fat stranding and and the diarrhea has no relationship to eating. He also has peripancreatic fluid collections. He was discharged after a 1-year history of type 2 diabetes mellitus, treated with 12 days. Two weeks before follow-up he had abdominal lifestyle interventions until 4 months ago, and hypothy- pain, and contrast-enhanced pancreas-protocol CT was per- roidism, diagnosed 10 years ago. He completed a course of formed. The scan demonstrated several hypodense lesions amoxicillin for pneumonia 6 months ago. Current medica- throughout the pancreas, including a 12-cm hypodense tions are metformin and levothyroxine. structure with a well-defined wall and no solid debris. The On physical examination, vital signs are normal and pancreatic duct was normal and no mass was identified. other findings are unremarkable. His abdomen is soft, Today the patient reports feeling well; he has abstained nontender, and nondistended; active bowel sounds are from alcohol since hospitalization. normal. On physical examination today, vital signs and other Erythrocyte sedimentation rate is 15 mm/h, leukocyte findings are normal. count is 4900/uL (4.9 x 10°/L), and hematocrit is 44%. Which of the following is the most appropriate Which of the following is the most likely cause of the management? patient’s diarrhea? (A) Endoscopic cystogastrostomy and necrosectomy (A) Clostridioides difficile colitis (B) Endoscopic retrograde pancreatography (B) Crohn disease (C) Endoscopic ultrasonography with fine-needle aspira- (C) Metformin tion (D) Microscopic colitis (D) Surgical drainage (E) Observation Item 35

(A) Endoscopic cystogastrostomy and necrosectomy (A) Clostridioides difficile colitis (B) Endoscopic retrograde pancreatography (B) Crohn disease (C) Endoscopic ultrasonography with fine-needle aspira- (C) Metformin tion (D) Microscopic colitis (D) Surgical drainage (E) Observation Item 35 Item 33 A 60-year-old man is evaluated at follow-up for elevated aminotransferase levels noted on laboratory testing for A 69-year-old man is evaluated in the ICU for the sud- asymptomatic hepatomegaly. He has type 2 diabetes mel- den onset of severe, constant periumbilical pain. He was litus, hypertension, and hyperlipidemia. Current medica- admitted 2 days ago for new-onset atrial fibrillation with tions are metformin, hydrochlorothiazide, losartan, and rapid ventricular rate and heart failure. He reports an urge atorvastatin. He consumes one to two alcoholic beverages to defecate but has not had a bowel movement in 2 days. weekly. Current medications are metoprolol, furosemide, losartan, On physical examination, blood pressure is 143/80 mm and heparin. Hg; other vital signs are normal. BMI is 37. Abdominal On physical examination, blood pressure is 110/60 mm examination reveals hepatomegaly, no tenderness to pal- Hg, pulse rate is 112/min and irregular, and respiration rate pation, and no splenomegaly. is 24/min. The patient appears to have significant pain. Alkaline phosphatase level is 180 U/L, alanine amino- Cardiac examination discloses an irregularly irregular transferase level is 64 U/L, and aspartate aminotransferase rhythm. The abdomen is nondistended and soft, with mild level is 42 U/L. Complete blood count, serum albumin, and tenderness to deep palpation in the mid abdomen; bowel serum total bilirubin are normal. sounds are present. Rectal examination reveals brown Ultrasound shows a normal gallbladder without stones; stool. normal-size bile ducts; and an enlarged, echogenic liver. Laboratory studies: Hemoglobin 13 g/dL (130 g/L) Which of the following is the most appropriate next step in Leukocyte count 13,000/uL (13.0 x 10°/L), with 70% management? polymorphonuclear cells Bicarbonate 17 mEq/L (17 mmol/L) (A) Alcohol cessation Lactate 2.1 mEq/L (2.1 mmol/L) (B) Discontinuation of atorvastatin

Item 33 A 60-year-old man is evaluated at follow-up for elevated aminotransferase levels noted on laboratory testing for A 69-year-old man is evaluated in the ICU for the sud- asymptomatic hepatomegaly. He has type 2 diabetes mel- den onset of severe, constant periumbilical pain. He was litus, hypertension, and hyperlipidemia. Current medica- admitted 2 days ago for new-onset atrial fibrillation with tions are metformin, hydrochlorothiazide, losartan, and rapid ventricular rate and heart failure. He reports an urge atorvastatin. He consumes one to two alcoholic beverages to defecate but has not had a bowel movement in 2 days. weekly. Current medications are metoprolol, furosemide, losartan, On physical examination, blood pressure is 143/80 mm and heparin. Hg; other vital signs are normal. BMI is 37. Abdominal On physical examination, blood pressure is 110/60 mm examination reveals hepatomegaly, no tenderness to pal- Hg, pulse rate is 112/min and irregular, and respiration rate pation, and no splenomegaly. is 24/min. The patient appears to have significant pain. Alkaline phosphatase level is 180 U/L, alanine amino- Cardiac examination discloses an irregularly irregular transferase level is 64 U/L, and aspartate aminotransferase rhythm. The abdomen is nondistended and soft, with mild level is 42 U/L. Complete blood count, serum albumin, and tenderness to deep palpation in the mid abdomen; bowel serum total bilirubin are normal. sounds are present. Rectal examination reveals brown Ultrasound shows a normal gallbladder without stones; stool. normal-size bile ducts; and an enlarged, echogenic liver. Laboratory studies: Hemoglobin 13 g/dL (130 g/L) Which of the following is the most appropriate next step in Leukocyte count 13,000/uL (13.0 x 10°/L), with 70% management? polymorphonuclear cells Bicarbonate 17 mEq/L (17 mmol/L) (A) Alcohol cessation Lactate 2.1 mEq/L (2.1 mmol/L) (B) Discontinuation of atorvastatin An abdominopelvic CT scan obtained without intrave- (C) Initiation of pioglitazone nous contrast is normal. (D) Weight loss

Item 33 A 60-year-old man is evaluated at follow-up for elevated aminotransferase levels noted on laboratory testing for A 69-year-old man is evaluated in the ICU for the sud- asymptomatic hepatomegaly. He has type 2 diabetes mel- den onset of severe, constant periumbilical pain. He was litus, hypertension, and hyperlipidemia. Current medica- admitted 2 days ago for new-onset atrial fibrillation with tions are metformin, hydrochlorothiazide, losartan, and rapid ventricular rate and heart failure. He reports an urge atorvastatin. He consumes one to two alcoholic beverages to defecate but has not had a bowel movement in 2 days. weekly. Current medications are metoprolol, furosemide, losartan, On physical examination, blood pressure is 143/80 mm and heparin. Hg; other vital signs are normal. BMI is 37. Abdominal On physical examination, blood pressure is 110/60 mm examination reveals hepatomegaly, no tenderness to pal- Hg, pulse rate is 112/min and irregular, and respiration rate pation, and no splenomegaly. is 24/min. The patient appears to have significant pain. Alkaline phosphatase level is 180 U/L, alanine amino- Cardiac examination discloses an irregularly irregular transferase level is 64 U/L, and aspartate aminotransferase rhythm. The abdomen is nondistended and soft, with mild level is 42 U/L. Complete blood count, serum albumin, and tenderness to deep palpation in the mid abdomen; bowel serum total bilirubin are normal. sounds are present. Rectal examination reveals brown Ultrasound shows a normal gallbladder without stones; stool. normal-size bile ducts; and an enlarged, echogenic liver. Laboratory studies: Hemoglobin 13 g/dL (130 g/L) Which of the following is the most appropriate next step in Leukocyte count 13,000/uL (13.0 x 10°/L), with 70% management? polymorphonuclear cells Bicarbonate 17 mEq/L (17 mmol/L) (A) Alcohol cessation Lactate 2.1 mEq/L (2.1 mmol/L) (B) Discontinuation of atorvastatin An abdominopelvic CT scan obtained without intrave- (C) Initiation of pioglitazone nous contrast is normal. (D) Weight loss 93

Self-Assessment Test wn 2 Sal Item 36 creatinine level of 1.9 mg/dL (167.9 pmol/L) and sodium b= level of 137 mEq/L (137 mmol/L). wn A 23-year-old woman is evaluated in the emergency wn @o Abdominal ultrasound shows a shrunken, irregular, wn department for a 3-day history of abdominal discomfort, and nodular liver; dilated portal vein; patent hepatic and = @o nausea and vomiting, and pruritus. She is pregnant at 36 weeks’ gestation. portal vasculature; and ascites. a Assessment of urine output, urinalysis, and urine sodium me On physical examination, temperature is 36.9 °C (98.4 °F), concentration and results of a paracentesis are pending. _ blood pressure is 160/110 mm Hg, pulse rate is 98/min, and oO wn ~ respiration rate is 22/min. Scleral icterus is noted. She has a gravid uterus. Which of the following is the most appropriate initial management? Laboratory studies: Hemoglobin 8.6 g/dL (860 g/L) (A) Discontinue diuretics Platelet count 75,000/uL (75 x 10°/L) (B) Initiate fluid restriction Alanine aminotransferase 130 U/L (C) Initiate propranolol Aspartate aminotransferase 110 U/L (D) Liberalize sodium intake Total bilirubin 3.4 mg/dL (58.1 umol/L) Direct bilirubin 1.6 mg/dL (27.4 umol/L) Lactate dehydrogenase 1600 U/L Item 39

wn 2 Sal Item 36 creatinine level of 1.9 mg/dL (167.9 pmol/L) and sodium b= level of 137 mEq/L (137 mmol/L). wn A 23-year-old woman is evaluated in the emergency wn @o Abdominal ultrasound shows a shrunken, irregular, wn department for a 3-day history of abdominal discomfort, and nodular liver; dilated portal vein; patent hepatic and = @o nausea and vomiting, and pruritus. She is pregnant at 36 weeks’ gestation. portal vasculature; and ascites. a Assessment of urine output, urinalysis, and urine sodium me On physical examination, temperature is 36.9 °C (98.4 °F), concentration and results of a paracentesis are pending. _ blood pressure is 160/110 mm Hg, pulse rate is 98/min, and oO wn ~ respiration rate is 22/min. Scleral icterus is noted. She has a gravid uterus. Which of the following is the most appropriate initial management? Laboratory studies: Hemoglobin 8.6 g/dL (860 g/L) (A) Discontinue diuretics Platelet count 75,000/uL (75 x 10°/L) (B) Initiate fluid restriction Alanine aminotransferase 130 U/L (C) Initiate propranolol Aspartate aminotransferase 110 U/L (D) Liberalize sodium intake Total bilirubin 3.4 mg/dL (58.1 umol/L) Direct bilirubin 1.6 mg/dL (27.4 umol/L) Lactate dehydrogenase 1600 U/L Item 39 Which of the following is the most appropriate A 59-year-old woman is evaluated in the emergency management? department for fever and jaundice. She has decompensated alcoholic cirrhosis with ascites. Current medications are (A Cc Delivery of the fetus furosemide and spironolactone. Plasma exchange On physical examination, temperature is 38.1 °C

Which of the following is the most appropriate A 59-year-old woman is evaluated in the emergency management? department for fever and jaundice. She has decompensated alcoholic cirrhosis with ascites. Current medications are (A Cc Delivery of the fetus furosemide and spironolactone. Plasma exchange On physical examination, temperature is 38.1 °C Platelet transfusion (100.7 °F ), blood pressure is 100/60 mm Hg, and pulse rate is 60/min. Jaundice is present. Abdominal examination shows (D) Ursodeoxycholic acid therapy ascites and splenomegaly. Laboratory evaluation shows a serum creatinine level of 1 mg/dL (88.4 pmol/L), blood urea nitrogen level of Item 37 30 mg/dL (10.7 mol/L), and total bilirubin level of 4.1 mg/dL A 21-year-old man is evaluated for a 4-month history of (70.1 mmol/L). diarrhea. Bowel movements are liquid and nonbloody and Diagnostic paracentesis for evaluation of ascitic fluid sometimes are preceded by lower abdominal cramps. He shows neutrophil count of 350/uL (0.35 x 10°/L). has near-daily bloating. Symptoms do not awaken him at night but improve with fasting. He reports no recent travel, Which of the following is the most appropriate initial antibiotic use, or weight loss. treatment? On physical examination, vital signs are normal. Abdominal examination is normal. (A) Fluoroquinolone Laboratory evaluation shows a hematocrit of 41% and (B) Intravenous albumin negative fecal calprotectin level. (C) Intravenous albumin and cefotaxime (D) Trimethoprim-sulfamethoxazole Which of the following is the most appropriate management? Item 40 (A) Colonoscopy A 44-year-old woman is evaluated for a 6-month history of (B) Fructose breath test nonbloody liquid stools five or six times daily. She reports a (C) Stool culture good appetite and no weight loss. She underwent cholecyst- (D) Trial of lactose-free diet ectomy for acute cholecystitis 5 years ago. On physical examination, vital signs are normal. Her abdomen is soft, nontender, and nondistended, with Item 38 hyperactive bowel sounds. A 60-year-old woman is evaluated for follow-up of cirrhosis Laboratory studies reveal a stool sodium level of due to nonalcoholic steatohepatitis. Her cirrhosis has been 85 mEq/L (85 mmol/L) and stool potassium level of 4.5 mEq/L complicated by ascites that has persisted despite escalating (4.5 mmol/L). Complete blood count and thyroid-stimulating diuretic treatment. She has been adhering to a low-sodium hormone level are normal. diet. Current medications are furosemide and spironolactone. On physical examination, temperature is 36.9 °C Which of the following conditions is most consistent with (98.4 °F), blood pressure is 98/58 mm Hg, pulse rate is this patient’s stool studies? 68/min, and respiration rate is 16/min. She has scleral (A) Bile salt-induced diarrhea icterus and spider angiomas over her chest and upper back. Easily detectable ascites is present. ( B) Enterotoxigenic Escherichia coli infection

Platelet transfusion (100.7 °F ), blood pressure is 100/60 mm Hg, and pulse rate is 60/min. Jaundice is present. Abdominal examination shows (D) Ursodeoxycholic acid therapy ascites and splenomegaly. Laboratory evaluation shows a serum creatinine level of 1 mg/dL (88.4 pmol/L), blood urea nitrogen level of Item 37 30 mg/dL (10.7 mol/L), and total bilirubin level of 4.1 mg/dL A 21-year-old man is evaluated for a 4-month history of (70.1 mmol/L). diarrhea. Bowel movements are liquid and nonbloody and Diagnostic paracentesis for evaluation of ascitic fluid sometimes are preceded by lower abdominal cramps. He shows neutrophil count of 350/uL (0.35 x 10°/L). has near-daily bloating. Symptoms do not awaken him at night but improve with fasting. He reports no recent travel, Which of the following is the most appropriate initial antibiotic use, or weight loss. treatment? On physical examination, vital signs are normal. Abdominal examination is normal. (A) Fluoroquinolone Laboratory evaluation shows a hematocrit of 41% and (B) Intravenous albumin negative fecal calprotectin level. (C) Intravenous albumin and cefotaxime (D) Trimethoprim-sulfamethoxazole Which of the following is the most appropriate management? Item 40 (A) Colonoscopy A 44-year-old woman is evaluated for a 6-month history of (B) Fructose breath test nonbloody liquid stools five or six times daily. She reports a (C) Stool culture good appetite and no weight loss. She underwent cholecyst- (D) Trial of lactose-free diet ectomy for acute cholecystitis 5 years ago. On physical examination, vital signs are normal. Her abdomen is soft, nontender, and nondistended, with Item 38 hyperactive bowel sounds. A 60-year-old woman is evaluated for follow-up of cirrhosis Laboratory studies reveal a stool sodium level of due to nonalcoholic steatohepatitis. Her cirrhosis has been 85 mEq/L (85 mmol/L) and stool potassium level of 4.5 mEq/L complicated by ascites that has persisted despite escalating (4.5 mmol/L). Complete blood count and thyroid-stimulating diuretic treatment. She has been adhering to a low-sodium hormone level are normal. diet. Current medications are furosemide and spironolactone. On physical examination, temperature is 36.9 °C Which of the following conditions is most consistent with (98.4 °F), blood pressure is 98/58 mm Hg, pulse rate is this patient’s stool studies? 68/min, and respiration rate is 16/min. She has scleral (A) Bile salt-induced diarrhea icterus and spider angiomas over her chest and upper back. Easily detectable ascites is present. ( B) Enterotoxigenic Escherichia coli infection Serum creatinine level 2 weeks ago was 0.9 mg/dL (C) Fructose malabsorption (79.6 umol/L). Current laboratory studies show a serum (D) VIPoma

Platelet transfusion (100.7 °F ), blood pressure is 100/60 mm Hg, and pulse rate is 60/min. Jaundice is present. Abdominal examination shows (D) Ursodeoxycholic acid therapy ascites and splenomegaly. Laboratory evaluation shows a serum creatinine level of 1 mg/dL (88.4 pmol/L), blood urea nitrogen level of Item 37 30 mg/dL (10.7 mol/L), and total bilirubin level of 4.1 mg/dL A 21-year-old man is evaluated for a 4-month history of (70.1 mmol/L). diarrhea. Bowel movements are liquid and nonbloody and Diagnostic paracentesis for evaluation of ascitic fluid sometimes are preceded by lower abdominal cramps. He shows neutrophil count of 350/uL (0.35 x 10°/L). has near-daily bloating. Symptoms do not awaken him at night but improve with fasting. He reports no recent travel, Which of the following is the most appropriate initial antibiotic use, or weight loss. treatment? On physical examination, vital signs are normal. Abdominal examination is normal. (A) Fluoroquinolone Laboratory evaluation shows a hematocrit of 41% and (B) Intravenous albumin negative fecal calprotectin level. (C) Intravenous albumin and cefotaxime (D) Trimethoprim-sulfamethoxazole Which of the following is the most appropriate management? Item 40 (A) Colonoscopy A 44-year-old woman is evaluated for a 6-month history of (B) Fructose breath test nonbloody liquid stools five or six times daily. She reports a (C) Stool culture good appetite and no weight loss. She underwent cholecyst- (D) Trial of lactose-free diet ectomy for acute cholecystitis 5 years ago. On physical examination, vital signs are normal. Her abdomen is soft, nontender, and nondistended, with Item 38 hyperactive bowel sounds. A 60-year-old woman is evaluated for follow-up of cirrhosis Laboratory studies reveal a stool sodium level of due to nonalcoholic steatohepatitis. Her cirrhosis has been 85 mEq/L (85 mmol/L) and stool potassium level of 4.5 mEq/L complicated by ascites that has persisted despite escalating (4.5 mmol/L). Complete blood count and thyroid-stimulating diuretic treatment. She has been adhering to a low-sodium hormone level are normal. diet. Current medications are furosemide and spironolactone. On physical examination, temperature is 36.9 °C Which of the following conditions is most consistent with (98.4 °F), blood pressure is 98/58 mm Hg, pulse rate is this patient’s stool studies? 68/min, and respiration rate is 16/min. She has scleral (A) Bile salt-induced diarrhea icterus and spider angiomas over her chest and upper back. Easily detectable ascites is present. ( B) Enterotoxigenic Escherichia coli infection Serum creatinine level 2 weeks ago was 0.9 mg/dL (C) Fructose malabsorption (79.6 umol/L). Current laboratory studies show a serum (D) VIPoma 94

Self-Assessment Test = cH Item 41 type 2 diabetes mellitus, and hypertension. She underwent — — sleeve gastrectomy 4 months ago. Current medications are = A 50-year-old woman is evaluated for worsening reflux. During the past 18 months she has experienced regurgita- omeprazole, promethazine, metformin, and lisinopril. Vital signs and other physical examination findings are S wn tion after every meal. She has dysphagia with solid food and n unremarkable. BMI is 35. wo liquids. She has lost 2.3 kg (5.0 lb). Her symptoms have not wn Upper endoscopy findings are notable only for gastric wn responded to proton pump inhibitor therapy. sleeve anatomy. Gastric biopsy specimens are negative for = Vital signs and other physical examination findings are = Helicobacter pylori. Duodenal biopsy specimens (for celiac dis- @ normal. ” ease) are normal. Result of a gastric emptying study is normal. Esophagography demonstrates poor motility, with loss of the primary peristaltic wave and tapering at the distal esophagus associated with delayed clearance of the esopha- Which of the following is the most appropriate treatment? gus. Her esophagram is shown. (A) Acarbose (B) Metoclopramide (C) Rifaximin (D) Smaller, more frequent meals

cH Item 41 type 2 diabetes mellitus, and hypertension. She underwent — — sleeve gastrectomy 4 months ago. Current medications are = A 50-year-old woman is evaluated for worsening reflux. During the past 18 months she has experienced regurgita- omeprazole, promethazine, metformin, and lisinopril. Vital signs and other physical examination findings are S wn tion after every meal. She has dysphagia with solid food and n unremarkable. BMI is 35. wo liquids. She has lost 2.3 kg (5.0 lb). Her symptoms have not wn Upper endoscopy findings are notable only for gastric wn responded to proton pump inhibitor therapy. sleeve anatomy. Gastric biopsy specimens are negative for = Vital signs and other physical examination findings are = Helicobacter pylori. Duodenal biopsy specimens (for celiac dis- @ normal. ” ease) are normal. Result of a gastric emptying study is normal. Esophagography demonstrates poor motility, with loss of the primary peristaltic wave and tapering at the distal esophagus associated with delayed clearance of the esopha- Which of the following is the most appropriate treatment? gus. Her esophagram is shown. (A) Acarbose (B) Metoclopramide (C) Rifaximin (D) Smaller, more frequent meals Item 43 A 55-year-old man is evaluated at a follow-up appointment. He had been experiencing intermittent epigastric abdominal pain for 3 months, and gallbladder ultrasound incidentally revealed a 4-cm lesion in his left liver. The gallbladder was normal, and his abdominal pain has spontaneously abated. On physical examination, vital signs and other findings are unremarkable. MRI with gadoxetate sodium contrast reveals a 4-cm mass consistent with a hepatic adenoma.

Item 43 A 55-year-old man is evaluated at a follow-up appointment. He had been experiencing intermittent epigastric abdominal pain for 3 months, and gallbladder ultrasound incidentally revealed a 4-cm lesion in his left liver. The gallbladder was normal, and his abdominal pain has spontaneously abated. On physical examination, vital signs and other findings are unremarkable. MRI with gadoxetate sodium contrast reveals a 4-cm mass consistent with a hepatic adenoma. Which of the following is the most appropriate management? (A) Liver biopsy (B) Serial abdominal imaging (C) Surgical resection (D) Clinical observation Item 44 A 40-year-old man is evaluated following discharge 6 weeks after hospitalization for an episode of upper gastrointestinal bleeding. During hospitalization, a proton pump inhibitor was initiated and subsequent upper endoscopy showed a healing Mallory-Weiss tear. He is currently asymptomatic. His only medication is omeprazole. Which of the following is the most likely diagnosis? Physical examination findings are normal.

Item 44 A 40-year-old man is evaluated following discharge 6 weeks after hospitalization for an episode of upper gastrointestinal bleeding. During hospitalization, a proton pump inhibitor was initiated and subsequent upper endoscopy showed a healing Mallory-Weiss tear. He is currently asymptomatic. His only medication is omeprazole. Which of the following is the most likely diagnosis? Physical examination findings are normal. (A) Achalasia Which of the following is the most appropriate (B) Barrett esophagus management? (C) Eosinophilic esophagitis (A) Barium esophagography (D) Refractory gastroesophageal reflux disease (B) Discontinuation of omeprazole (E) Viral esophagitis (C) Helicobacter pylori testing (D) Upper endoscopy Item 42 A 40-year-old woman is evaluated for a 3-month history of epigastric pain, bloating, abdominal fullness, nausea, and Item 45 diarrhea 30 to 60 minutes after meals that is worse with A 57-year-old man is evaluated for recurrent diarrhea and larger meals. She sometimes experiences headaches and abdominal pain over the past 2 months. He was diagnosed feels sweaty after larger meals. Symptoms usually improve with celiac disease 10 years ago when he presented with gradually 30 minutes to 2 hours after eating. She has obesity, similar symptoms; at that time, symptoms resolved within 95

Self-Assusamant'Test rn Le = 1 month of starting a gluten-free diet, which he has main- Item 48 > tained since then. He has unintentionally lost 2 kg (5 lb) in wn A 26-year-old woman is evaluated for a 4-week history of nn the past 2 months. @o intermittent bright red blood per rectum and the feeling of 72) On physical examination, vital signs and other findings 3 incomplete evacuation. She has loose and blood-streaked are normal. @o bowel movements four or five times daily. She reports no = Laboratory testing reveals a tissue transglutaminase ome other symptoms. IgA level more than 30 times the upper limit of normal. Vital signs and the remainder of the physical examina- ry wn oP tion are normal. Assessment for which of the following conditions is the Laboratory studies reveal a hemoglobin level of 11 g/dL most appropriate initial management? (110 g/L) and a normal leukocyte count. Colonoscopy reveals diffuse and symmetric inflam- (A) Inadvertent gluten exposure matory mucosal changes characterized by erythema and Microscopic colitis friability, with absent mucosal vascular pattern from the Pancreatic insufficiency rectum to mid sigmoid. Biopsy specimens obtained from D) Small-bowel lymphoma sigmoid and rectum show chronic colitis. Results of testing for Clostridioides difficile toxin are negative.

Self-Assusamant'Test rn Le = 1 month of starting a gluten-free diet, which he has main- Item 48 > tained since then. He has unintentionally lost 2 kg (5 lb) in wn A 26-year-old woman is evaluated for a 4-week history of nn the past 2 months. @o intermittent bright red blood per rectum and the feeling of 72) On physical examination, vital signs and other findings 3 incomplete evacuation. She has loose and blood-streaked are normal. @o bowel movements four or five times daily. She reports no = Laboratory testing reveals a tissue transglutaminase ome other symptoms. IgA level more than 30 times the upper limit of normal. Vital signs and the remainder of the physical examina- ry wn oP tion are normal. Assessment for which of the following conditions is the Laboratory studies reveal a hemoglobin level of 11 g/dL most appropriate initial management? (110 g/L) and a normal leukocyte count. Colonoscopy reveals diffuse and symmetric inflam- (A) Inadvertent gluten exposure matory mucosal changes characterized by erythema and Microscopic colitis friability, with absent mucosal vascular pattern from the Pancreatic insufficiency rectum to mid sigmoid. Biopsy specimens obtained from D) Small-bowel lymphoma sigmoid and rectum show chronic colitis. Results of testing for Clostridioides difficile toxin are negative. ltem 46 Which of the following is the most appropriate treatment? A 55-year-old man is evaluated for a 2-week history of intermittent bright red blood per rectum and pain with (A) 5-Aminosalicylate (5-ASA) enemas defecation. He has marked anorectal discomfort with wip- (B) 5-ASA suppositories ing, and blood is visualized in the toilet water and on toilet (C) Glucocorticoid enemas paper. His stools are firm and brown with bloody streaks. (D) Oral 5-ASAs He also has chronic constipation treated with over-the- counter psyllium fiber supplement. Inspection of the perineum reveals no thrombosed Item 49 external hemorrhoid; however, while gently spreading the buttocks for inspection of the perianal region, the patient A 63-year-old woman is evaluated for heartburn, frequent experiences exquisite pain. nocturnal regurgitation, and solid food dysphagia of 5 years’ Findings on screening colonoscopy 2 years ago were duration. She has systemic sclerosis. Her only medication is

ltem 46 Which of the following is the most appropriate treatment? A 55-year-old man is evaluated for a 2-week history of intermittent bright red blood per rectum and pain with (A) 5-Aminosalicylate (5-ASA) enemas defecation. He has marked anorectal discomfort with wip- (B) 5-ASA suppositories ing, and blood is visualized in the toilet water and on toilet (C) Glucocorticoid enemas paper. His stools are firm and brown with bloody streaks. (D) Oral 5-ASAs He also has chronic constipation treated with over-the- counter psyllium fiber supplement. Inspection of the perineum reveals no thrombosed Item 49 external hemorrhoid; however, while gently spreading the buttocks for inspection of the perianal region, the patient A 63-year-old woman is evaluated for heartburn, frequent experiences exquisite pain. nocturnal regurgitation, and solid food dysphagia of 5 years’ Findings on screening colonoscopy 2 years ago were duration. She has systemic sclerosis. Her only medication is normal. omeprazole. On physical examination, vital signs are normal. Dilated capillary vessels are noted on the face and palmar Which of the following is the most likely diagnosis? surface of the hands. Distal aspects of the fingers appear (A) Anal fissure thick and inflamed. (B) Angiodysplasia Esophagram demonstrates poor motility with loss of the primary peristaltic wave, a patulous gastroesophageal junc- (C) Internal hemorrhoids tion, and gastroesophageal reflux to the level of the clavicles. (D) Rectal cancer Endoscopy shows a mildly dilated esophagus with pat- ulous lower esophageal sphincter. Stomach and duodenum Item 47 appear normal.

normal. omeprazole. On physical examination, vital signs are normal. Dilated capillary vessels are noted on the face and palmar Which of the following is the most likely diagnosis? surface of the hands. Distal aspects of the fingers appear (A) Anal fissure thick and inflamed. (B) Angiodysplasia Esophagram demonstrates poor motility with loss of the primary peristaltic wave, a patulous gastroesophageal junc- (C) Internal hemorrhoids tion, and gastroesophageal reflux to the level of the clavicles. (D) Rectal cancer Endoscopy shows a mildly dilated esophagus with pat- ulous lower esophageal sphincter. Stomach and duodenum Item 47 appear normal. A 29-year-old woman is evaluated at routine follow-up for chronic hepatitis B virus infection. She is asymptomatic, has Which of the following is the most appropriate treatment?

normal. omeprazole. On physical examination, vital signs are normal. Dilated capillary vessels are noted on the face and palmar Which of the following is the most likely diagnosis? surface of the hands. Distal aspects of the fingers appear (A) Anal fissure thick and inflamed. (B) Angiodysplasia Esophagram demonstrates poor motility with loss of the primary peristaltic wave, a patulous gastroesophageal junc- (C) Internal hemorrhoids tion, and gastroesophageal reflux to the level of the clavicles. (D) Rectal cancer Endoscopy shows a mildly dilated esophagus with pat- ulous lower esophageal sphincter. Stomach and duodenum Item 47 appear normal. A 29-year-old woman is evaluated at routine follow-up for chronic hepatitis B virus infection. She is asymptomatic, has Which of the following is the most appropriate treatment? no other medical conditions, and does not take any medica- (A) Diltiazem tions. She is negative for hepatitis C virus and HIV infections. (B) Lifestyle changes and proton pump inhibitor On physical examination, vital signs and other findings are normal. (C) Metoclopramide (D) Laparoscopic fundoplication Laboratory studies: Alanine aminotransferase 89 U/L Hepatitis B core antibody Positive Item 50 Hepatitis B e antibody Negative Hepatitis B e antigen Positive A 57-year-old man is evaluated for dysphagia. During the Hepatitis B virus DNA 80,000 U/mL past year, he has noticed that swallowed meat occasionally gets stuck in his throat. More recently, softer foods have Liver ultrasound is normal. also been slow to move down after swallowing. He has lost 4.5 kg (9.9 Ib) in the past 6 months. He has a many-year his- Which of the following is the most appropriate management? tory of gastroesophageal reflux disease. His only medication is omeprazole. (A) Antiviral therapy On physical examination, vital signs are normal. BMI is (B) Clinical observation and surveillance 30. Other physical examination findings are unremarkable. (C) Hepatitis B virus immune globulin Laboratory evaluation reveals a mean corpuscular vol- (D) Liver biopsy ume of 70 fL.

no other medical conditions, and does not take any medica- (A) Diltiazem tions. She is negative for hepatitis C virus and HIV infections. (B) Lifestyle changes and proton pump inhibitor On physical examination, vital signs and other findings are normal. (C) Metoclopramide (D) Laparoscopic fundoplication Laboratory studies: Alanine aminotransferase 89 U/L Hepatitis B core antibody Positive Item 50 Hepatitis B e antibody Negative Hepatitis B e antigen Positive A 57-year-old man is evaluated for dysphagia. During the Hepatitis B virus DNA 80,000 U/mL past year, he has noticed that swallowed meat occasionally gets stuck in his throat. More recently, softer foods have Liver ultrasound is normal. also been slow to move down after swallowing. He has lost 4.5 kg (9.9 Ib) in the past 6 months. He has a many-year his- Which of the following is the most appropriate management? tory of gastroesophageal reflux disease. His only medication is omeprazole. (A) Antiviral therapy On physical examination, vital signs are normal. BMI is (B) Clinical observation and surveillance 30. Other physical examination findings are unremarkable. (C) Hepatitis B virus immune globulin Laboratory evaluation reveals a mean corpuscular vol- (D) Liver biopsy ume of 70 fL. 96

Self-Assessment Test Sed Which of the following is the most appropriate diagnostic (C) CT angiography cH — ind test to perform next? (D) Upper endoscopy <= so (A) Barium esophagography = wn (B) CT of the chest 72) Item 53 ist) wn (C) Endoscopy with biopsy A 70-year-old man is evaluated for follow-up 8 weeks w (D) Esophageal motility study = after hospitalization for a bleeding duodenal ulcer. Upper = Q endoscopy revealed multiple duodenal ulcers. Results of n”

(D) Esophageal motility study = after hospitalization for a bleeding duodenal ulcer. Upper = Q endoscopy revealed multiple duodenal ulcers. Results of n” tests for Helicobacter pylori (gastric biopsy and serology) Item 51 were negative. He currently has no abdominal pain or A 56-year-old man is evaluated for right-upper-quadrant melena. He has osteoarthritis, with pain in the neck, hips, abdominal pain of several months’ duration. He otherwise knees, and feet, which he had been treating with ibupro- has been well. He does not drink alcohol, has not been fen. The ibuprofen was discontinued during hospitalization exposed to other hepatotoxins, and takes no medications. and replaced with acetaminophen. His only other medi- On physical examination, vital signs are normal. cation is omeprazole. He would like to resume an NSAID Abdominal examination reveals hepatosplenomegaly. The because acetaminophen is ineffective. remainder of the physical examination is normal.

tests for Helicobacter pylori (gastric biopsy and serology) Item 51 were negative. He currently has no abdominal pain or A 56-year-old man is evaluated for right-upper-quadrant melena. He has osteoarthritis, with pain in the neck, hips, abdominal pain of several months’ duration. He otherwise knees, and feet, which he had been treating with ibupro- has been well. He does not drink alcohol, has not been fen. The ibuprofen was discontinued during hospitalization exposed to other hepatotoxins, and takes no medications. and replaced with acetaminophen. His only other medi- On physical examination, vital signs are normal. cation is omeprazole. He would like to resume an NSAID Abdominal examination reveals hepatosplenomegaly. The because acetaminophen is ineffective. remainder of the physical examination is normal. Laboratory studies: Which of the following is the most effective ulcer Platelet count 109,000/uL (109 x 109/L) preventive strategy for this patient? Alkaline phosphatase 450 U/L (A) Celecoxib and famotidine Alanine aminotransferase 105 U/L Aspartate aminotransferase 103 U/L (B) Celecoxib and omeprazole (C) Naproxen and misoprostol Chest radiograph shows bilateral hilar lymphadenopa- thy. Result of an interferon-y release assay is negative. (D) Switch from ibuprofen to naproxen Abdominal ultrasound shows a slightly enlarged, mildly nodular liver, with normal bile ducts. Spleen is 14cm Item 54 in length. Liver biopsy reveals changes of non-necrotizing hepatic granulomas without hepatic fibrosis. A 64-year-old man is evaluated in the emergency depart- Culture results of liver biopsy specimens are negative ment for ascites. He has diabetes mellitus and cirrhosis asso- for fungal, Brucella, and Coxiella burnetii infections. ciated with hemochromatosis, as well as a history of hepatic encephalopathy. Current medications are metformin, cana- Which of the following is the most appropriate diagnostic gliflozin, lactulose, and rifaximin.

Laboratory studies: Which of the following is the most effective ulcer Platelet count 109,000/uL (109 x 109/L) preventive strategy for this patient? Alkaline phosphatase 450 U/L (A) Celecoxib and famotidine Alanine aminotransferase 105 U/L Aspartate aminotransferase 103 U/L (B) Celecoxib and omeprazole (C) Naproxen and misoprostol Chest radiograph shows bilateral hilar lymphadenopa- thy. Result of an interferon-y release assay is negative. (D) Switch from ibuprofen to naproxen Abdominal ultrasound shows a slightly enlarged, mildly nodular liver, with normal bile ducts. Spleen is 14cm Item 54 in length. Liver biopsy reveals changes of non-necrotizing hepatic granulomas without hepatic fibrosis. A 64-year-old man is evaluated in the emergency depart- Culture results of liver biopsy specimens are negative ment for ascites. He has diabetes mellitus and cirrhosis asso- for fungal, Brucella, and Coxiella burnetii infections. ciated with hemochromatosis, as well as a history of hepatic encephalopathy. Current medications are metformin, cana- Which of the following is the most appropriate diagnostic gliflozin, lactulose, and rifaximin. test to perform next? On physical examination, blood pressure is 106/76 mm Hg and pulse rate is 60/min; other vital signs are nor- (A) CT of abdomen mal. The patient is alert. Jaundice, spider telangiectasia, (B) Hepatobiliary iminodiacetic acid scintigraphy and palmar erythema are present. Jugular venous disten- (C) Magnetic resonance cholangiopancreatography sion and peripheral edema are present. Cardiac sounds are indistinct and lung sounds are diminished. Ascites is (D) Upper endoscopy present. Abdominal ultrasound showsa cirrhotic liver, spleno-

test to perform next? On physical examination, blood pressure is 106/76 mm Hg and pulse rate is 60/min; other vital signs are nor- (A) CT of abdomen mal. The patient is alert. Jaundice, spider telangiectasia, (B) Hepatobiliary iminodiacetic acid scintigraphy and palmar erythema are present. Jugular venous disten- (C) Magnetic resonance cholangiopancreatography sion and peripheral edema are present. Cardiac sounds are indistinct and lung sounds are diminished. Ascites is (D) Upper endoscopy present. Abdominal ultrasound showsa cirrhotic liver, spleno- Item 52 megaly, and abdominal ascites. Paracentesis with analysis of ascitic fluid shows a A 68-year-old man is evaluated during hospitalization for leukocyte count of 100/uL (100 x 10°/L), albumin level of epigastric abdominal pain and a 1-week history of black, 2.2 g/dL (22 g/L), and total protein level of 2.6 g/dL (26 g/L). tarry stools. His only medication is ibuprofen for osteoar- Serum albumin level is 3.5 g/dL (35 g/L). thritis. On physical examination, blood pressure is 110/60 mm Which of the following is the most appropriate Hg and pulse rate is 105/min. Other vital signs are normal. management? Abdominal examination reveals epigastric tenderness with- out guarding. Anorectal examination shows no blood or (A) Ascitic fluid cytology stool in the rectal vault. (B) Ascitic fluid triglyceride measurement Laboratory studies show a hemoglobin level of 10 g/dL (C) Echocardiography (100 g/L). Volume repletion with intravenous 0.9% saline is (D) Liver biopsy

Item 52 megaly, and abdominal ascites. Paracentesis with analysis of ascitic fluid shows a A 68-year-old man is evaluated during hospitalization for leukocyte count of 100/uL (100 x 10°/L), albumin level of epigastric abdominal pain and a 1-week history of black, 2.2 g/dL (22 g/L), and total protein level of 2.6 g/dL (26 g/L). tarry stools. His only medication is ibuprofen for osteoar- Serum albumin level is 3.5 g/dL (35 g/L). thritis. On physical examination, blood pressure is 110/60 mm Which of the following is the most appropriate Hg and pulse rate is 105/min. Other vital signs are normal. management? Abdominal examination reveals epigastric tenderness with- out guarding. Anorectal examination shows no blood or (A) Ascitic fluid cytology stool in the rectal vault. (B) Ascitic fluid triglyceride measurement Laboratory studies show a hemoglobin level of 10 g/dL (C) Echocardiography (100 g/L). Volume repletion with intravenous 0.9% saline is (D) Liver biopsy begun, along with intravenous administration of a proton pump inhibitor. Item 55 Which of the following is the most appropriate diagnostic A 72-year-old woman is hospitalized for subacute onset of test to perform next? jaundice that developed 5 days ago on the second day of a cruise to Central America. She has no known liver disease (A) Capsule endoscopy and reports consuming fewer than three drinks per week. (B) Colonoscopy She has no abdominal pain, nausea, or vomiting. Five weeks oF

Self-Assessment Test wn ue = ago she was treated with amoxicillin-clavulanate for an Which of the following is the most appropriate = episode of acute diverticulitis. management? un n CONT. On physical examination, vital signs are normal. Icterus @ wn (A) Initiate protease inhibitor-based direct-acting antivi- and jaundice are observed. There are no signs of chronic 2 liver disease. Mental status is normal, and no asterixis is ral therapy @o seen. (B) Initiate rifaximin therapy = (C) Limit dietary protein -€ Laboratory studies: o (D) Refer for liver transplantation H Alkaline phosphatase 200 U/L - Alanine aminotransferase 97 U/L Aspartate aminotransferase 70 U/L Total bilirubin 15 mg/dL (256.5 umol/L) Item 58 INR 1.0 A 58-year-old woman is evaluated for treatment of hepatitis Right-upper-quadrant ultrasound shows no gallblad C virus (HCV) infection. She has unresectable metastatic der stones or biliary dilation, a normal-size liver, and no pancreatic adenocarcinoma. She requests treatment of her masses. HCV infection. On physical examination, vital signs are normal. She Which of the following is the most likely diagnosis? has jaundice, icterus, and cachexia.

Laboratory studies: o (D) Refer for liver transplantation H Alkaline phosphatase 200 U/L - Alanine aminotransferase 97 U/L Aspartate aminotransferase 70 U/L Total bilirubin 15 mg/dL (256.5 umol/L) Item 58 INR 1.0 A 58-year-old woman is evaluated for treatment of hepatitis Right-upper-quadrant ultrasound shows no gallblad C virus (HCV) infection. She has unresectable metastatic der stones or biliary dilation, a normal-size liver, and no pancreatic adenocarcinoma. She requests treatment of her masses. HCV infection. On physical examination, vital signs are normal. She Which of the following is the most likely diagnosis? has jaundice, icterus, and cachexia. (A) Autoimmune hepatitis Which of the following is the most appropriate (B) Drug-induced liver injury management? (C) Hepatitis A virus infection (A) HCV antiviral treatment (D) Primary biliary cholangitis (B) HCV viral load measurement and genotyping (C) Testing for hepatitis B virus and HIV infections Item 56 (D) No further HCV-related testing or treatment A 75-year-old man is evaluated for choking that started 3 months ago and has progressively worsened. He has trouble initiating the swallowing of pills and coughs when Item 59 drinking liquids. He can eat soft foods without choking. A 39-year-old man is evaluated for diarrhea, characterized He reports no heartburn, regurgitation, or chest pain. as passing five liquid stools daily for 3 months, accom- Parkinson disease was diagnosed 3 months ago. His only panied by urgency and abdominal cramps. He reports no medication is carbidopa-levodopa. weight loss or rectal bleeding. He has a history of migraines. On physical examination, vital signs are normal. A He has self-imposed a strict gluten-free diet for the past right, resting hand tremor, bradykinesia, rigidity, slow 5 years to prevent migraine. His only medication is daily speech, and evidence of balance impairment are noted. The ibuprofen to prevent migraine. remainder of the examination is normal. Vital signs and other findings on physical examination are normal. Which of the following is the most likely diagnosis? Laboratory evaluation shows a hematocrit of 40% and normal fecal calprotectin level. (A) Achalasia (B) Incarcerated paraesophageal hernia Which of the following is the most appropriate (C) Oropharyngeal dysphagia management? (D) Peptic stricture (A) Colonoscopy (B) Discontinuation of ibuprofen

(A) Autoimmune hepatitis Which of the following is the most appropriate (B) Drug-induced liver injury management? (C) Hepatitis A virus infection (A) HCV antiviral treatment (D) Primary biliary cholangitis (B) HCV viral load measurement and genotyping (C) Testing for hepatitis B virus and HIV infections Item 56 (D) No further HCV-related testing or treatment A 75-year-old man is evaluated for choking that started 3 months ago and has progressively worsened. He has trouble initiating the swallowing of pills and coughs when Item 59 drinking liquids. He can eat soft foods without choking. A 39-year-old man is evaluated for diarrhea, characterized He reports no heartburn, regurgitation, or chest pain. as passing five liquid stools daily for 3 months, accom- Parkinson disease was diagnosed 3 months ago. His only panied by urgency and abdominal cramps. He reports no medication is carbidopa-levodopa. weight loss or rectal bleeding. He has a history of migraines. On physical examination, vital signs are normal. A He has self-imposed a strict gluten-free diet for the past right, resting hand tremor, bradykinesia, rigidity, slow 5 years to prevent migraine. His only medication is daily speech, and evidence of balance impairment are noted. The ibuprofen to prevent migraine. remainder of the examination is normal. Vital signs and other findings on physical examination are normal. Which of the following is the most likely diagnosis? Laboratory evaluation shows a hematocrit of 40% and normal fecal calprotectin level. (A) Achalasia (B) Incarcerated paraesophageal hernia Which of the following is the most appropriate (C) Oropharyngeal dysphagia management? (D) Peptic stricture (A) Colonoscopy (B) Discontinuation of ibuprofen Item 57 (C) Tissue transglutaminase IgA measurement A 48-year-old man is evaluated for follow-up of cirrhosis due (D) Video capsule endoscopy to hepatitis C virus (HCV) infection. He has ascites respon- sive to furosemide and spironolactone and recent-onset hepatic encephalopathy treated with lactulose. He has a Item 60 MELD-Na (Model for End-Stage Liver Disease-sodium) A 55-year-old man is evaluated at follow-up for iron score of 12. He takes no additional medications. deficiency anemia and positive result on stool guaiac On physical examination, vital signs are normal. Physi- testing. Despite excellent preparation and visualiza- cal examination reveals spider angiomas, abdominal disten- tion, upper endoscopy and colonoscopy performed tion, and a palpable liver edge below the right costal margin. last week did not find the source of bleeding. He has Laboratory studies: no melena, hematochezia, or localizing symptoms. He Prothrombin time 14.6s has no other medical conditions and takes no medica- Total bilirubin 2.6 mg/dL (44.5 umol/L) tions. Creatinine 0.8 mg/dL (70.7 umol/L) Vital signs and other findings on physical examination HCV DNA 600,000 U/mL are normal.

Item 57 (C) Tissue transglutaminase IgA measurement A 48-year-old man is evaluated for follow-up of cirrhosis due (D) Video capsule endoscopy to hepatitis C virus (HCV) infection. He has ascites respon- sive to furosemide and spironolactone and recent-onset hepatic encephalopathy treated with lactulose. He has a Item 60 MELD-Na (Model for End-Stage Liver Disease-sodium) A 55-year-old man is evaluated at follow-up for iron score of 12. He takes no additional medications. deficiency anemia and positive result on stool guaiac On physical examination, vital signs are normal. Physi- testing. Despite excellent preparation and visualiza- cal examination reveals spider angiomas, abdominal disten- tion, upper endoscopy and colonoscopy performed tion, and a palpable liver edge below the right costal margin. last week did not find the source of bleeding. He has Laboratory studies: no melena, hematochezia, or localizing symptoms. He Prothrombin time 14.6s has no other medical conditions and takes no medica- Total bilirubin 2.6 mg/dL (44.5 umol/L) tions. Creatinine 0.8 mg/dL (70.7 umol/L) Vital signs and other findings on physical examination HCV DNA 600,000 U/mL are normal. 98

Self-Assessment Test Ged cH Which of the following is the most appropriate diagnostic Vital signs are normal. BMI is 24. Physical examination — ~~ test to perform next? reveals epigastric tenderness and an abdominal bruit. = wo Upper endoscopy findings are normal. (A) CT angiography = w wn (B) Barium small-bowel follow-through Which of the following is the most appropriate diagnostic ao wn (C) Tagged red cell scintigraphy test to perform next? wn (D) Video capsule endoscopy - — (A) Capsule endoscopy Y 7) (B) CT mesenteric angiography Item 61 (C) Gastric emptying study

(D) Video capsule endoscopy - — (A) Capsule endoscopy Y 7) (B) CT mesenteric angiography Item 61 (C) Gastric emptying study A 32-year-old man is evaluated for a relapse of ulcer- (D) Ultrasonography of gallbladder ative colitis unresponsive to increasing dosage of a 5-aminosalicylate. Symptoms remitted after 1 week of prednisone; after tapering the prednisone, however, Item 64 symptoms returned. A 75-year-old man is evaluated in the emergency depart- On physical examination, vital signs are normal. Abdo- ment for several episodes of maroon blood per rectum men is nondistended, with left-lower-quadrant discomfort and cramping abdominal pain of 18 hours’ duration. He is on deep palpation and no abdominal guarding. admitted to the hospital and colonoscopy preparation is ini Results of tests for tuberculosis, hepatitis B virus tiated. He has hypertension, atrial fibrillation, and coronary infection, and stool enteric pathogen panel are nega- artery disease. At a colonoscopy performed 1 week ago, a tive. Thiopurine methyltransferase enzyme activity is 1-cm pedunculated polyp was removed from the transverse normal. colon. Medications are apixaban, low-dose aspirin, metop Colonoscopy shows changes consistent with ulcerative rolol, and atorvastatin. colitis from the rectum to the splenic flexure. Biopsy speci- On initial physical examination, blood pressure was mens show severe active chronic colitis without evidence of 95/40 mm Hg and pulse rate was 105/min and irregular. cytomegalovirus infection. The abdomen was soft, with lower abdominal tender ness.

A 32-year-old man is evaluated for a relapse of ulcer- (D) Ultrasonography of gallbladder ative colitis unresponsive to increasing dosage of a 5-aminosalicylate. Symptoms remitted after 1 week of prednisone; after tapering the prednisone, however, Item 64 symptoms returned. A 75-year-old man is evaluated in the emergency depart- On physical examination, vital signs are normal. Abdo- ment for several episodes of maroon blood per rectum men is nondistended, with left-lower-quadrant discomfort and cramping abdominal pain of 18 hours’ duration. He is on deep palpation and no abdominal guarding. admitted to the hospital and colonoscopy preparation is ini Results of tests for tuberculosis, hepatitis B virus tiated. He has hypertension, atrial fibrillation, and coronary infection, and stool enteric pathogen panel are nega- artery disease. At a colonoscopy performed 1 week ago, a tive. Thiopurine methyltransferase enzyme activity is 1-cm pedunculated polyp was removed from the transverse normal. colon. Medications are apixaban, low-dose aspirin, metop Colonoscopy shows changes consistent with ulcerative rolol, and atorvastatin. colitis from the rectum to the splenic flexure. Biopsy speci- On initial physical examination, blood pressure was mens show severe active chronic colitis without evidence of 95/40 mm Hg and pulse rate was 105/min and irregular. cytomegalovirus infection. The abdomen was soft, with lower abdominal tender ness. Which of the following is the most appropriate After admission and administration of 2 L of intrave- treatment? nous fluid. blood pressure is 110/60 mm Hg and pulse rate is 80/min. (A) Azathioprine Hemoglobin is 9 g/dL (90 g/L). (B) Azathioprine and infliximab (C) Certolizumab Which of the following is the most appropriate (D) Multimatrix budesonide management of this patient’s antiplatelet and anticoagulant therapy?

Which of the following is the most appropriate After admission and administration of 2 L of intrave- treatment? nous fluid. blood pressure is 110/60 mm Hg and pulse rate is 80/min. (A) Azathioprine Hemoglobin is 9 g/dL (90 g/L). (B) Azathioprine and infliximab (C) Certolizumab Which of the following is the most appropriate (D) Multimatrix budesonide management of this patient’s antiplatelet and anticoagulant therapy? (A) Hold apixaban Item 62 (B) Hold apixaban and administer andexanet A 55-year-old man is evaluated for follow-up after colonos- (C) Hold aspirin and apixaban copy. He recently underwent colonoscopy for colon cancer screening, which revealed an 11-mm tubular adenoma. He (D) Hold aspirin and apixaban and administer andexanet has no family history of colorectal cancer. He has no symp- toms and is taking no medications. Item 65 Which of the following is the most appropriate An 80-year-old woman is evaluated in the emergency surveillance approach? department. She has a 48-hour history of six maroon stools and mild lower abdominal pain. No bleeding is witnessed (A) Colonoscopy in 3 years during 6 hours in the emergency department. She has (B ) Colonoscopy in 10 years hypertension and coronary artery disease. Current medi (C ) Fecal DNA-based testing every 3 years cations are atorvastatin, metoprolol, lisinopril, omeprazole, ( D) Fecal occult blood testing annually and low-dose aspirin. On physical examination, blood pressure is 150/85 mm Hg and pulse rate is 70/min. Abdomen is soft and nontender. Item 63 Hemoglobin level is 10 g/dL (100 g/L).

(A) Hold apixaban Item 62 (B) Hold apixaban and administer andexanet A 55-year-old man is evaluated for follow-up after colonos- (C) Hold aspirin and apixaban copy. He recently underwent colonoscopy for colon cancer screening, which revealed an 11-mm tubular adenoma. He (D) Hold aspirin and apixaban and administer andexanet has no family history of colorectal cancer. He has no symp- toms and is taking no medications. Item 65 Which of the following is the most appropriate An 80-year-old woman is evaluated in the emergency surveillance approach? department. She has a 48-hour history of six maroon stools and mild lower abdominal pain. No bleeding is witnessed (A) Colonoscopy in 3 years during 6 hours in the emergency department. She has (B ) Colonoscopy in 10 years hypertension and coronary artery disease. Current medi (C ) Fecal DNA-based testing every 3 years cations are atorvastatin, metoprolol, lisinopril, omeprazole, ( D) Fecal occult blood testing annually and low-dose aspirin. On physical examination, blood pressure is 150/85 mm Hg and pulse rate is 70/min. Abdomen is soft and nontender. Item 63 Hemoglobin level is 10 g/dL (100 g/L). A 54-year-old man is evaluated for an 8-week history of postprandial, gnawing, epigastric abdominal pain after Which of the following is the most appropriate diagnostic every meal. Pain begins 30 minutes after eating, persists test? for 1 hour, and gradually resolves. He has had an asso- (A) Colonoscopy ciated 4.5-kg (9.9-Ib) weight loss. He has hypertension, (B) CT angiography coronary artery disease, and peripheral vascular disease. Current medications are aspirin, atorvastatin, lisinopril, (C) Tagged red cell scintigraphy and metoprolol. (D) Upper endoscopy

A 54-year-old man is evaluated for an 8-week history of postprandial, gnawing, epigastric abdominal pain after Which of the following is the most appropriate diagnostic every meal. Pain begins 30 minutes after eating, persists test? for 1 hour, and gradually resolves. He has had an asso- (A) Colonoscopy ciated 4.5-kg (9.9-Ib) weight loss. He has hypertension, (B) CT angiography coronary artery disease, and peripheral vascular disease. Current medications are aspirin, atorvastatin, lisinopril, (C) Tagged red cell scintigraphy and metoprolol. (D) Upper endoscopy 99

2) <. = Item 66 Which of the following is the most appropriate > management? wn A 25-year-old woman is hospitalized with a severe relapse wn oO of Crohn disease. Ileocolonic Crohn disease was diagnosed (A) Intravenous proton pump inhibitor (PPI) and hospital 2) wn 2 years ago; it responded to dose-optimized azathioprine observation for 72 hours =) with prednisone. During the past year, three disease flares oO (B) Once-daily oral PPI, feeding, and hospital discharge = necessitated reintroduction of prednisone despite continu- oa (C) Once-daily oral PPI, no feeding, and hospital observa- ation of azathioprine. Her only medication is azathioprine. > tion for 72 hours wn oe On physical examination, vital signs are normal. Abdominal examination reveals right-lower- quadrant ten- (D) Upper endoscopy repeated in 24 hours derness, with no mass. Anorectal examination is normal. Abdominal CT scan shows only bowel wall thickening Item 69 without significant luminal narrowing of the distal 8 cm of the terminal ileum and proximal colon. Colonoscopy shows A 65-year-old woman is evaluated at a follow-up visit. She severe mucosal inflammatory changes, with ulcerations in presented to the emergency department 2 weeks ago with the terminal ileum and proximal colon. a 2-day history of left-lower-quadrant abdominal pain. CT revealed diverticulitis and a 15-mm cystic structure Which of the following is the most appropriate treatment? in the body of the pancreas. She was discharged on oral antibiotics and now feels well. Colonoscopy is scheduled (A) Add budesonide in 6 weeks. She has no other medical conditions and takes (B) Add infliximab no medications. The radiology report indicates that the (C) Change azathioprine to 6-mercaptopurine pancreatic cyst has all the imaging features of a serous cystadenoma. (D) Change azathioprine to sulfasalazine Vital signs and other physical examination findings are normal.

2) <. = Item 66 Which of the following is the most appropriate > management? wn A 25-year-old woman is hospitalized with a severe relapse wn oO of Crohn disease. Ileocolonic Crohn disease was diagnosed (A) Intravenous proton pump inhibitor (PPI) and hospital 2) wn 2 years ago; it responded to dose-optimized azathioprine observation for 72 hours =) with prednisone. During the past year, three disease flares oO (B) Once-daily oral PPI, feeding, and hospital discharge = necessitated reintroduction of prednisone despite continu- oa (C) Once-daily oral PPI, no feeding, and hospital observa- ation of azathioprine. Her only medication is azathioprine. > tion for 72 hours wn oe On physical examination, vital signs are normal. Abdominal examination reveals right-lower- quadrant ten- (D) Upper endoscopy repeated in 24 hours derness, with no mass. Anorectal examination is normal. Abdominal CT scan shows only bowel wall thickening Item 69 without significant luminal narrowing of the distal 8 cm of the terminal ileum and proximal colon. Colonoscopy shows A 65-year-old woman is evaluated at a follow-up visit. She severe mucosal inflammatory changes, with ulcerations in presented to the emergency department 2 weeks ago with the terminal ileum and proximal colon. a 2-day history of left-lower-quadrant abdominal pain. CT revealed diverticulitis and a 15-mm cystic structure Which of the following is the most appropriate treatment? in the body of the pancreas. She was discharged on oral antibiotics and now feels well. Colonoscopy is scheduled (A) Add budesonide in 6 weeks. She has no other medical conditions and takes (B) Add infliximab no medications. The radiology report indicates that the (C) Change azathioprine to 6-mercaptopurine pancreatic cyst has all the imaging features of a serous cystadenoma. (D) Change azathioprine to sulfasalazine Vital signs and other physical examination findings are normal. ltem 67 Which of the following is the most appropriate A 70-year-old man is evaluated for a 5-month history of management? bloating and nonbloody diarrhea. Diarrhea occurs three times daily. Bowel movements include oil droplets and (A) Endoscopic ultrasonography and fine-needle aspira- require multiple flushes. He reports no abdominal pain. He tion has lost 2.3 kg (5 Ib) since symptom onset. (B) MRI On physical examination, vital signs are normal. (C) Surgical resection Abdominal examination reveals diffuse tenderness to pal- (D) No further evaluation or intervention pation without guarding. On laboratory evaluation, hematocrit is 39%, tissue transglutaminase IgA level is normal, and the result of a Item 70 Giardia enzyme immunoassay is negative. Findings on colonoscopy with biopsy are normal. A 25-year-old woman is evaluated for a 6-month history Abdominal CT obtained with oral and intravenous contrast of dyspepsia associated with early satiety, occasional epi- shows multiple diverticula in the jejunum. gastric burning, rare nausea, and postprandial bloating and belching. She has no melena or weight loss. She was

ltem 67 Which of the following is the most appropriate A 70-year-old man is evaluated for a 5-month history of management? bloating and nonbloody diarrhea. Diarrhea occurs three times daily. Bowel movements include oil droplets and (A) Endoscopic ultrasonography and fine-needle aspira- require multiple flushes. He reports no abdominal pain. He tion has lost 2.3 kg (5 Ib) since symptom onset. (B) MRI On physical examination, vital signs are normal. (C) Surgical resection Abdominal examination reveals diffuse tenderness to pal- (D) No further evaluation or intervention pation without guarding. On laboratory evaluation, hematocrit is 39%, tissue transglutaminase IgA level is normal, and the result of a Item 70 Giardia enzyme immunoassay is negative. Findings on colonoscopy with biopsy are normal. A 25-year-old woman is evaluated for a 6-month history Abdominal CT obtained with oral and intravenous contrast of dyspepsia associated with early satiety, occasional epi- shows multiple diverticula in the jejunum. gastric burning, rare nausea, and postprandial bloating and belching. She has no melena or weight loss. She was Which of the following is the most appropriate born in the United States, has not recently traveled outside management? the country, and has no family history of gastrointestinal cancer. (A) Eluxadoline On physical examination, vital signs are normal. Mild (B) Glucose breath test diffuse tenderness to palpation of abdomen is noted.

management? the country, and has no family history of gastrointestinal cancer. (A) Eluxadoline On physical examination, vital signs are normal. Mild (B) Glucose breath test diffuse tenderness to palpation of abdomen is noted. (C) Stool testing for Clostridioides difficile toxin Complete blood count and results of liver function tests are normal. (D) Upper endoscopy with duodenal biopsy Which of the following is the most appropriate Item 68 management? A 49-year-old man is hospitalized for a 1-day history of ( ) Abdominal CT 3 melenic stools. He is taking ibuprofen daily to prevent (B ) Daily proton pump inhibitor migraine headaches. ( ) Helicobacter pylori serology On physical examination, vital signs and physical examination findings are normal. ( ) Stool antigen testing for H. pylori oO Laboratory studies reveal a hemoglobin level of ( E) Upper endoscopy 11.2 g/dL (112 g/dL). Upper endoscopy shows a 1.5-cm, clean-based, superfi- cial duodenal ulcer. Findings from gastric biopsy specimens Item 71 for assessment of Helicobacter pylori infection are pending. A 35-year-old woman is evaluated for follow-up of abdom- Ibuprofen is stopped. inal pain, which has prompted multiple emergency 100

oa) department visits. CT scans have revealed intussusception. On physical examination, vital signs are normal. The ci — Her mother was diagnosed with breast cancer at age abdomen is soft and nontender. be i= 40 years. The rest of her family history is unknown. a On physical examination, vital signs are normal. Find- £ Which of the following is the most appropriate next step wn wn ings on lips are shown. in management? w w 72) (A) Endoscopy after 8 weeks of proton pump inhibitor = therapy — -F) ” (B) Endoscopy after 12 weeks of proton pump inhibitor therapy (C) Endoscopy in 6 to 12 months (D) No follow-up endoscopy needed

On physical examination, vital signs are normal. Find- £ Which of the following is the most appropriate next step wn wn ings on lips are shown. in management? w w 72) (A) Endoscopy after 8 weeks of proton pump inhibitor = therapy — -F) ” (B) Endoscopy after 12 weeks of proton pump inhibitor therapy (C) Endoscopy in 6 to 12 months (D) No follow-up endoscopy needed Item 74 A 42-year-old woman is evaluated in the emergency depart- ment for right-upper-quadrant pain that has worsened over the preceding 2 days. She has otherwise been well and takes no medications. On physical examination, temperature is 38.4 °C (101.2 °F). All other vital signs are normal. Abdominal examination reveals right-upper-quadrant tenderness and guarding. Laboratory studies show normal hemoglobin level, ele- Which of the following is the most likely diagnosis? vated leukocyte count, and normal liver chemistries and lipase values. (A) Adenomatous polyposis An ultrasound demonstrates gallbladder wall thick- (B) Hamartoma syndrome (Cowden syndrome) ening; a sonographic Murphy sign is present. There is no (C) Juvenile polyposis syndrome common bile duct dilation.

Item 74 A 42-year-old woman is evaluated in the emergency depart- ment for right-upper-quadrant pain that has worsened over the preceding 2 days. She has otherwise been well and takes no medications. On physical examination, temperature is 38.4 °C (101.2 °F). All other vital signs are normal. Abdominal examination reveals right-upper-quadrant tenderness and guarding. Laboratory studies show normal hemoglobin level, ele- Which of the following is the most likely diagnosis? vated leukocyte count, and normal liver chemistries and lipase values. (A) Adenomatous polyposis An ultrasound demonstrates gallbladder wall thick- (B) Hamartoma syndrome (Cowden syndrome) ening; a sonographic Murphy sign is present. There is no (C) Juvenile polyposis syndrome common bile duct dilation. (D) Peutz-Jeghers syndrome Piperacillin-tazobactam is initiated.

Item 74 A 42-year-old woman is evaluated in the emergency depart- ment for right-upper-quadrant pain that has worsened over the preceding 2 days. She has otherwise been well and takes no medications. On physical examination, temperature is 38.4 °C (101.2 °F). All other vital signs are normal. Abdominal examination reveals right-upper-quadrant tenderness and guarding. Laboratory studies show normal hemoglobin level, ele- Which of the following is the most likely diagnosis? vated leukocyte count, and normal liver chemistries and lipase values. (A) Adenomatous polyposis An ultrasound demonstrates gallbladder wall thick- (B) Hamartoma syndrome (Cowden syndrome) ening; a sonographic Murphy sign is present. There is no (C) Juvenile polyposis syndrome common bile duct dilation. (D) Peutz-Jeghers syndrome Piperacillin-tazobactam is initiated. Which of the following is the most appropriate treatment? Item 72 (A) Cholecystectomy before hospital discharge A 55-year-old man is evaluated for follow-up of fundic (B) Cholecystectomy in 4 weeks gland polyps. Upper endoscopy was performed to screen for Barrett esophagus; it revealed a normal esophagus and (C) Emergent cholecystectomy approximately 10 to 15 polyps with a similar appearance (D) Endoscopic retrograde cholangiopancreatography in the gastric body (1-8 mm). Multiple biopsy specimens (E) Percutaneous gallbladder drainage revealed fundic gland polyps without dysplasia. His only medication is omeprazole. Findings on colonoscopy are normal. Item 75 A 56-year-old man is evaluated in the emergency depart- When should follow-up upper endoscopy be ment for symptoms of progressive confusion for the past performed? 2 days. He has a history of cirrhosis due to alcohol use but has been abstinent for the past 5 years. He also has a history (A) lyear of depression and anxiety. Escitalopram is listed as his only (B) 3to5 years medication on the electronic medical record. (C) 10 years On physical examination, vital signs are normal. He ( D) No follow-up endoscopy is oriented to self but not time or place. Scleral icterus and asterixis are noted. The remainder of the examination is noncontributory. Item 73 Specimens are obtained for blood and urine cultures

Which of the following is the most appropriate treatment? Item 72 (A) Cholecystectomy before hospital discharge A 55-year-old man is evaluated for follow-up of fundic (B) Cholecystectomy in 4 weeks gland polyps. Upper endoscopy was performed to screen for Barrett esophagus; it revealed a normal esophagus and (C) Emergent cholecystectomy approximately 10 to 15 polyps with a similar appearance (D) Endoscopic retrograde cholangiopancreatography in the gastric body (1-8 mm). Multiple biopsy specimens (E) Percutaneous gallbladder drainage revealed fundic gland polyps without dysplasia. His only medication is omeprazole. Findings on colonoscopy are normal. Item 75 A 56-year-old man is evaluated in the emergency depart- When should follow-up upper endoscopy be ment for symptoms of progressive confusion for the past performed? 2 days. He has a history of cirrhosis due to alcohol use but has been abstinent for the past 5 years. He also has a history (A) lyear of depression and anxiety. Escitalopram is listed as his only (B) 3to5 years medication on the electronic medical record. (C) 10 years On physical examination, vital signs are normal. He ( D) No follow-up endoscopy is oriented to self but not time or place. Scleral icterus and asterixis are noted. The remainder of the examination is noncontributory. Item 73 Specimens are obtained for blood and urine cultures A 60-year-old man is evaluated for follow-up of a gastric and a comprehensive metabolic profile. ulcer. He is asymptomatic. Upper endoscopy performed 4 weeks ago revealed a 1-cm, clean-based, cratered ulcer in Which of the following is the most appropriate next step the gastric antrum. Biopsy specimens from the ulcer margin in evaluation? were negative for malignancy. Random biopsy specimens (A) CT of the head from the stomach were negative for Helicobacter pylori. He has discontinued daily ibuprofen, previously used for (B) Electroencephalography osteoarthritis of the knees. Current medications are acet- (C) Medication review and reconciliation aminophen and omeprazole. (D) Neuropsychiatric testing

A 60-year-old man is evaluated for follow-up of a gastric and a comprehensive metabolic profile. ulcer. He is asymptomatic. Upper endoscopy performed 4 weeks ago revealed a 1-cm, clean-based, cratered ulcer in Which of the following is the most appropriate next step the gastric antrum. Biopsy specimens from the ulcer margin in evaluation? were negative for malignancy. Random biopsy specimens (A) CT of the head from the stomach were negative for Helicobacter pylori. He has discontinued daily ibuprofen, previously used for (B) Electroencephalography osteoarthritis of the knees. Current medications are acet- (C) Medication review and reconciliation aminophen and omeprazole. (D) Neuropsychiatric testing 101

Self-Assessment Test ~ 2. = Item 76 Item 79 > wn A 40-year-old woman is evaluated for intestinal metaplasia A 40-year-old woman is evaluated at follow-up for stage I ~” © found on recent upper endoscopy to assess postprandial endometrial cancer diagnosed 6 weeks ago. Colon cancer wn ~” pain. No ulcers were visualized but generalized erythema was diagnosed in her mother at age 55 years and her mater- = and irregular mucosal pattern was noted. Biopsy speci- nal aunt at age 60 years. @ =! mens from the gastric antrum and gastric body showed The patient has had total abdominal hysterectomy and - extensive metaplasia, no dysplasia, and no Helicobacter bilateral oophorectomy. Germline genetic testing confirmed o nn emp pylori. Her father died of gastric cancer. Her only medica- a pathogenic mutation in MSH2. tion is omeprazole. She is of Korean descent. Which of the following is the most appropriate screening strategy for this patient? Which of the following is the most appropriate next step in management? (A) Fecal DNA testing (A) Discontinue omeprazole (B) Fecal immunochemical test (B) Initiate chemoprophylaxis with ascorbic acid (C) Upper endoscopy and colonoscopy (C) Initiate chemoprophylaxis with aspirin ( D) Upper endoscopy, colonoscopy, and wireless capsule endoscopy (D) Perform surveillance endoscopy

(B) Initiate chemoprophylaxis with ascorbic acid (C) Upper endoscopy and colonoscopy (C) Initiate chemoprophylaxis with aspirin ( D) Upper endoscopy, colonoscopy, and wireless capsule endoscopy (D) Perform surveillance endoscopy Item 80 Item 77 A 60-year-old woman is evaluated for 6 months of progres- A 64-year-old man is evaluated in the hospital 2 hours after sive symptoms of dyspnea on exertion. She has cirrhosis due diagnosis of a bleeding gastric ulcer and treatment with to nonalcoholic steatohepatitis complicated by ascites and endoscopic clips. He also has atrial fibrillation, hyperten- esophageal varices. Current medications include proprano- sion, and hyperlipidemia. Outpatient medications are war- lol, furosemide, and spironolactone. farin, rosuvastatin, losartan, and hydrochlorothiazide. On On physical examination, vital signs are normal. Oxy- hospitalization, intravenous omeprazole was initiated and gen saturation is 99% with the patient breathing ambient warfarin was withheld. air. On cardiac examination, central venous pressure is ele- On physical examination, vital signs are stable. Heart vated. The pulmonic component of S, is increased in inten- rhythm is irregularly irregular. The remainder of the exam sity. The lungs are clear to auscultation. The liver is enlarged ination is normal. and tender, and ascites is present. Laboratory studies reveal a hemoglobin level of 8 g/dL Posteroanterior and lateral radiographs of the chest are (80 g/L) and an INR of 2.2. normal.

Item 80 Item 77 A 60-year-old woman is evaluated for 6 months of progres- A 64-year-old man is evaluated in the hospital 2 hours after sive symptoms of dyspnea on exertion. She has cirrhosis due diagnosis of a bleeding gastric ulcer and treatment with to nonalcoholic steatohepatitis complicated by ascites and endoscopic clips. He also has atrial fibrillation, hyperten- esophageal varices. Current medications include proprano- sion, and hyperlipidemia. Outpatient medications are war- lol, furosemide, and spironolactone. farin, rosuvastatin, losartan, and hydrochlorothiazide. On On physical examination, vital signs are normal. Oxy- hospitalization, intravenous omeprazole was initiated and gen saturation is 99% with the patient breathing ambient warfarin was withheld. air. On cardiac examination, central venous pressure is ele- On physical examination, vital signs are stable. Heart vated. The pulmonic component of S, is increased in inten- rhythm is irregularly irregular. The remainder of the exam sity. The lungs are clear to auscultation. The liver is enlarged ination is normal. and tender, and ascites is present. Laboratory studies reveal a hemoglobin level of 8 g/dL Posteroanterior and lateral radiographs of the chest are (80 g/L) and an INR of 2.2. normal. Which of the following is the most appropriate management? Which of the following is the most appropriate diagnostic test to perform next? ( A) Begin intravenous heparin bridging therapy (B) Discontinue warfarin permanently (A) CT of chest (B) Echocardiography ( C) Reinitiate warfarin after 30 days (D) Reinitiate warfarin within 7 days (C) Echocardiography with agitated saline (D) Ventilation-perfusion scanning

Which of the following is the most appropriate management? Which of the following is the most appropriate diagnostic test to perform next? ( A) Begin intravenous heparin bridging therapy (B) Discontinue warfarin permanently (A) CT of chest (B) Echocardiography ( C) Reinitiate warfarin after 30 days (D) Reinitiate warfarin within 7 days (C) Echocardiography with agitated saline (D) Ventilation-perfusion scanning Item 78 Item 81 A 46-year-old woman is evaluated at a follow-up visit after A 35-year-old woman is evaluated for nocturnal heartburn being diagnosed with gallstones. She was evaluated in the and regurgitation. She has a 5-year history of gastroesophageal emergency department 4 days ago for bothersome early reflux disease. She takes omeprazole every day 30 minutes satiation and postprandial fullness. A right-upper-quadrant before breakfast. She works as a musician and has concerts on ultrasound revealed several gallstones. weekends. After her concerts, she eats heavy meals at a late On physical examination, vital signs are normal. BMI is hour and experiences nocturnal symptoms that interfere with 37. Abdomen is nontender to palpation. sleep. During the week, she has minimal symptoms when she The ultrasound report describes multiple stones maintains her normal routine. She has no other concerning approximately 1 cm without gallbladder calcification, pol- symptoms. She does not smoke cigarettes. yps, or biliary dilation. On physical examination, BMI is 25.

Item 78 Item 81 A 46-year-old woman is evaluated at a follow-up visit after A 35-year-old woman is evaluated for nocturnal heartburn being diagnosed with gallstones. She was evaluated in the and regurgitation. She has a 5-year history of gastroesophageal emergency department 4 days ago for bothersome early reflux disease. She takes omeprazole every day 30 minutes satiation and postprandial fullness. A right-upper-quadrant before breakfast. She works as a musician and has concerts on ultrasound revealed several gallstones. weekends. After her concerts, she eats heavy meals at a late On physical examination, vital signs are normal. BMI is hour and experiences nocturnal symptoms that interfere with 37. Abdomen is nontender to palpation. sleep. During the week, she has minimal symptoms when she The ultrasound report describes multiple stones maintains her normal routine. She has no other concerning approximately 1 cm without gallbladder calcification, pol- symptoms. She does not smoke cigarettes. yps, or biliary dilation. On physical examination, BMI is 25. Which of the following is the most appropriate management Which of the following is the most appropriate additional of the gallstones? management?

Item 78 Item 81 A 46-year-old woman is evaluated at a follow-up visit after A 35-year-old woman is evaluated for nocturnal heartburn being diagnosed with gallstones. She was evaluated in the and regurgitation. She has a 5-year history of gastroesophageal emergency department 4 days ago for bothersome early reflux disease. She takes omeprazole every day 30 minutes satiation and postprandial fullness. A right-upper-quadrant before breakfast. She works as a musician and has concerts on ultrasound revealed several gallstones. weekends. After her concerts, she eats heavy meals at a late On physical examination, vital signs are normal. BMI is hour and experiences nocturnal symptoms that interfere with 37. Abdomen is nontender to palpation. sleep. During the week, she has minimal symptoms when she The ultrasound report describes multiple stones maintains her normal routine. She has no other concerning approximately 1 cm without gallbladder calcification, pol- symptoms. She does not smoke cigarettes. yps, or biliary dilation. On physical examination, BMI is 25. Which of the following is the most appropriate management Which of the following is the most appropriate additional of the gallstones? management? ( A) Cholecystectomy (A) Increase omeprazole to twice daily ( B) Endoscopic retrograde cholangiopancreatography (B) Laparoscopic fundoplication (C ) Magnetic resonance cholangiopancreatography (C) Lifestyle modifications ( D) Ursodeoxycholic acid (D) Upper endoscopy (E) Clinical observation (E) Wireless pH testing

( A) Cholecystectomy (A) Increase omeprazole to twice daily ( B) Endoscopic retrograde cholangiopancreatography (B) Laparoscopic fundoplication (C ) Magnetic resonance cholangiopancreatography (C) Lifestyle modifications ( D) Ursodeoxycholic acid (D) Upper endoscopy (E) Clinical observation (E) Wireless pH testing 102

Self-Assessment Test -— Item 82 Which of the following is the most appropriate i o shot A 66-year-old man is evaluated for relief of chronic back management? | cE pain from a lumbar vertebral compression fracture docu- (A) Cholecystectomy = mented on a recent radiograph. He has a history of cirrhosis, wn (B) Endoscopic retrograde cholangiopancreatography wn osteoporosis, and stage 2 chronic kidney disease. His only a medication is a bisphosphonate. (C) Hepatobiliary iminodiacetic acid scanning a On physical examination, vital signs are normal. The (D) Ultrasonography in 6 months mi inde

medication is a bisphosphonate. (C) Hepatobiliary iminodiacetic acid scanning a On physical examination, vital signs are normal. The (D) Ultrasonography in 6 months mi inde patient appears in mild distress because of back pain, with ao 2) point tenderness over the fourth lumbar vertebra. Laboratory studies show a serum total bilirubin level Item 85 of 1.5 mg/dL (25.6 mol/L) and serum creatinine level of A 30-year-old man is evaluated for epigastric pain that is more 1.3 mg/dL (114.9 umol/L). severe with eating and has progressively worsened over the past 6 months. He has diminished oral intake, as well as occa- Which of the following is the most appropriate treatment? sional nausea and diarrhea. Family history includes stomach cancer in his father. A Helicobacter pylori test is negative, and (A) Duloxetine proton pump inhibitor therapy with omeprazole has been (B) Ibuprofen ineffective. His only other medication is loperamide. (C) Low-dose opioid On physical examination, vital signs are normal. BMI is (D) Physical therapy 24. The abdomen is tender to palpation. No guarding is noted. Upper endoscopy findings are normal, as are biopsy specimens obtained from the stomach (for H. pylori) and Item 83 duodenum (for celiac disease). Omeprazole is discontinued.

patient appears in mild distress because of back pain, with ao 2) point tenderness over the fourth lumbar vertebra. Laboratory studies show a serum total bilirubin level Item 85 of 1.5 mg/dL (25.6 mol/L) and serum creatinine level of A 30-year-old man is evaluated for epigastric pain that is more 1.3 mg/dL (114.9 umol/L). severe with eating and has progressively worsened over the past 6 months. He has diminished oral intake, as well as occa- Which of the following is the most appropriate treatment? sional nausea and diarrhea. Family history includes stomach cancer in his father. A Helicobacter pylori test is negative, and (A) Duloxetine proton pump inhibitor therapy with omeprazole has been (B) Ibuprofen ineffective. His only other medication is loperamide. (C) Low-dose opioid On physical examination, vital signs are normal. BMI is (D) Physical therapy 24. The abdomen is tender to palpation. No guarding is noted. Upper endoscopy findings are normal, as are biopsy specimens obtained from the stomach (for H. pylori) and Item 83 duodenum (for celiac disease). Omeprazole is discontinued. A 37-year-old man is evaluated in the emergency depart- ment for right-upper-quadrant pain, fever, and malaise of Which of the following is the most appropriate next step in 3 days’ duration. Until now he had been well. treatment?

patient appears in mild distress because of back pain, with ao 2) point tenderness over the fourth lumbar vertebra. Laboratory studies show a serum total bilirubin level Item 85 of 1.5 mg/dL (25.6 mol/L) and serum creatinine level of A 30-year-old man is evaluated for epigastric pain that is more 1.3 mg/dL (114.9 umol/L). severe with eating and has progressively worsened over the past 6 months. He has diminished oral intake, as well as occa- Which of the following is the most appropriate treatment? sional nausea and diarrhea. Family history includes stomach cancer in his father. A Helicobacter pylori test is negative, and (A) Duloxetine proton pump inhibitor therapy with omeprazole has been (B) Ibuprofen ineffective. His only other medication is loperamide. (C) Low-dose opioid On physical examination, vital signs are normal. BMI is (D) Physical therapy 24. The abdomen is tender to palpation. No guarding is noted. Upper endoscopy findings are normal, as are biopsy specimens obtained from the stomach (for H. pylori) and Item 83 duodenum (for celiac disease). Omeprazole is discontinued. A 37-year-old man is evaluated in the emergency depart- ment for right-upper-quadrant pain, fever, and malaise of Which of the following is the most appropriate next step in 3 days’ duration. Until now he had been well. treatment? On physical examination, his temperature is (A) Citalopram 38.9 °C (102.0 °F), blood pressure is 100/40 mm Hg, and (B) Famotidine pulse rate is 94/min. Jaundice is present. Abdominal examination reveals right-upper-quadrant tenderness (C) Metoclopramide and guarding. (D) Nortriptyline Laboratory evaluation shows a normal hemoglobin value, an elevated leukocyte count, a total serum biliru- bin level of 9 mg/dL (153.9 umol/L), and normal lipase Item 86 level. A 56-year-old man is evaluated for a 2-day history of mild Right-upper-quadrant ultrasound demonstrates a gall watery diarrhea occurring two or three times daily. He has bladder with stones and no gallbladder wall thickening or not lost weight. Two days before symptoms developed, he pericolic fluid; common bile duct is somewhat dilated. A returned from a 2-week trip to Southeast Asia. stone is visualized in the distal common bile duct. On physical examination, temperature is 37.4 °C Antibiotic therapy with piperacillin-tazobactam is initiated. (99.4 °F), blood pressure is 120/80 mm Hg, pulse rate is 92/min, and respiration rate is 16/min. Abdomen is soft, nontender, Which of the following is the most appropriate next step in and nondistended. Bowel sounds are normal. management? Information regarding oral rehydration therapy is provided. (A) Laparoscopic biliary drainage (B) Magnetic resonance cholangiopancreatography Which of the following is the most appropriate additional (C) Urgent cholecystectomy management? (D) Urgent endoscopic retrograde cholangiopancreatography (A) Levofloxacin (B) Loperamide Item 84 (C) Stool culture A 67-year-old man is evaluated for a 1-year history of vague, (D) Stool molecular testing periodic epigastric pain. He reports no other symptoms. A trial of proton pump inhibitor therapy has not relieved symptoms. Item 87 Vital signs and other physical examination findings are A 45-year-old man is evaluated after a positive result on unremarkable. fecal antigen testing for Helicobacter pylori, obtained An abdominal ultrasound reveals a 1.5-cm polyp in 2 months after he completed eradication therapy for H. pylori the gallbladder, with no gallbladder wall thickening, fluid, gastritis, and duodenal ulcer documented by upper endos- stones, or sludge. No common bile duct dilation is seen. copy. The patient was adherent to the initial eradication Findings on upper endoscopy with gastric biopsy are therapy, consisting of clarithromycin, amoxicillin, and normal. omeprazole for 10 days. He is asymptomatic.

On physical examination, his temperature is (A) Citalopram 38.9 °C (102.0 °F), blood pressure is 100/40 mm Hg, and (B) Famotidine pulse rate is 94/min. Jaundice is present. Abdominal examination reveals right-upper-quadrant tenderness (C) Metoclopramide and guarding. (D) Nortriptyline Laboratory evaluation shows a normal hemoglobin value, an elevated leukocyte count, a total serum biliru- bin level of 9 mg/dL (153.9 umol/L), and normal lipase Item 86 level. A 56-year-old man is evaluated for a 2-day history of mild Right-upper-quadrant ultrasound demonstrates a gall watery diarrhea occurring two or three times daily. He has bladder with stones and no gallbladder wall thickening or not lost weight. Two days before symptoms developed, he pericolic fluid; common bile duct is somewhat dilated. A returned from a 2-week trip to Southeast Asia. stone is visualized in the distal common bile duct. On physical examination, temperature is 37.4 °C Antibiotic therapy with piperacillin-tazobactam is initiated. (99.4 °F), blood pressure is 120/80 mm Hg, pulse rate is 92/min, and respiration rate is 16/min. Abdomen is soft, nontender, Which of the following is the most appropriate next step in and nondistended. Bowel sounds are normal. management? Information regarding oral rehydration therapy is provided. (A) Laparoscopic biliary drainage (B) Magnetic resonance cholangiopancreatography Which of the following is the most appropriate additional (C) Urgent cholecystectomy management? (D) Urgent endoscopic retrograde cholangiopancreatography (A) Levofloxacin (B) Loperamide Item 84 (C) Stool culture A 67-year-old man is evaluated for a 1-year history of vague, (D) Stool molecular testing periodic epigastric pain. He reports no other symptoms. A trial of proton pump inhibitor therapy has not relieved symptoms. Item 87 Vital signs and other physical examination findings are A 45-year-old man is evaluated after a positive result on unremarkable. fecal antigen testing for Helicobacter pylori, obtained An abdominal ultrasound reveals a 1.5-cm polyp in 2 months after he completed eradication therapy for H. pylori the gallbladder, with no gallbladder wall thickening, fluid, gastritis, and duodenal ulcer documented by upper endos- stones, or sludge. No common bile duct dilation is seen. copy. The patient was adherent to the initial eradication Findings on upper endoscopy with gastric biopsy are therapy, consisting of clarithromycin, amoxicillin, and normal. omeprazole for 10 days. He is asymptomatic. 103

rn 2 ane Which of the following is the most appropriate next step in Which of the following is the most appropriate treatment? > management? n wn (A) Ganciclovir @o 2) (A) Bismuth, tetracycline, metronidazole, and omeprazole Intravenous caspofungin wn for 14 days 3 Oral fluconazole Gs) (B Clarithromycin, amoxicillin, and omeprazole for 14 days s Oral fluconazole and oral acyclovir =

rn 2 ane Which of the following is the most appropriate next step in Which of the following is the most appropriate treatment? > management? n wn (A) Ganciclovir @o 2) (A) Bismuth, tetracycline, metronidazole, and omeprazole Intravenous caspofungin wn for 14 days 3 Oral fluconazole Gs) (B Clarithromycin, amoxicillin, and omeprazole for 14 days s Oral fluconazole and oral acyclovir = vr S Clarithromycin, metronidazole, amoxicillin, and BSos E) Upper endoscopy with biopsy and cytologic brushings o omeprazole for 14 days wn or Repeat fecal antigen test in 4 weeks aS Repeat upper endoscopy and biopsy Item 90 A 60-year-old woman is evaluated at follow-up for daily nausea, bloating and occasional vomiting after large meals, Item 88 epigastric pain, and fullness. Upper endoscopy last week A 58-year-old man is hospitalized after having three black, revealed some retained food in the stomach but no other loose stools in 1 day. He has no other medical conditions, significant findings, including Helicobacter pylori infec- takes no medications, and does not drink alcohol. tion. She has a 10-year history of type 2 diabetes mellitus. On physical examination, vital signs are normal. The Current medications are metformin and canagliflozin. patient appears comfortable, with a normal abdominal The hemoglobin A,, level is 9%. examination. Anorectal examination shows a small amount of black tarry stool in the rectal vault. The remainder of the Which of the following is the most appropriate next step in examination is normal. management? Upper endoscopy reveals a 1.5-cm gastric ulcer with a nonbleeding visible vessel, which is treated with endoscopic ( A) Initiate erythromycin clips. Biopsy of the ulcer is performed, and results of testing (B) Initiate metoclopramide for Helicobacter pylori infection are pending. (C) Obtain 4-hour gastric scintigraphy ( D) Obtain upper gastrointestinal barium series Which of the following is the most appropriate immediate ( E) Repeat upper endoscopy once hemoglobin A,, level is treatment? less than 7%

vr S Clarithromycin, metronidazole, amoxicillin, and BSos E) Upper endoscopy with biopsy and cytologic brushings o omeprazole for 14 days wn or Repeat fecal antigen test in 4 weeks aS Repeat upper endoscopy and biopsy Item 90 A 60-year-old woman is evaluated at follow-up for daily nausea, bloating and occasional vomiting after large meals, Item 88 epigastric pain, and fullness. Upper endoscopy last week A 58-year-old man is hospitalized after having three black, revealed some retained food in the stomach but no other loose stools in 1 day. He has no other medical conditions, significant findings, including Helicobacter pylori infec- takes no medications, and does not drink alcohol. tion. She has a 10-year history of type 2 diabetes mellitus. On physical examination, vital signs are normal. The Current medications are metformin and canagliflozin. patient appears comfortable, with a normal abdominal The hemoglobin A,, level is 9%. examination. Anorectal examination shows a small amount of black tarry stool in the rectal vault. The remainder of the Which of the following is the most appropriate next step in examination is normal. management? Upper endoscopy reveals a 1.5-cm gastric ulcer with a nonbleeding visible vessel, which is treated with endoscopic ( A) Initiate erythromycin clips. Biopsy of the ulcer is performed, and results of testing (B) Initiate metoclopramide for Helicobacter pylori infection are pending. (C) Obtain 4-hour gastric scintigraphy ( D) Obtain upper gastrointestinal barium series Which of the following is the most appropriate immediate ( E) Repeat upper endoscopy once hemoglobin A,, level is treatment? less than 7% (A) Broad-spectrum antibiotics (B) Esomeprazole, intravenously twice daily Item 91 (C) Octreotide, intravenously by continuous infusion A 56-year-old woman is evaluated for a 3-month history of (D) Omeprazole, orally once daily watery, nonbloody diarrhea that occurs four times daily, usually after meals. Abdominal cramping precedes each bowel movement. She occasionally experiences rectal Item 89 urgency. She has not lost weight. She also has osteoarthritis A 43-year-old man is evaluated for difficulty with swallowing of the knees, self-treated with daily ibuprofen for the past and painful swallowing. The pain began approximately 5 days 5 years. ago and occurs with both solids and liquids. He has recently On physical examination, vital signs and other findings diagnosed HIV infection and is receiving antiretroviral therapy. are normal. On physical examination, vital signs are normal. Colonoscopy reveals a normal-appearing colon. Biopsy Oropharynx findings are shown. specimens of normal-appearing ascending and sigmoid colon are notable for a marked increase in intraepithelial lymphocytes.

(A) Broad-spectrum antibiotics (B) Esomeprazole, intravenously twice daily Item 91 (C) Octreotide, intravenously by continuous infusion A 56-year-old woman is evaluated for a 3-month history of (D) Omeprazole, orally once daily watery, nonbloody diarrhea that occurs four times daily, usually after meals. Abdominal cramping precedes each bowel movement. She occasionally experiences rectal Item 89 urgency. She has not lost weight. She also has osteoarthritis A 43-year-old man is evaluated for difficulty with swallowing of the knees, self-treated with daily ibuprofen for the past and painful swallowing. The pain began approximately 5 days 5 years. ago and occurs with both solids and liquids. He has recently On physical examination, vital signs and other findings diagnosed HIV infection and is receiving antiretroviral therapy. are normal. On physical examination, vital signs are normal. Colonoscopy reveals a normal-appearing colon. Biopsy Oropharynx findings are shown. specimens of normal-appearing ascending and sigmoid colon are notable for a marked increase in intraepithelial lymphocytes. Which of the following is the most appropriate management? (A) Check fecal calprotectin (B) Discontinue ibuprofen (C) Initiate oral budesonide (D) Initiate oral prednisone

(A) Check fecal calprotectin (B) Discontinue ibuprofen (C) Initiate oral budesonide (D) Initiate oral prednisone Item 92 A 27-year-old man is evaluated for a pruritic rash on his elbows and knees of 3 years’ duration. Celiac disease was diagnosed 7 months ago. He started a gluten-free diet, and The remainder of the examination is normal. the diarrhea resolved but the rash has persisted. He is oth- Previous laboratory studies revealed a CD4 cell count erwise well and describes no additional symptoms. He is of 128/uL. taking no medications. 104

Self-Assessment Test ot On physical examination, vital signs are normal. Skin associated hypotension and tachycardia. The bleeding cH i findings are shown. chet was attributed to diverticulosis, which was successfully ij a treated during colonoscopy. He also has hypertension, type 2 diabetes mellitus, and hyperlipidemia. His medications = wn nn include low-dose aspirin, hydrochlorothiazide, metformin, Q wn and rosuvastatin. Aspirin was held at the time of hospital 2)

findings are shown. chet was attributed to diverticulosis, which was successfully ij a treated during colonoscopy. He also has hypertension, type 2 diabetes mellitus, and hyperlipidemia. His medications = wn nn include low-dose aspirin, hydrochlorothiazide, metformin, Q wn and rosuvastatin. Aspirin was held at the time of hospital 2) admission. Family history includes stroke in his father. a = a rn Which of the following is the most appropriate management of this patient’s aspirin therapy?

admission. Family history includes stroke in his father. a = a rn Which of the following is the most appropriate management of this patient’s aspirin therapy? (A) Discontinue indefinitely (B) Restart in 30 days (C) Restart now (D) Restart now and add omeprazole

(A) Discontinue indefinitely (B) Restart in 30 days (C) Restart now (D) Restart now and add omeprazole Item 95 A 25-year-old woman is evaluated for frequent watery, nonbloody diarrhea that began 5 years ago. She has a 2-year Laboratory testing reveals a tissue transglutaminase history of arthralgia and headaches. Diarrhea, arthralgia, IgA level of 2 U/mL (normal, 0-3 U/mL). and headaches resolved after the patient started a glu- Skin biopsy findings are consistent with dermatitis ten-free diet 1 year ago. Symptoms occasionally return if herpetiformis. she accidentally consumes gluten. Vital signs and other physical examination findings are Which of the following is the most appropriate normal. management? Laboratory studies show a normal tissue transglutam- inase IgA level. Results of testing for haplotypes HLA-DQ2 ( = Dapsone and HLA-DQ8 are positive for HLA-DQ2. (B Hydrocortisone cream ( Hydroxychloroquine S eee) Which of the following is the most appropriate diagnostic ( Measurement of glucose-6-phosphate dehydrogenase test to perform next? activity (A) Clostridioides difficile testing (B) Repeat HLA testing after resumption of a gluten- Item 93 containing diet

( Hydroxychloroquine S eee) Which of the following is the most appropriate diagnostic ( Measurement of glucose-6-phosphate dehydrogenase test to perform next? activity (A) Clostridioides difficile testing (B) Repeat HLA testing after resumption of a gluten- Item 93 containing diet A 68-year-old man is evaluated in follow-up for constant, (C) Repeat tissue transglutaminase IgA measurement moderate epigastric pain that radiates to the back. Chronic after resumption of gluten-containing diet

( Hydroxychloroquine S eee) Which of the following is the most appropriate diagnostic ( Measurement of glucose-6-phosphate dehydrogenase test to perform next? activity (A) Clostridioides difficile testing (B) Repeat HLA testing after resumption of a gluten- Item 93 containing diet A 68-year-old man is evaluated in follow-up for constant, (C) Repeat tissue transglutaminase IgA measurement moderate epigastric pain that radiates to the back. Chronic after resumption of gluten-containing diet pancreatitis was diagnosed 1 week ago. He is a 45-pack-year (D) Upper endoscopy and biopsy smoker. He does not currently drink alcohol. On physical examination, vital signs are normal. Deep abdominal palpation elicits mild epigastric tenderness. Item 96 | A pancreas-protocol CT scan demonstrated an atrophic A 40-year-old woman was hospitalized 3 days ago with pancreas with calcifications throughout, no masses, and no gallstone pancreatitis. Abdominal ultrasound at admis- cystic lesions. The pancreatic duct caliber is normal. sion revealed multiple small gallstones in the gallbladder, NSAIDs and acetaminophen are recommended for a common bile duct that is normal in size (3 mm), and pain. no choledocholithiasis. She was treated with intravenous fluids; her pain has resolved and she is now tolerating an Which of the following is the most appropriate additional oral diet. treatment for pain? On physical examination, vital signs and other findings are normal. (A) Oxycodone Current laboratory results are normal. (B) ) Pancreatic enzyme therapy (C) Surgical pancreatic duct decompression Which of the following is the most appropriate (D) Tobacco cessation management?

pancreatitis was diagnosed 1 week ago. He is a 45-pack-year (D) Upper endoscopy and biopsy smoker. He does not currently drink alcohol. On physical examination, vital signs are normal. Deep abdominal palpation elicits mild epigastric tenderness. Item 96 | A pancreas-protocol CT scan demonstrated an atrophic A 40-year-old woman was hospitalized 3 days ago with pancreas with calcifications throughout, no masses, and no gallstone pancreatitis. Abdominal ultrasound at admis- cystic lesions. The pancreatic duct caliber is normal. sion revealed multiple small gallstones in the gallbladder, NSAIDs and acetaminophen are recommended for a common bile duct that is normal in size (3 mm), and pain. no choledocholithiasis. She was treated with intravenous fluids; her pain has resolved and she is now tolerating an Which of the following is the most appropriate additional oral diet. treatment for pain? On physical examination, vital signs and other findings are normal. (A) Oxycodone Current laboratory results are normal. (B) ) Pancreatic enzyme therapy (C) Surgical pancreatic duct decompression Which of the following is the most appropriate (D) Tobacco cessation management? (A) Endoscopic retrograde cholangiopancreatography

pancreatitis was diagnosed 1 week ago. He is a 45-pack-year (D) Upper endoscopy and biopsy smoker. He does not currently drink alcohol. On physical examination, vital signs are normal. Deep abdominal palpation elicits mild epigastric tenderness. Item 96 | A pancreas-protocol CT scan demonstrated an atrophic A 40-year-old woman was hospitalized 3 days ago with pancreas with calcifications throughout, no masses, and no gallstone pancreatitis. Abdominal ultrasound at admis- cystic lesions. The pancreatic duct caliber is normal. sion revealed multiple small gallstones in the gallbladder, NSAIDs and acetaminophen are recommended for a common bile duct that is normal in size (3 mm), and pain. no choledocholithiasis. She was treated with intravenous fluids; her pain has resolved and she is now tolerating an Which of the following is the most appropriate additional oral diet. treatment for pain? On physical examination, vital signs and other findings are normal. (A) Oxycodone Current laboratory results are normal. (B) ) Pancreatic enzyme therapy (C) Surgical pancreatic duct decompression Which of the following is the most appropriate (D) Tobacco cessation management? (A) Endoscopic retrograde cholangiopancreatography Item 94 (B) ) Endoscopic ultrasonography (C) Laparoscopic cholecystectomy before hospital discharge A 65-year-old man is evaluated before hospital discharge. During hospitalization, he was treated for massive lower (D) Laparoscopic cholecystectomy in 4 to 6 weeks gastrointestinal bleeding. Fluid resuscitation relieved (E) Magnetic resonance cholangiopancreatography

Item 94 (B) ) Endoscopic ultrasonography (C) Laparoscopic cholecystectomy before hospital discharge A 65-year-old man is evaluated before hospital discharge. During hospitalization, he was treated for massive lower (D) Laparoscopic cholecystectomy in 4 to 6 weeks gastrointestinal bleeding. Fluid resuscitation relieved (E) Magnetic resonance cholangiopancreatography 105

Answers and Critiques C) ltem 1 Answer: C Educational Objective: Treat autoimmune pancreatitis. ¢ CT findings that strongly suggest type 1 autoimmune pancreatitis include a diffusely enlarged pancreas with The most appropriate management is prednisone (Option C). indistinct borders and delayed contrast enhancement. The patient has painless jaundice with imaging features sug- gestive of type 1 autoimmune pancreatitis (AIP). CT find- ¢ Initial treatment of type 1 autoimmune pancreatitis is ings that strongly suggest type 1 AIP include a diffusely high-dose oral prednisone tapered over 2 to 3 months. w enlarged pancreas with indistinct borders and delayed con- o 3 trast enhancement. In comparison, imaging characteristics Bibliography =: of pancreatic cancer include a low-density mass and dil- de Pretis N, De Marchi G, Frulloni L. Diagnosis and treatment of autoim- = theses atation and/or compression of the pancreatic duct associ- mune pancreatitis. Curr Opin Gastroenterol. 2018;34(5):362-366. [PMID: rw) 29901516] doi:10.1097/MOG.0000000000000454 a) ated with distal pancreatic atrophy. Endoscopic ultrasound = with fine-needle aspiration, if pursued, shows greater than © w 10 IgG4-positive cells/hpf; this finding is consistent with Item 2 Answer: A ome o a diagnosis of type 1 AIP, a manifestation of IgG4 disease. = Educational Objective: Diagnose primary biliary Ww A significant elevation of serum IgG4 level is also helpful = cholangitis. << in diagnosing type 1 AIP. Most IgG4-related conditions are characterized by plasma cell infiltration of the tissues and The most appropriate diagnostic test to perform next is an anti- subsequent clinical manifestations. AIP is a frequent mani- mitochondrial antibody (AMA) test (Option A). This patient festation of IgG4-related disease, but nearly any organ may most likely has primary biliary cholangitis (PBC), a diagnosis be involved, including lymph nodes, salivary glands, and the that is best established by positive results for AMA. PBC is an biliary system. Retroperitoneal fibrosis may also be related autoimmune disease affecting the small and medium bile to IgG4 disease. Initial treatment includes high-dose predni- ducts. It is often asymptomatic but can present with pruri- sone tapered over 2 to 3 months. Symptoms typically resolve tus and fatigue. PBC is more common in women than men within 2 to 4 weeks of therapy. Approximately 90% of patients (female-to-male ratio is 9:1). Typically, the alkaline phospha- achieve remission with oral glucocorticoids. Failure of clinical tase level is elevated in PBC; if it is at least 1.5 times the upper symptoms to respond to glucocorticoids suggests an incorrect limit of normal, a positive result on an AMA test establishes diagnosis, and other causes should be investigated. Up to the diagnosis without the need for liver biopsy. Patients with 60% of patients may relapse. Readministration of glucocor- PBC who are negative for AMA may test positive for other PBC- ticoids or immunomodulators, such as 6-mercaptopurine, specific autoantibodies, including sp100 and gp210. Once azathioprine, mycophenolate, or rituximab, may be used to PBC is diagnosed, first-line treatment is ursodeoxycholic acid, treat recurrent AIP. Diagnostic criteria for AIP are known which results in histologic improvement, improves survival by the acronym HISORt (diagnostic Histology, suggestive rates, and diminishes the need for liver transplantation. Imaging, Serology with elevated serum IgG4, Other organ Primary sclerosing cholangitis (PSC) is an autoimmune involvement, or Response to therapy with glucocorticoids). fibroinflammatory disease, primarily of large bile ducts. PSC Type 2 AIP, or idiopathic duct-centric pancreatitis, does not is more common in men than in women and is associated demonstrate IgG4-positive cells but is instead characterized with inflammatory bowel disease (IBD) in about 85% of by granulocytic lesions. Type 2 AIP may be associated with cases. PSC should be suspected in patients with IBD who inflammatory bowel disease. have elevated alkaline phosphatase levels. Some patients The immunosuppressant azathioprine (Option A) may may also have elevated serum total bilirubin levels or total be used as a glucocorticoid-sparing agent to treat relapsing protein, reflecting the presence of hypergammaglobulin- IgG4-related disease. Because of its slow onset, azathioprine emia. PSC is associated with many autoantibodies, including is not used for induction therapy but is useful in the mainte- anti-smooth muscle antibody (Option B). This otherwise nance phase of therapy for recurrent disease. well woman is more likely to have PBC than PSC, and mea- Endoscopic retrograde cholangiopancreatography with surement of anti-smooth muscle antibody is not indicated. biliary stent placement (Option B) is not required in AIP Autoimmune hepatitis is a chronic inflammatory hepatitis because jaundice should respond to glucocorticoids. that is more common in women than men and typically Although pancreatic adenocarcinoma and autoimmune presents with abnormal aminotransferase enzyme levels. A pancreatitis may be mistaken for each other, in this patient positive antinuclear or anti-smooth muscle antibody result the diagnosis appears certain on the basis of imaging char- is more common in autoimmune hepatitis. acteristics and needle biopsy results. Total pancreatectomy Liver biopsy (Option C) is not indicated because PBC (Option D) for pancreatic carcinoma is not indicated. is most often diagnosed noninvasively by serology. Only

C) ltem 1 Answer: C Educational Objective: Treat autoimmune pancreatitis. ¢ CT findings that strongly suggest type 1 autoimmune pancreatitis include a diffusely enlarged pancreas with The most appropriate management is prednisone (Option C). indistinct borders and delayed contrast enhancement. The patient has painless jaundice with imaging features sug- gestive of type 1 autoimmune pancreatitis (AIP). CT find- ¢ Initial treatment of type 1 autoimmune pancreatitis is ings that strongly suggest type 1 AIP include a diffusely high-dose oral prednisone tapered over 2 to 3 months. w enlarged pancreas with indistinct borders and delayed con- o 3 trast enhancement. In comparison, imaging characteristics Bibliography =: of pancreatic cancer include a low-density mass and dil- de Pretis N, De Marchi G, Frulloni L. Diagnosis and treatment of autoim- = theses atation and/or compression of the pancreatic duct associ- mune pancreatitis. Curr Opin Gastroenterol. 2018;34(5):362-366. [PMID: rw) 29901516] doi:10.1097/MOG.0000000000000454 a) ated with distal pancreatic atrophy. Endoscopic ultrasound = with fine-needle aspiration, if pursued, shows greater than © w 10 IgG4-positive cells/hpf; this finding is consistent with Item 2 Answer: A ome o a diagnosis of type 1 AIP, a manifestation of IgG4 disease. = Educational Objective: Diagnose primary biliary Ww A significant elevation of serum IgG4 level is also helpful = cholangitis. << in diagnosing type 1 AIP. Most IgG4-related conditions are characterized by plasma cell infiltration of the tissues and The most appropriate diagnostic test to perform next is an anti- subsequent clinical manifestations. AIP is a frequent mani- mitochondrial antibody (AMA) test (Option A). This patient festation of IgG4-related disease, but nearly any organ may most likely has primary biliary cholangitis (PBC), a diagnosis be involved, including lymph nodes, salivary glands, and the that is best established by positive results for AMA. PBC is an biliary system. Retroperitoneal fibrosis may also be related autoimmune disease affecting the small and medium bile to IgG4 disease. Initial treatment includes high-dose predni- ducts. It is often asymptomatic but can present with pruri- sone tapered over 2 to 3 months. Symptoms typically resolve tus and fatigue. PBC is more common in women than men within 2 to 4 weeks of therapy. Approximately 90% of patients (female-to-male ratio is 9:1). Typically, the alkaline phospha- achieve remission with oral glucocorticoids. Failure of clinical tase level is elevated in PBC; if it is at least 1.5 times the upper symptoms to respond to glucocorticoids suggests an incorrect limit of normal, a positive result on an AMA test establishes diagnosis, and other causes should be investigated. Up to the diagnosis without the need for liver biopsy. Patients with 60% of patients may relapse. Readministration of glucocor- PBC who are negative for AMA may test positive for other PBC- ticoids or immunomodulators, such as 6-mercaptopurine, specific autoantibodies, including sp100 and gp210. Once azathioprine, mycophenolate, or rituximab, may be used to PBC is diagnosed, first-line treatment is ursodeoxycholic acid, treat recurrent AIP. Diagnostic criteria for AIP are known which results in histologic improvement, improves survival by the acronym HISORt (diagnostic Histology, suggestive rates, and diminishes the need for liver transplantation. Imaging, Serology with elevated serum IgG4, Other organ Primary sclerosing cholangitis (PSC) is an autoimmune involvement, or Response to therapy with glucocorticoids). fibroinflammatory disease, primarily of large bile ducts. PSC Type 2 AIP, or idiopathic duct-centric pancreatitis, does not is more common in men than in women and is associated demonstrate IgG4-positive cells but is instead characterized with inflammatory bowel disease (IBD) in about 85% of by granulocytic lesions. Type 2 AIP may be associated with cases. PSC should be suspected in patients with IBD who inflammatory bowel disease. have elevated alkaline phosphatase levels. Some patients The immunosuppressant azathioprine (Option A) may may also have elevated serum total bilirubin levels or total be used as a glucocorticoid-sparing agent to treat relapsing protein, reflecting the presence of hypergammaglobulin- IgG4-related disease. Because of its slow onset, azathioprine emia. PSC is associated with many autoantibodies, including is not used for induction therapy but is useful in the mainte- anti-smooth muscle antibody (Option B). This otherwise nance phase of therapy for recurrent disease. well woman is more likely to have PBC than PSC, and mea- Endoscopic retrograde cholangiopancreatography with surement of anti-smooth muscle antibody is not indicated. biliary stent placement (Option B) is not required in AIP Autoimmune hepatitis is a chronic inflammatory hepatitis because jaundice should respond to glucocorticoids. that is more common in women than men and typically Although pancreatic adenocarcinoma and autoimmune presents with abnormal aminotransferase enzyme levels. A pancreatitis may be mistaken for each other, in this patient positive antinuclear or anti-smooth muscle antibody result the diagnosis appears certain on the basis of imaging char- is more common in autoimmune hepatitis. acteristics and needle biopsy results. Total pancreatectomy Liver biopsy (Option C) is not indicated because PBC (Option D) for pancreatic carcinoma is not indicated. is most often diagnosed noninvasively by serology. Only 107

Answers and Critiques patients with strong suspicion for PBC and negative antibody Nonabsorbed disaccharides, such as lactulose (Option results should undergo liver biopsy. C), are initiated for the management of hepatic encephalop- Autoimmune pancreatitis is a frequent manifestation of athy. This manifestation of cirrhosis can develop in the same IgG4-related disease. Patients with autoimmune pancreatitis population as patients with ascites. However, this cathartic may present with abdominal pain or obstructive jaundice is poorly tolerated and should not be initiated in a patient with or without a mass. Autoimmune pancreatitis may also without symptoms referable to hepatic encephalopathy. be associated with secondary sclerosing cholangitis. This Patients with cirrhosis typically develop catabolic patient does not have abdominal pain or jaundice, and mea- changes to their metabolism. The dietary protein needs suring serum IgG4 level (Option D) is not indicated. of patients with decompensated cirrhosis exceed those of healthy persons, and dietary protein supplementa- tion is indicated in this patient population. Therefore, a e Primary biliary cirrhosis is most commonly diagnosed low-protein diet (Option D) should not be initiated for > in women, it is often asymptomatic but can present this patient. =] “a with pruritus and fatigue. = oe e Diagnosis of primary biliary cholangitis is confirmed 7) ¢ Medications that decrease renal perfusion pressures, by elevation of the serum alkaline phosphatase level » such as ACE inhibitors, can worsen ascites in patients s 1.5 times the upper limit of normal and the presence 2. with portal hypertension. ra) of antimitochondrial antibody. = e 6-Blockers and NSAIDs should be used with caution t= 2 Bibliography or discontinued in patients with portal hypertension = © Lindor KD, Bowlus CL, Boyer J, et al. Primary biliary cholangitis: 2018 prac- and ascites. “a tice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2019;69:394-419. [PMID: 30070375] doi:10.1002 hep.30145 Bibliography Adebayo D, Neong SF, Wong F. Ascites and hepatorenal syndrome. Clin Liver Dis. 2019;23:659-682. [PMID: 31563217] doi:10.1016 /j.cld.2019.06.002

patients with strong suspicion for PBC and negative antibody Nonabsorbed disaccharides, such as lactulose (Option results should undergo liver biopsy. C), are initiated for the management of hepatic encephalop- Autoimmune pancreatitis is a frequent manifestation of athy. This manifestation of cirrhosis can develop in the same IgG4-related disease. Patients with autoimmune pancreatitis population as patients with ascites. However, this cathartic may present with abdominal pain or obstructive jaundice is poorly tolerated and should not be initiated in a patient with or without a mass. Autoimmune pancreatitis may also without symptoms referable to hepatic encephalopathy. be associated with secondary sclerosing cholangitis. This Patients with cirrhosis typically develop catabolic patient does not have abdominal pain or jaundice, and mea- changes to their metabolism. The dietary protein needs suring serum IgG4 level (Option D) is not indicated. of patients with decompensated cirrhosis exceed those of healthy persons, and dietary protein supplementa- tion is indicated in this patient population. Therefore, a e Primary biliary cirrhosis is most commonly diagnosed low-protein diet (Option D) should not be initiated for > in women, it is often asymptomatic but can present this patient. =] “a with pruritus and fatigue. = oe e Diagnosis of primary biliary cholangitis is confirmed 7) ¢ Medications that decrease renal perfusion pressures, by elevation of the serum alkaline phosphatase level » such as ACE inhibitors, can worsen ascites in patients s 1.5 times the upper limit of normal and the presence 2. with portal hypertension. ra) of antimitochondrial antibody. = e 6-Blockers and NSAIDs should be used with caution t= 2 Bibliography or discontinued in patients with portal hypertension = © Lindor KD, Bowlus CL, Boyer J, et al. Primary biliary cholangitis: 2018 prac- and ascites. “a tice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2019;69:394-419. [PMID: 30070375] doi:10.1002 hep.30145 Bibliography Adebayo D, Neong SF, Wong F. Ascites and hepatorenal syndrome. Clin Liver Dis. 2019;23:659-682. [PMID: 31563217] doi:10.1016 /j.cld.2019.06.002 Item 3 Answer: B

patients with strong suspicion for PBC and negative antibody Nonabsorbed disaccharides, such as lactulose (Option results should undergo liver biopsy. C), are initiated for the management of hepatic encephalop- Autoimmune pancreatitis is a frequent manifestation of athy. This manifestation of cirrhosis can develop in the same IgG4-related disease. Patients with autoimmune pancreatitis population as patients with ascites. However, this cathartic may present with abdominal pain or obstructive jaundice is poorly tolerated and should not be initiated in a patient with or without a mass. Autoimmune pancreatitis may also without symptoms referable to hepatic encephalopathy. be associated with secondary sclerosing cholangitis. This Patients with cirrhosis typically develop catabolic patient does not have abdominal pain or jaundice, and mea- changes to their metabolism. The dietary protein needs suring serum IgG4 level (Option D) is not indicated. of patients with decompensated cirrhosis exceed those of healthy persons, and dietary protein supplementa- tion is indicated in this patient population. Therefore, a e Primary biliary cirrhosis is most commonly diagnosed low-protein diet (Option D) should not be initiated for > in women, it is often asymptomatic but can present this patient. =] “a with pruritus and fatigue. = oe e Diagnosis of primary biliary cholangitis is confirmed 7) ¢ Medications that decrease renal perfusion pressures, by elevation of the serum alkaline phosphatase level » such as ACE inhibitors, can worsen ascites in patients s 1.5 times the upper limit of normal and the presence 2. with portal hypertension. ra) of antimitochondrial antibody. = e 6-Blockers and NSAIDs should be used with caution t= 2 Bibliography or discontinued in patients with portal hypertension = © Lindor KD, Bowlus CL, Boyer J, et al. Primary biliary cholangitis: 2018 prac- and ascites. “a tice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2019;69:394-419. [PMID: 30070375] doi:10.1002 hep.30145 Bibliography Adebayo D, Neong SF, Wong F. Ascites and hepatorenal syndrome. Clin Liver Dis. 2019;23:659-682. [PMID: 31563217] doi:10.1016 /j.cld.2019.06.002 Item 3 Answer: B Educational Objective: Treat ascites in a patient with Item 4 Answer: B cirrhosis by stopping an ACE inhibitor. Educational Objective: Categorize the phase of chronic hepatitis B virus infection. The most appropriate treatment is discontinuation of lisinopril (Option B). The development of ascites is often the first man- This patient is in the immune control phase of chronic hepa- ifestation of decompensation of cirrhosis. Ascites results from titis B virus (HBV) infection (Option B). Screening for chronic portal hypertension and functional renal impairment, which HBV infection is indicated in persons born or raised in regions leads to ineffective natriuresis and retention of sodium. In with high rates of HBV infection, including Asia, Africa, the patients with ascites due to cirrhosis, the initial management of South Pacific, European Mediterranean countries, Eastern ascites consists of dietary sodium restriction, which may equal- Europe, most of South America, Honduras, Guatemala, and ize the sodium balance in patients and prevent ascites. If this the Middle East (except Israel and Cyprus). Screening will treatment does not resolve the sodium imbalance, a diuretic detect those who may benefit from treatment. Treatment regimen with spironolactone and furosemide can be prescribed is offered to selected patients in the immune active phase to increase natriuresis. Medications that decrease renal perfu- of infection. The four phases of infection are categorized on sion pressures, such as ACE inhibitors and angiotensin receptor the basis of immune response to the virus: immune toler- blockers, can worsen ascites in patients with portal hyperten- ant, immune active, immune control, and reactivation. The sion. Therefore, discontinuation of the ACE inhibitor lisinopril immune control phase of chronic HBV infection is also known is the correct next step in the treatment of this patient. Other as inactive chronic HBV infection. The immune control phase medications that should be used with caution or discontinued is characterized by normal serum alanine aminotransferase include B-blockers and NSAIDs. Propranolol has been shown (ALT) measurement, indicating absence of liver inflamma- to shorten survival in patients with refractory ascites. Prosta- tion; positive results for hepatitis B core (HBc) antigen IgG glandin inhibitors, such as NSAIDs, can reduce urinary sodium antibody, indicating previous infection; hepatitis B e antigen excretion in patients with cirrhosis and can induce azotemia. (HBeAg) -negative and anti-HBe-positive serology, indicating Statins (Option A) for the treatment of dyslipidemia lack of viral replication and infectivity; and HBV DNA level may increase hepatic aminotransferase levels. However, the less than 2000 U/mL, indicating immune control of viral rep- overall benefits of these medications typically outweigh the lication and infection. This patient meets all the criteria for the potential harms, especially in patients with risk factors for immune control phase of chronic HBV infection. She does not coronary artery disease, such as in this patient with non- require treatment. alcoholic steatohepatitis, type 2 diabetes, dyslipidemia, and The immune active phase of chronic HBV infection hypertension. Therefore, discontinuation of atorvastatin is (Option A) is characterized by evidence of liver inflamma- not appropriate. tion (elevated ALT level) and uncontrolled infection (HBV

Educational Objective: Treat ascites in a patient with Item 4 Answer: B cirrhosis by stopping an ACE inhibitor. Educational Objective: Categorize the phase of chronic hepatitis B virus infection. The most appropriate treatment is discontinuation of lisinopril (Option B). The development of ascites is often the first man- This patient is in the immune control phase of chronic hepa- ifestation of decompensation of cirrhosis. Ascites results from titis B virus (HBV) infection (Option B). Screening for chronic portal hypertension and functional renal impairment, which HBV infection is indicated in persons born or raised in regions leads to ineffective natriuresis and retention of sodium. In with high rates of HBV infection, including Asia, Africa, the patients with ascites due to cirrhosis, the initial management of South Pacific, European Mediterranean countries, Eastern ascites consists of dietary sodium restriction, which may equal- Europe, most of South America, Honduras, Guatemala, and ize the sodium balance in patients and prevent ascites. If this the Middle East (except Israel and Cyprus). Screening will treatment does not resolve the sodium imbalance, a diuretic detect those who may benefit from treatment. Treatment regimen with spironolactone and furosemide can be prescribed is offered to selected patients in the immune active phase to increase natriuresis. Medications that decrease renal perfu- of infection. The four phases of infection are categorized on sion pressures, such as ACE inhibitors and angiotensin receptor the basis of immune response to the virus: immune toler- blockers, can worsen ascites in patients with portal hyperten- ant, immune active, immune control, and reactivation. The sion. Therefore, discontinuation of the ACE inhibitor lisinopril immune control phase of chronic HBV infection is also known is the correct next step in the treatment of this patient. Other as inactive chronic HBV infection. The immune control phase medications that should be used with caution or discontinued is characterized by normal serum alanine aminotransferase include B-blockers and NSAIDs. Propranolol has been shown (ALT) measurement, indicating absence of liver inflamma- to shorten survival in patients with refractory ascites. Prosta- tion; positive results for hepatitis B core (HBc) antigen IgG glandin inhibitors, such as NSAIDs, can reduce urinary sodium antibody, indicating previous infection; hepatitis B e antigen excretion in patients with cirrhosis and can induce azotemia. (HBeAg) -negative and anti-HBe-positive serology, indicating Statins (Option A) for the treatment of dyslipidemia lack of viral replication and infectivity; and HBV DNA level may increase hepatic aminotransferase levels. However, the less than 2000 U/mL, indicating immune control of viral rep- overall benefits of these medications typically outweigh the lication and infection. This patient meets all the criteria for the potential harms, especially in patients with risk factors for immune control phase of chronic HBV infection. She does not coronary artery disease, such as in this patient with non- require treatment. alcoholic steatohepatitis, type 2 diabetes, dyslipidemia, and The immune active phase of chronic HBV infection hypertension. Therefore, discontinuation of atorvastatin is (Option A) is characterized by evidence of liver inflamma- not appropriate. tion (elevated ALT level) and uncontrolled infection (HBV 108

_DREWete bie Sritiques DNA >2000 U/mL). HBeAg may be positive or negative in in diameter typically do not resolve with antibiotic therapy this phase. Depending on other factors, treatment may be alone, and aspiration of the abscess by percutaneous needle indicated. approach is warranted. In addition to aspiration, the patient The immune tolerant phase (Option C) is acquired should undergo evaluation to determine the cause of the through vertical transmission. In this phase, HBeAg is pos- abscess with abdominal imaging and diagnostic imaging of itive, anti-HBeAg is negative, ALT level is normal, but HBV the biliary tree. DNA level exceeds 1 million U/mL. Treatment is not recom- Hepatic abscesses that are less than 5 cm are not typ- mended in this phase. ically amenable to placement of a percutaneous drain The reactivation phase (Option D) is characterized by (Option B). loss of HBV immune control. It is recognized by a rising HBV Before the availability of interventional radiologic pro- DNA level compared with baseline or seroconversion of hep- cedures, such as needle aspiration and drainage catheter atitis B surface antigen (HBsAg) from negative to positive in placement, hepatic abscesses were often treated with sur- patients who were previously HBsAg negative and anti-HBc gical resection (Option C). This intervention is now rarely 2) a positive. Reactivation may be the result of immunosuppres- needed. =]

DNA >2000 U/mL). HBeAg may be positive or negative in in diameter typically do not resolve with antibiotic therapy this phase. Depending on other factors, treatment may be alone, and aspiration of the abscess by percutaneous needle indicated. approach is warranted. In addition to aspiration, the patient The immune tolerant phase (Option C) is acquired should undergo evaluation to determine the cause of the through vertical transmission. In this phase, HBeAg is pos- abscess with abdominal imaging and diagnostic imaging of itive, anti-HBeAg is negative, ALT level is normal, but HBV the biliary tree. DNA level exceeds 1 million U/mL. Treatment is not recom- Hepatic abscesses that are less than 5 cm are not typ- mended in this phase. ically amenable to placement of a percutaneous drain The reactivation phase (Option D) is characterized by (Option B). loss of HBV immune control. It is recognized by a rising HBV Before the availability of interventional radiologic pro- DNA level compared with baseline or seroconversion of hep- cedures, such as needle aspiration and drainage catheter atitis B surface antigen (HBsAg) from negative to positive in placement, hepatic abscesses were often treated with sur- patients who were previously HBsAg negative and anti-HBc gical resection (Option C). This intervention is now rarely 2) a positive. Reactivation may be the result of immunosuppres- needed. =] sion with immune modulators, cytotoxic chemotherapy, Continuation of antibiotics without drainage (Option = and drugs that deplete B lymphocytes, such as rituximab. D) is not appropriate because the size of the hepatic 7 rs) Prophylactic treatment is typically recommended for select abscess (3.5 cm) requires drainage. Abscesses less than s e patients in the immune control phase who are at risk for 3 cm in diameter typically resolve without additional inter- c wn reactivation. vention. al o > wn = e The four phases of chronic hepatitis B virus (HBV) e In patients with pyogenic liver abscess, empiric <= infection are differentiated on the basis of immune broad-spectrum parenteral antibiotics that cover response: immune tolerant, immune active, immune streptococci, enteric gram-negative bacilli, and anaer- control, and reactivation. obes should be initiated.

sion with immune modulators, cytotoxic chemotherapy, Continuation of antibiotics without drainage (Option = and drugs that deplete B lymphocytes, such as rituximab. D) is not appropriate because the size of the hepatic 7 rs) Prophylactic treatment is typically recommended for select abscess (3.5 cm) requires drainage. Abscesses less than s e patients in the immune control phase who are at risk for 3 cm in diameter typically resolve without additional inter- c wn reactivation. vention. al o > wn = e The four phases of chronic hepatitis B virus (HBV) e In patients with pyogenic liver abscess, empiric <= infection are differentiated on the basis of immune broad-spectrum parenteral antibiotics that cover response: immune tolerant, immune active, immune streptococci, enteric gram-negative bacilli, and anaer- control, and reactivation. obes should be initiated. e Patients in the immune control phase of chronic HBV e Hepatic abscesses 3 cm or greater in diameter typi- infection, also known as inactive chronic HBV infec- cally do not resolve with antibiotic therapy alone, and tion, generally do not require treatment. aspiration of the abscess by percutaneous needle approach is warranted. Bibliography Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, Bibliography and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Longworth S, Han J. Pyogenic liver abscess. Clin Liver Dis (Hoboken). 2015; Hepatology. 2018;67:1560-1599. [PMID: 29405329] doi:10.1002/hep. 6:51-54. [PMID: 31040988] doi:10.1002/cld.487 29800

e Patients in the immune control phase of chronic HBV e Hepatic abscesses 3 cm or greater in diameter typi- infection, also known as inactive chronic HBV infec- cally do not resolve with antibiotic therapy alone, and tion, generally do not require treatment. aspiration of the abscess by percutaneous needle approach is warranted. Bibliography Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, Bibliography and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Longworth S, Han J. Pyogenic liver abscess. Clin Liver Dis (Hoboken). 2015; Hepatology. 2018;67:1560-1599. [PMID: 29405329] doi:10.1002/hep. 6:51-54. [PMID: 31040988] doi:10.1002/cld.487 29800 Item 5 Answer: A Item 6 Answer: C Educational Objective: Treat hepatic abscess. Educational Objective: Treat acute diverticulitis with hospitalization and intravenous antibiotics. The most appropriate additional treatment is needle aspira- tion (Option A). Hepatic abscesses are typically found when The most appropriate management for this patient with acute patients present with fever, right-upper-quadrant abdominal diverticulitis is hospitalization for intravenous antibiotics pain, and malaise. Despite sometimes impressive findings (Option C). Diverticulitis results from a diverticulum (herni- on imaging, patients often have relatively mild and nontoxic ation of the mucosa and submucosa through a weakness in symptoms. If an abscess is left untreated, septic shock can the muscle wall) becoming blocked, trapping bacteria, and ultimately develop. Hepatic abscesses typically result from subsequently developing inflammation. This immunosup- direct spread to the liver in the setting of biliary infection or pressed patient has acute uncomplicated diverticulitis (no portal venous spread of bacteria from abdominal infections, abscess, obstruction, or fistula). The medical management of such as diverticulitis. Patients who are from areas of the world diverticulitis is based on the degree of the patient’s symptoms where amoeba are endemic, or patients who have traveled and severity ofdisease. Uncomplicated diverticulitis is treated to these areas, should have serologic evaluation for Entam- with oral antibiotics (ciprofloxacin or metronidazole) and oeba histolytica. Serologic testing combined with abdominal a liquid diet. Intravenous antibiotics with activities against imaging will confirm this diagnosis. In patients with pyogenic gram-negative rods and anaerobic organisms are required in liver abscess, empiric broad-spectrum parenteral antibiotics patients who cannot tolerate an oral diet; patients with severe that cover streptococci, enteric gram-negative bacilli, and comorbidities, advanced age, or immunosuppression; and anaerobes should be initiated before needle aspiration. Anti patients for whom oral antibiotics have been ineffective. Typ- biotic therapy can be modified on the basis of culture results ical regimens include ceftriaxone plus metronidazole, single- but is continued for several weeks. Abscesses 3 cm or greater agent therapy with a B-lactam or B-lactam/®-lactamase

Item 5 Answer: A Item 6 Answer: C Educational Objective: Treat hepatic abscess. Educational Objective: Treat acute diverticulitis with hospitalization and intravenous antibiotics. The most appropriate additional treatment is needle aspira- tion (Option A). Hepatic abscesses are typically found when The most appropriate management for this patient with acute patients present with fever, right-upper-quadrant abdominal diverticulitis is hospitalization for intravenous antibiotics pain, and malaise. Despite sometimes impressive findings (Option C). Diverticulitis results from a diverticulum (herni- on imaging, patients often have relatively mild and nontoxic ation of the mucosa and submucosa through a weakness in symptoms. If an abscess is left untreated, septic shock can the muscle wall) becoming blocked, trapping bacteria, and ultimately develop. Hepatic abscesses typically result from subsequently developing inflammation. This immunosup- direct spread to the liver in the setting of biliary infection or pressed patient has acute uncomplicated diverticulitis (no portal venous spread of bacteria from abdominal infections, abscess, obstruction, or fistula). The medical management of such as diverticulitis. Patients who are from areas of the world diverticulitis is based on the degree of the patient’s symptoms where amoeba are endemic, or patients who have traveled and severity ofdisease. Uncomplicated diverticulitis is treated to these areas, should have serologic evaluation for Entam- with oral antibiotics (ciprofloxacin or metronidazole) and oeba histolytica. Serologic testing combined with abdominal a liquid diet. Intravenous antibiotics with activities against imaging will confirm this diagnosis. In patients with pyogenic gram-negative rods and anaerobic organisms are required in liver abscess, empiric broad-spectrum parenteral antibiotics patients who cannot tolerate an oral diet; patients with severe that cover streptococci, enteric gram-negative bacilli, and comorbidities, advanced age, or immunosuppression; and anaerobes should be initiated before needle aspiration. Anti patients for whom oral antibiotics have been ineffective. Typ- biotic therapy can be modified on the basis of culture results ical regimens include ceftriaxone plus metronidazole, single- but is continued for several weeks. Abscesses 3 cm or greater agent therapy with a B-lactam or B-lactam/®-lactamase 109

Answers and Critiques inhibitor combination, or meropenem. This patient, who is gastrointestinal bleeding. This patient’s MDF score is 35, and immunosuppressed because of her prednisone and mycophe prednisolone should be considered. Prednisolone should be CONT. nolate mofetil therapy, should be hospitalized for intravenous discontinued if there is no or only minimal response to ther antibiotics. apy by day 7, as determined by the Lille model score (https: // Colonoscopy now (Option A) is contraindicated in acute www.mdcalc.com/lille-model-alcoholic-hepatitis). diverticulitis. Guidelines recommend colonoscopy after the Although infections are common in patients with acute resolution of acute diverticulitis if a high-quality examina- alcoholic hepatitis, in the absence of infection or suspicion tion has not been performed recently; however, “recently” of active infection, antibiotics (Option A) are not recom- is not defined in the guidelines. Consideration of follow-up mended. colonoscopy would be reasonable if more than 2 to 3 years Acute alcoholic hepatitis is most often diagnosed clin- have elapsed since the last examination. ically, with liver biopsy (Option B) reserved for cases with Oral antibiotics (Option B) are considered adequate diagnostic uncertainty. In this patient, the presence of fever, > for stable, immunocompetent patients with uncomplicated jaundice, tender hepatomegaly, and leukocytosis and a his- = w diverticulitis. Clinical trials have failed to demonstrate supe- tory of substantial alcohol consumption obviate the need for = riority of intravenous antibiotics over oral antibiotics in this liver biopsy. Oo =e wn patient population. However, hospitalization and intrave- The 2018 American College of Gastroenterology guide- gy nous antibiotics are recommended for patients at higher risk line on alcoholic liver disease makes a conditional recom- J Qa. for poor outcomes, such as patients with perforation, large mendation against the use of pentoxifylline (Option C) oO me abscesses, sepsis, or bowel obstruction or those who cannot for patients with severe alcoholic hepatitis. Pentoxifylline = tolerate liquid intake or have significant comorbid disease. should not be selected as initial therapy for this patient. 2 = Surgery (Option D) is indicated for patients present- oO wn ing with, or who develop, peritonitis or persistent sepsis. Surgery is not necessary in this patient with uncomplicated e Prednisolone is the treatment for severe alcoholic diverticulitis. hepatitis, defined as a Maddrey discriminant function score of 32 or greater or the presence of hepatic encephalopathy. e¢ Uncomplicated diverticulitis is treated with oral anti- e Patients with alcoholic hepatitis treated with predni- biotics (ciprofloxacin or metronidazole) and a liquid solone who do not respond after 7 days should have diet. the prednisolone discontinued; otherwise, predniso- e Hospitalization and intravenous antibiotics are required lone should be continued for 28 days. to treat acute diverticulitis in patients who cannot tolerate an oral diet; patients with severe comorbidities, Bibliography advanced age, or immunosuppression; and patients for Crabb DW, Im GY, Szabo G, et al. Diagnosis and treatment of alcohol-associ- whom oral antibiotics have been ineffective. ated liver diseases: 2019 practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2020;71:306-333. [PMID: 31314133] doi:10.1002/hep.30866 Bibliography Young-Fadok TM. Diverticulitis. N Engl J Med. 2018;379:1635-1642. [PMID: 30354951] doi:10.1056/NEJMcp1800468 Item 8 Answer: B

inhibitor combination, or meropenem. This patient, who is gastrointestinal bleeding. This patient’s MDF score is 35, and immunosuppressed because of her prednisone and mycophe prednisolone should be considered. Prednisolone should be CONT. nolate mofetil therapy, should be hospitalized for intravenous discontinued if there is no or only minimal response to ther antibiotics. apy by day 7, as determined by the Lille model score (https: // Colonoscopy now (Option A) is contraindicated in acute www.mdcalc.com/lille-model-alcoholic-hepatitis). diverticulitis. Guidelines recommend colonoscopy after the Although infections are common in patients with acute resolution of acute diverticulitis if a high-quality examina- alcoholic hepatitis, in the absence of infection or suspicion tion has not been performed recently; however, “recently” of active infection, antibiotics (Option A) are not recom- is not defined in the guidelines. Consideration of follow-up mended. colonoscopy would be reasonable if more than 2 to 3 years Acute alcoholic hepatitis is most often diagnosed clin- have elapsed since the last examination. ically, with liver biopsy (Option B) reserved for cases with Oral antibiotics (Option B) are considered adequate diagnostic uncertainty. In this patient, the presence of fever, > for stable, immunocompetent patients with uncomplicated jaundice, tender hepatomegaly, and leukocytosis and a his- = w diverticulitis. Clinical trials have failed to demonstrate supe- tory of substantial alcohol consumption obviate the need for = riority of intravenous antibiotics over oral antibiotics in this liver biopsy. Oo =e wn patient population. However, hospitalization and intrave- The 2018 American College of Gastroenterology guide- gy nous antibiotics are recommended for patients at higher risk line on alcoholic liver disease makes a conditional recom- J Qa. for poor outcomes, such as patients with perforation, large mendation against the use of pentoxifylline (Option C) oO me abscesses, sepsis, or bowel obstruction or those who cannot for patients with severe alcoholic hepatitis. Pentoxifylline = tolerate liquid intake or have significant comorbid disease. should not be selected as initial therapy for this patient. 2 = Surgery (Option D) is indicated for patients present- oO wn ing with, or who develop, peritonitis or persistent sepsis. Surgery is not necessary in this patient with uncomplicated e Prednisolone is the treatment for severe alcoholic diverticulitis. hepatitis, defined as a Maddrey discriminant function score of 32 or greater or the presence of hepatic encephalopathy. e¢ Uncomplicated diverticulitis is treated with oral anti- e Patients with alcoholic hepatitis treated with predni- biotics (ciprofloxacin or metronidazole) and a liquid solone who do not respond after 7 days should have diet. the prednisolone discontinued; otherwise, predniso- e Hospitalization and intravenous antibiotics are required lone should be continued for 28 days. to treat acute diverticulitis in patients who cannot tolerate an oral diet; patients with severe comorbidities, Bibliography advanced age, or immunosuppression; and patients for Crabb DW, Im GY, Szabo G, et al. Diagnosis and treatment of alcohol-associ- whom oral antibiotics have been ineffective. ated liver diseases: 2019 practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2020;71:306-333. [PMID: 31314133] doi:10.1002/hep.30866 Bibliography Young-Fadok TM. Diverticulitis. N Engl J Med. 2018;379:1635-1642. [PMID: 30354951] doi:10.1056/NEJMcp1800468 Item 8 Answer: B Educational Objective: Identify the proper surveillance interval following removal of a serrated polyp. Item 7 Answer: D The most appropriate screening test to perform next is colo- Educational Objective: Treat alcoholic hepatitis. noscopy in 5 to 10 years (Option B). A surveillance interval of The most appropriate management is prednisolone (Option 5 to 10 years is appropriate for patients with one or two small D). This patient has acute alcoholic hepatitis, a distinct clinical (<10 mm) sessile serrated polyps without dysplasia. As the syndrome of severe steatohepatitis in the setting of chronic number or size of sessile serrated polyps increases, the sur- alcoholic liver disease. Acute alcoholic hepatitis often presents veillance interval decreases (3-5 years for 3-4 polyps or 3 years with fever, jaundice, tender hepatomegaly, and leukocyto- for 5-10 polyps, all <10 mm) and 3 years for polyps 10 mm or sis. The short-term mortality rate is high. In severe cases, as greater. This patient’s colonoscopy revealed a single 7-mm defined by a Maddrey discriminant function (MDF) score of 32 sessile serrated polyp. It is critical that a polyp be completely or greater or the presence of hepatic encephalopathy, treatment removed during colonoscopy. Research suggests that up to with prednisolone can be considered. The MDF score = 4.6 27% of interval colon cancers occur in the same colon section (prothrombin time [s] — control prothrombin time [s]) + as the previous polypectomy, and another analysis that reex- serum total bilirubin (mg/dL). A meta-analysis of randomized amined the colon of patients with sessile polyps greater than studies showed that glucocorticoids were effective in reducing 2 cm demonstrated that 17.6% had residual neoplastic tissue, short-term mortality by 46%. This treatment should be con- suggesting that incomplete polyp removal may be a cause for sidered in patients who do not have evidence of infection or interval cancers. Quality of the baseline colonoscopy, which

Educational Objective: Identify the proper surveillance interval following removal of a serrated polyp. Item 7 Answer: D The most appropriate screening test to perform next is colo- Educational Objective: Treat alcoholic hepatitis. noscopy in 5 to 10 years (Option B). A surveillance interval of The most appropriate management is prednisolone (Option 5 to 10 years is appropriate for patients with one or two small D). This patient has acute alcoholic hepatitis, a distinct clinical (<10 mm) sessile serrated polyps without dysplasia. As the syndrome of severe steatohepatitis in the setting of chronic number or size of sessile serrated polyps increases, the sur- alcoholic liver disease. Acute alcoholic hepatitis often presents veillance interval decreases (3-5 years for 3-4 polyps or 3 years with fever, jaundice, tender hepatomegaly, and leukocyto- for 5-10 polyps, all <10 mm) and 3 years for polyps 10 mm or sis. The short-term mortality rate is high. In severe cases, as greater. This patient’s colonoscopy revealed a single 7-mm defined by a Maddrey discriminant function (MDF) score of 32 sessile serrated polyp. It is critical that a polyp be completely or greater or the presence of hepatic encephalopathy, treatment removed during colonoscopy. Research suggests that up to with prednisolone can be considered. The MDF score = 4.6 27% of interval colon cancers occur in the same colon section (prothrombin time [s] — control prothrombin time [s]) + as the previous polypectomy, and another analysis that reex- serum total bilirubin (mg/dL). A meta-analysis of randomized amined the colon of patients with sessile polyps greater than studies showed that glucocorticoids were effective in reducing 2 cm demonstrated that 17.6% had residual neoplastic tissue, short-term mortality by 46%. This treatment should be con- suggesting that incomplete polyp removal may be a cause for sidered in patients who do not have evidence of infection or interval cancers. Quality of the baseline colonoscopy, which 110

Answers and Critiques includes factors such as bowel preparation and adenoma Testing for anti-gliadin antibodies (IgA and IgG) (Option detection rate by the endoscopist, may also affect risk for B) should not be done because of its low sensitivity and spec- interval colon cancer. ificity compared with testing for antibodies to deamidated The surveillance interval for multiple (<20) small (<10 mm) gliadin peptide. hyperplastic polyps in the rectum or sigmoid colon or proxi- Before a gluten-free diet (Option C) is recommended, mal to the sigmoid or rectum is 10 years, which is identical to it is crucial to determine the celiac disease status of the the interval for colonoscopy in patient without polyps. Cer- patient because the sensitivity of serologies and duodenal tain factors, however, may alter this recommendation. Ser- biopsy declines after institution of a gluten-free diet. This rated polyposis syndrome (SPS) is characterized by multiple patient’s celiac disease status has not yet been clarified—she serrated polyps throughout the colon. This syndrome has has selective IgA deficiency, and IgG serologies have not yet an uncertain genetic basis and can be diagnosed if a patient been performed. has either of the following during their lifetime: (1) five or Current guidelines recommend that HLA-DQ2 and more serrated polyps proximal to the rectum, all at least HLA-DQ8 testing (Option D) should not be used routinely wn Y 5 mm in size, with two or more at least 10 mm in size, or as part of the initial diagnosis of celiac disease; if this test- s Zs (2) more than 20 serrated polyps throughout the colon, at ing is done and results are positive, patients should still be =

includes factors such as bowel preparation and adenoma Testing for anti-gliadin antibodies (IgA and IgG) (Option detection rate by the endoscopist, may also affect risk for B) should not be done because of its low sensitivity and spec- interval colon cancer. ificity compared with testing for antibodies to deamidated The surveillance interval for multiple (<20) small (<10 mm) gliadin peptide. hyperplastic polyps in the rectum or sigmoid colon or proxi- Before a gluten-free diet (Option C) is recommended, mal to the sigmoid or rectum is 10 years, which is identical to it is crucial to determine the celiac disease status of the the interval for colonoscopy in patient without polyps. Cer- patient because the sensitivity of serologies and duodenal tain factors, however, may alter this recommendation. Ser- biopsy declines after institution of a gluten-free diet. This rated polyposis syndrome (SPS) is characterized by multiple patient’s celiac disease status has not yet been clarified—she serrated polyps throughout the colon. This syndrome has has selective IgA deficiency, and IgG serologies have not yet an uncertain genetic basis and can be diagnosed if a patient been performed. has either of the following during their lifetime: (1) five or Current guidelines recommend that HLA-DQ2 and more serrated polyps proximal to the rectum, all at least HLA-DQ8 testing (Option D) should not be used routinely wn Y 5 mm in size, with two or more at least 10 mm in size, or as part of the initial diagnosis of celiac disease; if this test- s Zs (2) more than 20 serrated polyps throughout the colon, at ing is done and results are positive, patients should still be = least five located proximal to the rectum. Colonoscopy is serologically tested for celiac disease. Genetic testing is most = oO recommended every year (Option A) in SPS, with removal valuable for patients who have not had serologic testing for =} = of all polyps greater than 5 mm. celiac disease before starting a gluten-free diet and when G Interval stool-based testing with DNA testing (Option C) the results of celiac-specific serology and histology are dis- w* Ree o or fecal occult blood testing (Option D) is not recommended crepant. = for patients with polyps identified and removed during wa = colonoscopy. <t e In patients with selective IgA deficiency undergoing testing for celiac disease, IgG antibodies to deami- ¢ Colon cancer surveillance with colonoscopy every 5 to dated gliadin peptide or tissue transglutaminase 10 years is appropriate for patients with one or two ses- should be used. sile serrated polyps less than 10 mm without dysplasia.

least five located proximal to the rectum. Colonoscopy is serologically tested for celiac disease. Genetic testing is most = oO recommended every year (Option A) in SPS, with removal valuable for patients who have not had serologic testing for =} = of all polyps greater than 5 mm. celiac disease before starting a gluten-free diet and when G Interval stool-based testing with DNA testing (Option C) the results of celiac-specific serology and histology are dis- w* Ree o or fecal occult blood testing (Option D) is not recommended crepant. = for patients with polyps identified and removed during wa = colonoscopy. <t e In patients with selective IgA deficiency undergoing testing for celiac disease, IgG antibodies to deami- ¢ Colon cancer surveillance with colonoscopy every 5 to dated gliadin peptide or tissue transglutaminase 10 years is appropriate for patients with one or two ses- should be used. sile serrated polyps less than 10 mm without dysplasia. e As the number (>2) or size (=10 mm) of sessile serrated Bibliography Husby S, Murray JA, Katzka DA. AGA clinical practice update on diagnosis polyps increases, the colon cancer surveillance interval and monitoring of celiac disease-changing utility of serology and histo- decreases. logic measures: expert review. Gastroenterology. 2019;156:885-889. [PMID: 30578783] doi:10.1053/j.gastro.2018.12.010

e As the number (>2) or size (=10 mm) of sessile serrated Bibliography Husby S, Murray JA, Katzka DA. AGA clinical practice update on diagnosis polyps increases, the colon cancer surveillance interval and monitoring of celiac disease-changing utility of serology and histo- decreases. logic measures: expert review. Gastroenterology. 2019;156:885-889. [PMID: 30578783] doi:10.1053/j.gastro.2018.12.010 Bibliography Gupta S, Lieberman D, Anderson JC, et al. Recommendations for follow-up after colonoscopy and polypectomy: a consensus update by the US Multi- society Task Force on Colorectal Cancer. Am J Gastroenterol. Item 10 Answer: A 2020;115:415-434. [PMID: 32039982] doi:10.14309/ajg.0000000000 Educational Objective: Diagnose Budd-Chiari 000544 syndrome. The most appropriate diagnostic test to perform next is

Bibliography Gupta S, Lieberman D, Anderson JC, et al. Recommendations for follow-up after colonoscopy and polypectomy: a consensus update by the US Multi- society Task Force on Colorectal Cancer. Am J Gastroenterol. Item 10 Answer: A 2020;115:415-434. [PMID: 32039982] doi:10.14309/ajg.0000000000 Educational Objective: Diagnose Budd-Chiari 000544 syndrome. The most appropriate diagnostic test to perform next is Item 9 Answer: A abdominal Doppler ultrasonography (Option A). The devel- opment of Budd-Chiari syndrome is heralded by right-up- Educational Objective: Diagnose celiac disease in a per-quadrant abdominal discomfort, hepatomegaly, and patient with IgA deficiency. ascites. Thrombosis of the hepatic veins leads to hepatic con- The most appropriate management is measurement of serum gestion and increased portal pressures, resulting in ascites. anti-deamidated gliadin peptide IgG antibodies (Option A). Risk factors for Budd-Chiari syndrome include hypercoagu- This patient is at high risk for celiac disease, given her chronic lable states, such as myeloproliferative neoplasms, pregnancy, diarrhea, low weight, osteoporosis, and family history. Tissue and the use of oral contraceptives. Budd-Chiari syndrome can transglutaminase IgA antibody is the preferred serologic test be diagnosed with Doppler ultrasonography of the abdomen, for celiac disease in general, but its sensitivity is diminished which demonstrates absence of flow in the hepatic veins as in the setting of selective IgA deficiency. This patient’s unde- well as hepatic congestion. Typically, the caudate lobe of the tectable total IgA level indicates that she has selective IgA liver will develop hypertrophy because the venous drainage of deficiency, so IgG serology should be used. Available IgG serol- this segment of the liver is directly into the inferior vena cava ogies are antibodies to deamidated gliadin peptide or tissue rather than through the hepatic veins. Long-term anticoag- transglutaminase. If the anti-deamidated gliadin peptide IgG ulation is required in patients with Budd-Chiari syndrome, antibody level is elevated, upper endoscopy with duodenal although bleeding risks are significant in patients with acute biopsy should be performed; the presence of villus atrophy or chronic liver disease, portal hypertension, and esophageal indicates a diagnosis of celiac disease, for which a gluten-free varices. Angioplasty of the hepatic veins and/or placement of diet should be prescribed. a transjugular intrahepatic portosystemic shunt (TIPS) can be

Item 9 Answer: A abdominal Doppler ultrasonography (Option A). The devel- opment of Budd-Chiari syndrome is heralded by right-up- Educational Objective: Diagnose celiac disease in a per-quadrant abdominal discomfort, hepatomegaly, and patient with IgA deficiency. ascites. Thrombosis of the hepatic veins leads to hepatic con- The most appropriate management is measurement of serum gestion and increased portal pressures, resulting in ascites. anti-deamidated gliadin peptide IgG antibodies (Option A). Risk factors for Budd-Chiari syndrome include hypercoagu- This patient is at high risk for celiac disease, given her chronic lable states, such as myeloproliferative neoplasms, pregnancy, diarrhea, low weight, osteoporosis, and family history. Tissue and the use of oral contraceptives. Budd-Chiari syndrome can transglutaminase IgA antibody is the preferred serologic test be diagnosed with Doppler ultrasonography of the abdomen, for celiac disease in general, but its sensitivity is diminished which demonstrates absence of flow in the hepatic veins as in the setting of selective IgA deficiency. This patient’s unde- well as hepatic congestion. Typically, the caudate lobe of the tectable total IgA level indicates that she has selective IgA liver will develop hypertrophy because the venous drainage of deficiency, so IgG serology should be used. Available IgG serol- this segment of the liver is directly into the inferior vena cava ogies are antibodies to deamidated gliadin peptide or tissue rather than through the hepatic veins. Long-term anticoag- transglutaminase. If the anti-deamidated gliadin peptide IgG ulation is required in patients with Budd-Chiari syndrome, antibody level is elevated, upper endoscopy with duodenal although bleeding risks are significant in patients with acute biopsy should be performed; the presence of villus atrophy or chronic liver disease, portal hypertension, and esophageal indicates a diagnosis of celiac disease, for which a gluten-free varices. Angioplasty of the hepatic veins and/or placement of diet should be prescribed. a transjugular intrahepatic portosystemic shunt (TIPS) can be 111

Answers and Critiques used to reestablish adequate hepatic venous drainage. If liver recommended for prophylaxis in persons aged 12 months or failure develops, liver transplantation may be considered. older. For long-term immunity, the HAV vaccine series should Abdominal radiography (Option B) can demonstrate be completed with a second dose at least 6 months after the bowel obstruction or intestinal ileus but would not be help- first dose; however, the second dose is not necessary for post- ful in the diagnosis of hepatic vein thrombosis. exposure prophylaxis. Hepatobiliary iminodiacetic acid scintigraphy (Option According to the CDC, the HAV vaccine for postexposure C) is used to evaluate for gallbladder obstruction or a bile prophylaxis provides numerous public health advantages leak after an intervention on the biliary tree. This patient’s compared with HAV immune globulin (Option B), includ- acute onset of tender hepatomegaly and ascites is not com- ing the induction of active immunity and longer duration of patible with intermittent, colicky gallbladder pain, and protection, ease of administration, and greater acceptability hepatobiliary scintigraphy is not indicated. and availability. Noncontrast abdominal CT (Option D) is not helpful For exposed patients older than 40 years, HAV vaccine > when there is concern for vascular disease in the abdo- and HAV immune globulin (Option C) may be coadminis- = an men. Intravenous contrast is essential for evaluating the tered, depending on individual risk assessment. Combined = patency of the hepatic artery, portal veins, and hepatic veins. therapy (administered at different sites) is a consideration @o = wn Contrast-enhanced abdominal CT can help elucidate the because of the limited vaccine efficacy in this age group and a = extent of vascular thrombosis and potential use of a TIPS for the greater severity of illness in older adults. HAV immune 2. opening the hepatic veins to decompress the liver; without globulin may also be administered to persons at high risk (2) = intravenous contrast, however, CT would not be appropriate for complications, including those with chronic liver disease =. in this setting. In most patients, Doppler ultrasonography is and immunosuppression. Because this young patient does 2 a adequate for evaluation of Budd-Chiari syndrome and does not have these risk factors, HAV immune globulin is not @o wn not require contrast administration or radiation exposure. necessary.

used to reestablish adequate hepatic venous drainage. If liver recommended for prophylaxis in persons aged 12 months or failure develops, liver transplantation may be considered. older. For long-term immunity, the HAV vaccine series should Abdominal radiography (Option B) can demonstrate be completed with a second dose at least 6 months after the bowel obstruction or intestinal ileus but would not be help- first dose; however, the second dose is not necessary for post- ful in the diagnosis of hepatic vein thrombosis. exposure prophylaxis. Hepatobiliary iminodiacetic acid scintigraphy (Option According to the CDC, the HAV vaccine for postexposure C) is used to evaluate for gallbladder obstruction or a bile prophylaxis provides numerous public health advantages leak after an intervention on the biliary tree. This patient’s compared with HAV immune globulin (Option B), includ- acute onset of tender hepatomegaly and ascites is not com- ing the induction of active immunity and longer duration of patible with intermittent, colicky gallbladder pain, and protection, ease of administration, and greater acceptability hepatobiliary scintigraphy is not indicated. and availability. Noncontrast abdominal CT (Option D) is not helpful For exposed patients older than 40 years, HAV vaccine > when there is concern for vascular disease in the abdo- and HAV immune globulin (Option C) may be coadminis- = an men. Intravenous contrast is essential for evaluating the tered, depending on individual risk assessment. Combined = patency of the hepatic artery, portal veins, and hepatic veins. therapy (administered at different sites) is a consideration @o = wn Contrast-enhanced abdominal CT can help elucidate the because of the limited vaccine efficacy in this age group and a = extent of vascular thrombosis and potential use of a TIPS for the greater severity of illness in older adults. HAV immune 2. opening the hepatic veins to decompress the liver; without globulin may also be administered to persons at high risk (2) = intravenous contrast, however, CT would not be appropriate for complications, including those with chronic liver disease =. in this setting. In most patients, Doppler ultrasonography is and immunosuppression. Because this young patient does 2 a adequate for evaluation of Budd-Chiari syndrome and does not have these risk factors, HAV immune globulin is not @o wn not require contrast administration or radiation exposure. necessary. Although HAV infection is usually a self-limited illness, patients may experience considerable morbidity; fulminant ¢ Budd-Chiari syndrome is suggested by right-upper- hepatic failure, although rare, can occur. Postexposure vac- quadrant abdominal discomfort, hepatomegaly, and cination will effectively prevent infection in this patient ascites. and is recommended rather than providing no preventive

Although HAV infection is usually a self-limited illness, patients may experience considerable morbidity; fulminant ¢ Budd-Chiari syndrome is suggested by right-upper- hepatic failure, although rare, can occur. Postexposure vac- quadrant abdominal discomfort, hepatomegaly, and cination will effectively prevent infection in this patient ascites. and is recommended rather than providing no preventive e Budd-Chiari syndrome can be diagnosed with measures (Option D). Doppler ultrasonography of the abdomen; it demon- strates absence of flow in the hepatic veins as well as e Nonimmune persons exposed to hepatitis A virus hepatic congestion. (HAV) should receive postexposure prophylaxis with HAV vaccine as soon as possible after exposure. Bibliography Das CJ, Soneja M, Tayal S, et al. Role of radiological imaging and interven- e Postexposure prophylaxis with both HAV vaccine and tions in management of Budd-Chiari syndrome. Clin Radiol. 2018:73:610- HAV immune globulin may be considered for nonim- 624. [PMID: 29549997] doi:10.1016/j.crad.2018.02.003 mune patients older than 40 years.

e Budd-Chiari syndrome can be diagnosed with measures (Option D). Doppler ultrasonography of the abdomen; it demon- strates absence of flow in the hepatic veins as well as e Nonimmune persons exposed to hepatitis A virus hepatic congestion. (HAV) should receive postexposure prophylaxis with HAV vaccine as soon as possible after exposure. Bibliography Das CJ, Soneja M, Tayal S, et al. Role of radiological imaging and interven- e Postexposure prophylaxis with both HAV vaccine and tions in management of Budd-Chiari syndrome. Clin Radiol. 2018:73:610- HAV immune globulin may be considered for nonim- 624. [PMID: 29549997] doi:10.1016/j.crad.2018.02.003 mune patients older than 40 years. Item 11 Answer: A Bibliography Nelson NP, Link-Gelles R, Hofmeister MG, et al. Update: recommendations Educational Objective: Prevent transmission of of the Advisory Committee on Immunization Practices for use of hepati- hepatitis A virus. tis A vaccine for postexposure prophylaxis and for preexposure prophy- laxis for international travel MMWR Morb Mortal Wkly Rep. The most appropriate preventive measure is administration 2018;67:1216-1220. [PMID: 30383742] doi:10.15585/mmwr.mm6743a5

Item 11 Answer: A Bibliography Nelson NP, Link-Gelles R, Hofmeister MG, et al. Update: recommendations Educational Objective: Prevent transmission of of the Advisory Committee on Immunization Practices for use of hepati- hepatitis A virus. tis A vaccine for postexposure prophylaxis and for preexposure prophy- laxis for international travel MMWR Morb Mortal Wkly Rep. The most appropriate preventive measure is administration 2018;67:1216-1220. [PMID: 30383742] doi:10.15585/mmwr.mm6743a5 of the hepatitis A virus (HAV) vaccine (Option A). HAV is transmitted by the fecal-oral route and causes a self-limited illness. Risk factors for transmission include international Item 12 Answer: A travel, contact with household members with HAV infection, Educational Objective: Diagnose acute pancreatitis. men who have sex with men, homelessness, and exposure to day care or institutionalized settings. HAV incidence declined The most appropriate management is contrast-enhanced CT dramatically after introduction of universal childhood HAV (Option A). This patient probably has acute pancreatitis, the vaccination, but rates have recently increased among unvac- diagnosis of which requires at least two of the following: cinated people, especially those reporting homelessness or (1) acute-onset abdominal pain characteristic of pancreatitis drug use. This unvaccinated patient has been exposed to (severe, persistent for hours to days, and epigastric in loca a roommate with acute HAV infection and so is at risk for tion, often radiating to the back); (2) elevation in pancre infection. Persons who have recently been exposed to HAV atic enzymes (typically lipase) three times the upper limit and have not been immunized should receive postexposure of normal or higher: and (3) imaging findings characteristic prophylaxis, consisting of the HAV vaccine, as soon as possible of acute pancreatitis, including peripancreatic fat stranding after exposure, preferably within 2 weeks. The HAV vaccine is and inflammation as well as peripancreatic edema. Serum

of the hepatitis A virus (HAV) vaccine (Option A). HAV is transmitted by the fecal-oral route and causes a self-limited illness. Risk factors for transmission include international Item 12 Answer: A travel, contact with household members with HAV infection, Educational Objective: Diagnose acute pancreatitis. men who have sex with men, homelessness, and exposure to day care or institutionalized settings. HAV incidence declined The most appropriate management is contrast-enhanced CT dramatically after introduction of universal childhood HAV (Option A). This patient probably has acute pancreatitis, the vaccination, but rates have recently increased among unvac- diagnosis of which requires at least two of the following: cinated people, especially those reporting homelessness or (1) acute-onset abdominal pain characteristic of pancreatitis drug use. This unvaccinated patient has been exposed to (severe, persistent for hours to days, and epigastric in loca a roommate with acute HAV infection and so is at risk for tion, often radiating to the back); (2) elevation in pancre infection. Persons who have recently been exposed to HAV atic enzymes (typically lipase) three times the upper limit and have not been immunized should receive postexposure of normal or higher: and (3) imaging findings characteristic prophylaxis, consisting of the HAV vaccine, as soon as possible of acute pancreatitis, including peripancreatic fat stranding after exposure, preferably within 2 weeks. The HAV vaccine is and inflammation as well as peripancreatic edema. Serum 112

Answers and Critiques C) atic conditions (e.g., kidney disease, acute appendicitis) and amylase and lipase levels may be elevated in nonpancre- MEN1, von Hippel-Lindau syndrome, neurofibromatosis type 1, and tuberous sclerosis. Among these inherited endo- CONT. * therefore are not specific for acute pancreatitis. This patient crinopathies, MEN1 is most frequently associated with pan- has typical symptoms, but his lipase levels do not meet the creatic NETs (80%), whereas pancreatic NETs occur in 1% to threshold for diagnosis. Therefore, cross-sectional imaging 20% of the other inherited endocrinopathies. MEN] is a rare is recommended to confirm the diagnosis. Cross-sectional heritable disorder classically characterized by a predisposition imaging is also helpful to assess patients for other condi- to tumors of the parathyroid glands, anterior pituitary, and tions that might mimic acute pancreatitis and to evaluate pancreatic islet cells, including insulinoma, as seen in this patients with atypical symptoms. Preferred imaging modali- patient. MEN1 is clinically diagnosed by the presence of two ties include contrast-enhanced CT and MRI. or more primary MENI1 tumor types. In patients who have Routine use of antibiotics (Option B) is not warranted in family members with a diagnosis of MEN1, the presence of a acute pancreatitis unless there is evidence of extrapancreatic single MEN1-associated tumor satisfies the diagnostic criteria infection, such as ascending cholangitis, bacteremia, urinary for MEN1. Pancreatic NETs account for the greatest propor- w wo tract infection, or pneumonia. Prophylactic antibiotics do tion of deaths in patients with MEN1, and gastrinoma is the =

C) atic conditions (e.g., kidney disease, acute appendicitis) and amylase and lipase levels may be elevated in nonpancre- MEN1, von Hippel-Lindau syndrome, neurofibromatosis type 1, and tuberous sclerosis. Among these inherited endo- CONT. * therefore are not specific for acute pancreatitis. This patient crinopathies, MEN1 is most frequently associated with pan- has typical symptoms, but his lipase levels do not meet the creatic NETs (80%), whereas pancreatic NETs occur in 1% to threshold for diagnosis. Therefore, cross-sectional imaging 20% of the other inherited endocrinopathies. MEN] is a rare is recommended to confirm the diagnosis. Cross-sectional heritable disorder classically characterized by a predisposition imaging is also helpful to assess patients for other condi- to tumors of the parathyroid glands, anterior pituitary, and tions that might mimic acute pancreatitis and to evaluate pancreatic islet cells, including insulinoma, as seen in this patients with atypical symptoms. Preferred imaging modali- patient. MEN1 is clinically diagnosed by the presence of two ties include contrast-enhanced CT and MRI. or more primary MENI1 tumor types. In patients who have Routine use of antibiotics (Option B) is not warranted in family members with a diagnosis of MEN1, the presence of a acute pancreatitis unless there is evidence of extrapancreatic single MEN1-associated tumor satisfies the diagnostic criteria infection, such as ascending cholangitis, bacteremia, urinary for MEN1. Pancreatic NETs account for the greatest propor- w wo tract infection, or pneumonia. Prophylactic antibiotics do tion of deaths in patients with MEN1, and gastrinoma is the = not affect the rates of important outcomes, such as organ most common of the functioning NETs. However, most gas- <2 = - failure and hospital length of stay. trinomas are located in the duodenal wall, not the pancreas. 1S) Endoscopic ultrasonography (Option C), in which an Insulinomas are the second most common NET and the most cs t ultrasound probe is placed in the stomach and small intes- common pancreatic NET; they tend to be small and may be cs

not affect the rates of important outcomes, such as organ most common of the functioning NETs. However, most gas- <2 = - failure and hospital length of stay. trinomas are located in the duodenal wall, not the pancreas. 1S) Endoscopic ultrasonography (Option C), in which an Insulinomas are the second most common NET and the most cs t ultrasound probe is placed in the stomach and small intes- common pancreatic NET; they tend to be small and may be cs tine to better visualize the pancreas and biliary system, is not multiple. Sporadic insulinomas occur in patients age 40 years w ee <t typically used in the initial diagnosis of pancreatitis because and older; therefore, the diagnosis of insulinoma in a younger S of its invasive nature. patient is cause to screen for MEN1. a = Once a diagnosis of pancreatitis is confirmed, patients A defect of the RET proto-oncogene is responsible for i 4 should undergo an assessment for the cause of acute pan- the clinical variations of MEN type 2 (MEN2) (Option B), creatitis. Biliary disease and alcohol are the most common which involve tumors of the thyroid, parathyroid, and adre- causes of acute pancreatitis. Transabdominal ultrasonogra- nal glands. MEN2 is not associated with NETs of the pan- phy is the preferred imaging modality to assess for a biliary creas, and genetic testing for the MEN2 gene is not indicated. cause of acute pancreatitis. Triglyceride levels (Option D) Neurofibromas present as soft, skin-colored papules. should be measured in patients without a biliary cause of Other cutaneous manifestations of neurofibromatosis type 1 acute pancreatitis; a triglyceride level exceeding 1000 mg/dL (Option C) include café-au-lait macules and axillary freck- (11.3 mmol/L) can be considered the cause of the acute pan- ling. Nearly all patients with tuberous sclerosis (Option D) creatitis. Because the diagnosis of acute pancreatitis has not have one or more of the characteristic skin lesions, including been established and the biliary tree has not been evaluated, hypopigmented macules, angiofibromas, or a brown fibrous measurement of triglyceride levels is premature. plaque on the forehead. Genetic testing for these disorders is not indicated in the absence of these cutaneous findings.

tine to better visualize the pancreas and biliary system, is not multiple. Sporadic insulinomas occur in patients age 40 years w ee <t typically used in the initial diagnosis of pancreatitis because and older; therefore, the diagnosis of insulinoma in a younger S of its invasive nature. patient is cause to screen for MEN1. a = Once a diagnosis of pancreatitis is confirmed, patients A defect of the RET proto-oncogene is responsible for i 4 should undergo an assessment for the cause of acute pan- the clinical variations of MEN type 2 (MEN2) (Option B), creatitis. Biliary disease and alcohol are the most common which involve tumors of the thyroid, parathyroid, and adre- causes of acute pancreatitis. Transabdominal ultrasonogra- nal glands. MEN2 is not associated with NETs of the pan- phy is the preferred imaging modality to assess for a biliary creas, and genetic testing for the MEN2 gene is not indicated. cause of acute pancreatitis. Triglyceride levels (Option D) Neurofibromas present as soft, skin-colored papules. should be measured in patients without a biliary cause of Other cutaneous manifestations of neurofibromatosis type 1 acute pancreatitis; a triglyceride level exceeding 1000 mg/dL (Option C) include café-au-lait macules and axillary freck- (11.3 mmol/L) can be considered the cause of the acute pan- ling. Nearly all patients with tuberous sclerosis (Option D) creatitis. Because the diagnosis of acute pancreatitis has not have one or more of the characteristic skin lesions, including been established and the biliary tree has not been evaluated, hypopigmented macules, angiofibromas, or a brown fibrous measurement of triglyceride levels is premature. plaque on the forehead. Genetic testing for these disorders is not indicated in the absence of these cutaneous findings. e The diagnosis of acute pancreatitis requires at least two of the following: (1) acute-onset abdominal pain ¢ Sporadic insulinomas tend to occur in patients age characteristic of pancreatitis, (2) elevation in pancre- 40 years and older; therefore, the diagnosis of insu- atic enzymes at least three times the upper limit of linoma in a younger patient is cause to screen for normal, and (3) findings on cross-sectional imaging multiple endocrine neoplasia type 1. characteristic of acute pancreatitis.

e The diagnosis of acute pancreatitis requires at least two of the following: (1) acute-onset abdominal pain ¢ Sporadic insulinomas tend to occur in patients age characteristic of pancreatitis, (2) elevation in pancre- 40 years and older; therefore, the diagnosis of insu- atic enzymes at least three times the upper limit of linoma in a younger patient is cause to screen for normal, and (3) findings on cross-sectional imaging multiple endocrine neoplasia type 1. characteristic of acute pancreatitis. e Routine use of antibiotics is not warranted in acute Bibliography Scott AT, Howe JR. Evaluation and management of neuroendocrine tumors pancreatitis. of the pancreas. Surg Clin North Am. 2019;99:793-814. [PMID: 31255207] doi:10.1016/j.suc.2019.04.014 Bibliography Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med. 2016: 375:1972-1981. [PMID: 27959604] Item 14 Answer: A Educational Objective: Evaluate chronic constipation.

Bibliography Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med. 2016: 375:1972-1981. [PMID: 27959604] Item 14 Answer: A Educational Objective: Evaluate chronic constipation. Item 13 Answer: A The most appropriate management is colonoscopy (Option A). Constipation is one of the most common gastrointestinal Educational Objective: Diagnose multiple endocrine symptoms, affecting 20% of the general population. Constipa- neoplasia type 1. tion can present with symptoms including infrequent, diffi- This patient should undergo genetic testing for multiple cult, or incomplete defecation, and it can be acute or chronic. endocrine neoplasia type 1 (MEN1) (Option A). Although The patient’s history is compatible with chronic constipation. most pancreatic neuroendocrine tumors (NETs) are sporadic, Constipation can be secondary or functional (idiopathic). some are associated with hereditary endocrinopathies, such Medications are the most common cause of secondary 113

Answers and Critiques constipation. Other causes of this common condition include others are diagnosed after an evaluation of abnormal labora- mechanical obstruction, systemic illnesses, altered physio- tory test results demonstrating a cholestatic pattern of liver logic states, and psychosocial conditions. Once secondary injury. Symptomatic patients present with fatigue and pru- causes have been excluded, chronic constipation is considered ritus. Clinical findings vary as well. Asymptomatic patients functional. Functional constipation is subtyped into catego- may have no findings, and others may have jaundice, hepato- ries of slow transit, normal transit, or dyssynergic defecation. megaly, splenomegaly, and excoriations related to pruritus. Slow-transit constipation is defined as the delayed passage of PSC is associated with inflammatory bowel disease (IBD) in fecal contents through the colon based on objective transit approximately 85% of cases. Therefore, all patients with PSC testing. Normal-transit constipation is functional constipa- without known IBD should have colonoscopy with biopsies at tion in which colonic transit times are adequate. Dyssynergic the time of PSC diagnosis. Common colonoscopy findings in defecation refers to difficulty with or inability to expel stool as patients with PSC and IBD include mild pancolitis with rectal a result of some combination of abnormalities in contraction sparing and backwash ileitis. Because of the higher risk for b and/or relaxation of the muscles of the pelvic floor during def- colon cancer in these patients, surveillance colonoscopy with = wn ecation. Colonoscopy is the initial evaluation of constipation biopsies is also recommended every1 to 2 years. Patients with = in elderly patients with acute constipation and patients with PSC have a 15% lifetime risk for cholangiocarcinoma. Annual Oo = wa unintentional weight loss, family history of colorectal cancer, or biannual magnetic resonance cholangiopancreatography o J unexplained anemia, and age older than 50 years with no (MRCP) and measurement of the carbohydrate antigen 19-9 a. previous colonoscopy. This patient is age 52 years, and colo- level are recommended for cholangiocarcinoma surveillance. (a) =e noscopy should be performed as the initial study to evaluate The incidence of cholangiocarcinoma is highest in the first = for mechanical causes of constipation. 2 years after PSC is diagnosed. There is also an increased risk 2 = Treatment options for chronic constipation include for gallbladder cancer in PSC, and regular annual screening @ ~” serotonergic prokinetic agents (prucalopride [Option B)), with ultrasonography is recommended. bulking agents (psyllium [Option C]), stimulant laxatives PSC is most commonly diagnosed by MRCP. Endoscopic (senna, bisacodyl), osmotic laxatives (polyethylene glycol, retrograde cholangiopancreatography (ERCP) (Option B) is lactulose, sorbitol), stool softeners (docusate), secretagogues indicated in patients who have associated jaundice, worsening (lubiprostone, linaclotide, plecanatide), and/or biofeedback. pruritus, cholangitis, or a dominant stricture or bile duct mass These therapeutic modalities are appropriate after evaluation on MRCP This patient has no indication for ERCP at this time. for a cause of constipation. Liver biopsy (Option C) is useful in patients for whom Physiologic testing, including colon transit testing with PSC is suspected but the MRCP result is normal. In this situ- a radiopaque marker study (Option D), scintigraphy, or the ation, small-duct PSC not seen on MRCP may be diagnosed wireless motility capsule, is reserved for patients with con- with liver biopsy. This patient has no indication for liver stipation symptoms that do not respond to initial trials of biopsy because MRCP established the diagnosis. lifestyle modification and laxative therapy. Liver transplantation (Option D) should be considered for patients with PSC and decompensated cirrhosis, recurrent bacterial cholangitis, and hilar cholangiocarcinoma. Trans- ¢ Constipation can be secondary or functional (idio- plant outcomes for patients with PSC are excellent, with pathic); medications are the most common cause of 1-year survival rates of at least 90% and recurrence rates of secondary constipation. approximately 20% at 5 years after liver transplantation. This ¢ Colonoscopy is the initial evaluation of constipation in patient does not have an indication for liver transplantation.

constipation. Other causes of this common condition include others are diagnosed after an evaluation of abnormal labora- mechanical obstruction, systemic illnesses, altered physio- tory test results demonstrating a cholestatic pattern of liver logic states, and psychosocial conditions. Once secondary injury. Symptomatic patients present with fatigue and pru- causes have been excluded, chronic constipation is considered ritus. Clinical findings vary as well. Asymptomatic patients functional. Functional constipation is subtyped into catego- may have no findings, and others may have jaundice, hepato- ries of slow transit, normal transit, or dyssynergic defecation. megaly, splenomegaly, and excoriations related to pruritus. Slow-transit constipation is defined as the delayed passage of PSC is associated with inflammatory bowel disease (IBD) in fecal contents through the colon based on objective transit approximately 85% of cases. Therefore, all patients with PSC testing. Normal-transit constipation is functional constipa- without known IBD should have colonoscopy with biopsies at tion in which colonic transit times are adequate. Dyssynergic the time of PSC diagnosis. Common colonoscopy findings in defecation refers to difficulty with or inability to expel stool as patients with PSC and IBD include mild pancolitis with rectal a result of some combination of abnormalities in contraction sparing and backwash ileitis. Because of the higher risk for b and/or relaxation of the muscles of the pelvic floor during def- colon cancer in these patients, surveillance colonoscopy with = wn ecation. Colonoscopy is the initial evaluation of constipation biopsies is also recommended every1 to 2 years. Patients with = in elderly patients with acute constipation and patients with PSC have a 15% lifetime risk for cholangiocarcinoma. Annual Oo = wa unintentional weight loss, family history of colorectal cancer, or biannual magnetic resonance cholangiopancreatography o J unexplained anemia, and age older than 50 years with no (MRCP) and measurement of the carbohydrate antigen 19-9 a. previous colonoscopy. This patient is age 52 years, and colo- level are recommended for cholangiocarcinoma surveillance. (a) =e noscopy should be performed as the initial study to evaluate The incidence of cholangiocarcinoma is highest in the first = for mechanical causes of constipation. 2 years after PSC is diagnosed. There is also an increased risk 2 = Treatment options for chronic constipation include for gallbladder cancer in PSC, and regular annual screening @ ~” serotonergic prokinetic agents (prucalopride [Option B)), with ultrasonography is recommended. bulking agents (psyllium [Option C]), stimulant laxatives PSC is most commonly diagnosed by MRCP. Endoscopic (senna, bisacodyl), osmotic laxatives (polyethylene glycol, retrograde cholangiopancreatography (ERCP) (Option B) is lactulose, sorbitol), stool softeners (docusate), secretagogues indicated in patients who have associated jaundice, worsening (lubiprostone, linaclotide, plecanatide), and/or biofeedback. pruritus, cholangitis, or a dominant stricture or bile duct mass These therapeutic modalities are appropriate after evaluation on MRCP This patient has no indication for ERCP at this time. for a cause of constipation. Liver biopsy (Option C) is useful in patients for whom Physiologic testing, including colon transit testing with PSC is suspected but the MRCP result is normal. In this situ- a radiopaque marker study (Option D), scintigraphy, or the ation, small-duct PSC not seen on MRCP may be diagnosed wireless motility capsule, is reserved for patients with con- with liver biopsy. This patient has no indication for liver stipation symptoms that do not respond to initial trials of biopsy because MRCP established the diagnosis. lifestyle modification and laxative therapy. Liver transplantation (Option D) should be considered for patients with PSC and decompensated cirrhosis, recurrent bacterial cholangitis, and hilar cholangiocarcinoma. Trans- ¢ Constipation can be secondary or functional (idio- plant outcomes for patients with PSC are excellent, with pathic); medications are the most common cause of 1-year survival rates of at least 90% and recurrence rates of secondary constipation. approximately 20% at 5 years after liver transplantation. This ¢ Colonoscopy is the initial evaluation of constipation in patient does not have an indication for liver transplantation. elderly patients with acute constipation and patients with unintentional weight loss, family history of colo- e Primary sclerosing cholangitis (PSC) is associated rectal cancer, unexplained anemia, and age older than with inflammatory bowel disease (IBD) in approxi- 50 years with no previous colonoscopy. mately 85% of cases; therefore, all patients with PSC without known IBD should have colonoscopy with Bibliography biopsies at the time of PSC diagnosis. Bharucha AE, Wald A. Chronic constipation. Mayo Clin Proc. 2019;94:2340- 2357. [PMID: 31054770] doi:10.1016/j.mayocp.2019.01.031 e Patients with PSC have a 15% lifetime risk for cholan- giocarcinoma; annual or biannual magnetic reso- nance cholangiopancreatography and carbohydrate Item 15 Answer: A antigen 19-9 measurement is recommended for chol-

elderly patients with acute constipation and patients with unintentional weight loss, family history of colo- e Primary sclerosing cholangitis (PSC) is associated rectal cancer, unexplained anemia, and age older than with inflammatory bowel disease (IBD) in approxi- 50 years with no previous colonoscopy. mately 85% of cases; therefore, all patients with PSC without known IBD should have colonoscopy with Bibliography biopsies at the time of PSC diagnosis. Bharucha AE, Wald A. Chronic constipation. Mayo Clin Proc. 2019;94:2340- 2357. [PMID: 31054770] doi:10.1016/j.mayocp.2019.01.031 e Patients with PSC have a 15% lifetime risk for cholan- giocarcinoma; annual or biannual magnetic reso- nance cholangiopancreatography and carbohydrate Item 15 Answer: A antigen 19-9 measurement is recommended for chol- Educational Objective: Evaluate for inflammatory angiocarcinoma surveillance.

elderly patients with acute constipation and patients with unintentional weight loss, family history of colo- e Primary sclerosing cholangitis (PSC) is associated rectal cancer, unexplained anemia, and age older than with inflammatory bowel disease (IBD) in approxi- 50 years with no previous colonoscopy. mately 85% of cases; therefore, all patients with PSC without known IBD should have colonoscopy with Bibliography biopsies at the time of PSC diagnosis. Bharucha AE, Wald A. Chronic constipation. Mayo Clin Proc. 2019;94:2340- 2357. [PMID: 31054770] doi:10.1016/j.mayocp.2019.01.031 e Patients with PSC have a 15% lifetime risk for cholan- giocarcinoma; annual or biannual magnetic reso- nance cholangiopancreatography and carbohydrate Item 15 Answer: A antigen 19-9 measurement is recommended for chol- Educational Objective: Evaluate for inflammatory angiocarcinoma surveillance. bowel disease in a patient with primary sclerosing cholangitis. Bibliography The most appropriate management is colonoscopy (Option Bowlus CL, Lim JK, Lindor KD. AGA clinical practice update on surveillance for hepatobiliary cancers in patients with primary sclerosing cholangitis: A). The clinical presentation of primary sclerosing cholan- expert review. Clin Gastroenterol Hepatol. 2019;17:2416-2422. [PMID: gitis (PSC) varies. Many patients are asymptomatic, whereas 31306801] doi:10.1016 /j.cgh.2019.07.011

bowel disease in a patient with primary sclerosing cholangitis. Bibliography The most appropriate management is colonoscopy (Option Bowlus CL, Lim JK, Lindor KD. AGA clinical practice update on surveillance for hepatobiliary cancers in patients with primary sclerosing cholangitis: A). The clinical presentation of primary sclerosing cholan- expert review. Clin Gastroenterol Hepatol. 2019;17:2416-2422. [PMID: gitis (PSC) varies. Many patients are asymptomatic, whereas 31306801] doi:10.1016 /j.cgh.2019.07.011 114

Answers and Critiques EC] Item 16 Answer: B Bibliography Crockett SD, Wani S, Gardner TB, et al; American Gastroenterological Educational Objective: Treat acute pancreatitis with Association Institute Clinical Guidelines Committee. American initiation of oral feeding. Gastroenterological Association Institute guideline on initial manage- ment of acute pancreatitis. Gastroenterology. 2018;154:1096-1101. [PMID: The most appropriate management is initiation of oral feeding 29409760] doi:10.1053/j.gastro.2018.01.032 (Option B). The patient has acute pancreatitis. The diagnosis of acute pancreatitis requires two of the following three crite- ria: (1) acute-onset abdominal pain characteristic of pancre- Item 17 Answer: D atitis, (2) serum lipase or amylase levels elevated at least three Educational Objective: Screen for Barrett esophagus. times the upper limit of normal, and (3) characteristic imag- ing findings. She received intravenous resuscitation overnight, The most appropriate management is upper endoscopy which typically consists of 250 to 500 mL/h of normal saline (Option D). This patient has longstanding (5 years) gas- or lactated Ringer solution, with fluid boluses as needed for troesophageal reflux disease (GERD) along with multiple wn

which typically consists of 250 to 500 mL/h of normal saline (Option D). This patient has longstanding (5 years) gas- or lactated Ringer solution, with fluid boluses as needed for troesophageal reflux disease (GERD) along with multiple wn severe volume depletion. Treatment with intravenous fluids risk factors for esophageal cancer, including male sex, age a = should be aimed at avoiding hypovolemia and maintaining older than 50 years, hiatal hernia, obesity with intraab- = adequate organ perfusion. Goal-directed therapy allows for dominal distribution of fat, and tobacco use. Endoscopy to ‘iS Oo titration of fluids to particular biochemical and clinical tar- assess for Barrett esophagus is indicated. The diagnosis of sc gets, including blood pressure, pulse rate, urine output, blood Barrett esophagus is confirmed by the finding of salmon- = cs urea nitrogen, and hematocrit. This patient initially had risk colored mucosa on endoscopy with columnar epithelium wn hoe factors for severe disease, including a hematocrit greater than with acid-mucin-containing goblet cells on histopathology. o

severe volume depletion. Treatment with intravenous fluids risk factors for esophageal cancer, including male sex, age a = should be aimed at avoiding hypovolemia and maintaining older than 50 years, hiatal hernia, obesity with intraab- = adequate organ perfusion. Goal-directed therapy allows for dominal distribution of fat, and tobacco use. Endoscopy to ‘iS Oo titration of fluids to particular biochemical and clinical tar- assess for Barrett esophagus is indicated. The diagnosis of sc gets, including blood pressure, pulse rate, urine output, blood Barrett esophagus is confirmed by the finding of salmon- = cs urea nitrogen, and hematocrit. This patient initially had risk colored mucosa on endoscopy with columnar epithelium wn hoe factors for severe disease, including a hematocrit greater than with acid-mucin-containing goblet cells on histopathology. o Barrett esophagus progresses as follows: intestinal metapla- = 44%, which has improved with volume resuscitation. Overall, vn = her pain is improving and oral feeding should therefore be sia, indefinite for dysplasia, low-grade dysplasia, high-grade q

Barrett esophagus progresses as follows: intestinal metapla- = 44%, which has improved with volume resuscitation. Overall, vn = her pain is improving and oral feeding should therefore be sia, indefinite for dysplasia, low-grade dysplasia, high-grade q considered. Patients with acute pancreatitis should resume dysplasia, intramucosal carcinoma, and, finally, invasive feeding when pain improves and any nausea or vomiting sub- adenocarcinoma. Patients with high-grade dysplasia and sides. Oral feeding is preferred, and guidelines recommend confirmed low-grade dysplasia should undergo treatment to starting oral feeding within 24 hours. eradicate all neoplastic and at-risk epithelium. Patients with If patients with acute pancreatitis do not tolerate oral Barrett esophagus without dysplasia should undergo surveil- feeding, enteral tube feeding (Option A) should be considered lance endoscopy every 3 to 5 years to monitor for dysplasia or within 72 hours. Historically, this approach included place- precancerous changes. ment of a nasojejunal tube to avoid stimulation of the pancreas. Bariatric surgery (Option A) might be a reasonable More recent data suggest that nasogastric tube placement and option to treat this patient’s obesity. However, before that feedings are easier to administer than nasojejunal feeding decision is made, screening this higher-risk patient for and are as efficacious. In this patient, however, oral feeding esophageal cancer should be performed and cancer should should be attempted before enteral feeding is considered. be treated, if found. In the past, management of acute pancreatitis included In the setting of GERD, an esophageal motility study

and are as efficacious. In this patient, however, oral feeding esophageal cancer should be performed and cancer should should be attempted before enteral feeding is considered. be treated, if found. In the past, management of acute pancreatitis included In the setting of GERD, an esophageal motility study keeping patients on nothing-by-mouth status (Option C) to (Option B), such as esophageal manometry, would be indi- prevent stimulation of the pancreas. However, more recent evi- cated to rule out a motility disorder before antireflux surgery. dence has demonstrated a benefit to early feeding; this approach This patient reports good symptom control with medical may promote a healthy mucosal barrier and avoid translocation therapy, however, and does not require antireflux surgery. of gut bacteria, which can result in local and systemic infection. Furthermore, he has no other symptoms, such as dysphagia, Transfusion of packed red blood cells (Option D) is not that suggest a motility disorder. Therefore, a motility study required at this time. Although complications of pancreati- is not indicated. tis may include gastrointestinal bleeding (e.g., splenic vein Surgery is not required because this patient’s GERD is thrombus leading to varices or pseudoaneurysm formation currently well controlled with medical therapy. Surgery is followed by rupture of an arterial wall), this patient is hemo- infrequently required for GERD; indications include fail- dynamically stable and does not exhibit signs or symptoms ure of optimal proton pump inhibitor therapy, desire to of acute gastrointestinal bleeding. She was intravascularly stop medication, and intolerable medication side effects. depleted at the time of hospitalization, and fluid resuscita- Surgical treatments for GERD are laparoscopic fundopli-

dynamically stable and does not exhibit signs or symptoms ure of optimal proton pump inhibitor therapy, desire to of acute gastrointestinal bleeding. She was intravascularly stop medication, and intolerable medication side effects. depleted at the time of hospitalization, and fluid resuscita- Surgical treatments for GERD are laparoscopic fundopli- tion led to an expected decrease in hematocrit. cation (Option C) or bariatric surgery for obesity, as well as magnetic sphincter augmentation (a magnetic ring is placed around the lower esophageal sphincter without sur- e Patients with acute pancreatitis should resume oral gical alteration of the stomach). Surgery is most effective in feedings when pain improves and any nausea or vom- patients with typical symptoms of heartburn and regurgi- iting subsides. tation that respond to therapy. However, about one third of patients require resumption of a proton pump inhibitor 5 to e If patients with acute pancreatitis do not tolerate oral 10 years after surgery. Postoperative complications include feeding, enteral feeding should be considered within dysphagia, diarrhea, and inability to belch because of a tight 72 hours. fundoplication. 115

Answers and Critiques e Men with gastroesophageal reflux disease symptoms e The mainstay of treatment of autoimmune hepatitis is for 5 years and additional risk factors (nocturnal reflux immunosuppression with prednisone or a combination symptoms, hiatal hernia, elevated BMI, intra-abdominal of prednisone and azathioprine. distribution of body fat, tobacco use) should be ¢ Because autoimmune hepatitis has a high rate of screened for Barrett esophagus. relapse, therapy is recommended for at least 2 to 3 years before discontinuation of the medications. Bibliography Clermont M, Falk GW. Clinical guidelines update on the diagnosis and man- Bibliography agement of Barrett’s esophagus. Dig Dis Sci. 2018;63:2122-2128. [PMID: 29671159] doi:10.1007/s10620-018-5070-z Liwinski T, Schramm C. Autoimmune hepatitis—update on clinical man- agement in 2017. Clin Res Hepatol Gastroenterol. 2017;41:617-625. [PMID: 28882739] doi:10.1016/j.clinre.2017.07.002 > = wn Item 18 Answer: A = @o Item 19 Answer: C = Educational Objective: Treat autoimmune hepatitis. wn gy Educational Objective: Diagnose colonic ischemia. = The most appropriate management is continuation of immu- 2. nosuppressant therapy (Option A). Autoimmune hepatitis is The most likely diagnosis is colonic ischemia (Option C). (=) =e a chronic, inflammatory liver disease that has variable pre- This form of ischemic bowel disease is the most common a. 2 sentation, from asymptomatic elevation of aminotransferase and usually results from a nonocclusive low-flow state in = @o levels to extrahepatic symptoms (e.g., myalgia and malaise) to microvessels. The term colonic ischemia is preferred to ische- n” acute liver failure. Diagnosis is based on laboratory test results, mic colitis because some patients do not have a documented including the presence of antinuclear and smooth-muscle inflammatory phase of disease. Risk factors for colonic ische- antibodies and elevated IgG levels, exclusion of other diag- mia include age (>60 years), female sex, vasoconstrictive and noses (e.g., Wilson disease, viral hepatitis, and drug-induced antihypertension medications, constipation, and thrombo- liver injury), and liver biopsy. Patients with severe presenta- philia. Colonic ischemia presents with abrupt onset of lower tions require management by a hepatologist. The mainstay abdominal discomfort that is mild to moderate and cramping, of treatment is immunosuppression. Induction of remission followed within 24 hours by hematochezia (passage of fresh is typically with prednisone or a combination of prednisone blood or clots from the colon). Physical examination usually and azathioprine. Depending on response, maintenance ther- reveals lower abdominal tenderness over the involved colonic apy may consist of prednisone or azathioprine monotherapy segment without peritoneal signs. Leukocyte count and blood or combination therapy. Because of the high rate of relapse, urea nitrogen may be mildly elevated. Abdominal CT is indi- therapy is recommended for at least 2 to 3 years. Biochemical cated to assess the severity, phase, and distribution of colonic response may occur within 3 to 8 months of treatment in 85% ischemia. CT findings are nonspecific, including segmental of patients whose disease responds to standard treatment, but bowel wall thickening and pericolonic fat stranding, often in histologic response can lag by several months. Therefore, a the distribution of the “watershed” areas of the colon (splenic liver biopsy is recommended to demonstrate absence of active flexure and rectosigmoid junction). Colonoscopy is the pri- inflammation before cessation of therapy. mary method to diagnose colonic ischemia, usually after CT If the patient is doing well and aminotransferase levels has shown a thickened segment of colon. have normalized, a biopsy is not necessary to monitor therapy Acute diverticulitis (Option A) often presents with col- (Option B). A biopsy is typically performed before attempted icky lower abdominal pain and left-lower-quadrant abdom- withdrawal of immunosuppressant therapy to assess risk for inal tenderness on physical examination. However, acute relapse. This patient has no indication for biopsy at this time. diverticulitis does not present with rectal bleeding, making Normalization of liver test results is insufficient to this diagnosis unlikely. In addition, CT scans in acute diver- determine when it is safe to stop therapy. Stopping immu- ticulitis typically show pericolonic fat stranding of the sig- nosuppressant therapy before completion of at least 2 years moid colon with associated diverticulosis, which is not seen of therapy, regardless of aminotransferase levels, is associ- on this patient’s CT scan. ated with an increased risk for relapse. Therefore, stopping Clostridioides difficile infection (Option B) can mimic azathioprine therapy now and tapering prednisone (Option the presentation of colonic ischemia and must be excluded C) and stopping azathioprine now, tapering prednisone, and by stool tests. However, bloody diarrhea is uncommon in performing a liver biopsy (Option D) are not recommended. C. difficile colitis, and the infection often involves the colon Because of the adverse effects of immunosuppressant ther- in a diffuse fashion rather than the segmental pattern seen apy, indefinite treatment is avoided if possible. Some patients on this patient’s CT scan. will require indefinite maintenance therapy because of Ulcerative colitis (Option D) can present with abdomi- relapsing disease. However, it is too soon to know whether nal pain and bloody stools. However, it usually involves the this patient will remain in remission or relapse after discon- rectum and extends proximally in a continuous and sym- tinuation of immunosuppressant therapy. metric pattern. This patient’s CT scan, showing segmental

e Men with gastroesophageal reflux disease symptoms e The mainstay of treatment of autoimmune hepatitis is for 5 years and additional risk factors (nocturnal reflux immunosuppression with prednisone or a combination symptoms, hiatal hernia, elevated BMI, intra-abdominal of prednisone and azathioprine. distribution of body fat, tobacco use) should be ¢ Because autoimmune hepatitis has a high rate of screened for Barrett esophagus. relapse, therapy is recommended for at least 2 to 3 years before discontinuation of the medications. Bibliography Clermont M, Falk GW. Clinical guidelines update on the diagnosis and man- Bibliography agement of Barrett’s esophagus. Dig Dis Sci. 2018;63:2122-2128. [PMID: 29671159] doi:10.1007/s10620-018-5070-z Liwinski T, Schramm C. Autoimmune hepatitis—update on clinical man- agement in 2017. Clin Res Hepatol Gastroenterol. 2017;41:617-625. [PMID: 28882739] doi:10.1016/j.clinre.2017.07.002 > = wn Item 18 Answer: A = @o Item 19 Answer: C = Educational Objective: Treat autoimmune hepatitis. wn gy Educational Objective: Diagnose colonic ischemia. = The most appropriate management is continuation of immu- 2. nosuppressant therapy (Option A). Autoimmune hepatitis is The most likely diagnosis is colonic ischemia (Option C). (=) =e a chronic, inflammatory liver disease that has variable pre- This form of ischemic bowel disease is the most common a. 2 sentation, from asymptomatic elevation of aminotransferase and usually results from a nonocclusive low-flow state in = @o levels to extrahepatic symptoms (e.g., myalgia and malaise) to microvessels. The term colonic ischemia is preferred to ische- n” acute liver failure. Diagnosis is based on laboratory test results, mic colitis because some patients do not have a documented including the presence of antinuclear and smooth-muscle inflammatory phase of disease. Risk factors for colonic ische- antibodies and elevated IgG levels, exclusion of other diag- mia include age (>60 years), female sex, vasoconstrictive and noses (e.g., Wilson disease, viral hepatitis, and drug-induced antihypertension medications, constipation, and thrombo- liver injury), and liver biopsy. Patients with severe presenta- philia. Colonic ischemia presents with abrupt onset of lower tions require management by a hepatologist. The mainstay abdominal discomfort that is mild to moderate and cramping, of treatment is immunosuppression. Induction of remission followed within 24 hours by hematochezia (passage of fresh is typically with prednisone or a combination of prednisone blood or clots from the colon). Physical examination usually and azathioprine. Depending on response, maintenance ther- reveals lower abdominal tenderness over the involved colonic apy may consist of prednisone or azathioprine monotherapy segment without peritoneal signs. Leukocyte count and blood or combination therapy. Because of the high rate of relapse, urea nitrogen may be mildly elevated. Abdominal CT is indi- therapy is recommended for at least 2 to 3 years. Biochemical cated to assess the severity, phase, and distribution of colonic response may occur within 3 to 8 months of treatment in 85% ischemia. CT findings are nonspecific, including segmental of patients whose disease responds to standard treatment, but bowel wall thickening and pericolonic fat stranding, often in histologic response can lag by several months. Therefore, a the distribution of the “watershed” areas of the colon (splenic liver biopsy is recommended to demonstrate absence of active flexure and rectosigmoid junction). Colonoscopy is the pri- inflammation before cessation of therapy. mary method to diagnose colonic ischemia, usually after CT If the patient is doing well and aminotransferase levels has shown a thickened segment of colon. have normalized, a biopsy is not necessary to monitor therapy Acute diverticulitis (Option A) often presents with col- (Option B). A biopsy is typically performed before attempted icky lower abdominal pain and left-lower-quadrant abdom- withdrawal of immunosuppressant therapy to assess risk for inal tenderness on physical examination. However, acute relapse. This patient has no indication for biopsy at this time. diverticulitis does not present with rectal bleeding, making Normalization of liver test results is insufficient to this diagnosis unlikely. In addition, CT scans in acute diver- determine when it is safe to stop therapy. Stopping immu- ticulitis typically show pericolonic fat stranding of the sig- nosuppressant therapy before completion of at least 2 years moid colon with associated diverticulosis, which is not seen of therapy, regardless of aminotransferase levels, is associ- on this patient’s CT scan. ated with an increased risk for relapse. Therefore, stopping Clostridioides difficile infection (Option B) can mimic azathioprine therapy now and tapering prednisone (Option the presentation of colonic ischemia and must be excluded C) and stopping azathioprine now, tapering prednisone, and by stool tests. However, bloody diarrhea is uncommon in performing a liver biopsy (Option D) are not recommended. C. difficile colitis, and the infection often involves the colon Because of the adverse effects of immunosuppressant ther- in a diffuse fashion rather than the segmental pattern seen apy, indefinite treatment is avoided if possible. Some patients on this patient’s CT scan. will require indefinite maintenance therapy because of Ulcerative colitis (Option D) can present with abdomi- relapsing disease. However, it is too soon to know whether nal pain and bloody stools. However, it usually involves the this patient will remain in remission or relapse after discon- rectum and extends proximally in a continuous and sym- tinuation of immunosuppressant therapy. metric pattern. This patient’s CT scan, showing segmental 116

Answers and Critiques thickening of the descending and sigmoid colon with spar- effects of glucocorticoids and the limited extent of disease ing of the rectum, makes ulcerative colitis unlikely, as do the in this patient, oral glucocorticoids would not be an appro- I abrupt symptom onset and older patient age. priate treatment. ¢ Colonic ischemia is the most common form of e Patients with ulcerative proctitis should receive topi- ischemic bowel disease and usually results from a cal therapy with 5-aminosalicylate suppositories; nonocclusive low-flow state in microvessels. once remission is achieved, 5-aminosalicylates are ¢ Colonic ischemia presents with abrupt-onset lower effective in maintaining it.

¢ Colonic ischemia is the most common form of e Patients with ulcerative proctitis should receive topi- ischemic bowel disease and usually results from a cal therapy with 5-aminosalicylate suppositories; nonocclusive low-flow state in microvessels. once remission is achieved, 5-aminosalicylates are ¢ Colonic ischemia presents with abrupt-onset lower effective in maintaining it. abdominal discomfort and cramping, followed within ¢ Combined 5-ASA therapy (oral and topical) is superior 24 hours by hematochezia. for inducing remission in patients with left-sided or extensive ulcerative colitis compared with oral or wn Bibliography topical therapies alone. cf 3 Brandt LJ, Feuerstadt P, Longstreth GF, et al; American College of Gastroenterology. ACG clinical guideline: epidemiology, risk factors, pat- = terns of presentation, diagnosis, and management of colon ischemia (CI). Bibliography = Am J Gastroenterol. 2015;110:18-44; quiz 45. [PMID: 25559486] doi:10. rs) Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: 1038/ajg.2014.395 =) ulcerative colitis in adults. AmJ Gastroenterol. 2019;114:384-413. [PMID: = 30840605] doi:10.14309/ajg.0000000000000152 cs wn Soe o Item 20 Answer: A = wn

abdominal discomfort and cramping, followed within ¢ Combined 5-ASA therapy (oral and topical) is superior 24 hours by hematochezia. for inducing remission in patients with left-sided or extensive ulcerative colitis compared with oral or wn Bibliography topical therapies alone. cf 3 Brandt LJ, Feuerstadt P, Longstreth GF, et al; American College of Gastroenterology. ACG clinical guideline: epidemiology, risk factors, pat- = terns of presentation, diagnosis, and management of colon ischemia (CI). Bibliography = Am J Gastroenterol. 2015;110:18-44; quiz 45. [PMID: 25559486] doi:10. rs) Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: 1038/ajg.2014.395 =) ulcerative colitis in adults. AmJ Gastroenterol. 2019;114:384-413. [PMID: = 30840605] doi:10.14309/ajg.0000000000000152 cs wn Soe o Item 20 Answer: A = wn Educational Objective: Treat ulcerative proctitis with Item 21 Answer: C = <= topical 5-aminosalicylate. Educational Objective: Diagnose hereditary hemochromatosis. The most appropriate treatment is a 5-aminosalicylate (5-ASA) suppository (Option A). Categories of the extent of The most appropriate diagnostic test to perform next is trans- ulcerative colitis include proctitis (within 18 cm of the anal ferrin saturation measurement (Option C). This patient’s verge, distal to the rectosigmoid junction), left-sided colitis elevated ferritin level suggests a diagnosis of hereditary hemo- (extending from the sigmoid to the splenic flexure), and chromatosis, an autosomal recessive disorder of excessive extensive colitis (beyond the splenic flexure). This patient accumulation of iron in the liver due to a mutation in the has findings consistent with mild ulcerative proctitis. Three genes that control hepcidin synthesis. Cirrhosis and cardio- factors must be considered in choosing therapy for ulcerative myopathy are major causes of morbidity; small-joint arthritis colitis: disease severity, distribution of disease, and previ- is common; and diabetes mellitus and other endocrinopathies ous therapies, including response and adherence. 5-ASAs may be seen. Early diagnosis may be made through evaluation are anti-inflammatory medications and the mainstay of of abnormal aminotransferase levels. In these patients, the treatment of mild to moderate ulcerative colitis. Patients diagnosis is suspected by finding elevated transferrin satura- with proctitis should receive topical therapy with 5-ASA tion greater than 45% (guidelines vary) and an elevated serum suppositories. Patients with left-sided colitis should receive ferritin level; diagnosis is confirmed through genetic testing. topical therapy with 5-ASA enemas. In mild to moderate left- Typically, patients have homozygosity of C282Y polymor- sided or extensive ulcerative colitis, combined 5-ASA therapy phism of the HFE gene, but other polymorphisms, such as (oral and topical) is superior for inducing remission com- H63D, may be present. pared with oral or topical therapies alone. Once remission is o,-Antitrypsin (AAT) (Option A) deficiency is an auto- achieved, 5-ASAs are effective in maintaining it. somal co-dominant genetic disorder that results in accumu- A glucocorticoid suppository (Option B) would be effec- lation of a variant protein in the liver. Homozygosity for this tive in inducing remission of ulcerative proctitis, but topical condition may result in liver injury and eventual cirrhosis. 5-ASA therapy is superior for this purpose. Topical gluco- The hepatic accumulation of AAT results in decreased circu- corticoid therapy may be considered in patients with disease lating AAT, leading to lung disease. AAT deficiency does not limited to the rectum but intolerant of topical or oral 5-ASA cause elevations of serum ferritin. therapy. In addition, 5-ASAs are effective in maintenance of MRI with special software is used to noninvasively remission, whereas topical glucocorticoids are effective only assess the extent of cardiac and liver iron overload and gen- for induction. erally obviates the need to perform organ biopsy to quanti- Oral therapy with 5-ASA (Option C) would be less opti- tate iron deposits. Liver biopsy (Option B) is used if it is also mal than topical 5-ASA in this patient given the limited dis- necessary to grade the degree of fibrosis or evaluate for other tribution of disease in the rectum. Oral 5-ASA would be an liver diseases. Liver biopsy is not indicated for this patient option if the patient declines use of a suppository. at this time and is not the appropriate next diagnostic test. Oral glucocorticoids (Option D) are commonly used to Porphyria cutanea tarda is diagnosed by plasma or treat moderate to severe ulcerative colitis and are effective in urine porphyrin measurement (Option D). This disorder is inducing remission. However, given the significant adverse a less common cause of secondary iron overload associated

Educational Objective: Treat ulcerative proctitis with Item 21 Answer: C = <= topical 5-aminosalicylate. Educational Objective: Diagnose hereditary hemochromatosis. The most appropriate treatment is a 5-aminosalicylate (5-ASA) suppository (Option A). Categories of the extent of The most appropriate diagnostic test to perform next is trans- ulcerative colitis include proctitis (within 18 cm of the anal ferrin saturation measurement (Option C). This patient’s verge, distal to the rectosigmoid junction), left-sided colitis elevated ferritin level suggests a diagnosis of hereditary hemo- (extending from the sigmoid to the splenic flexure), and chromatosis, an autosomal recessive disorder of excessive extensive colitis (beyond the splenic flexure). This patient accumulation of iron in the liver due to a mutation in the has findings consistent with mild ulcerative proctitis. Three genes that control hepcidin synthesis. Cirrhosis and cardio- factors must be considered in choosing therapy for ulcerative myopathy are major causes of morbidity; small-joint arthritis colitis: disease severity, distribution of disease, and previ- is common; and diabetes mellitus and other endocrinopathies ous therapies, including response and adherence. 5-ASAs may be seen. Early diagnosis may be made through evaluation are anti-inflammatory medications and the mainstay of of abnormal aminotransferase levels. In these patients, the treatment of mild to moderate ulcerative colitis. Patients diagnosis is suspected by finding elevated transferrin satura- with proctitis should receive topical therapy with 5-ASA tion greater than 45% (guidelines vary) and an elevated serum suppositories. Patients with left-sided colitis should receive ferritin level; diagnosis is confirmed through genetic testing. topical therapy with 5-ASA enemas. In mild to moderate left- Typically, patients have homozygosity of C282Y polymor- sided or extensive ulcerative colitis, combined 5-ASA therapy phism of the HFE gene, but other polymorphisms, such as (oral and topical) is superior for inducing remission com- H63D, may be present. pared with oral or topical therapies alone. Once remission is o,-Antitrypsin (AAT) (Option A) deficiency is an auto- achieved, 5-ASAs are effective in maintaining it. somal co-dominant genetic disorder that results in accumu- A glucocorticoid suppository (Option B) would be effec- lation of a variant protein in the liver. Homozygosity for this tive in inducing remission of ulcerative proctitis, but topical condition may result in liver injury and eventual cirrhosis. 5-ASA therapy is superior for this purpose. Topical gluco- The hepatic accumulation of AAT results in decreased circu- corticoid therapy may be considered in patients with disease lating AAT, leading to lung disease. AAT deficiency does not limited to the rectum but intolerant of topical or oral 5-ASA cause elevations of serum ferritin. therapy. In addition, 5-ASAs are effective in maintenance of MRI with special software is used to noninvasively remission, whereas topical glucocorticoids are effective only assess the extent of cardiac and liver iron overload and gen- for induction. erally obviates the need to perform organ biopsy to quanti- Oral therapy with 5-ASA (Option C) would be less opti- tate iron deposits. Liver biopsy (Option B) is used if it is also mal than topical 5-ASA in this patient given the limited dis- necessary to grade the degree of fibrosis or evaluate for other tribution of disease in the rectum. Oral 5-ASA would be an liver diseases. Liver biopsy is not indicated for this patient option if the patient declines use of a suppository. at this time and is not the appropriate next diagnostic test. Oral glucocorticoids (Option D) are commonly used to Porphyria cutanea tarda is diagnosed by plasma or treat moderate to severe ulcerative colitis and are effective in urine porphyrin measurement (Option D). This disorder is inducing remission. However, given the significant adverse a less common cause of secondary iron overload associated 117

Answers and Critiques with acquired abnormalities in porphyrin metabolism and underlying liver disease, especially hepatitis C virus infec- e The diagnosis of irritable bowel syndrome requires tion. Porphyria cutanea tarda is characterized by cutaneous symptoms of recurrent abdominal pain at least 1 day blisters, often on the hands, and hypertrichosis. This patient a week for 3 months, along with at least two of the has no findings of porphyria cutanea tarda. following: pain related to defecation, change in stool frequency, or change in stool consistency. e Hereditary hemochromatosis is suggested by the pres- e Fecal calprotectin testing to assess for inflammatory ence of an elevated serum ferritin level and transferrin bowel disease and stool testing for giardiasis and saturation. celiac disease should be considered in patients with e The diagnosis of hereditary hemochromatosis is con- chronic diarrhea. firmed by testing for mutations in the HFE gene. > Bibliography = wn Bibliography Smalley W, Falck-Ytter C, Carrasco-Labra A, et al. AGA clinical practice = guidelines on the laboratory evaluation of functional diarrhea and @o Kowdley KV, Brown KE, Ahn J, et al. ACG clinical guideline: hereditary = diarrhea-predominant irritable bowel syndrome in adults (IBS-D). wn hemochromatosis. Am J Gastroenterol. 2019;114:1202-1218. [PMID: Gastroenterology. 2019;157:851-854. [PMID: 31302098] doi:10.1053/ pel) 31335359] doi:10.14309/ajg.0000000000000315 j.gastro.2019.07.004 i] Qa. a me Item 22 Answer: D Item 23 Answer: C =. 2 SS Educational Objective: Diagnose irritable bowel Educational Objective: Evaluate unstable lower Oo syndrome. gastrointestinal bleeding. “a

with acquired abnormalities in porphyrin metabolism and underlying liver disease, especially hepatitis C virus infec- e The diagnosis of irritable bowel syndrome requires tion. Porphyria cutanea tarda is characterized by cutaneous symptoms of recurrent abdominal pain at least 1 day blisters, often on the hands, and hypertrichosis. This patient a week for 3 months, along with at least two of the has no findings of porphyria cutanea tarda. following: pain related to defecation, change in stool frequency, or change in stool consistency. e Hereditary hemochromatosis is suggested by the pres- e Fecal calprotectin testing to assess for inflammatory ence of an elevated serum ferritin level and transferrin bowel disease and stool testing for giardiasis and saturation. celiac disease should be considered in patients with e The diagnosis of hereditary hemochromatosis is con- chronic diarrhea. firmed by testing for mutations in the HFE gene. > Bibliography = wn Bibliography Smalley W, Falck-Ytter C, Carrasco-Labra A, et al. AGA clinical practice = guidelines on the laboratory evaluation of functional diarrhea and @o Kowdley KV, Brown KE, Ahn J, et al. ACG clinical guideline: hereditary = diarrhea-predominant irritable bowel syndrome in adults (IBS-D). wn hemochromatosis. Am J Gastroenterol. 2019;114:1202-1218. [PMID: Gastroenterology. 2019;157:851-854. [PMID: 31302098] doi:10.1053/ pel) 31335359] doi:10.14309/ajg.0000000000000315 j.gastro.2019.07.004 i] Qa. a me Item 22 Answer: D Item 23 Answer: C =. 2 SS Educational Objective: Diagnose irritable bowel Educational Objective: Evaluate unstable lower Oo syndrome. gastrointestinal bleeding. “a The most appropriate diagnostic test is stool testing for Giar- The most appropriate next diagnostic test is CT angiography dia (Option D). The patient meets the clinical criteria for (CTA) (Option C). This patient has active lower gastrointes- irritable bowel syndrome with abdominal pain at least 1 day tinal bleeding with associated hemodynamic instability. In a week for 3 months and at least two of the following: pain addition to continued intravenous fluid resuscitation, rapid related to defecation, change in stool frequency, or change identification of the bleeding source is essential. CTA is the in stool consistency. IBS is a common cause of diarrhea and study of choice in this setting because it can be performed can be diagnosed on clinical grounds, including history quickly and has the greatest likelihood of localizing the site and physical examination. Although an extensive workup of bleeding (with an accuracy of nearly 100%). CTA can detect for structural abnormalities is not indicated in the absence bleeding at a rate of 0.3 mL/min. of alarm symptoms, fecal calprotectin testing to assess for Although conventional angiography (Option A) allows inflammatory bowel disease and stool testing for giardiasis transarterial embolization at time of diagnosis, it is limited and celiac disease should be considered in patients with by the need for a higher rate of bleeding (0.5-1.0 mL/min) chronic diarrhea. than that for CTA to identify a bleeding source. Complica- Abdominal ultrasonography (Option A) visualizes the tions of conventional angiography, including acute kidney gallbladder and biliary tree, and its role in the evaluation injury and thromboembolic events, have been reported in of abdominal pain is principally to exclude choledocholi- up to 10% of case series. Catheter angiography and possible thiasis or biliary obstruction. Biliary colic pain is typically embolization should be performed as soon as possible after postprandial, particularly after fatty meals. Diarrhea is not a a positive CTA finding. feature of biliary colic. Given the patient’s symptoms, ultra- In hemodynamically stable patients without evidence sonography is not indicated. of rapid bleeding, colonoscopy (Option B) is the first study Colonoscopy with biopsy of the right and left colon of choice in patients with lower gastrointestinal bleeding. It (Option B) is performed to investigate for microscopic colitis, should be performed within 24 hours of presentation after a form of inflammatory bowel disease that most commonly adequate colon preparation. Colonoscopy identifies a source affects women in the seventh or eighth decades of life. It is of bleeding in two thirds of patients. characterized by watery diarrhea and is sometimes associ- Upper endoscopy (Option D) should be performed ated with medication use, including NSAIDs. Microscopic immediately if no bleeding source is identified by initial colitis does not have to be ruled out in a patient meeting CTA. Upper endoscopy may be the first procedure per- clinical criteria for IBS without alarm symptoms. formed if suspicion for upper gastrointestinal bleeding is Escherichia coli 0157:H7 (Option C) can cause acute high. Upper gastrointestinal bleeding is a consideration inflammatory diarrhea via toxin-mediated injury to the in this patient taking aspirin and an NSAID. However, the colon. Clinical manifestations include bloody diarrhea, presence of bilious fluid without blood following nasogas- tenesmus, and leukocytosis. This condition can progress to tric tube lavage suggests that the pylorus is open and there hemolytic uremic syndrome. The chronic time course and is no active upper gastrointestinal bleeding proximal to the nonbloody nature of diarrhea in this patient make this diag- ligament of Treitz. In this patient, CTA is the preferred initial nosis unlikely. diagnostic test.

The most appropriate diagnostic test is stool testing for Giar- The most appropriate next diagnostic test is CT angiography dia (Option D). The patient meets the clinical criteria for (CTA) (Option C). This patient has active lower gastrointes- irritable bowel syndrome with abdominal pain at least 1 day tinal bleeding with associated hemodynamic instability. In a week for 3 months and at least two of the following: pain addition to continued intravenous fluid resuscitation, rapid related to defecation, change in stool frequency, or change identification of the bleeding source is essential. CTA is the in stool consistency. IBS is a common cause of diarrhea and study of choice in this setting because it can be performed can be diagnosed on clinical grounds, including history quickly and has the greatest likelihood of localizing the site and physical examination. Although an extensive workup of bleeding (with an accuracy of nearly 100%). CTA can detect for structural abnormalities is not indicated in the absence bleeding at a rate of 0.3 mL/min. of alarm symptoms, fecal calprotectin testing to assess for Although conventional angiography (Option A) allows inflammatory bowel disease and stool testing for giardiasis transarterial embolization at time of diagnosis, it is limited and celiac disease should be considered in patients with by the need for a higher rate of bleeding (0.5-1.0 mL/min) chronic diarrhea. than that for CTA to identify a bleeding source. Complica- Abdominal ultrasonography (Option A) visualizes the tions of conventional angiography, including acute kidney gallbladder and biliary tree, and its role in the evaluation injury and thromboembolic events, have been reported in of abdominal pain is principally to exclude choledocholi- up to 10% of case series. Catheter angiography and possible thiasis or biliary obstruction. Biliary colic pain is typically embolization should be performed as soon as possible after postprandial, particularly after fatty meals. Diarrhea is not a a positive CTA finding. feature of biliary colic. Given the patient’s symptoms, ultra- In hemodynamically stable patients without evidence sonography is not indicated. of rapid bleeding, colonoscopy (Option B) is the first study Colonoscopy with biopsy of the right and left colon of choice in patients with lower gastrointestinal bleeding. It (Option B) is performed to investigate for microscopic colitis, should be performed within 24 hours of presentation after a form of inflammatory bowel disease that most commonly adequate colon preparation. Colonoscopy identifies a source affects women in the seventh or eighth decades of life. It is of bleeding in two thirds of patients. characterized by watery diarrhea and is sometimes associ- Upper endoscopy (Option D) should be performed ated with medication use, including NSAIDs. Microscopic immediately if no bleeding source is identified by initial colitis does not have to be ruled out in a patient meeting CTA. Upper endoscopy may be the first procedure per- clinical criteria for IBS without alarm symptoms. formed if suspicion for upper gastrointestinal bleeding is Escherichia coli 0157:H7 (Option C) can cause acute high. Upper gastrointestinal bleeding is a consideration inflammatory diarrhea via toxin-mediated injury to the in this patient taking aspirin and an NSAID. However, the colon. Clinical manifestations include bloody diarrhea, presence of bilious fluid without blood following nasogas- tenesmus, and leukocytosis. This condition can progress to tric tube lavage suggests that the pylorus is open and there hemolytic uremic syndrome. The chronic time course and is no active upper gastrointestinal bleeding proximal to the nonbloody nature of diarrhea in this patient make this diag- ligament of Treitz. In this patient, CTA is the preferred initial nosis unlikely. diagnostic test. 118

Answers and Critiques of the stomach. Band ligation is effective in these types of varices because of their predictable anatomy and more e For active lower gastrointestinal bleeding with associ- superficial location, which permits thorough eradication. In ated hemodynamic instability, CT angiography is the this patient, band ligation is not a good option because vari- study of choice. ces in the gastric fundus are not amenable to this approach. e For active lower gastrointestinal bleeding, catheter angiography and possible embolization should be performed as soon as possible after positive results on e In patients with gastric varices, contrast-enhanced CT angiography. cross-sectional imaging should be performed to determine the best treatment.

of the stomach. Band ligation is effective in these types of varices because of their predictable anatomy and more e For active lower gastrointestinal bleeding with associ- superficial location, which permits thorough eradication. In ated hemodynamic instability, CT angiography is the this patient, band ligation is not a good option because vari- study of choice. ces in the gastric fundus are not amenable to this approach. e For active lower gastrointestinal bleeding, catheter angiography and possible embolization should be performed as soon as possible after positive results on e In patients with gastric varices, contrast-enhanced CT angiography. cross-sectional imaging should be performed to determine the best treatment. Bibliography Gralnek IM, Neeman Z, Strate LL. Acute lower gastrointestinal bleeding. Bibliography N Engl J Med. 2017;376:1054-1063. [PMID: 28296600] doi:10.1056/ Koch D. Update in the management of gastric varices. Curr Opin wn NEJMcp1603455 Gastroenterol. 2016;32:166-71. [PMID: 27054775] doi:10.1097/MOG. a =] 0000000000000267 = 4 en Item 24 Answer: A 1S) <3 Educational Objective: Evaluate gastric varices in a Item 25 Answer: A e © patient with cirrhosis. Educational Objective: Treat colon cancer in patient wn = with familial adenomatous polyposis. o The most appropriate next step in management is abdom- 2 wn inal CT with contrast (Option A). Gastric varices occur in The most appropriate treatment is colectomy (Option A). = up to 20% of patients with cirrhosis and can be challenging This patient likely has a de novo mutation in the APC gene =

Bibliography Gralnek IM, Neeman Z, Strate LL. Acute lower gastrointestinal bleeding. Bibliography N Engl J Med. 2017;376:1054-1063. [PMID: 28296600] doi:10.1056/ Koch D. Update in the management of gastric varices. Curr Opin wn NEJMcp1603455 Gastroenterol. 2016;32:166-71. [PMID: 27054775] doi:10.1097/MOG. a =] 0000000000000267 = 4 en Item 24 Answer: A 1S) <3 Educational Objective: Evaluate gastric varices in a Item 25 Answer: A e © patient with cirrhosis. Educational Objective: Treat colon cancer in patient wn = with familial adenomatous polyposis. o The most appropriate next step in management is abdom- 2 wn inal CT with contrast (Option A). Gastric varices occur in The most appropriate treatment is colectomy (Option A). = up to 20% of patients with cirrhosis and can be challenging This patient likely has a de novo mutation in the APC gene = to manage. Typically, octreotide is administered to reduce causing familial adenomatous polyposis (FAP). Classic FAP portal pressures, and antibiotics are provided to reduce risk is characterized by more than 100 adenomatous polyps in for infectious complications of gastrointestinal bleeding. the colon, and lifetime risk for colon cancer approaches These complications include bacteremia, which can increase 100%. Other intestinal manifestations of FAP include benign morbidity and mortality from variceal bleeding. Treatment fundic gland polyps of the stomach, duodenal adenomas, options for gastric varices along the greater curvature of the and ampullary adenomas. Extracolonic manifestations stomach depend on the anatomy of the abdominal vascula- include desmoid tumors, papillary thyroid cancer, extra ture. For isolated gastric varices due to splenic vein throm- teeth, cysts, osteomas, and congenital hypertrophy of the bosis, splenectomy can be performed to decompress varices. retinal pigmented epithelium. De novo mutations are found If the portal vein is patent and a suitable splenorenal shunt is in up to 25% of FAP cases. The patient should undergo available, balloon-occluded retrograde transvenous oblitera- genetic counseling and germline genetic testing, which tion of varices can be considered. If the anatomy of the hepatic would confirm a diagnosis of FAP. Her unaffected parents veins and portal vein branches is favorable, a transjugular should also undergo genetic testing to confirm that this intrahepatic portosystemic shunt may be an option. To deter- finding is a de novo mutation. If her parents have FAP, they mine the best therapy, contrast-enhanced cross-sectional should undergo upper endoscopy with a side-viewing imaging is required. Therefore, abdominal CT with contrast is endoscope (duodenoscope), colonoscopy, and thyroid the best next action. ultrasonography. Because mutations in APC behave in an Gastric fundal varices are much more frequent in autosomal dominant fashion, each child of an affected indi- patients with portal vein and/or splenic vein thrombosis, vidual should be counseled that they have a 50% chance of and the finding of these varices should prompt cross-sec- inheriting the APC mutation. The timing of genetic testing tional imaging to investigate the presence of such thrombo- for offspring can be discussed with providers, but sigmoid- ses. Endovascular obliteration is an option in patients with a oscopy or colonoscopy should begin at ages 10 to 12 years. large gastro- or splenorenal collateral; therefore, cross-sec- If adenomas are detected, even children who have not had tional vascular imaging with contrast-enhanced CT is pre- genetic testing should be screened as if they have a con- ferred over abdominal ultrasonography (Option B) because firmed mutation. The treatment of choice in FAP is colec- it would investigate both thrombosis and the presence of tomy. The surgical approach depends on the rectal polyp such collaterals and would guide management accordingly. burden. In this patient, the rectum is relatively spared, and Balloon tamponade (Option C) provides only short- the patient may be a candidate for a subtotal colectomy with term tamponade of bleeding varices. It is best used in unsta- sparing of the rectum. Following colectomy, she should have ble patients as a temporizing device while more definitive annual sigmoidoscopy, as well as surveillance of her upper therapy is pending. In this hemodynamically stable patient, gastrointestinal tract and thyroid. balloon tamponade is not necessary. Endoscopic removal of the adenocarcinoma (Option B) Band ligation (Option D) is an effective therapy for is not recommended because it would not provide adequate esophageal varices, as well as varices in the gastric cardia, lymph node sampling and would leave the remaining colon which extend from the esophagus into the lesser curvature at risk for future cancers.

to manage. Typically, octreotide is administered to reduce causing familial adenomatous polyposis (FAP). Classic FAP portal pressures, and antibiotics are provided to reduce risk is characterized by more than 100 adenomatous polyps in for infectious complications of gastrointestinal bleeding. the colon, and lifetime risk for colon cancer approaches These complications include bacteremia, which can increase 100%. Other intestinal manifestations of FAP include benign morbidity and mortality from variceal bleeding. Treatment fundic gland polyps of the stomach, duodenal adenomas, options for gastric varices along the greater curvature of the and ampullary adenomas. Extracolonic manifestations stomach depend on the anatomy of the abdominal vascula- include desmoid tumors, papillary thyroid cancer, extra ture. For isolated gastric varices due to splenic vein throm- teeth, cysts, osteomas, and congenital hypertrophy of the bosis, splenectomy can be performed to decompress varices. retinal pigmented epithelium. De novo mutations are found If the portal vein is patent and a suitable splenorenal shunt is in up to 25% of FAP cases. The patient should undergo available, balloon-occluded retrograde transvenous oblitera- genetic counseling and germline genetic testing, which tion of varices can be considered. If the anatomy of the hepatic would confirm a diagnosis of FAP. Her unaffected parents veins and portal vein branches is favorable, a transjugular should also undergo genetic testing to confirm that this intrahepatic portosystemic shunt may be an option. To deter- finding is a de novo mutation. If her parents have FAP, they mine the best therapy, contrast-enhanced cross-sectional should undergo upper endoscopy with a side-viewing imaging is required. Therefore, abdominal CT with contrast is endoscope (duodenoscope), colonoscopy, and thyroid the best next action. ultrasonography. Because mutations in APC behave in an Gastric fundal varices are much more frequent in autosomal dominant fashion, each child of an affected indi- patients with portal vein and/or splenic vein thrombosis, vidual should be counseled that they have a 50% chance of and the finding of these varices should prompt cross-sec- inheriting the APC mutation. The timing of genetic testing tional imaging to investigate the presence of such thrombo- for offspring can be discussed with providers, but sigmoid- ses. Endovascular obliteration is an option in patients with a oscopy or colonoscopy should begin at ages 10 to 12 years. large gastro- or splenorenal collateral; therefore, cross-sec- If adenomas are detected, even children who have not had tional vascular imaging with contrast-enhanced CT is pre- genetic testing should be screened as if they have a con- ferred over abdominal ultrasonography (Option B) because firmed mutation. The treatment of choice in FAP is colec- it would investigate both thrombosis and the presence of tomy. The surgical approach depends on the rectal polyp such collaterals and would guide management accordingly. burden. In this patient, the rectum is relatively spared, and Balloon tamponade (Option C) provides only short- the patient may be a candidate for a subtotal colectomy with term tamponade of bleeding varices. It is best used in unsta- sparing of the rectum. Following colectomy, she should have ble patients as a temporizing device while more definitive annual sigmoidoscopy, as well as surveillance of her upper therapy is pending. In this hemodynamically stable patient, gastrointestinal tract and thyroid. balloon tamponade is not necessary. Endoscopic removal of the adenocarcinoma (Option B) Band ligation (Option D) is an effective therapy for is not recommended because it would not provide adequate esophageal varices, as well as varices in the gastric cardia, lymph node sampling and would leave the remaining colon which extend from the esophagus into the lesser curvature at risk for future cancers. 119

Left hemicolectomy (Option C) may be considered of this condition is for a suspected lesion being monitored for sporadic colon cancer but not for FAP because of the for growth at short intervals in the context of potential liver increased cancer risk in the remaining colon. transplantation. In this patient with potentially resectable Sulindac (Option D) is an NSAID that may be con- hepatocellular carcinoma, surveillance is not warranted. sidered to reduce rectal polyp burden after surgery or as chemoprevention in addition to endoscopic management of colon polyps. It is not appropriate therapy for colon cancer. ¢ Patients with hepatocellular carcinoma who have well-compensated cirrhosis, no symptoms referable to liver disease, no evidence of portal hypertension, and e The treatment of choice in familial adenomatous normal liver function markers should be referred for polyposis is colectomy. surgical resection.

Left hemicolectomy (Option C) may be considered of this condition is for a suspected lesion being monitored for sporadic colon cancer but not for FAP because of the for growth at short intervals in the context of potential liver increased cancer risk in the remaining colon. transplantation. In this patient with potentially resectable Sulindac (Option D) is an NSAID that may be con- hepatocellular carcinoma, surveillance is not warranted. sidered to reduce rectal polyp burden after surgery or as chemoprevention in addition to endoscopic management of colon polyps. It is not appropriate therapy for colon cancer. ¢ Patients with hepatocellular carcinoma who have well-compensated cirrhosis, no symptoms referable to liver disease, no evidence of portal hypertension, and e The treatment of choice in familial adenomatous normal liver function markers should be referred for polyposis is colectomy. surgical resection. e Liver transplantation for hepatocellular cancer is the > Bibliography best therapy for patients who also have portal hyper- i] w Kidambi TD, Kohli DR, Samadder NJ, et al. Hereditary polyposis syndromes. Curr Treat Options Gastroenterol. 2019;17:650-665. [PMID: 31705372] tension or features of liver dysfunction. = @o doi:10.1007/s11938-019-00251-4 = wn Bibliography » = Marrero JA, Kulik LM, Sirlin CB, et al. Diagnosis, staging, and management a of hepatocellular carcinoma: 2018 practice guidance by the American (=) Item 26 Answer: 8B Association for the Study of Liver Diseases. Hepatology. 2018;68:723-750. = [PMID: 29624699] doi:10.1002/hep.29913 =. Educational Objective: Treat hepatocellular carcinoma 2 with surgical resection. = @o wn The most appropriate management is surgical resection Item 27 Answer: C (Option B). Patients with hepatocellular carcinoma who have Educational Objective: Diagnose small-duct primary well-compensated cirrhosis, no symptoms referable to liver sclerosing cholangitis. disease, no evidence of portal hypertension, and normal liver function markers, like this patient, typically can tolerate sur- The most appropriate next step in management is liver biopsy gical resection. The left liver is smaller than the right liver; (Option C). Primary sclerosing cholangitis (PSC) is an auto- therefore, in this patient, resection of cancer that spares the immune fibroinflammatory disease of the intrahepatic bile right liver should be undertaken. Screening for hepatocellular ducts; it most commonly affects the large ducts but can carcinoma is important in patients with cirrhosis, even those also affect the small intrahepatic ducts. It is associated with who have undergone successful antiviral therapy for hepa- inflammatory bowel disease in about 85% of cases and occurs titis C virus infection. Although successful antiviral therapy in approximately 7.5% of patients with ulcerative colitis. PSC decreases the risk for hepatocellular carcinoma, the risk is can be diagnosed with magnetic resonance cholangiopan- not eliminated and screening with abdominal ultrasonogra- creatography (MRCP). Althougha liver biopsy is rarely needed phy should be performed indefinitely at 6-month intervals. to diagnose PSC, diagnosis of small-duct PSC requires a liver Patients who undergo surgical resection are at risk for recur- biopsy. In this patient at risk for sclerosing cholangitis, with rent hepatocellular cancer, and surveillance imaging should liver enzyme levels indicating cholestatic liver disease and a continue after resection. normal MRCP result, a liver biopsy should be performed to Liver transplantation (Option A) for hepatocellular evaluate for small-duct PSC. cancer is the best therapy for patients who also have por- Drug-induced liver injury encompasses a spectrum of tal hypertension or features of liver dysfunction, such as liver injury and can be induced by many medications. This jaundice, and cannot undergo liver resection. This patient patient demonstrates cholestatic injury characterized by a has well-compensated cirrhosis and should be referred for disproportionate elevation in the alkaline phosphatase level resection rather than liver transplantation. compared with serum aminotransferase levels. Levofloxacin Liver-directed cytoreductive therapies, including is more commonly associated with a hepatocellular pattern transarterial chemoembolization (Option C), transarterial of injury characterized primarily by elevations of amino- radioembolization, stereotactic body radiotherapy, and transferase levels. More importantly, the cholestatic pattern radiofrequency ablation, are considered when patients are of liver injury was discovered before initiation of levofloxa- not candidates for surgical resection or liver transplanta- cin, strongly suggesting another cause for the patient’s liver tion. These locoregional procedures typically decrease the injury. Therefore, discontinuation of levofloxacin (Option A) size of liver tumors and may be curative, but they are not as is not necessary. definitive as resection and thus are considered second-line In patients with sclerosing cholangitis, endoscopic ret- therapies. This patient is a candidate for surgical resection as rograde cholangiopancreatography (ERCP) (Option B) can be first-line therapy. used to dilate strictures and remove stones in symptomatic Ongoing surveillance (Option D) is not appropriate in a patients with jaundice and pruritus or bacterial cholangitis. patient who can be considered for resection of hepatocellular ERCP can also be performed after MRCP to investigate a bile carcinoma. The only potential role for ongoing surveillance duct mass. This patient does not have indications for ERCP.

e Liver transplantation for hepatocellular cancer is the > Bibliography best therapy for patients who also have portal hyper- i] w Kidambi TD, Kohli DR, Samadder NJ, et al. Hereditary polyposis syndromes. Curr Treat Options Gastroenterol. 2019;17:650-665. [PMID: 31705372] tension or features of liver dysfunction. = @o doi:10.1007/s11938-019-00251-4 = wn Bibliography » = Marrero JA, Kulik LM, Sirlin CB, et al. Diagnosis, staging, and management a of hepatocellular carcinoma: 2018 practice guidance by the American (=) Item 26 Answer: 8B Association for the Study of Liver Diseases. Hepatology. 2018;68:723-750. = [PMID: 29624699] doi:10.1002/hep.29913 =. Educational Objective: Treat hepatocellular carcinoma 2 with surgical resection. = @o wn The most appropriate management is surgical resection Item 27 Answer: C (Option B). Patients with hepatocellular carcinoma who have Educational Objective: Diagnose small-duct primary well-compensated cirrhosis, no symptoms referable to liver sclerosing cholangitis. disease, no evidence of portal hypertension, and normal liver function markers, like this patient, typically can tolerate sur- The most appropriate next step in management is liver biopsy gical resection. The left liver is smaller than the right liver; (Option C). Primary sclerosing cholangitis (PSC) is an auto- therefore, in this patient, resection of cancer that spares the immune fibroinflammatory disease of the intrahepatic bile right liver should be undertaken. Screening for hepatocellular ducts; it most commonly affects the large ducts but can carcinoma is important in patients with cirrhosis, even those also affect the small intrahepatic ducts. It is associated with who have undergone successful antiviral therapy for hepa- inflammatory bowel disease in about 85% of cases and occurs titis C virus infection. Although successful antiviral therapy in approximately 7.5% of patients with ulcerative colitis. PSC decreases the risk for hepatocellular carcinoma, the risk is can be diagnosed with magnetic resonance cholangiopan- not eliminated and screening with abdominal ultrasonogra- creatography (MRCP). Althougha liver biopsy is rarely needed phy should be performed indefinitely at 6-month intervals. to diagnose PSC, diagnosis of small-duct PSC requires a liver Patients who undergo surgical resection are at risk for recur- biopsy. In this patient at risk for sclerosing cholangitis, with rent hepatocellular cancer, and surveillance imaging should liver enzyme levels indicating cholestatic liver disease and a continue after resection. normal MRCP result, a liver biopsy should be performed to Liver transplantation (Option A) for hepatocellular evaluate for small-duct PSC. cancer is the best therapy for patients who also have por- Drug-induced liver injury encompasses a spectrum of tal hypertension or features of liver dysfunction, such as liver injury and can be induced by many medications. This jaundice, and cannot undergo liver resection. This patient patient demonstrates cholestatic injury characterized by a has well-compensated cirrhosis and should be referred for disproportionate elevation in the alkaline phosphatase level resection rather than liver transplantation. compared with serum aminotransferase levels. Levofloxacin Liver-directed cytoreductive therapies, including is more commonly associated with a hepatocellular pattern transarterial chemoembolization (Option C), transarterial of injury characterized primarily by elevations of amino- radioembolization, stereotactic body radiotherapy, and transferase levels. More importantly, the cholestatic pattern radiofrequency ablation, are considered when patients are of liver injury was discovered before initiation of levofloxa- not candidates for surgical resection or liver transplanta- cin, strongly suggesting another cause for the patient’s liver tion. These locoregional procedures typically decrease the injury. Therefore, discontinuation of levofloxacin (Option A) size of liver tumors and may be curative, but they are not as is not necessary. definitive as resection and thus are considered second-line In patients with sclerosing cholangitis, endoscopic ret- therapies. This patient is a candidate for surgical resection as rograde cholangiopancreatography (ERCP) (Option B) can be first-line therapy. used to dilate strictures and remove stones in symptomatic Ongoing surveillance (Option D) is not appropriate in a patients with jaundice and pruritus or bacterial cholangitis. patient who can be considered for resection of hepatocellular ERCP can also be performed after MRCP to investigate a bile carcinoma. The only potential role for ongoing surveillance duct mass. This patient does not have indications for ERCP. 120

Liver ultrasonography (Option D) can be useful in the The Infectious Diseases Society of America suggests screen- initial evaluation of cholestasis. The presence of biliary dil- ing patients with genital warts, men who have sex with atation on ultrasonography indicates gallstones, strictures, men, and women who have a history of abnormal cervical or malignancy, whereas the absence of biliary dilatation is cytology results or participate in receptive anal intercourse. compatible with intrahepatic cholestasis. In this patient with The presence of IBD is not an indication to routinely screen ulcerative colitis and a pattern of cholestatic injury, MRCP for anal cancer. was appropriately performed and had normal results. MRCP Patients with IBD are at increased risk for colorectal is more sensitive in the diagnosis of sclerosing cholangitis cancer through longstanding colorectal inflammation. In than is ultrasonography. Liver ultrasonography will not pro- patients who have ulcerative colitis with disease proximal to vide any additional useful information. The most helpful the sigmoid colon or Crohn disease with more than one third diagnostic test will be a liver biopsy. of the colon involved, surveillance colonoscopy (Option C) should be done 8 years after diagnosis and then every 1 to MY ROUTES 5 eerie ES ee 2 years thereafter. Because this patient has had IBD for only w e Primary sclerosing cholangitis is an autoimmune rf) 2 years, surveillance colonoscopy is not yet necessary. a fibroinflammatory disease that most commonly Patients with IBD also have elevated risk for metabolic = affects the large bile ducts but can also affect the small bone disease through use of glucocorticoids and diminished = oO intrahepatic ducts; it can be diagnosed with magnetic vitamin D and calcium absorption. Bone mineral density sc resonance cholangiopancreatography. = testing with dual-energy x-ray absorptiometry (Option D) ce

Liver ultrasonography (Option D) can be useful in the The Infectious Diseases Society of America suggests screen- initial evaluation of cholestasis. The presence of biliary dil- ing patients with genital warts, men who have sex with atation on ultrasonography indicates gallstones, strictures, men, and women who have a history of abnormal cervical or malignancy, whereas the absence of biliary dilatation is cytology results or participate in receptive anal intercourse. compatible with intrahepatic cholestasis. In this patient with The presence of IBD is not an indication to routinely screen ulcerative colitis and a pattern of cholestatic injury, MRCP for anal cancer. was appropriately performed and had normal results. MRCP Patients with IBD are at increased risk for colorectal is more sensitive in the diagnosis of sclerosing cholangitis cancer through longstanding colorectal inflammation. In than is ultrasonography. Liver ultrasonography will not pro- patients who have ulcerative colitis with disease proximal to vide any additional useful information. The most helpful the sigmoid colon or Crohn disease with more than one third diagnostic test will be a liver biopsy. of the colon involved, surveillance colonoscopy (Option C) should be done 8 years after diagnosis and then every 1 to MY ROUTES 5 eerie ES ee 2 years thereafter. Because this patient has had IBD for only w e Primary sclerosing cholangitis is an autoimmune rf) 2 years, surveillance colonoscopy is not yet necessary. a fibroinflammatory disease that most commonly Patients with IBD also have elevated risk for metabolic = affects the large bile ducts but can also affect the small bone disease through use of glucocorticoids and diminished = oO intrahepatic ducts; it can be diagnosed with magnetic vitamin D and calcium absorption. Bone mineral density sc resonance cholangiopancreatography. = testing with dual-energy x-ray absorptiometry (Option D) ce ¢ Liver biopsy is needed to diagnose small-duct primary is recommended in all patients starting oral glucocorticoid wn ome o sclerosing cholangitis. therapy. Otherwise, patients with IBD should be screened = for osteoporosis on the basis of established guidelines for the wn < general population. Performing dual-energy x-ray absorp- <= Bibliography tiometry in this patient is not indicated because she is not Dyson JK, Beuers U, Jones DEJ, et al. Primary sclerosing cholangitis. Lancet. 2018;391:2547-2559. [PMID: 29452711] doi:10.1016/S0140-6736 (18) starting glucocorticoid therapy and has no conventional risk 30300-3 factors for osteoporosis.

¢ Liver biopsy is needed to diagnose small-duct primary is recommended in all patients starting oral glucocorticoid wn ome o sclerosing cholangitis. therapy. Otherwise, patients with IBD should be screened = for osteoporosis on the basis of established guidelines for the wn < general population. Performing dual-energy x-ray absorp- <= Bibliography tiometry in this patient is not indicated because she is not Dyson JK, Beuers U, Jones DEJ, et al. Primary sclerosing cholangitis. Lancet. 2018;391:2547-2559. [PMID: 29452711] doi:10.1016/S0140-6736 (18) starting glucocorticoid therapy and has no conventional risk 30300-3 factors for osteoporosis. Item 28 Answer: B ¢ Women with inflammatory bowel disease receiving Educational Objective: Provide appropriate health care immunosuppressive therapy should undergo Pap maintenance in a patient with inflammatory bowel testing annually. disease. The most appropriate health maintenance screening to per- Bibliography

Item 28 Answer: B ¢ Women with inflammatory bowel disease receiving Educational Objective: Provide appropriate health care immunosuppressive therapy should undergo Pap maintenance in a patient with inflammatory bowel testing annually. disease. The most appropriate health maintenance screening to per- Bibliography form is cervical cancer screening (Option B). Patients with Farraye FA, Melmed Gy, Lichtenstein GR, et al. ACG clinical guideline: preventive care in inflammatory bowel disease. Am J Gastroenterol. inflammatory bowel disease (IBD) have increased risk for 2017;112:241-258. [PMID: 28071656] doi:10.1038/ajg.2016.537 colorectal, cervical, and skin cancers. The U.S. Preventive Services Task Force recommends screening women aged 21 to 65 years every 3 years with cytology (Pap test). In women Item 29 Answer: B aged 30 to 65 years who want to extend the screening interval, Educational Objective: Diagnose eosinophilic high-risk human papillomavirus (HPV) testing (preferred) esophagitis. or cytology combined with high-risk HPV testing can be performed every 5 years. However, women with IBD have The most likely diagnosis is eosinophilic esophagitis (EoE) increased risk for cervical dysplasia; this risk is greater in (Option B). This patient presented with a food impaction that women using immunosuppressive therapy. Women with IBD resolved spontaneously. Most patients with EoE are men diag- receiving immunosuppressive therapy should undergo Pap nosed between the second and fifth decades of life, and many testing annually. Patients with IBD also have increased risk have other atopic conditions, such as asthma, rhinitis, der- for vaccine-preventable illnesses. Inactivated vaccines can matitis, and seasonal or food allergies. The diagnostic criteria be safely administered to all patients with IBD, regardless for EoE are symptoms of esophageal dysfunction, esophageal of immunosuppression. Depression and anxiety are more biopsy specimens showing persistent eosinophil counts of at common in patients with IBD than in the general popula- least 15/hpf, and exclusion of other causes of eosinophilia. tion, and screening is recommended. Patients with ulcerative Examples of other causes of esophageal eosinophilia include colitis and Crohn disease should undergo yearly melanoma gastroesophageal reflux disease, hypereosinophilic syndrome, screening, and those receiving immunomodulators should infections (i-e., fungal, viral), autoimmune and connective be screened for nonmelanoma squamous cell cancer while tissue disorders, Crohn disease with esophageal involvement, using these agents. and drug hypersensitivity reactions. Peripheral eosinophilia Evidence is insufficient to recommend routine anal can- is not a diagnostic criterion for EoE. Upper endoscopy with cer screening (Option A) in average-risk populations, but biopsies to confirm this diagnosis is appropriate. Treatment such screening may be considered in high-risk populations. options include a proton pump inhibitor, swallowed topical

form is cervical cancer screening (Option B). Patients with Farraye FA, Melmed Gy, Lichtenstein GR, et al. ACG clinical guideline: preventive care in inflammatory bowel disease. Am J Gastroenterol. inflammatory bowel disease (IBD) have increased risk for 2017;112:241-258. [PMID: 28071656] doi:10.1038/ajg.2016.537 colorectal, cervical, and skin cancers. The U.S. Preventive Services Task Force recommends screening women aged 21 to 65 years every 3 years with cytology (Pap test). In women Item 29 Answer: B aged 30 to 65 years who want to extend the screening interval, Educational Objective: Diagnose eosinophilic high-risk human papillomavirus (HPV) testing (preferred) esophagitis. or cytology combined with high-risk HPV testing can be performed every 5 years. However, women with IBD have The most likely diagnosis is eosinophilic esophagitis (EoE) increased risk for cervical dysplasia; this risk is greater in (Option B). This patient presented with a food impaction that women using immunosuppressive therapy. Women with IBD resolved spontaneously. Most patients with EoE are men diag- receiving immunosuppressive therapy should undergo Pap nosed between the second and fifth decades of life, and many testing annually. Patients with IBD also have increased risk have other atopic conditions, such as asthma, rhinitis, der- for vaccine-preventable illnesses. Inactivated vaccines can matitis, and seasonal or food allergies. The diagnostic criteria be safely administered to all patients with IBD, regardless for EoE are symptoms of esophageal dysfunction, esophageal of immunosuppression. Depression and anxiety are more biopsy specimens showing persistent eosinophil counts of at common in patients with IBD than in the general popula- least 15/hpf, and exclusion of other causes of eosinophilia. tion, and screening is recommended. Patients with ulcerative Examples of other causes of esophageal eosinophilia include colitis and Crohn disease should undergo yearly melanoma gastroesophageal reflux disease, hypereosinophilic syndrome, screening, and those receiving immunomodulators should infections (i-e., fungal, viral), autoimmune and connective be screened for nonmelanoma squamous cell cancer while tissue disorders, Crohn disease with esophageal involvement, using these agents. and drug hypersensitivity reactions. Peripheral eosinophilia Evidence is insufficient to recommend routine anal can- is not a diagnostic criterion for EoE. Upper endoscopy with cer screening (Option A) in average-risk populations, but biopsies to confirm this diagnosis is appropriate. Treatment such screening may be considered in high-risk populations. options include a proton pump inhibitor, swallowed topical 121

Answers and Critiques glucocorticoids (e.g., fluticasone, budesonide), and/or endo- to ultrasonography increases the sensitivity of HCC detection scopic dilation. An empiric elimination diet may help treat but also increases the false-positive rate. No available infor- and prevent flares in EoE. mation indicates that the addition of AFP measurement to Barrett esophagus (Option A) is a complication of biannual ultrasonography leads to improved survival. There- chronic acid reflux disease and is a risk factor for esopha- fore, the American Association for the Study of Liver Disease geal cancer. However, it does not cause dysphagia with food (AASLD) recommends surveillance using ultrasonography impaction. with or without AFP every 6 months. Although esophageal cancer (Option C) can cause solid The AASLD does not recommend MRI (Option A) or food dysphagia in older patients, it is often persistent and CT (Option B) as the primary modality for the surveillance progressive but not intermittent with spontaneous resolu- of HCC in patients with cirrhosis. Although these modal- tion as seen in this young patient. ities are more sensitive than ultrasonography, there is no Patients with symptomatic peptic strictures (Option D) evidence that this translates to improved survival. How- > often have long-standing reflux or heartburn, which are not ever, the AASLD notes that in select patients with a high = wn present in this patient. likelihood of having an inadequate ultrasound or in whom = Symptoms of esophageal dysmotility and reflux are ultrasonography is attempted but inadequate, MRI or CT @o ed wn common in all forms of systemic sclerosis (Option E). Dys- may be used. <3) = phagia is the result of incomplete peristalsis, and reflux No surveillance (Option D) is inappropriate because a. results from decreased lower esophageal sphincter pressure. patients with cirrhosis, such as this patient, are at increased oO =e Patients with systemic sclerosis usually have associated skin risk for HCC. The AASLD recommends surveillance of adults = findings and sclerodactyly. This patient lacks these charac- with cirrhosis because it improves overall survival. <2 < teristics. @o wa

glucocorticoids (e.g., fluticasone, budesonide), and/or endo- to ultrasonography increases the sensitivity of HCC detection scopic dilation. An empiric elimination diet may help treat but also increases the false-positive rate. No available infor- and prevent flares in EoE. mation indicates that the addition of AFP measurement to Barrett esophagus (Option A) is a complication of biannual ultrasonography leads to improved survival. There- chronic acid reflux disease and is a risk factor for esopha- fore, the American Association for the Study of Liver Disease geal cancer. However, it does not cause dysphagia with food (AASLD) recommends surveillance using ultrasonography impaction. with or without AFP every 6 months. Although esophageal cancer (Option C) can cause solid The AASLD does not recommend MRI (Option A) or food dysphagia in older patients, it is often persistent and CT (Option B) as the primary modality for the surveillance progressive but not intermittent with spontaneous resolu- of HCC in patients with cirrhosis. Although these modal- tion as seen in this young patient. ities are more sensitive than ultrasonography, there is no Patients with symptomatic peptic strictures (Option D) evidence that this translates to improved survival. How- > often have long-standing reflux or heartburn, which are not ever, the AASLD notes that in select patients with a high = wn present in this patient. likelihood of having an inadequate ultrasound or in whom = Symptoms of esophageal dysmotility and reflux are ultrasonography is attempted but inadequate, MRI or CT @o ed wn common in all forms of systemic sclerosis (Option E). Dys- may be used. <3) = phagia is the result of incomplete peristalsis, and reflux No surveillance (Option D) is inappropriate because a. results from decreased lower esophageal sphincter pressure. patients with cirrhosis, such as this patient, are at increased oO =e Patients with systemic sclerosis usually have associated skin risk for HCC. The AASLD recommends surveillance of adults = findings and sclerodactyly. This patient lacks these charac- with cirrhosis because it improves overall survival. <2 < teristics. @o wa e Patients with cirrhosis who have undergone virologic ¢ Eosinophilic esophagitis is a condition commonly cure for hepatitis C virus infection should undergo associated with dysphagia and food bolus obstruction, surveillance for hepatocellular carcinoma every 6 months usually found in younger men with atopic conditions. with ultrasonography.

e Patients with cirrhosis who have undergone virologic ¢ Eosinophilic esophagitis is a condition commonly cure for hepatitis C virus infection should undergo associated with dysphagia and food bolus obstruction, surveillance for hepatocellular carcinoma every 6 months usually found in younger men with atopic conditions. with ultrasonography. ¢ Diagnostic criteria for eosinophilic esophagitis are e No information indicates that the addition of dysphagia, esophageal biopsy specimens with eosino- o-fetoprotein (AFP) to ultrasonography screening for phil counts of at least 15/hpf, and exclusion of other hepatocellular carcinoma leads to improved survival; causes of eosinophilia. therefore, surveillance using ultrasonography may be performed with or without AFP measurement every Bibliography 6 months. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated international con- sensus diagnostic criteria for eosinophilic esophagitis: proceedings of the AGREE conference. Gastroenterology. 2018;155:1022-1033.e10. [PMID: Bibliography 30009819] doi:10.1053/j.gastro.2018.07.009 Marrero JA, Kulik LM, Sirlin CB, et al. Diagnosis, staging, and management of hepatocellular carcinoma: 2018 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2018;68:723-750. [PMID: 29624699] doi:10.1002/hep.29913 Item 30 Answer: C

¢ Diagnostic criteria for eosinophilic esophagitis are e No information indicates that the addition of dysphagia, esophageal biopsy specimens with eosino- o-fetoprotein (AFP) to ultrasonography screening for phil counts of at least 15/hpf, and exclusion of other hepatocellular carcinoma leads to improved survival; causes of eosinophilia. therefore, surveillance using ultrasonography may be performed with or without AFP measurement every Bibliography 6 months. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated international con- sensus diagnostic criteria for eosinophilic esophagitis: proceedings of the AGREE conference. Gastroenterology. 2018;155:1022-1033.e10. [PMID: Bibliography 30009819] doi:10.1053/j.gastro.2018.07.009 Marrero JA, Kulik LM, Sirlin CB, et al. Diagnosis, staging, and management of hepatocellular carcinoma: 2018 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2018;68:723-750. [PMID: 29624699] doi:10.1002/hep.29913 Item 30 Answer: C Educational Objective: Screen for hepatocellular carcinoma in a patient with cirrhosis. Item 31 Answer: D Educational Objective: Manage narcotic bowel The most appropriate surveillance modality for hepatocellu- syndrome. lar carcinoma (HCC) is ultrasonography of the liver (Option C) every 6 months. Adults with cirrhosis are at the high- The most appropriate management is opioid discontinuation est risk for HCC and should undergo surveillance regardless (Option D). The patient has progressively severe abdominal of the cause of cirrhosis. In most patients with hepatitis C pain that requires escalating narcotic doses. The paradoxical virus (HCV) infection, cure rates seen with direct-acting worsening of her pain despite dose escalation is consistent antiviral agents exceed 90%. Sustained virologic response is with narcotic bowel syndrome, also known as opiate-induced defined as a negative HCV RNA result 12 weeks after therapy gastrointestinal hyperalgesia. The proposed cause of narcotic and defines virologic cure. Virologic cure is associated with bowel syndrome is centrally mediated opioid-induced hyper- reduced risk for progression to cirrhosis, cirrhosis complica- algesia, but the pathophysiological mechanism is not well tions, hepatocellular carcinoma, and liver-related mortality. defined. The condition is characterized by a patient’s fear of The risk for HCC in patients with HCV-related cirrhosis who tapering narcotics; however, the only effective treatment is achieve virologic cure after antiviral treatment is lowered, but complete cessation of narcotic use, which is most successfully not eliminated; therefore, patients with cirrhosis and treated achieved in a supervised detoxification program. During the HCV infection should undergo surveillance for HCC every detoxification process, nonpharmacologic therapies, such as 6 months. The addition of «-fetoprotein (AFP) measurement stress reduction and exercise, are introduced and adjuvant

Educational Objective: Screen for hepatocellular carcinoma in a patient with cirrhosis. Item 31 Answer: D Educational Objective: Manage narcotic bowel The most appropriate surveillance modality for hepatocellu- syndrome. lar carcinoma (HCC) is ultrasonography of the liver (Option C) every 6 months. Adults with cirrhosis are at the high- The most appropriate management is opioid discontinuation est risk for HCC and should undergo surveillance regardless (Option D). The patient has progressively severe abdominal of the cause of cirrhosis. In most patients with hepatitis C pain that requires escalating narcotic doses. The paradoxical virus (HCV) infection, cure rates seen with direct-acting worsening of her pain despite dose escalation is consistent antiviral agents exceed 90%. Sustained virologic response is with narcotic bowel syndrome, also known as opiate-induced defined as a negative HCV RNA result 12 weeks after therapy gastrointestinal hyperalgesia. The proposed cause of narcotic and defines virologic cure. Virologic cure is associated with bowel syndrome is centrally mediated opioid-induced hyper- reduced risk for progression to cirrhosis, cirrhosis complica- algesia, but the pathophysiological mechanism is not well tions, hepatocellular carcinoma, and liver-related mortality. defined. The condition is characterized by a patient’s fear of The risk for HCC in patients with HCV-related cirrhosis who tapering narcotics; however, the only effective treatment is achieve virologic cure after antiviral treatment is lowered, but complete cessation of narcotic use, which is most successfully not eliminated; therefore, patients with cirrhosis and treated achieved in a supervised detoxification program. During the HCV infection should undergo surveillance for HCC every detoxification process, nonpharmacologic therapies, such as 6 months. The addition of «-fetoprotein (AFP) measurement stress reduction and exercise, are introduced and adjuvant 122

Answers and Critiques treatments with nonopioid analgesics, such as antidepres- or in the peripancreatic tissues. Walled-off necrosis occurs sants, are added. Psychotherapy may be beneficial. when necrotic areas liquefy and become encapsulated with CONT. Lubiprostone (Option A) activates type 2 chloride chan- a well-defined wall surrounding the necrotic area. Because nels on enterocytes lining the gut lumen, causing chloride of the semi-solid nature of the debris in walled-off necrosis, ions to move into the colonic lumen with sodium and water these lesions are not typically amenable to simple endo- following the ionic gradient. It is used to treat constipa- scopic needle drainage and may require endoscopic drain- tion-predominant irritable bowel syndrome and chronic age, such as endoscopic cystogastrostomy and necrosectomy idiopathic constipation. Lubiprostone is not indicated (Option A), or surgical drainage. Because this patient has a because this patient’s constipation is controlled with poly- pseudocyst, he does not require these procedures. ethylene glycol and her symptoms are not likely related to Endoscopic retrograde pancreatography (Option B) is irritable bowel syndrome. not recommended for pancreatic fluid collections. Instru- Methadone (Option B), an opiate with a long half-life, mentation of the pancreatic duct carries a risk for pancreati- is used for management of chronic pain or maintenance tis. Although this procedure may provide information, such wn go therapy for opiate abuse. Because pain in narcotic bowel as connection of the fluid collection to the pancreatic duct, =

treatments with nonopioid analgesics, such as antidepres- or in the peripancreatic tissues. Walled-off necrosis occurs sants, are added. Psychotherapy may be beneficial. when necrotic areas liquefy and become encapsulated with CONT. Lubiprostone (Option A) activates type 2 chloride chan- a well-defined wall surrounding the necrotic area. Because nels on enterocytes lining the gut lumen, causing chloride of the semi-solid nature of the debris in walled-off necrosis, ions to move into the colonic lumen with sodium and water these lesions are not typically amenable to simple endo- following the ionic gradient. It is used to treat constipa- scopic needle drainage and may require endoscopic drain- tion-predominant irritable bowel syndrome and chronic age, such as endoscopic cystogastrostomy and necrosectomy idiopathic constipation. Lubiprostone is not indicated (Option A), or surgical drainage. Because this patient has a because this patient’s constipation is controlled with poly- pseudocyst, he does not require these procedures. ethylene glycol and her symptoms are not likely related to Endoscopic retrograde pancreatography (Option B) is irritable bowel syndrome. not recommended for pancreatic fluid collections. Instru- Methadone (Option B), an opiate with a long half-life, mentation of the pancreatic duct carries a risk for pancreati- is used for management of chronic pain or maintenance tis. Although this procedure may provide information, such wn go therapy for opiate abuse. Because pain in narcotic bowel as connection of the fluid collection to the pancreatic duct, = syndrome worsens with continued or escalating opiate dos- this information will not change management. Therefore, = = ing and can be treated only by discontinuing opiate use, the procedure is not appropriate for this patient. =) methadone is not an effective treatment in this condition. If a patient is symptomatic or there is concern for infec- cs t Colonoscopy with biopsy (Option C) of the right and tion, endoscopic ultrasonography with fine-needle aspiration Cc wn left colon is performed to assess for microscopic colitis, a (Option C) can be considered. For symptomatic pancreatic ao form of inflammatory bowel disease that causes watery diar- pseudocysts, endoscopic drainage is preferred over surgical > 2) rhea. Although abdominal pain can be present in patients drainage (Option D) given its lesser morbidity. This patient <= with microscopic colitis, this patient’s history of constipa- is asymptomatic and thus does not need to undergo ultra- <

syndrome worsens with continued or escalating opiate dos- this information will not change management. Therefore, = = ing and can be treated only by discontinuing opiate use, the procedure is not appropriate for this patient. =) methadone is not an effective treatment in this condition. If a patient is symptomatic or there is concern for infec- cs t Colonoscopy with biopsy (Option C) of the right and tion, endoscopic ultrasonography with fine-needle aspiration Cc wn left colon is performed to assess for microscopic colitis, a (Option C) can be considered. For symptomatic pancreatic ao form of inflammatory bowel disease that causes watery diar- pseudocysts, endoscopic drainage is preferred over surgical > 2) rhea. Although abdominal pain can be present in patients drainage (Option D) given its lesser morbidity. This patient <= with microscopic colitis, this patient’s history of constipa- is asymptomatic and thus does not need to undergo ultra- < tion treated with polyethylene glycol make this diagnosis sonography and fine-needle aspiration. unlikely.

syndrome worsens with continued or escalating opiate dos- this information will not change management. Therefore, = = ing and can be treated only by discontinuing opiate use, the procedure is not appropriate for this patient. =) methadone is not an effective treatment in this condition. If a patient is symptomatic or there is concern for infec- cs t Colonoscopy with biopsy (Option C) of the right and tion, endoscopic ultrasonography with fine-needle aspiration Cc wn left colon is performed to assess for microscopic colitis, a (Option C) can be considered. For symptomatic pancreatic ao form of inflammatory bowel disease that causes watery diar- pseudocysts, endoscopic drainage is preferred over surgical > 2) rhea. Although abdominal pain can be present in patients drainage (Option D) given its lesser morbidity. This patient <= with microscopic colitis, this patient’s history of constipa- is asymptomatic and thus does not need to undergo ultra- < tion treated with polyethylene glycol make this diagnosis sonography and fine-needle aspiration. unlikely. e Pancreatic pseudocysts are peripancreatic fluid collec- ¢ Narcotic bowel syndrome is characterized by paradox- tions that occur with acute pancreatitis and do not ical worsening of abdominal pain despite dose escala- contain solid material or debris. tion; complete cessation of narcotic use is the only ¢ Pancreatic pseudocysts do not require drainage unless effective treatment. the patient is symptomatic or the pseudocysts become infected. Bibliography Farmer AD, Gallagher J, Bruckner-Holt C, et al. Narcotic bowel syndrome. Bibliography Lancet Gastroenterol Hepatol. 2017;2:361-368. [PMID: 28397700] doi:10.1016/S2468-1253(16)30217-5 Hines OJ, Pandol SJ. Management of severe acute pancreatitis. BMJ. 2019; 367:16227. [PMID: 31791953] doi:10.1136/bmj.16227

e Pancreatic pseudocysts are peripancreatic fluid collec- ¢ Narcotic bowel syndrome is characterized by paradox- tions that occur with acute pancreatitis and do not ical worsening of abdominal pain despite dose escala- contain solid material or debris. tion; complete cessation of narcotic use is the only ¢ Pancreatic pseudocysts do not require drainage unless effective treatment. the patient is symptomatic or the pseudocysts become infected. Bibliography Farmer AD, Gallagher J, Bruckner-Holt C, et al. Narcotic bowel syndrome. Bibliography Lancet Gastroenterol Hepatol. 2017;2:361-368. [PMID: 28397700] doi:10.1016/S2468-1253(16)30217-5 Hines OJ, Pandol SJ. Management of severe acute pancreatitis. BMJ. 2019; 367:16227. [PMID: 31791953] doi:10.1136/bmj.16227 Item 32 Answer: E

e Pancreatic pseudocysts are peripancreatic fluid collec- ¢ Narcotic bowel syndrome is characterized by paradox- tions that occur with acute pancreatitis and do not ical worsening of abdominal pain despite dose escala- contain solid material or debris. tion; complete cessation of narcotic use is the only ¢ Pancreatic pseudocysts do not require drainage unless effective treatment. the patient is symptomatic or the pseudocysts become infected. Bibliography Farmer AD, Gallagher J, Bruckner-Holt C, et al. Narcotic bowel syndrome. Bibliography Lancet Gastroenterol Hepatol. 2017;2:361-368. [PMID: 28397700] doi:10.1016/S2468-1253(16)30217-5 Hines OJ, Pandol SJ. Management of severe acute pancreatitis. BMJ. 2019; 367:16227. [PMID: 31791953] doi:10.1136/bmj.16227 Item 32 Answer: E Educational Objective: Manage asymptomatic Item 33 Answer: B pancreatic pseudocysts. Educational Objective: Diagnose acute mesenteric ischemia. The most appropriate management is observation (Option E). This patient has recovered from alcohol-induced pancreatitis The most appropriate diagnostic test to perform next is CT and now has a pancreatic pseudocyst. Pancreatic pseudocysts angiography (Option B). This patient has acute mesenteric are one of the four types of fluid collections seen in acute pan- ischemia (AMI) caused by an abrupt decrease in blood flow to creatitis; the others are acute peripancreatic fluid collections, the small intestine, likely due to an embolus related to atrial acute necrotic collections, and walled-off necrosis. Pancreatic fibrillation. AMI most commonly presents with abrupt onset pseudocysts are defined as peripancreatic fluid collections of severe periumbilical abdominal pain followed by the urge to that persist beyond 4 weeks. They develop a well-defined wall, defecate. Although the patient reports severe abdominal pain, but this wall lacks the epithelial layer required of a true cyst. physical examination reveals a soft, nontender, nondistended Pseudocysts do not contain solid material or debris and do abdomen without peritoneal signs. Pain that is dispropor- not require drainage unless the patient is symptomatic or the tionate to physical examination findings should immediately pseudocysts become infected. This patient feels well and thus raise suspicion for early AMI. With late presentation, intes- does not require drainage. Ongoing expectant management tinal ischemia progresses to infarction and peritoneal signs and observation are appropriate. develop. This late presentation of AMI is associated with a Acute necrotic collections are areas of pancreatic necro- high mortality rate. Results of laboratory studies and abdom- sis that develop within the first 4 weeks of acute pancreati- inal imaging in early AMI are nonspecific. Most patients will tis. Necrosis may occur within the pancreatic parenchyma have an elevated leukocyte count. Serum lactate level may be

Educational Objective: Manage asymptomatic Item 33 Answer: B pancreatic pseudocysts. Educational Objective: Diagnose acute mesenteric ischemia. The most appropriate management is observation (Option E). This patient has recovered from alcohol-induced pancreatitis The most appropriate diagnostic test to perform next is CT and now has a pancreatic pseudocyst. Pancreatic pseudocysts angiography (Option B). This patient has acute mesenteric are one of the four types of fluid collections seen in acute pan- ischemia (AMI) caused by an abrupt decrease in blood flow to creatitis; the others are acute peripancreatic fluid collections, the small intestine, likely due to an embolus related to atrial acute necrotic collections, and walled-off necrosis. Pancreatic fibrillation. AMI most commonly presents with abrupt onset pseudocysts are defined as peripancreatic fluid collections of severe periumbilical abdominal pain followed by the urge to that persist beyond 4 weeks. They develop a well-defined wall, defecate. Although the patient reports severe abdominal pain, but this wall lacks the epithelial layer required of a true cyst. physical examination reveals a soft, nontender, nondistended Pseudocysts do not contain solid material or debris and do abdomen without peritoneal signs. Pain that is dispropor- not require drainage unless the patient is symptomatic or the tionate to physical examination findings should immediately pseudocysts become infected. This patient feels well and thus raise suspicion for early AMI. With late presentation, intes- does not require drainage. Ongoing expectant management tinal ischemia progresses to infarction and peritoneal signs and observation are appropriate. develop. This late presentation of AMI is associated with a Acute necrotic collections are areas of pancreatic necro- high mortality rate. Results of laboratory studies and abdom- sis that develop within the first 4 weeks of acute pancreati- inal imaging in early AMI are nonspecific. Most patients will tis. Necrosis may occur within the pancreatic parenchyma have an elevated leukocyte count. Serum lactate level may be 123

normal and does not exclude the diagnosis. CT angiography is metformin to have triggered the patient’s symptoms given the recommended imaging modality to diagnose AMI. the temporal relationship between symptom onset and CONT. Colonoscopy with biopsy (Option A) is the test of choice commencement of metformin. Moreover, the normal eryth- to confirm the diagnosis of colonic ischemia. This ischemia rocyte sedimentation rate and lack of abdominal pain or presents with the abrupt onset of lower abdominal discom- tenderness on physical examination argue against Crohn fort that is mild to moderate and cramping, followed within disease. 24 hours by hematochezia (passage of fresh blood or clots Microscopic colitis (Option D) is a distinct type of from the colon). This patient’s presentation is not consistent inflammatory bowel disease characterized by macroscop- with colonic ischemia, and colonoscopy is not indicated. ically normal mucosa with inflammatory changes seen on Doppler ultrasonography (Option C) is an effective, histopathology of colon biopsy specimens. It is subclassified low-cost method to assess the proximal mesenteric vessels. into lymphocytic colitis and collagenous colitis on the basis of However, adequate ultrasonography often cannot be per- predominating histologic features. Microscopic colitis pre- me formed in patients with AMI, making it an inferior option to dominantly affects middle-aged women. Medications, = wn CT angiography. including NSAIDs, selective serotonin reuptake inhibitors, = Although magnetic resonance angiography (Option D) and proton pump inhibitors, have been associated with © = wn avoids the risks of radiation and contrast exposure, it takes the development of microscopic colitis. = *) = longer and is less sensitive for distal and nonocclusive dis- a. ease in patients suspected of having AMI. 2) e Acute diarrhea is usually caused by infectious = = agents, whereas chronic diarrhea is more commonly <2 i e Early acute mesenteric ischemia most commonly noninfectious. oO wn presents with abrupt onset of severe periumbilical e Patients with chronic diarrhea should be asked about abdominal pain followed by the urge to defecate and new medications and the timing of the initiation of an unremarkable abdominal examination. medication in relation to the onset of diarrhea; met- ¢ CT angiography is the recommended imaging modal- formin is a common cause of chronic watery diarrhea. ity for the diagnosis of acute mesenteric ischemia. Bibliography Bibliography Arasaradnam RP, Brown §, Forbes A, et al. Guidelines for the investigation of chronic diarrhoea in adults: British Society of Gastroenterology, 3rd Clair DG, Beach JM. Mesenteric ischemia. N EnglJ Med. 2016;374:959-68. edition. Gut. 2018;67:1380-1399. [PMID: 29653941] doi:10.1136/gutjnl- [PMID: 26962730] doi:10.1056/NEJMra1503884 2017-315909

normal and does not exclude the diagnosis. CT angiography is metformin to have triggered the patient’s symptoms given the recommended imaging modality to diagnose AMI. the temporal relationship between symptom onset and CONT. Colonoscopy with biopsy (Option A) is the test of choice commencement of metformin. Moreover, the normal eryth- to confirm the diagnosis of colonic ischemia. This ischemia rocyte sedimentation rate and lack of abdominal pain or presents with the abrupt onset of lower abdominal discom- tenderness on physical examination argue against Crohn fort that is mild to moderate and cramping, followed within disease. 24 hours by hematochezia (passage of fresh blood or clots Microscopic colitis (Option D) is a distinct type of from the colon). This patient’s presentation is not consistent inflammatory bowel disease characterized by macroscop- with colonic ischemia, and colonoscopy is not indicated. ically normal mucosa with inflammatory changes seen on Doppler ultrasonography (Option C) is an effective, histopathology of colon biopsy specimens. It is subclassified low-cost method to assess the proximal mesenteric vessels. into lymphocytic colitis and collagenous colitis on the basis of However, adequate ultrasonography often cannot be per- predominating histologic features. Microscopic colitis pre- me formed in patients with AMI, making it an inferior option to dominantly affects middle-aged women. Medications, = wn CT angiography. including NSAIDs, selective serotonin reuptake inhibitors, = Although magnetic resonance angiography (Option D) and proton pump inhibitors, have been associated with © = wn avoids the risks of radiation and contrast exposure, it takes the development of microscopic colitis. = *) = longer and is less sensitive for distal and nonocclusive dis- a. ease in patients suspected of having AMI. 2) e Acute diarrhea is usually caused by infectious = = agents, whereas chronic diarrhea is more commonly <2 i e Early acute mesenteric ischemia most commonly noninfectious. oO wn presents with abrupt onset of severe periumbilical e Patients with chronic diarrhea should be asked about abdominal pain followed by the urge to defecate and new medications and the timing of the initiation of an unremarkable abdominal examination. medication in relation to the onset of diarrhea; met- ¢ CT angiography is the recommended imaging modal- formin is a common cause of chronic watery diarrhea. ity for the diagnosis of acute mesenteric ischemia. Bibliography Bibliography Arasaradnam RP, Brown §, Forbes A, et al. Guidelines for the investigation of chronic diarrhoea in adults: British Society of Gastroenterology, 3rd Clair DG, Beach JM. Mesenteric ischemia. N EnglJ Med. 2016;374:959-68. edition. Gut. 2018;67:1380-1399. [PMID: 29653941] doi:10.1136/gutjnl- [PMID: 26962730] doi:10.1056/NEJMra1503884 2017-315909 Item 34 Answer: C Item 35 Answer: D Educational Objective: Diagnose medication-induced Educational Objective: Treat nonalcoholic fatty liver chronic diarrhea. disease.

Item 34 Answer: C Item 35 Answer: D Educational Objective: Diagnose medication-induced Educational Objective: Treat nonalcoholic fatty liver chronic diarrhea. disease. The most likely cause of this patient’s diarrhea is metformin The most appropriate next step in management is weight (Option C). The patient reports a 4-month history of diarrhea loss (Option D). This patient likely has nonalcoholic fatty characterized by watery, nonbloody bowel movements. This liver disease (NAFLD) given the presence of diabetes, obe- duration of symptoms (>4 weeks) is classified as chronic diar- sity, hypertension, and hyperlipidemia. Diabetes is associated thea. In contrast to acute diarrhea, which is usually caused by with the development of NAFLD, including its more severe infectious agents, chronic diarrhea is more commonly non- manifestations of nonalcoholic steatohepatitis (NASH), liver infectious. Patients with diarrhea should be asked about new fibrosis, cirrhosis, and hepatocellular carcinoma. Elevations medications and the timing of the initiation of medication of hepatic aminotransferase concentrations are associated in relation to diarrhea onset. Metformin is a common cause with higher BMI, waist circumference, and triglyceride levels of chronic watery diarrhea, possibly related to a promotility and lower HDL cholesterol levels. Patients with type 2 dia- effect and stimulation of intestinal chloride secretion. The betes or prediabetes and elevated liver enzyme levels or fatty temporal association with the commencement of metformin liver on ultrasound should be evaluated for presence of NASH (which was started 4 months ago, coinciding with symp- and liver fibrosis. Noninvasive tests, such as elastography or tom onset) strongly suggests that metformin is the cause of fibrosis biomarkers, may be used to assess risk for fibrosis, but diarrhea. referral to a liver specialist and liver biopsy may be required Although Clostridioides difficile colitis (Option A) can for definitive diagnosis. The mainstay of NAFLD management result from antibiotic use, the time between amoxicillin is weight loss. Weight loss of at least 5% improves steatosis, use and onset of diarrhea argues against amoxicillin as the whereas weight loss of 8% to 10% improves steatohepatitis and triggering event. fibrosis. No specific diet for NAFLD is recommended. Bariatric Crohn disease (Option B) can cause watery diarrhea surgery and concomitant weight loss improve inflammation or inflammatory diarrhea. However, it is less likely than and fibrosis associated with NAFLD.

The most likely cause of this patient’s diarrhea is metformin The most appropriate next step in management is weight (Option C). The patient reports a 4-month history of diarrhea loss (Option D). This patient likely has nonalcoholic fatty characterized by watery, nonbloody bowel movements. This liver disease (NAFLD) given the presence of diabetes, obe- duration of symptoms (>4 weeks) is classified as chronic diar- sity, hypertension, and hyperlipidemia. Diabetes is associated thea. In contrast to acute diarrhea, which is usually caused by with the development of NAFLD, including its more severe infectious agents, chronic diarrhea is more commonly non- manifestations of nonalcoholic steatohepatitis (NASH), liver infectious. Patients with diarrhea should be asked about new fibrosis, cirrhosis, and hepatocellular carcinoma. Elevations medications and the timing of the initiation of medication of hepatic aminotransferase concentrations are associated in relation to diarrhea onset. Metformin is a common cause with higher BMI, waist circumference, and triglyceride levels of chronic watery diarrhea, possibly related to a promotility and lower HDL cholesterol levels. Patients with type 2 dia- effect and stimulation of intestinal chloride secretion. The betes or prediabetes and elevated liver enzyme levels or fatty temporal association with the commencement of metformin liver on ultrasound should be evaluated for presence of NASH (which was started 4 months ago, coinciding with symp- and liver fibrosis. Noninvasive tests, such as elastography or tom onset) strongly suggests that metformin is the cause of fibrosis biomarkers, may be used to assess risk for fibrosis, but diarrhea. referral to a liver specialist and liver biopsy may be required Although Clostridioides difficile colitis (Option A) can for definitive diagnosis. The mainstay of NAFLD management result from antibiotic use, the time between amoxicillin is weight loss. Weight loss of at least 5% improves steatosis, use and onset of diarrhea argues against amoxicillin as the whereas weight loss of 8% to 10% improves steatohepatitis and triggering event. fibrosis. No specific diet for NAFLD is recommended. Bariatric Crohn disease (Option B) can cause watery diarrhea surgery and concomitant weight loss improve inflammation or inflammatory diarrhea. However, it is less likely than and fibrosis associated with NAFLD. 124

Answers and Critiques This patient does not excessively use alcohol, so alcohol high-molecular-weight von Willebrand factor multi- cessation (Option A) is unlikely to resolve his steatosis. No mers. These multimers accumulate, generating platelet-rich amount of alcohol use is safe in patients with liver disease. thrombi in small vessels. Initial treatment involves therapeu- Statins are safe in most patients with NAFLD and should tic plasma exchange (Option B) to remove the multimers and not be discontinued (Option B). Cardiovascular disease is replace the deficient ADAMTS13. Although this patient has the leading cause of death in patients with NAFLD, and hemolytic anemia and thrombocytopenia, a third-trimester initiation of therapy with statins should be considered in pregnancy and elevated liver enzyme levels are more compat- patients with NALD at high risk for cardiovascular events. ible with HELLP syndrome. There is no relationship between statin use and steatosis in If bleeding is not controlled, or if an invasive procedure NAFLD. is planned, transfusion of platelets (Option C) or plasma may No drugs have been approved by the FDA for the treat- be warranted. In the absence of bleeding, as in this patient, ment of NAFLD. Pioglitazone (Option C) and vitamin E administration of platelets is not necessary. Any intervention treatment of biopsy-proven nonalcoholic steatohepatitis that delays delivery of the fetus should be avoided. wn @ improve liver histology, but effects on longer-term clinical Intrahepatic cholestasis of pregnancy can develop =

This patient does not excessively use alcohol, so alcohol high-molecular-weight von Willebrand factor multi- cessation (Option A) is unlikely to resolve his steatosis. No mers. These multimers accumulate, generating platelet-rich amount of alcohol use is safe in patients with liver disease. thrombi in small vessels. Initial treatment involves therapeu- Statins are safe in most patients with NAFLD and should tic plasma exchange (Option B) to remove the multimers and not be discontinued (Option B). Cardiovascular disease is replace the deficient ADAMTS13. Although this patient has the leading cause of death in patients with NAFLD, and hemolytic anemia and thrombocytopenia, a third-trimester initiation of therapy with statins should be considered in pregnancy and elevated liver enzyme levels are more compat- patients with NALD at high risk for cardiovascular events. ible with HELLP syndrome. There is no relationship between statin use and steatosis in If bleeding is not controlled, or if an invasive procedure NAFLD. is planned, transfusion of platelets (Option C) or plasma may No drugs have been approved by the FDA for the treat- be warranted. In the absence of bleeding, as in this patient, ment of NAFLD. Pioglitazone (Option C) and vitamin E administration of platelets is not necessary. Any intervention treatment of biopsy-proven nonalcoholic steatohepatitis that delays delivery of the fetus should be avoided. wn @ improve liver histology, but effects on longer-term clinical Intrahepatic cholestasis of pregnancy can develop = outcomes are not known and routine use for NAFLD is not during earlier stages of pregnancy and causes pruritus. = recommended. Potential complications include premature labor and fetal — rs) death. Although ursodeoxycholic acid (Option D) can be =) = helpful in intrahepatic cholestasis of pregnancy, it has no c e Patients with type 2 diabetes or prediabetes and benefit in the HELLP syndrome and therefore is not an wn id o elevated liver enzymes or fatty liver on ultrasound appropriate choice for this patient. = should be evaluated for presence of nonalcoholic wn = steatohepatitis and liver fibrosis. Pe

outcomes are not known and routine use for NAFLD is not during earlier stages of pregnancy and causes pruritus. = recommended. Potential complications include premature labor and fetal — rs) death. Although ursodeoxycholic acid (Option D) can be =) = helpful in intrahepatic cholestasis of pregnancy, it has no c e Patients with type 2 diabetes or prediabetes and benefit in the HELLP syndrome and therefore is not an wn id o elevated liver enzymes or fatty liver on ultrasound appropriate choice for this patient. = should be evaluated for presence of nonalcoholic wn = steatohepatitis and liver fibrosis. Pe ¢ The HELLP (hemolysis, elevated liver enzymes, and e The mainstay of management of nonalcoholic fatty low platelets) syndrome typically presents with non- liver disease is weight loss. specific symptoms, such as abdominal pain, nausea with vomiting, pruritus, and jaundice. Bibliography Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of e The HELLP syndrome is treated by prompt delivery of nonalcoholic fatty liver disease: Practice guidance from the American the fetus. Association for the Study of Liver Diseases. Hepatology. 2018;67:328-357. [PMID: 28714183] doi:10.1002/hep.29367 Bibliography Chandrasekaran S, Simon R. Hepatic complications in preeclampsia. Clin Obstet Gynecol. 2020;63:165-174. [PMID: 31770122] doi:10.1097/GRF. Item 36 Answer: A 0000000000000501

¢ The HELLP (hemolysis, elevated liver enzymes, and e The mainstay of management of nonalcoholic fatty low platelets) syndrome typically presents with non- liver disease is weight loss. specific symptoms, such as abdominal pain, nausea with vomiting, pruritus, and jaundice. Bibliography Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of e The HELLP syndrome is treated by prompt delivery of nonalcoholic fatty liver disease: Practice guidance from the American the fetus. Association for the Study of Liver Diseases. Hepatology. 2018;67:328-357. [PMID: 28714183] doi:10.1002/hep.29367 Bibliography Chandrasekaran S, Simon R. Hepatic complications in preeclampsia. Clin Obstet Gynecol. 2020;63:165-174. [PMID: 31770122] doi:10.1097/GRF. Item 36 Answer: A 0000000000000501 Educational Objective: Treat the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Item 37 Answer: D The most appropriate management is delivery of the fetus Educational Objective: Manage lactase deficiency. (Option A). The third trimester of pregnancy can be com- plicated by potentially serious liver conditions. The HELLP The most appropriate management is a trial of a lactose-free (hemolysis, elevated liver enzymes, and low platelets) syn- diet (Option D). The patient describes diarrhea lasting longer drome is a serious manifestation of preeclampsia and must be than 4 weeks, thereby meeting the criteria for chronic diar- recognized promptly. HELLP typically presents with nonspe- thea. The lack of nocturnal symptoms and improvement of cific symptoms, such as abdominal pain, nausea with vom- symptoms with fasting suggest osmotic diarrhea. Osmotic iting, pruritus, and jaundice. The only definitive therapy is diarrhea results from a nonabsorbed, osmotically active delivery of the fetus. Prompt treatment is paramount because substance in the intestinal lumen, leading to luminal fluid rates of fetal and maternal mortality are high. Treatment with accumulation due to an osmotic gradient. This gradient is first-line agents for severe hypertension should occur as soon present after ingestion of an osmotically active substance and as possible to reduce the risk for maternal stroke. The goal is absent during fasting (including during sleep). A common is to rapidly achieve a blood pressure in the range of 140 to cause of osmotic diarrhea is lactase deficiency that results 150/90 to 100 mm Hg. Coagulopathy may increase the risk for in lactose malabsorption, which typically presents in young bleeding in the perinatal state. Liver dysfunction can worsen adulthood. In this condition, brush-border lactase is lost and in the 48 hours after delivery before resolving. Rarely, liver ingested lactose is no longer broken down to its constituent transplantation may be required if symptoms of liver failure monosaccharides. The persistent presence of this unabsorbed progress. disaccharide creates an osmotic gradient. Although a lactose Thrombotic thrombocytopenic (TTP) is characterized breath test is available to test for lactase deficiency, the diag- by microangiopathic hemolytic anemia and thrombocyto- nosis can typically be based on improvement after exclusion penia. Acquired TTP is caused by a deficiency in the metal- of dietary lactose or administration of lactase enzymes with loprotease ADAMTS13, which is responsible for cleaving meals.

Educational Objective: Treat the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Item 37 Answer: D The most appropriate management is delivery of the fetus Educational Objective: Manage lactase deficiency. (Option A). The third trimester of pregnancy can be com- plicated by potentially serious liver conditions. The HELLP The most appropriate management is a trial of a lactose-free (hemolysis, elevated liver enzymes, and low platelets) syn- diet (Option D). The patient describes diarrhea lasting longer drome is a serious manifestation of preeclampsia and must be than 4 weeks, thereby meeting the criteria for chronic diar- recognized promptly. HELLP typically presents with nonspe- thea. The lack of nocturnal symptoms and improvement of cific symptoms, such as abdominal pain, nausea with vom- symptoms with fasting suggest osmotic diarrhea. Osmotic iting, pruritus, and jaundice. The only definitive therapy is diarrhea results from a nonabsorbed, osmotically active delivery of the fetus. Prompt treatment is paramount because substance in the intestinal lumen, leading to luminal fluid rates of fetal and maternal mortality are high. Treatment with accumulation due to an osmotic gradient. This gradient is first-line agents for severe hypertension should occur as soon present after ingestion of an osmotically active substance and as possible to reduce the risk for maternal stroke. The goal is absent during fasting (including during sleep). A common is to rapidly achieve a blood pressure in the range of 140 to cause of osmotic diarrhea is lactase deficiency that results 150/90 to 100 mm Hg. Coagulopathy may increase the risk for in lactose malabsorption, which typically presents in young bleeding in the perinatal state. Liver dysfunction can worsen adulthood. In this condition, brush-border lactase is lost and in the 48 hours after delivery before resolving. Rarely, liver ingested lactose is no longer broken down to its constituent transplantation may be required if symptoms of liver failure monosaccharides. The persistent presence of this unabsorbed progress. disaccharide creates an osmotic gradient. Although a lactose Thrombotic thrombocytopenic (TTP) is characterized breath test is available to test for lactase deficiency, the diag- by microangiopathic hemolytic anemia and thrombocyto- nosis can typically be based on improvement after exclusion penia. Acquired TTP is caused by a deficiency in the metal- of dietary lactose or administration of lactase enzymes with loprotease ADAMTS13, which is responsible for cleaving meals. 125

Answer and Critiques s Colonoscopy (Option A) has a role in the evaluation of for oliguria, urinalysis (bland urinary sediment), and urine chronic diarrhea: to diagnose inflammatory bowel disease sodium concentration (low) is also appropriate in the evalua- (IBD) or, along with colonic biopsies, microscopic colitis. tion for suspected hepatorenal syndrome. Although IBD is a cause of chronic diarrhea, it is less com- Fluid restriction (Option B) can be useful in patients mon than lactase deficiency. In addition, this patient’s lack who develop dilutional, hypervolemic hyponatremia. of weight loss, anemia, and negative fecal calprotectin result Although this patient is hypervolemic, she does not have make IBD an unlikely diagnosis. Thus, colonoscopy is not hyponatremia; she has impaired natriuresis and requires necessary. dietary sodium restriction, not fluid restriction. Fructose (Option B), a monosaccharide found in fruit Nonselective B-blockers, such as propranolol (Option C), and as an added sweetener in processed foods, is absorbed are often used in patients with cirrhosis and portal hyper- via a fructose transporter on the luminal surface of entero- tension to decrease portal pressures and reduce risk for vari- cytes (epithelial cells of the small intestine). Defects in ceal hemorrhage. However, in the setting of refractory ascites > this transporter can lead to fructose malabsorption, and or hepatorenal syndrome, B-blocker therapy should not be = wn osmotic diarrhea may ensue. Fructose intolerance is less initiated because it can lower renal perfusion pressures and = common than lactase deficiency and is a controversial @ worsen clinical outcomes. B-Blockers that are already a part = 2) diagnosis. Empiric treatment for lactose malabsorption, a of a patient’s medication regimen should be discontinued y = well-established and common diagnosis, is the most rea- in this context. Q. sonable initial management for this patient. This hypervolemic patient already has excessive total- (a) =F Stool culture (Option C) may be performed in the set- body sodium, and liberalizing dietary sodium intake (Option D) a ting of diarrhea due to a suspected bacterial cause, such as <2 would not be expected to improve clinical outcomes. Rather, = Escherichia coli or Campylobacter jejuni. These infections an increase in dietary sodium intake would worsen volume oO wn typically cause acute diarrhea, not the chronic diarrhea seen overload yet not necessarily improve renal function. in this patient.

Colonoscopy (Option A) has a role in the evaluation of for oliguria, urinalysis (bland urinary sediment), and urine chronic diarrhea: to diagnose inflammatory bowel disease sodium concentration (low) is also appropriate in the evalua- (IBD) or, along with colonic biopsies, microscopic colitis. tion for suspected hepatorenal syndrome. Although IBD is a cause of chronic diarrhea, it is less com- Fluid restriction (Option B) can be useful in patients mon than lactase deficiency. In addition, this patient’s lack who develop dilutional, hypervolemic hyponatremia. of weight loss, anemia, and negative fecal calprotectin result Although this patient is hypervolemic, she does not have make IBD an unlikely diagnosis. Thus, colonoscopy is not hyponatremia; she has impaired natriuresis and requires necessary. dietary sodium restriction, not fluid restriction. Fructose (Option B), a monosaccharide found in fruit Nonselective B-blockers, such as propranolol (Option C), and as an added sweetener in processed foods, is absorbed are often used in patients with cirrhosis and portal hyper- via a fructose transporter on the luminal surface of entero- tension to decrease portal pressures and reduce risk for vari- cytes (epithelial cells of the small intestine). Defects in ceal hemorrhage. However, in the setting of refractory ascites > this transporter can lead to fructose malabsorption, and or hepatorenal syndrome, B-blocker therapy should not be = wn osmotic diarrhea may ensue. Fructose intolerance is less initiated because it can lower renal perfusion pressures and = common than lactase deficiency and is a controversial @ worsen clinical outcomes. B-Blockers that are already a part = 2) diagnosis. Empiric treatment for lactose malabsorption, a of a patient’s medication regimen should be discontinued y = well-established and common diagnosis, is the most rea- in this context. Q. sonable initial management for this patient. This hypervolemic patient already has excessive total- (a) =F Stool culture (Option C) may be performed in the set- body sodium, and liberalizing dietary sodium intake (Option D) a ting of diarrhea due to a suspected bacterial cause, such as <2 would not be expected to improve clinical outcomes. Rather, = Escherichia coli or Campylobacter jejuni. These infections an increase in dietary sodium intake would worsen volume oO wn typically cause acute diarrhea, not the chronic diarrhea seen overload yet not necessarily improve renal function. in this patient. ¢ The initial management of acute kidney injury in e The most common cause of osmotic diarrhea patients with cirrhosis is to stop diuretic therapy. is lactase deficiency that results in lactose e In patients with hepatorenal syndrome, B-blocker malabsorption. therapy should be discontinued. e Lactase deficiency can be diagnosed on the basis of improvement after exclusion of dietary lactose or Bibliography administration of lactase enzymes with meals. Adebayo D, Neong SF, Wong F. Ascites and hepatorenal syndrome. Clin Liver Dis. 2019;23:659-682. [PMID: 31563217] doi:10.1016/j.cld.2019.06.002

¢ The initial management of acute kidney injury in e The most common cause of osmotic diarrhea patients with cirrhosis is to stop diuretic therapy. is lactase deficiency that results in lactose e In patients with hepatorenal syndrome, B-blocker malabsorption. therapy should be discontinued. e Lactase deficiency can be diagnosed on the basis of improvement after exclusion of dietary lactose or Bibliography administration of lactase enzymes with meals. Adebayo D, Neong SF, Wong F. Ascites and hepatorenal syndrome. Clin Liver Dis. 2019;23:659-682. [PMID: 31563217] doi:10.1016/j.cld.2019.06.002 Bibliography Schiller LR, Pardi DS, Sellin JH. Chronic diarrhea: diagnosis and manage- Item 39 Answer: C ment. Clin Gastroenterol Hepatol. 2017;15:182-193.e3. [PMID: 27496381] doi:10.1016/j.cgh.2016.07.028 Educational Objective: Treat spontaneous bacterial peritonitis.

Bibliography Schiller LR, Pardi DS, Sellin JH. Chronic diarrhea: diagnosis and manage- Item 39 Answer: C ment. Clin Gastroenterol Hepatol. 2017;15:182-193.e3. [PMID: 27496381] doi:10.1016/j.cgh.2016.07.028 Educational Objective: Treat spontaneous bacterial peritonitis. Item 38 Answer: A The most appropriate initial treatment is intravenous albu- min and a third-generation cephalosporin, such as cefotax- Educational Objective: Manage renal dysfunction in a ime (Option C). Spontaneous bacterial peritonitis (SBP) is an patient with cirrhosis. infection of ascitic fluid in patients with portal hypertension. The most appropriate initial management is discontinuation SBP can present with fever, abdominal pain, and/or kidney of diuretics (Option A). In a patient with cirrhosis and portal dysfunction; it should be considered in any patient with asci- hypertension, ascites is a manifestation of inadequate natri- tes whose status declines. SBP is diagnosed by an ascitic fluid uresis, with increased splanchnic blood flow and reduced neutrophil count of 250/uL (0.25 x 10°/L) or greater. Bacte- renal perfusion. These factors contribute to accumulation of rial culture of ascitic fluid should also be performed but is fluid in the peritoneal space. Initial management of ascites often negative. Initial treatment of SBP entails prompt initia- includes dietary sodium restriction and diuretic therapy with tion of a third-generation cephalosporin and adjunctive albu- spironolactone and furosemide. As the splanchnic vascula- min therapy. Such treatment has a survival benefit. SBP has a ture progressively dilates and renal perfusion decreases with high mortality rate, and patients who develop SBP should be worsening of portal hypertension, hepatorenal syndrome considered for liver transplantation. can develop, which manifests as declining renal function. In patients with cirrhosis and ascites, long-term pro- ‘The initial evaluation of these patients is investigation for phylactic antibiotic therapy, typically with a fluoroquino- a decrease in intravascular volume and for infection and lone (Option A), is recommended to prevent SBP if the exclusion of other causes of acute kidney injury. In this ascitic fluid protein level is less than 1.5 g/dL (15 g/L) and is patient, furosemide and spironolactone may be exacerbating associated with impaired renal function (serum creatinine renal hypoperfusion and should be stopped. Assessment 21.2 mg/dL [106.1 umol/L], blood urea nitrogen >25 mg/dL

Item 38 Answer: A The most appropriate initial treatment is intravenous albu- min and a third-generation cephalosporin, such as cefotax- Educational Objective: Manage renal dysfunction in a ime (Option C). Spontaneous bacterial peritonitis (SBP) is an patient with cirrhosis. infection of ascitic fluid in patients with portal hypertension. The most appropriate initial management is discontinuation SBP can present with fever, abdominal pain, and/or kidney of diuretics (Option A). In a patient with cirrhosis and portal dysfunction; it should be considered in any patient with asci- hypertension, ascites is a manifestation of inadequate natri- tes whose status declines. SBP is diagnosed by an ascitic fluid uresis, with increased splanchnic blood flow and reduced neutrophil count of 250/uL (0.25 x 10°/L) or greater. Bacte- renal perfusion. These factors contribute to accumulation of rial culture of ascitic fluid should also be performed but is fluid in the peritoneal space. Initial management of ascites often negative. Initial treatment of SBP entails prompt initia- includes dietary sodium restriction and diuretic therapy with tion of a third-generation cephalosporin and adjunctive albu- spironolactone and furosemide. As the splanchnic vascula- min therapy. Such treatment has a survival benefit. SBP has a ture progressively dilates and renal perfusion decreases with high mortality rate, and patients who develop SBP should be worsening of portal hypertension, hepatorenal syndrome considered for liver transplantation. can develop, which manifests as declining renal function. In patients with cirrhosis and ascites, long-term pro- ‘The initial evaluation of these patients is investigation for phylactic antibiotic therapy, typically with a fluoroquino- a decrease in intravascular volume and for infection and lone (Option A), is recommended to prevent SBP if the exclusion of other causes of acute kidney injury. In this ascitic fluid protein level is less than 1.5 g/dL (15 g/L) and is patient, furosemide and spironolactone may be exacerbating associated with impaired renal function (serum creatinine renal hypoperfusion and should be stopped. Assessment 21.2 mg/dL [106.1 umol/L], blood urea nitrogen >25 mg/dL 126

Answers.and Gritiguis [8.9 mmol/L], or serum sodium <130 mEq/L [130 mmol/L]) cholecystectomy or after partial ileal resection because of or liver failure (Child-Turcotte-Pugh score >9 and bilirubin incomplete enterohepatic recirculation of bile acids. This CONT. level >3 mg/dL [51.3 wmol/L]). Fluoroquinolones are typi- form of diarrhea can be treated with a bile salt binder, such cally not used as initial treatment of SBP. as cholestyramine. Secretory diarrhea due to bile acid excess In general, large-volume paracentesis should be results in an osmotic gap less than 50 mOsm/kg; given this avoided when SBP is suspected because it may result in patient’s gap of 111 mOsm/kg, this cause is unlikely. fluid shifts from the intervascular space to the peritoneal Enterotoxigenic Escherichia coli infection (Option B) cavity, decreasing the effective circulating volume, activating is a common cause of traveler’s diarrhea, characterized as the renin-angiotensin system, and precipitating hepatorenal watery diarrhea of a secretory subtype. The presence of an syndrome. The infusion of albumin (Option B) following osmotic gap excludes this infection. paracentesis for therapeutic purposes is recommended for VIPoma (Option D) is a rare form of functional neuro- higher-volume paracentesis greater than 5 L. endocrine tumor that is usually located in the pancreas. The Trimethoprim-sulfamethoxazole (Option D) can be secretion of vasoactive intestinal peptide (VIP) by this tumor 4] v used for secondary prophylaxis of SBP but is not appropriate results in a secretory diarrhea. This patient’s stool studies are 2 zs as initial treatment. consistent with osmotic diarrhea. = = rs) cs e In patients with liquid stool, a calculated osmotic = e Spontaneous bacterial peritonitis is diagnosed by an co

[8.9 mmol/L], or serum sodium <130 mEq/L [130 mmol/L]) cholecystectomy or after partial ileal resection because of or liver failure (Child-Turcotte-Pugh score >9 and bilirubin incomplete enterohepatic recirculation of bile acids. This CONT. level >3 mg/dL [51.3 wmol/L]). Fluoroquinolones are typi- form of diarrhea can be treated with a bile salt binder, such cally not used as initial treatment of SBP. as cholestyramine. Secretory diarrhea due to bile acid excess In general, large-volume paracentesis should be results in an osmotic gap less than 50 mOsm/kg; given this avoided when SBP is suspected because it may result in patient’s gap of 111 mOsm/kg, this cause is unlikely. fluid shifts from the intervascular space to the peritoneal Enterotoxigenic Escherichia coli infection (Option B) cavity, decreasing the effective circulating volume, activating is a common cause of traveler’s diarrhea, characterized as the renin-angiotensin system, and precipitating hepatorenal watery diarrhea of a secretory subtype. The presence of an syndrome. The infusion of albumin (Option B) following osmotic gap excludes this infection. paracentesis for therapeutic purposes is recommended for VIPoma (Option D) is a rare form of functional neuro- higher-volume paracentesis greater than 5 L. endocrine tumor that is usually located in the pancreas. The Trimethoprim-sulfamethoxazole (Option D) can be secretion of vasoactive intestinal peptide (VIP) by this tumor 4] v used for secondary prophylaxis of SBP but is not appropriate results in a secretory diarrhea. This patient’s stool studies are 2 zs as initial treatment. consistent with osmotic diarrhea. = = rs) cs e In patients with liquid stool, a calculated osmotic = e Spontaneous bacterial peritonitis is diagnosed by an co ascitic fluid neutrophil count of 250/uL (0.25 x 10°/L) gap of greater than 100 mOsm/kg suggests osmotic wn td aw or higher. diarrhea. = wn e Treatment of spontaneous bacterial peritonitis e The fecal osmotic gap is calculated as follows: 290 - S <x includes a third-generation cephalosporin; albumin (2 x [stool sodium + stool potassium]). is infused in the presence of hepatic (bilirubin level >4 mg/dL [68.4 umol/L]) or kidney dysfunction. Bibliography Schiller LR, Pardi DS, Sellin JH. Chronic diarrhea: diagnosis and manage- ment. Clin Gastroenterol Hepatol. 2017;15:182-193.e3. [PMID: 27496381] Bibliography doi:10.1016/j.cgh.2016.07.028 Pericleous M, Sarnowski A, Moore A, et al. The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol. 2016;28:e10-8. [PMID: 26671516] doi:10.1097/ Item 41 Answer: A MEG.0000000000000548 Educational Objective: Diagnose achalasia.

ascitic fluid neutrophil count of 250/uL (0.25 x 10°/L) gap of greater than 100 mOsm/kg suggests osmotic wn td aw or higher. diarrhea. = wn e Treatment of spontaneous bacterial peritonitis e The fecal osmotic gap is calculated as follows: 290 - S <x includes a third-generation cephalosporin; albumin (2 x [stool sodium + stool potassium]). is infused in the presence of hepatic (bilirubin level >4 mg/dL [68.4 umol/L]) or kidney dysfunction. Bibliography Schiller LR, Pardi DS, Sellin JH. Chronic diarrhea: diagnosis and manage- ment. Clin Gastroenterol Hepatol. 2017;15:182-193.e3. [PMID: 27496381] Bibliography doi:10.1016/j.cgh.2016.07.028 Pericleous M, Sarnowski A, Moore A, et al. The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol. 2016;28:e10-8. [PMID: 26671516] doi:10.1097/ Item 41 Answer: A MEG.0000000000000548 Educational Objective: Diagnose achalasia. The most likely diagnosis is achalasia (Option A). Achalasia is Item 40 Answer: C associated with dysphagia with both solids and liquids, along with nonacidic regurgitation of undigested food. Additional Educational Objective: Diagnose osmotic diarrhea. symptoms include heartburn, weight loss, and chest pain The patient’s stool studies are most consistent with osmotic unresponsive to acid-reducing agents. It can be idiopathic diarrhea. Fructose malabsorption (Option C) is a common or associated with viral, autoimmune, and neurodegenera- cause of this form of diarrhea. Chronic diarrhea can be classi- tive disorders and infection (e.g., Chagas disease). The initial fied as osmotic, secretory, steatorrhea, inflammatory, motility, diagnostic test is barium esophagography or upper endoscopy, or miscellaneous. Classification allows narrowing the dif- which shows dilation of the esophagus with narrowing at the ferential diagnosis to guide selective laboratory testing and gastroesophageal junction. In classic achalasia, esophageal imaging. Stool electrolytes measured in liquid stool can help manometry shows incomplete relaxation of the lower esoph- identify osmotic diarrhea, as indicated by a fecal osmotic gap, ageal sphincter and aperistalsis; however, not all patients with which suggests an unmeasured osmotically active intralu- conditions on the spectrum of achalasia-type disorders have minal substance. The fecal osmotic gap can be calculated as these classic findings. Upper endoscopy reveals retained food follows: 290 - (2 x [stool sodium + stool potassium]). In this and saliva, no signs of mechanical obstruction, and “tight- patient, the fecal osmotic gap is: 290 - (2 x [85 + 4.5]) = 111 ness” at the gastroesophageal junction while the scope is mOsm/kg. An osmotic gap of greater than 100 mOsm/kg advanced into the stomach. Treatment of achalasia aims to suggests an unmeasured osmotically active substance. Such decrease lower esophageal sphincter pressure, which relieves substances include malabsorbed carbohydrates (e.g., lactose symptoms. Treatments include botulinum toxin injection, or fructose) and sorbitol. The latter is an artificial sweetener pneumatic balloon dilation, peroral endoscopic myotomy, or commonly found in sugar-free gum. Treatment of osmotic laparoscopic myotomy. Choice of therapy depends on patient diarrhea requires avoiding offending agents, such as following factors, type of disease, and available local expertise. a low-fermentable oligosaccharides, disaccharides, monosac- Barrett esophagus (Option B) is a risk factor for esoph- charides, and polyols (FODMAP) and a lactose-free diet. ageal cancer and a complication of reflux disease, but this Intraluminal bile acid excess (Option A) can cause condition alone does not cause symptoms or dysphagia and secretory diarrhea. This condition can develop after cannot account for this patient’s symptoms.

The most likely diagnosis is achalasia (Option A). Achalasia is Item 40 Answer: C associated with dysphagia with both solids and liquids, along with nonacidic regurgitation of undigested food. Additional Educational Objective: Diagnose osmotic diarrhea. symptoms include heartburn, weight loss, and chest pain The patient’s stool studies are most consistent with osmotic unresponsive to acid-reducing agents. It can be idiopathic diarrhea. Fructose malabsorption (Option C) is a common or associated with viral, autoimmune, and neurodegenera- cause of this form of diarrhea. Chronic diarrhea can be classi- tive disorders and infection (e.g., Chagas disease). The initial fied as osmotic, secretory, steatorrhea, inflammatory, motility, diagnostic test is barium esophagography or upper endoscopy, or miscellaneous. Classification allows narrowing the dif- which shows dilation of the esophagus with narrowing at the ferential diagnosis to guide selective laboratory testing and gastroesophageal junction. In classic achalasia, esophageal imaging. Stool electrolytes measured in liquid stool can help manometry shows incomplete relaxation of the lower esoph- identify osmotic diarrhea, as indicated by a fecal osmotic gap, ageal sphincter and aperistalsis; however, not all patients with which suggests an unmeasured osmotically active intralu- conditions on the spectrum of achalasia-type disorders have minal substance. The fecal osmotic gap can be calculated as these classic findings. Upper endoscopy reveals retained food follows: 290 - (2 x [stool sodium + stool potassium]). In this and saliva, no signs of mechanical obstruction, and “tight- patient, the fecal osmotic gap is: 290 - (2 x [85 + 4.5]) = 111 ness” at the gastroesophageal junction while the scope is mOsm/kg. An osmotic gap of greater than 100 mOsm/kg advanced into the stomach. Treatment of achalasia aims to suggests an unmeasured osmotically active substance. Such decrease lower esophageal sphincter pressure, which relieves substances include malabsorbed carbohydrates (e.g., lactose symptoms. Treatments include botulinum toxin injection, or fructose) and sorbitol. The latter is an artificial sweetener pneumatic balloon dilation, peroral endoscopic myotomy, or commonly found in sugar-free gum. Treatment of osmotic laparoscopic myotomy. Choice of therapy depends on patient diarrhea requires avoiding offending agents, such as following factors, type of disease, and available local expertise. a low-fermentable oligosaccharides, disaccharides, monosac- Barrett esophagus (Option B) is a risk factor for esoph- charides, and polyols (FODMAP) and a lactose-free diet. ageal cancer and a complication of reflux disease, but this Intraluminal bile acid excess (Option A) can cause condition alone does not cause symptoms or dysphagia and secretory diarrhea. This condition can develop after cannot account for this patient’s symptoms. 127

Answers and Critiques Eosinophilic esophagitis (Option C) may also present a meal for 30 minutes. The use of dietary supplements, such with dysphagia and may be initially misdiagnosed as reflux. as guar gum or pectin, to increase food viscosity can also be Patients with eosinophilic esophagitis, however, usually helpful. present with solid food dysphagia rather than solid and Pharmacologic interventions can be considered when liquid dysphagia and regurgitation symptoms. In addition, the previously mentioned measures fail, although no phar- most adult patients are men, typically in their fourth decade macologic treatment has been approved for dumping syn- of life, with a history of allergic disease. drome. The currently available options include acarbose Although this patient has not responded to proton (Option A) and, in severe cases, somatostatin analogues. pump inhibitor therapy, refractory gastroesophageal reflux Acarbose, an a-glycosidase hydrolase inhibitor that inter- disease (Option D) is unlikely to be the correct diagnosis feres with digestion of polysaccharides to monosaccharides, given the dysphagia and weight loss. Patients with a motil- can be used for late symptoms of dumping syndrome if ity disorder are often misdiagnosed with more common dietary intervention is only partially successful. > diseases, such as reflux. A careful history is needed to elicit Metoclopramide (Option B) is a prokinetic approved for = n regurgitation and dysphagia symptoms that suggest a motil- the treatment of gastroparesis. However, this patient does = ity disorder. not have gastroparesis, as documented by the normal results oO = wa Viral esophagitis (Option E) tends to present more of a gastric emptying study. ro) = often with odynophagia and is more often seen in immu- Rifaximin (Option C) is indicated for irritable bowel a. nosuppressed individuals. Viral esophagitis does not result syndrome with diarrhea, which this patient does not have. a = in regurgitation or dysphagia with both solids and liquids. ae 2 i= ¢ Dumping syndrome results from rapid gastric empty- @ w” e Achalasia is associated with dysphagia with both solids ing after gastric surgery; symptoms can include and liquids, along with nonacidic regurgitation of abdominal pain, epigastric fullness, diarrhea, nausea, undigested food. vomiting, borborygmi, and bloating.

Eosinophilic esophagitis (Option C) may also present a meal for 30 minutes. The use of dietary supplements, such with dysphagia and may be initially misdiagnosed as reflux. as guar gum or pectin, to increase food viscosity can also be Patients with eosinophilic esophagitis, however, usually helpful. present with solid food dysphagia rather than solid and Pharmacologic interventions can be considered when liquid dysphagia and regurgitation symptoms. In addition, the previously mentioned measures fail, although no phar- most adult patients are men, typically in their fourth decade macologic treatment has been approved for dumping syn- of life, with a history of allergic disease. drome. The currently available options include acarbose Although this patient has not responded to proton (Option A) and, in severe cases, somatostatin analogues. pump inhibitor therapy, refractory gastroesophageal reflux Acarbose, an a-glycosidase hydrolase inhibitor that inter- disease (Option D) is unlikely to be the correct diagnosis feres with digestion of polysaccharides to monosaccharides, given the dysphagia and weight loss. Patients with a motil- can be used for late symptoms of dumping syndrome if ity disorder are often misdiagnosed with more common dietary intervention is only partially successful. > diseases, such as reflux. A careful history is needed to elicit Metoclopramide (Option B) is a prokinetic approved for = n regurgitation and dysphagia symptoms that suggest a motil- the treatment of gastroparesis. However, this patient does = ity disorder. not have gastroparesis, as documented by the normal results oO = wa Viral esophagitis (Option E) tends to present more of a gastric emptying study. ro) = often with odynophagia and is more often seen in immu- Rifaximin (Option C) is indicated for irritable bowel a. nosuppressed individuals. Viral esophagitis does not result syndrome with diarrhea, which this patient does not have. a = in regurgitation or dysphagia with both solids and liquids. ae 2 i= ¢ Dumping syndrome results from rapid gastric empty- @ w” e Achalasia is associated with dysphagia with both solids ing after gastric surgery; symptoms can include and liquids, along with nonacidic regurgitation of abdominal pain, epigastric fullness, diarrhea, nausea, undigested food. vomiting, borborygmi, and bloating. ¢ Achalasia treatment includes botulinum toxin injec- ¢ First-line treatment of dumping syndrome is smaller, tion, pneumatic balloon dilation, peroral endoscopic more frequent meals. myotomy, or laparoscopic myotomy.

Eosinophilic esophagitis (Option C) may also present a meal for 30 minutes. The use of dietary supplements, such with dysphagia and may be initially misdiagnosed as reflux. as guar gum or pectin, to increase food viscosity can also be Patients with eosinophilic esophagitis, however, usually helpful. present with solid food dysphagia rather than solid and Pharmacologic interventions can be considered when liquid dysphagia and regurgitation symptoms. In addition, the previously mentioned measures fail, although no phar- most adult patients are men, typically in their fourth decade macologic treatment has been approved for dumping syn- of life, with a history of allergic disease. drome. The currently available options include acarbose Although this patient has not responded to proton (Option A) and, in severe cases, somatostatin analogues. pump inhibitor therapy, refractory gastroesophageal reflux Acarbose, an a-glycosidase hydrolase inhibitor that inter- disease (Option D) is unlikely to be the correct diagnosis feres with digestion of polysaccharides to monosaccharides, given the dysphagia and weight loss. Patients with a motil- can be used for late symptoms of dumping syndrome if ity disorder are often misdiagnosed with more common dietary intervention is only partially successful. > diseases, such as reflux. A careful history is needed to elicit Metoclopramide (Option B) is a prokinetic approved for = n regurgitation and dysphagia symptoms that suggest a motil- the treatment of gastroparesis. However, this patient does = ity disorder. not have gastroparesis, as documented by the normal results oO = wa Viral esophagitis (Option E) tends to present more of a gastric emptying study. ro) = often with odynophagia and is more often seen in immu- Rifaximin (Option C) is indicated for irritable bowel a. nosuppressed individuals. Viral esophagitis does not result syndrome with diarrhea, which this patient does not have. a = in regurgitation or dysphagia with both solids and liquids. ae 2 i= ¢ Dumping syndrome results from rapid gastric empty- @ w” e Achalasia is associated with dysphagia with both solids ing after gastric surgery; symptoms can include and liquids, along with nonacidic regurgitation of abdominal pain, epigastric fullness, diarrhea, nausea, undigested food. vomiting, borborygmi, and bloating. ¢ Achalasia treatment includes botulinum toxin injec- ¢ First-line treatment of dumping syndrome is smaller, tion, pneumatic balloon dilation, peroral endoscopic more frequent meals. myotomy, or laparoscopic myotomy. Bibliography Bibliography Vavricka SR, Greuter T. Gastroparesis and dumping syndrome: current con- Zaninotto G, Bennett C, Boeckxstaens G, et al. The 2018 ISDE achalasia cepts and management. J Clin Med. 2019;8. [PMID: 31362413] doi:10.3390/ guidelines. Dis Esophagus. 2018;31. [PMID: 30169645] doi:10.1093/dote/ jem8081127

Bibliography Bibliography Vavricka SR, Greuter T. Gastroparesis and dumping syndrome: current con- Zaninotto G, Bennett C, Boeckxstaens G, et al. The 2018 ISDE achalasia cepts and management. J Clin Med. 2019;8. [PMID: 31362413] doi:10.3390/ guidelines. Dis Esophagus. 2018;31. [PMID: 30169645] doi:10.1093/dote/ jem8081127 doy071 Item 43 Answer: C Item 42 Answer: D Educational Objective: Treat hepatic adenoma ina Educational Objective: Treat dumping syndrome. man.

Bibliography Bibliography Vavricka SR, Greuter T. Gastroparesis and dumping syndrome: current con- Zaninotto G, Bennett C, Boeckxstaens G, et al. The 2018 ISDE achalasia cepts and management. J Clin Med. 2019;8. [PMID: 31362413] doi:10.3390/ guidelines. Dis Esophagus. 2018;31. [PMID: 30169645] doi:10.1093/dote/ jem8081127 doy071 Item 43 Answer: C Item 42 Answer: D Educational Objective: Treat hepatic adenoma ina Educational Objective: Treat dumping syndrome. man. The most appropriate treatment is smaller, more frequent The most appropriate management is surgical resection meals (Option D). This patient most likely has dumping syn- (Option C). Hepatic adenomas are benign neoplasms that drome as a consequence of her sleeve gastrectomy. Dumping often are found incidentally. They can be differentiated from syndrome can followa variety of surgical procedures, includ- focal nodular hyperplasia by abdominal MRI with gadoxetate ing vagotomy, pyloroplasty, Roux-en-Y bypass, sleeve gastrec- sodium. This contrast agent is excreted in the bile ducts and tomy, and esophagectomy. Early dumping syndrome, as in therefore clarifies the presence of a hepatic adenoma, which this patient, results from the rapid transition of food into the does not typically excrete bile. Most hepatic adenomas are small intestine, causing a fluid shift and potential release of found in women (and are eight times more common than gastrointestinal hormones with vasoactive properties. Classic in men), particularly those using oral contraceptive agents. gastrointestinal symptoms can include abdominal pain, epi- Factors posing an increased risk for malignant transformation gastric fullness, diarrhea, nausea, vomiting, borborygmi, and of hepatic adenomas include adenomas greater than 5 cm in bloating. Classic vasomotor symptoms can include palpita- diameter and adenomas with B-catenin activation. Adenomas tions and tachycardia, faintness or syncope, diaphoresis, and in men commonly have B-catenin activation; therefore, sur- flushing and pallor. Symptoms typically occur within 1 hour gical resection of adenomas found in men is recommended. of eating. Treatment should be tiered, beginning with dietary Liver biopsy (Option A) is indicated in patients with modifications and patient education by a trained dietitian. diagnostic uncertainty but may increase the risk for bleed- Dietary interventions can include the pursuit of smaller and ing; therefore, it should be performed only if the diagnosis more frequent meals (at least six per day); delayed intake of will result in a meaningful change in management. In fluids by at least 30 minutes after intake of solids; avoidance patients with hepatic adenomas, liver biopsy can clarify the of rapidly absorbable carbohydrates and alcohol; increased expression of B-catenin. Because adenomas that express intake of high-fiber, high-protein foods; and lying down after activated B-catenin are at increased risk for malignancy, liver

The most appropriate treatment is smaller, more frequent The most appropriate management is surgical resection meals (Option D). This patient most likely has dumping syn- (Option C). Hepatic adenomas are benign neoplasms that drome as a consequence of her sleeve gastrectomy. Dumping often are found incidentally. They can be differentiated from syndrome can followa variety of surgical procedures, includ- focal nodular hyperplasia by abdominal MRI with gadoxetate ing vagotomy, pyloroplasty, Roux-en-Y bypass, sleeve gastrec- sodium. This contrast agent is excreted in the bile ducts and tomy, and esophagectomy. Early dumping syndrome, as in therefore clarifies the presence of a hepatic adenoma, which this patient, results from the rapid transition of food into the does not typically excrete bile. Most hepatic adenomas are small intestine, causing a fluid shift and potential release of found in women (and are eight times more common than gastrointestinal hormones with vasoactive properties. Classic in men), particularly those using oral contraceptive agents. gastrointestinal symptoms can include abdominal pain, epi- Factors posing an increased risk for malignant transformation gastric fullness, diarrhea, nausea, vomiting, borborygmi, and of hepatic adenomas include adenomas greater than 5 cm in bloating. Classic vasomotor symptoms can include palpita- diameter and adenomas with B-catenin activation. Adenomas tions and tachycardia, faintness or syncope, diaphoresis, and in men commonly have B-catenin activation; therefore, sur- flushing and pallor. Symptoms typically occur within 1 hour gical resection of adenomas found in men is recommended. of eating. Treatment should be tiered, beginning with dietary Liver biopsy (Option A) is indicated in patients with modifications and patient education by a trained dietitian. diagnostic uncertainty but may increase the risk for bleed- Dietary interventions can include the pursuit of smaller and ing; therefore, it should be performed only if the diagnosis more frequent meals (at least six per day); delayed intake of will result in a meaningful change in management. In fluids by at least 30 minutes after intake of solids; avoidance patients with hepatic adenomas, liver biopsy can clarify the of rapidly absorbable carbohydrates and alcohol; increased expression of B-catenin. Because adenomas that express intake of high-fiber, high-protein foods; and lying down after activated B-catenin are at increased risk for malignancy, liver 128

Answers and Critiques biopsy is potentially useful if surgical resection is being con- discharge is a cause of PPI overuse. The goal should be to use sidered. In this patient, whose risk for malignancy is already the lowest dose to control symptoms and discontinue therapy increased because he is male, liver biopsy is not necessary. if there is no appropriate indication. Adverse effects of PPI In women with hepatic adenomas that are 5 cm or may include headache and gastrointestinal distress. Vitamin smaller in diameter or that do not completely regress on ces- B,. deficiency, hypomagnesemia, and subsequent hypocal- sation of oral contraceptive agents, serial abdominal imaging cemia and hypokalemia may also be associated with PPI use. (Option B) every 6 months is recommended to evaluate for Risk for community-acquired pneumonia or Clostridioides growth that would increase the risk for malignancy or hem- difficile infection also may be increased. Additional concerns orrhage. This option would be reasonable if this patient were have been raised regarding hip fracture, kidney injury, and female but is not appropriate for a male patient. dementia, but causal relationships are unproven. Because this Benign lesions, including focal nodular hyperplasia, patient has no indication for PPI use, continuing this therapy hepatic hemangioma, and simple hepatic cysts, do not pose would be unnecessary. appreciable risk for malignant transformation. When these Barium esophagography (Option A) is useful in the wn ov lesions are diagnosed by abdominal imaging, biopsy or serial evaluation of esophageal dysphagia, especially when there =

biopsy is potentially useful if surgical resection is being con- discharge is a cause of PPI overuse. The goal should be to use sidered. In this patient, whose risk for malignancy is already the lowest dose to control symptoms and discontinue therapy increased because he is male, liver biopsy is not necessary. if there is no appropriate indication. Adverse effects of PPI In women with hepatic adenomas that are 5 cm or may include headache and gastrointestinal distress. Vitamin smaller in diameter or that do not completely regress on ces- B,. deficiency, hypomagnesemia, and subsequent hypocal- sation of oral contraceptive agents, serial abdominal imaging cemia and hypokalemia may also be associated with PPI use. (Option B) every 6 months is recommended to evaluate for Risk for community-acquired pneumonia or Clostridioides growth that would increase the risk for malignancy or hem- difficile infection also may be increased. Additional concerns orrhage. This option would be reasonable if this patient were have been raised regarding hip fracture, kidney injury, and female but is not appropriate for a male patient. dementia, but causal relationships are unproven. Because this Benign lesions, including focal nodular hyperplasia, patient has no indication for PPI use, continuing this therapy hepatic hemangioma, and simple hepatic cysts, do not pose would be unnecessary. appreciable risk for malignant transformation. When these Barium esophagography (Option A) is useful in the wn ov lesions are diagnosed by abdominal imaging, biopsy or serial evaluation of esophageal dysphagia, especially when there = imaging thereafter is not necessary. Hepatic adenomas pres- is a suspicion for motility disorders or proximal lesions (e.g., = = ent a risk for hemorrhage or malignant transformation, Zenker diverticulum). This test would be of little yield in fs) particularly if they grow to greater than 5 cm or are found this patient without dysphagia whose endoscopy showed no sc <= in men. Therefore, clinical observation (Option D) in this other structural issues. c

imaging thereafter is not necessary. Hepatic adenomas pres- is a suspicion for motility disorders or proximal lesions (e.g., = = ent a risk for hemorrhage or malignant transformation, Zenker diverticulum). This test would be of little yield in fs) particularly if they grow to greater than 5 cm or are found this patient without dysphagia whose endoscopy showed no sc <= in men. Therefore, clinical observation (Option D) in this other structural issues. c patient is not appropriate. Testing for Helicobacter pylori (Option C) would be wn Cd o warranted for peptic ulcer disease or gastritis. Because this = wn patient had an identified cause of his upper gastrointestinal S e Factors posing an increased risk for malignant trans- bleeding and has no additional pathology or risk factors, 4

patient is not appropriate. Testing for Helicobacter pylori (Option C) would be wn Cd o warranted for peptic ulcer disease or gastritis. Because this = wn patient had an identified cause of his upper gastrointestinal S e Factors posing an increased risk for malignant trans- bleeding and has no additional pathology or risk factors, 4 formation of hepatic adenomas include adenomas H. pylori testing is not indicated. greater than 5 cm in diameter, adenomas with In the absence of recurrent bleeding, repeat upper B-catenin activation, or adenomas found in men. endoscopy (Option D) to assess for healing in patients with ¢ Oral contraceptives should be discontinued in women Mallory-Weiss tear is not indicated. Repeat upper endo-

formation of hepatic adenomas include adenomas H. pylori testing is not indicated. greater than 5 cm in diameter, adenomas with In the absence of recurrent bleeding, repeat upper B-catenin activation, or adenomas found in men. endoscopy (Option D) to assess for healing in patients with ¢ Oral contraceptives should be discontinued in women Mallory-Weiss tear is not indicated. Repeat upper endo- with hepatic adenomas with follow-up CT or MRI at scopy in upper gastrointestinal bleeding is reserved for select patients with peptic ulcer disease (persistent symptoms after 6-month intervals to confirm stability or regression in 8 to 12 weeks of therapy, ulcers of unknown cause, or no the size of the lesion. gastric ulcer biopsy during initial endoscopy), patients with severe erosive esophagitis, and patients with esophageal Bibliography varices. Bioulac-Sage P, Sempoux C, Balabaud C. Hepatocellular adenoma: classifi- cation, variants and clinical relevance. Semin Diagn Pathol. 2017;34:112- 25. [PMID: 28131467] doi:10.1053/j.semdp.2016.12.007

with hepatic adenomas with follow-up CT or MRI at scopy in upper gastrointestinal bleeding is reserved for select patients with peptic ulcer disease (persistent symptoms after 6-month intervals to confirm stability or regression in 8 to 12 weeks of therapy, ulcers of unknown cause, or no the size of the lesion. gastric ulcer biopsy during initial endoscopy), patients with severe erosive esophagitis, and patients with esophageal Bibliography varices. Bioulac-Sage P, Sempoux C, Balabaud C. Hepatocellular adenoma: classifi- cation, variants and clinical relevance. Semin Diagn Pathol. 2017;34:112- 25. [PMID: 28131467] doi:10.1053/j.semdp.2016.12.007 ¢ Unnecessary continuation of proton pump inhibitors (PPIs) after hospital discharge is a cause of PPI overuse. Item 44 Answer: B e PPI therapy should be used at the lowest dose to Educational Objective: Avoid overuse of proton pump control symptoms and discontinued if there is no inhibitor therapy. appropriate indication. The most appropriate management is discontinuation of omeprazole (Option B). This patient had upper gastrointes- Bibliography tinal bleeding secondary to a Mallory-Weiss tear. This small Heidelbaugh JJ, Kim AH, Chang R, et al. Overutilization of proton-pump mucosal defect may occur after repeated vomiting and may inhibitors: what the clinician needs to know. Therap Adv Gastroenterol. 2012;5:219-32. [PMID: 22778788] doi:10.1177/1756283X12437358 cause bleeding, often self-limited. In this patient, a proton pump inhibitor (PPI), omeprazole, was started during hospi- talization for gastrointestinal bleeding, before endoscopy and Item 45 Answer: A the diagnosis of Mallory-Weiss tear, and the drug was never Educational Objective: Evaluate recurrent celiac disease discontinued. PPI therapy is given to all patients suspected of symptoms. having clinically significant upper gastrointestinal bleeding before endoscopy as part of their initial management and The most appropriate initial management is assessment for is continued following hospital discharge in patients with inadvertent gluten exposure (Option A). This patient with a bleeding due to peptic ulcer disease. In patients with Mallory- history of celiac disease now presents with recurrent symp- Weiss tear, PPI therapy to prevent recurrent bleeding is less toms. The most common cause of recurrent celiac disease well studied but is not commonly used. This patient does symptoms is gluten exposure. This exposure may be inad- not have a guideline-recommended indication for contin- vertent. This patient’s elevated tissue transglutaminase IgA ued PPI use, and it would be appropriate to discontinue the level 10 years after diagnosis is suspicious for ongoing gluten omeprazole. Unnecessary continuation of PPIs after hospital exposure because serologic results typically normalize within

¢ Unnecessary continuation of proton pump inhibitors (PPIs) after hospital discharge is a cause of PPI overuse. Item 44 Answer: B e PPI therapy should be used at the lowest dose to Educational Objective: Avoid overuse of proton pump control symptoms and discontinued if there is no inhibitor therapy. appropriate indication. The most appropriate management is discontinuation of omeprazole (Option B). This patient had upper gastrointes- Bibliography tinal bleeding secondary to a Mallory-Weiss tear. This small Heidelbaugh JJ, Kim AH, Chang R, et al. Overutilization of proton-pump mucosal defect may occur after repeated vomiting and may inhibitors: what the clinician needs to know. Therap Adv Gastroenterol. 2012;5:219-32. [PMID: 22778788] doi:10.1177/1756283X12437358 cause bleeding, often self-limited. In this patient, a proton pump inhibitor (PPI), omeprazole, was started during hospi- talization for gastrointestinal bleeding, before endoscopy and Item 45 Answer: A the diagnosis of Mallory-Weiss tear, and the drug was never Educational Objective: Evaluate recurrent celiac disease discontinued. PPI therapy is given to all patients suspected of symptoms. having clinically significant upper gastrointestinal bleeding before endoscopy as part of their initial management and The most appropriate initial management is assessment for is continued following hospital discharge in patients with inadvertent gluten exposure (Option A). This patient with a bleeding due to peptic ulcer disease. In patients with Mallory- history of celiac disease now presents with recurrent symp- Weiss tear, PPI therapy to prevent recurrent bleeding is less toms. The most common cause of recurrent celiac disease well studied but is not commonly used. This patient does symptoms is gluten exposure. This exposure may be inad- not have a guideline-recommended indication for contin- vertent. This patient’s elevated tissue transglutaminase IgA ued PPI use, and it would be appropriate to discontinue the level 10 years after diagnosis is suspicious for ongoing gluten omeprazole. Unnecessary continuation of PPIs after hospital exposure because serologic results typically normalize within 129

Answers and Critiques 1 year of starting a gluten-free diet. Before nonresponsive generally resolve within a few weeks with the use of sitz baths, celiac disease is diagnosed, a dietitian’s evaluation of the psyllium, bulking agents, and topical vasodilators (nifedipine patient’s exposure to dietary gluten is important. and nitroglycerin). Topical anesthetics and anti-inflammatory In patients who truly have unresponsive celiac dis- agents can be considered to address pain or bleeding, but their ease, other diagnoses should be considered. Some reports use is not required to promote fissure healing. suggest that approximately 10% of patients with celiac Angiodysplasia (Option B) can occur throughout the disease and recurrent symptoms have a concurrent diag- colon but is most common in the right colon. Angiodysplasia- nosis. Conditions to consider include HIV infection, irrita- related bleeding is typically painless and causes bleeding ble bowel syndrome, small intestinal bacterial overgrowth, episodes that are unrelated to defecation. Because this microscopic colitis (Option B), and pancreatic insufficiency patient has pain with defecation, angiodysplasia is not a (Option C). This patient does not appear to have risk factors likely cause of his symptoms. for small intestinal bacterial overgrowth or chronic pan- Hemorrhoids (Option C) are submucosal, arteriovenous S creatitis. Microscopic colitis deserves particular attention sinusoids that are part of normal anorectal anatomy and are = wn because approximately 4% of patients with celiac disease believed to play an important role in anal canal function. = have this condition, but it is more typically found in mid- Age-related changes can cause the hemorrhoid beds to slide oO back and forth during defecation, resulting in mucoid anal = rn dle-age and older women. Because inadvertent exposure oY) to gluten is the most common cause of recurrent celiac discharge, as well as perianal wetness, soiling, irritation, = a. disease symptoms, a referral to a dietitian and exploration and/or pruritus. Hemorrhoidal bleeding is most often asso- (2) =. of possible sources of gluten exposure is the best initial ciated with painless defecation. The presence of pain (as in =. management option. this patient) should raise suspicion for an alternative diagno- 2 = Upper endoscopy with duodenal biopsy is necessary to sis, such as anal fissure. © wn diagnose celiac disease. This procedure also plays a role in Rectal cancer (Option D) should always be considered the assessment for unresponsive celiac disease, including in a patient with new-onset rectal outlet bleeding. However, evaluation for intestinal lymphoma (Option D) or adenocar- painful defecation typically does not occur with rectal can- cinoma, which can complicate celiac disease and manifest as cer. In this patient, the presence of pain with defecation and unresponsive disease. However, unresponsive celiac disease the history of normal findings on screening colonoscopy is far less likely than inadvertent gluten intake as a cause of 2 years previously make rectal cancer unlikely. this patient’s recurrent symptoms.

1 year of starting a gluten-free diet. Before nonresponsive generally resolve within a few weeks with the use of sitz baths, celiac disease is diagnosed, a dietitian’s evaluation of the psyllium, bulking agents, and topical vasodilators (nifedipine patient’s exposure to dietary gluten is important. and nitroglycerin). Topical anesthetics and anti-inflammatory In patients who truly have unresponsive celiac dis- agents can be considered to address pain or bleeding, but their ease, other diagnoses should be considered. Some reports use is not required to promote fissure healing. suggest that approximately 10% of patients with celiac Angiodysplasia (Option B) can occur throughout the disease and recurrent symptoms have a concurrent diag- colon but is most common in the right colon. Angiodysplasia- nosis. Conditions to consider include HIV infection, irrita- related bleeding is typically painless and causes bleeding ble bowel syndrome, small intestinal bacterial overgrowth, episodes that are unrelated to defecation. Because this microscopic colitis (Option B), and pancreatic insufficiency patient has pain with defecation, angiodysplasia is not a (Option C). This patient does not appear to have risk factors likely cause of his symptoms. for small intestinal bacterial overgrowth or chronic pan- Hemorrhoids (Option C) are submucosal, arteriovenous S creatitis. Microscopic colitis deserves particular attention sinusoids that are part of normal anorectal anatomy and are = wn because approximately 4% of patients with celiac disease believed to play an important role in anal canal function. = have this condition, but it is more typically found in mid- Age-related changes can cause the hemorrhoid beds to slide oO back and forth during defecation, resulting in mucoid anal = rn dle-age and older women. Because inadvertent exposure oY) to gluten is the most common cause of recurrent celiac discharge, as well as perianal wetness, soiling, irritation, = a. disease symptoms, a referral to a dietitian and exploration and/or pruritus. Hemorrhoidal bleeding is most often asso- (2) =. of possible sources of gluten exposure is the best initial ciated with painless defecation. The presence of pain (as in =. management option. this patient) should raise suspicion for an alternative diagno- 2 = Upper endoscopy with duodenal biopsy is necessary to sis, such as anal fissure. © wn diagnose celiac disease. This procedure also plays a role in Rectal cancer (Option D) should always be considered the assessment for unresponsive celiac disease, including in a patient with new-onset rectal outlet bleeding. However, evaluation for intestinal lymphoma (Option D) or adenocar- painful defecation typically does not occur with rectal can- cinoma, which can complicate celiac disease and manifest as cer. In this patient, the presence of pain with defecation and unresponsive disease. However, unresponsive celiac disease the history of normal findings on screening colonoscopy is far less likely than inadvertent gluten intake as a cause of 2 years previously make rectal cancer unlikely. this patient’s recurrent symptoms. e Anal fissures are longitudinal mucosal tears in the e The most common cause of recurrent celiac disease anal canal characterized by anorectal pain worsened symptoms is gluten exposure. by bowel movements.

1 year of starting a gluten-free diet. Before nonresponsive generally resolve within a few weeks with the use of sitz baths, celiac disease is diagnosed, a dietitian’s evaluation of the psyllium, bulking agents, and topical vasodilators (nifedipine patient’s exposure to dietary gluten is important. and nitroglycerin). Topical anesthetics and anti-inflammatory In patients who truly have unresponsive celiac dis- agents can be considered to address pain or bleeding, but their ease, other diagnoses should be considered. Some reports use is not required to promote fissure healing. suggest that approximately 10% of patients with celiac Angiodysplasia (Option B) can occur throughout the disease and recurrent symptoms have a concurrent diag- colon but is most common in the right colon. Angiodysplasia- nosis. Conditions to consider include HIV infection, irrita- related bleeding is typically painless and causes bleeding ble bowel syndrome, small intestinal bacterial overgrowth, episodes that are unrelated to defecation. Because this microscopic colitis (Option B), and pancreatic insufficiency patient has pain with defecation, angiodysplasia is not a (Option C). This patient does not appear to have risk factors likely cause of his symptoms. for small intestinal bacterial overgrowth or chronic pan- Hemorrhoids (Option C) are submucosal, arteriovenous S creatitis. Microscopic colitis deserves particular attention sinusoids that are part of normal anorectal anatomy and are = wn because approximately 4% of patients with celiac disease believed to play an important role in anal canal function. = have this condition, but it is more typically found in mid- Age-related changes can cause the hemorrhoid beds to slide oO back and forth during defecation, resulting in mucoid anal = rn dle-age and older women. Because inadvertent exposure oY) to gluten is the most common cause of recurrent celiac discharge, as well as perianal wetness, soiling, irritation, = a. disease symptoms, a referral to a dietitian and exploration and/or pruritus. Hemorrhoidal bleeding is most often asso- (2) =. of possible sources of gluten exposure is the best initial ciated with painless defecation. The presence of pain (as in =. management option. this patient) should raise suspicion for an alternative diagno- 2 = Upper endoscopy with duodenal biopsy is necessary to sis, such as anal fissure. © wn diagnose celiac disease. This procedure also plays a role in Rectal cancer (Option D) should always be considered the assessment for unresponsive celiac disease, including in a patient with new-onset rectal outlet bleeding. However, evaluation for intestinal lymphoma (Option D) or adenocar- painful defecation typically does not occur with rectal can- cinoma, which can complicate celiac disease and manifest as cer. In this patient, the presence of pain with defecation and unresponsive disease. However, unresponsive celiac disease the history of normal findings on screening colonoscopy is far less likely than inadvertent gluten intake as a cause of 2 years previously make rectal cancer unlikely. this patient’s recurrent symptoms. e Anal fissures are longitudinal mucosal tears in the e The most common cause of recurrent celiac disease anal canal characterized by anorectal pain worsened symptoms is gluten exposure. by bowel movements. e For the assessment of recurrent symptoms of celiac e Marked anorectal pain with attempted inspection of disease, a dietitian should evaluate possible sources of the perianal area in the context of painful defecatory gluten exposure. bleeding is nearly diagnostic of anal fissure.

e For the assessment of recurrent symptoms of celiac e Marked anorectal pain with attempted inspection of disease, a dietitian should evaluate possible sources of the perianal area in the context of painful defecatory gluten exposure. bleeding is nearly diagnostic of anal fissure. Bibliography Bibliography Rubin JE, Crowe SE. Celiac disease. Ann Intern Med. 2020;172:ITC1-ITC16. Mathur N, Qureshi W. Anal fissure management by the gastroenterologist. [PMID: 31905394] doi:10.7326/AITC202001070 Curr Opin Gastroenterol. 2020;36:19-24. [PMID: 31688336] doi:10.1097/ MOG.0000000000000599

Bibliography Bibliography Rubin JE, Crowe SE. Celiac disease. Ann Intern Med. 2020;172:ITC1-ITC16. Mathur N, Qureshi W. Anal fissure management by the gastroenterologist. [PMID: 31905394] doi:10.7326/AITC202001070 Curr Opin Gastroenterol. 2020;36:19-24. [PMID: 31688336] doi:10.1097/ MOG.0000000000000599 Item 46 Answer: A Educational Objective: Diagnose anal fissure. Item 47 Answer: A Educational Objective: Treat hepatitis B virus infection The most likely diagnosis is an anal fissure (Option A). Anal in the immune-active phase. fissures are longitudinal mucosal tears in the anal canal char- acterized by anorectal pain worsened by bowel movements. The most appropriate management is antiviral therapy (Option A). Rectal bleeding with bowel movements or wiping is fre- Treatment for hepatitis B virus (HBV) infection is advised quently reported. Anal fissures are idiopathic or result from for patients with acute liver failure, chronic infection in the trauma due to the passage of hard stool; receptive anal inter- immune-active phase or reactivation phase, or cirrhosis and for course; or the insertion of a foreign body, such as an enema selected immunosuppressed patients. Chronic HBV infection or endoscope. In this patient, the marked anorectal pain with is diagnosed after 6 months in patients with persistent hepatitis attempted inspection of the perianal area in the context of B surface antigen detected in serum. Chronic HBV infection is painful defecatory bleeding is nearly diagnostic of anal fis- divided into phases of disease. Patients in the immune-active sure. A digital rectal examination is not needed in patients phase or reactivation phase have an elevated alanine amino- with severe anal pain, particularly when a thrombosed transferase (ALT) level, presence of hepatitis B core antibody, external hemorrhoid is excluded (as in this patient), because and an elevated HBV DNA level (>20,000 U/mL in hepati- the likely diagnosis is an anal fissure. Acute anal fissures tis B e antigen [HBeAg]-positive disease or >2000 U/mL in

Item 46 Answer: A Educational Objective: Diagnose anal fissure. Item 47 Answer: A Educational Objective: Treat hepatitis B virus infection The most likely diagnosis is an anal fissure (Option A). Anal in the immune-active phase. fissures are longitudinal mucosal tears in the anal canal char- acterized by anorectal pain worsened by bowel movements. The most appropriate management is antiviral therapy (Option A). Rectal bleeding with bowel movements or wiping is fre- Treatment for hepatitis B virus (HBV) infection is advised quently reported. Anal fissures are idiopathic or result from for patients with acute liver failure, chronic infection in the trauma due to the passage of hard stool; receptive anal inter- immune-active phase or reactivation phase, or cirrhosis and for course; or the insertion of a foreign body, such as an enema selected immunosuppressed patients. Chronic HBV infection or endoscope. In this patient, the marked anorectal pain with is diagnosed after 6 months in patients with persistent hepatitis attempted inspection of the perianal area in the context of B surface antigen detected in serum. Chronic HBV infection is painful defecatory bleeding is nearly diagnostic of anal fis- divided into phases of disease. Patients in the immune-active sure. A digital rectal examination is not needed in patients phase or reactivation phase have an elevated alanine amino- with severe anal pain, particularly when a thrombosed transferase (ALT) level, presence of hepatitis B core antibody, external hemorrhoid is excluded (as in this patient), because and an elevated HBV DNA level (>20,000 U/mL in hepati- the likely diagnosis is an anal fissure. Acute anal fissures tis B e antigen [HBeAg]-positive disease or >2000 U/mL in 130

Answers and Critiques HBeAg-negative disease; a rise above baseline HBV DNA level findings, and histopathologic features are diagnostic of mild, in the reactivation phase). This patient has chronic HBV infec- left-sided ulcerative colitis. The initial therapy of choice would tion in the immune-active, HBeAg-positive phase. First-line be 5-ASA enemas because they deliver active drug to the rec- antiviral treatment is entecavir or tenofovir for most patients. tum and sigmoid colon. 5-ASAs are anti-inflammatory med- Pegylated interferon can also be used. ications and the mainstay of treatment of mild to moderate Treatment is necessary to decrease hepatic inflamma- ulcerative colitis, with a dose-dependent response when used tion, the risk for progression to fibrosis, and the eventual cir- to induce disease remission. Of note, combined 5-ASA therapy rhosis that will occur without treatment. Clinical observation (oral and topical) is superior for induction of remission com- and surveillance (Option B) is not the best option for a patient pared with oral or topical therapies alone. Once remission is with chronic HBV infection in the immune-active phase. achieved, 5-ASAs are effective in maintaining it. Patients with chronic HBV infection should receive 5-ASA suppositories (Option B) deliver medication only appropriate immunizations, particularly hepatitis A virus to the rectum and therefore would be inadequate therapy for vaccination. HBV immune globulin (Option C) is indicated a patient with sigmoid inflammation, such as this patient. wn o for postexposure prophylaxis following acute exposure to A glucocorticoid enema (Option C) would be effec- =]

HBeAg-negative disease; a rise above baseline HBV DNA level findings, and histopathologic features are diagnostic of mild, in the reactivation phase). This patient has chronic HBV infec- left-sided ulcerative colitis. The initial therapy of choice would tion in the immune-active, HBeAg-positive phase. First-line be 5-ASA enemas because they deliver active drug to the rec- antiviral treatment is entecavir or tenofovir for most patients. tum and sigmoid colon. 5-ASAs are anti-inflammatory med- Pegylated interferon can also be used. ications and the mainstay of treatment of mild to moderate Treatment is necessary to decrease hepatic inflamma- ulcerative colitis, with a dose-dependent response when used tion, the risk for progression to fibrosis, and the eventual cir- to induce disease remission. Of note, combined 5-ASA therapy rhosis that will occur without treatment. Clinical observation (oral and topical) is superior for induction of remission com- and surveillance (Option B) is not the best option for a patient pared with oral or topical therapies alone. Once remission is with chronic HBV infection in the immune-active phase. achieved, 5-ASAs are effective in maintaining it. Patients with chronic HBV infection should receive 5-ASA suppositories (Option B) deliver medication only appropriate immunizations, particularly hepatitis A virus to the rectum and therefore would be inadequate therapy for vaccination. HBV immune globulin (Option C) is indicated a patient with sigmoid inflammation, such as this patient. wn o for postexposure prophylaxis following acute exposure to A glucocorticoid enema (Option C) would be effec- =] HBV. It is also recommended for prevention of HBV recur- tive in inducing remission of left-sided ulcerative colitis. it rence after liver transplantation in HBsAg-positive transplant However, topical 5-ASA therapy is superior to topical glu- — oO recipients. Hepatitis B immune globulin is not indicated for cocorticoids for this indication for several reasons. 5-ASAs sc = treatment of active HBV infection and is ineffective in the are effective in maintenance of remission, whereas topical c treatment of chronic active HBV infection. glucocorticoids are effective only for induction. In addition, = o A liver biopsy-confirmed diagnosis of cirrhosis can be glucocorticoids have significant adverse effects. However, = helpful in determining the need for antiviral treatment in guidelines recommend glucocorticoid enemas in patients rn = patients with chronic HBV infection. However, this patient with mild to moderate proctitis or left-sided colitis who are <=

HBV. It is also recommended for prevention of HBV recur- tive in inducing remission of left-sided ulcerative colitis. it rence after liver transplantation in HBsAg-positive transplant However, topical 5-ASA therapy is superior to topical glu- — oO recipients. Hepatitis B immune globulin is not indicated for cocorticoids for this indication for several reasons. 5-ASAs sc = treatment of active HBV infection and is ineffective in the are effective in maintenance of remission, whereas topical c treatment of chronic active HBV infection. glucocorticoids are effective only for induction. In addition, = o A liver biopsy-confirmed diagnosis of cirrhosis can be glucocorticoids have significant adverse effects. However, = helpful in determining the need for antiviral treatment in guidelines recommend glucocorticoid enemas in patients rn = patients with chronic HBV infection. However, this patient with mild to moderate proctitis or left-sided colitis who are <= with immune-active infection already has an indication for intolerant of or refractory to oral or topical 5-ASA therapy. treatment. Furthermore, cirrhosis is unlikely in an asymp- Oral 5-ASAs (Option D) are an alternative therapy if tomatic patient without evident complications from cirrho- the patient declines use of 5-ASA enemas or has insufficient sis and a normal hepatic ultrasound. Therefore, a liver biopsy response. Oral 5-ASAs alone would be less optimal than (Option D) is not needed. topical 5-ASAs in this patient given the limited distribution of disease in the rectum and sigmoid colon.

with immune-active infection already has an indication for intolerant of or refractory to oral or topical 5-ASA therapy. treatment. Furthermore, cirrhosis is unlikely in an asymp- Oral 5-ASAs (Option D) are an alternative therapy if tomatic patient without evident complications from cirrho- the patient declines use of 5-ASA enemas or has insufficient sis and a normal hepatic ultrasound. Therefore, a liver biopsy response. Oral 5-ASAs alone would be less optimal than (Option D) is not needed. topical 5-ASAs in this patient given the limited distribution of disease in the rectum and sigmoid colon. e Treatment of hepatitis B virus (HBV) infection is advised for patients with acute liver failure, chronic e 5-Aminosalicylate enemas are an appropriate and infection in the immune-active phase or reactivation effective treatment for mild, left-sided ulcerative phase, or cirrhosis and for selected immunosup- colitis. pressed patients. e 5-Aminosalicylate suppositories are an appropriate e Immune-active chronic HBV infection is defined by and effective treatment for mild to moderate ulcera- presence of hepatitis B core antibody, elevated alanine tive proctitis. aminotransferase level, and HBV viral load greater than 2000 U/mL in patients negative for hepatitis B e Bibliography antigen and greater than 20,000 U/mL in patients Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: ulcerative colitis in adults. Am J Gastroenterol. 2019;114:384-413. [PMID: positive for hepatitis B e antigen. 30840605] doi:10.14309/ajg.0000000000000152

e Treatment of hepatitis B virus (HBV) infection is advised for patients with acute liver failure, chronic e 5-Aminosalicylate enemas are an appropriate and infection in the immune-active phase or reactivation effective treatment for mild, left-sided ulcerative phase, or cirrhosis and for selected immunosup- colitis. pressed patients. e 5-Aminosalicylate suppositories are an appropriate e Immune-active chronic HBV infection is defined by and effective treatment for mild to moderate ulcera- presence of hepatitis B core antibody, elevated alanine tive proctitis. aminotransferase level, and HBV viral load greater than 2000 U/mL in patients negative for hepatitis B e Bibliography antigen and greater than 20,000 U/mL in patients Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: ulcerative colitis in adults. Am J Gastroenterol. 2019;114:384-413. [PMID: positive for hepatitis B e antigen. 30840605] doi:10.14309/ajg.0000000000000152 Bibliography Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, Item 49 Answer: B and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Hepatology. 2018;67:1560-1599. [PMID: 29405329] doi:10.1002/hep. Educational Objective: Treat hypomotility disorder. 29800 The most appropriate treatment is diet, lifestyle, and acid reduction therapy with a proton pump inhibitor (Option B).

Bibliography Terrault NA, Lok ASF, McMahon BJ, et al. Update on prevention, diagnosis, Item 49 Answer: B and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance. Hepatology. 2018;67:1560-1599. [PMID: 29405329] doi:10.1002/hep. Educational Objective: Treat hypomotility disorder. 29800 The most appropriate treatment is diet, lifestyle, and acid reduction therapy with a proton pump inhibitor (Option B). Item 48 Answer: A This patient has a hypomotility disorder. Esophageal hypo- motility is associated with poor peristalsis, causing symp- Educational Objective: Treat left-sided ulcerative toms of dysphagia, and a hypotensive lower esophageal colitis. sphincter, causing symptoms of reflux. Other symptoms can The most appropriate treatment is 5-aminosalicylate (5-ASA) include regurgitation of undigested food, in particular when enemas (Option A). Categories of the extent of ulcerative colitis the patient is in a recumbent position. Esophageal manom- include proctitis (within 18 cm of the anal verge, distal to the etry shows hypotonic, weak nonperistaltic contractions in rectosigmoid junction), left-sided colitis (extending from the the distal esophagus. In most cases, the cause of hypotonic sigmoid to the splenic flexure), and extensive colitis (beyond esophageal disease is unknown. However, secondary causes the splenic flexure). This patient’s symptoms, colonoscopy include smooth-muscle relaxants, anticholinergic agents, 131

estrogen, progesterone, connective tissue disorders (sclero- foods; other symptoms include weight loss, anorexia, anemia derma), and pregnancy. This patient has systemic sclerosis. Both caused by gastrointestinal bleeding, and chest pain. The two limited and diffuse systemic sclerosis are associated with hypo- types of esophageal carcinoma are squamous cell carcinoma tonic motility disorder. Treatment includes lifestyle changes, (most commonly located in the proximal esophagus) and ade- such as eating upright and consuming a liquid or semisolid nocarcinoma (usually found in the distal esophagus). Risk fac- diet rather than solid food. Medical therapy includes optimi- tors for adenocarcinoma include male sex, older age, GERD, zation of an antireflux regimen and low-dose antidepressants Barrett esophagus, obesity, and tobacco use. Risk factors for for chest pain if present. Esophageal chest pain symptoms may squamous cell carcinoma include tobacco and alcohol use, be alleviated by low doses of tricyclic antidepressants, such as caustic injury, achalasia, past thoracic radiation, nutritional amitriptyline, or serotonin modulators, such as trazodone. deficiencies (zinc, selenium), and poor socioeconomic status. Patients with medical disorders associated with hyper- Barium esophagography (Option A) is a useful test in peristalsis, such as diffuse (or distal) esophageal spasm and the evaluation of esophageal dysphagia in specific situations, = hypercontractile (nutcracker) esophagus with dysphagia may such as suspicion for motility disorders or proximal lesions = wn respond to smooth muscle relaxants, such as the calcium (e.g., Zenker diverticulum). In this case, however, the likeli- = channel blocker diltiazem (Option A). However, smooth hood of malignancy is high given the presence of weight loss @o = wn muscle relaxants will not help this patient with a hypotonic and anemia. Even if a peptic stricture secondary to GERD re') = motility disorder and may worsen the symptoms. Treatment were suspected, biopsy would still be necessary, making a. of this patient’s hypomotility disorder can be complicated by endoscopy the initial test of choice. (e) oy the presence of Raynaud phenomenon, which may necessi- CT of the chest (Option B) may be used to evaluate for =A tate treatment with a calcium channel blocker. extrinsic compression as a cause of dysphagia and for staging 2 =| Metoclopramide (Option C) is not recommended in the of established esophageal cancer. However, it is not a first-line © wn treatment of gastroesophageal reflux disease or esophageal test for dysphagia because it poorly visualizes the esophageal motor disorders because the risk outweighs the benefits. mucosa and does not provide the opportunity for biopsy. Adverse effects of metoclopramide include tardive dyskinesia. Dysphagia occurring with solids alone suggests a mechan- Laparoscopic fundoplication (Option D) is an antireflux ical obstruction, whereas dysphagia with either liquids alone surgery that creates a 360-degree wrap around the gastro- or the combination of liquids and solids favors a motility dis- esophageal junction and may benefit select patients with order. An esophageal motility study (Option D) is an important reflux. However, this surgery would cause an obstructive diagnostic test in patients with nonobstructive dysphagia. In pathology in a hypotonic motility disorder and likely would this case, however, the progression of dysphagia from solid worsen dysphagia symptoms. to soft foods suggests a mechanical obstruction rather than a motility disorder, making endoscopy the preferred test.

estrogen, progesterone, connective tissue disorders (sclero- foods; other symptoms include weight loss, anorexia, anemia derma), and pregnancy. This patient has systemic sclerosis. Both caused by gastrointestinal bleeding, and chest pain. The two limited and diffuse systemic sclerosis are associated with hypo- types of esophageal carcinoma are squamous cell carcinoma tonic motility disorder. Treatment includes lifestyle changes, (most commonly located in the proximal esophagus) and ade- such as eating upright and consuming a liquid or semisolid nocarcinoma (usually found in the distal esophagus). Risk fac- diet rather than solid food. Medical therapy includes optimi- tors for adenocarcinoma include male sex, older age, GERD, zation of an antireflux regimen and low-dose antidepressants Barrett esophagus, obesity, and tobacco use. Risk factors for for chest pain if present. Esophageal chest pain symptoms may squamous cell carcinoma include tobacco and alcohol use, be alleviated by low doses of tricyclic antidepressants, such as caustic injury, achalasia, past thoracic radiation, nutritional amitriptyline, or serotonin modulators, such as trazodone. deficiencies (zinc, selenium), and poor socioeconomic status. Patients with medical disorders associated with hyper- Barium esophagography (Option A) is a useful test in peristalsis, such as diffuse (or distal) esophageal spasm and the evaluation of esophageal dysphagia in specific situations, = hypercontractile (nutcracker) esophagus with dysphagia may such as suspicion for motility disorders or proximal lesions = wn respond to smooth muscle relaxants, such as the calcium (e.g., Zenker diverticulum). In this case, however, the likeli- = channel blocker diltiazem (Option A). However, smooth hood of malignancy is high given the presence of weight loss @o = wn muscle relaxants will not help this patient with a hypotonic and anemia. Even if a peptic stricture secondary to GERD re') = motility disorder and may worsen the symptoms. Treatment were suspected, biopsy would still be necessary, making a. of this patient’s hypomotility disorder can be complicated by endoscopy the initial test of choice. (e) oy the presence of Raynaud phenomenon, which may necessi- CT of the chest (Option B) may be used to evaluate for =A tate treatment with a calcium channel blocker. extrinsic compression as a cause of dysphagia and for staging 2 =| Metoclopramide (Option C) is not recommended in the of established esophageal cancer. However, it is not a first-line © wn treatment of gastroesophageal reflux disease or esophageal test for dysphagia because it poorly visualizes the esophageal motor disorders because the risk outweighs the benefits. mucosa and does not provide the opportunity for biopsy. Adverse effects of metoclopramide include tardive dyskinesia. Dysphagia occurring with solids alone suggests a mechan- Laparoscopic fundoplication (Option D) is an antireflux ical obstruction, whereas dysphagia with either liquids alone surgery that creates a 360-degree wrap around the gastro- or the combination of liquids and solids favors a motility dis- esophageal junction and may benefit select patients with order. An esophageal motility study (Option D) is an important reflux. However, this surgery would cause an obstructive diagnostic test in patients with nonobstructive dysphagia. In pathology in a hypotonic motility disorder and likely would this case, however, the progression of dysphagia from solid worsen dysphagia symptoms. to soft foods suggests a mechanical obstruction rather than a motility disorder, making endoscopy the preferred test. e Esophageal hypomotility disorder is associated with poor peristalsis, causing symptoms of dysphagia, and ¢ Dysphagia occurring with solids alone suggests a a hypotensive lower esophageal sphincter, causing mechanical obstruction, whereas dysphagia with symptoms of reflux. either liquids alone or the combination of liquids and

e Esophageal hypomotility disorder is associated with poor peristalsis, causing symptoms of dysphagia, and ¢ Dysphagia occurring with solids alone suggests a a hypotensive lower esophageal sphincter, causing mechanical obstruction, whereas dysphagia with symptoms of reflux. either liquids alone or the combination of liquids and e Treatment of esophageal hypomotility disorder solids favors a motility disorder. includes lifestyle changes, such as eating upright and e Dysphagia in the setting of weight loss, anemia, and consuming a liquid or semisolid diet rather than solid history of gastroesophageal reflux disease should food, and acid reduction with a proton pump inhibitor. prompt endoscopy to evaluate for malignancy. Bibliography Bibliography Valdovinos MA, Zavala-Solares MR, Coss-Adame E. Esophageal hypomotility Liu LWC, Andrews CN, Armstrong D, et al. Clinical practice guidelines for and spastic motor disorders: current diagnosis and treatment. Curr the assessment of uninvestigated esophageal dysphagia. J Can Assoc Gastroenterol Rep. 2014;16(11):421. [PMID: 25376746] doi:10.1007/s11894- Gastroenterol. 2018;1:5-19. [PMID: 31294391] doi:10.1093/jcag/gwx008- 014-0421-1

Bibliography Bibliography Valdovinos MA, Zavala-Solares MR, Coss-Adame E. Esophageal hypomotility Liu LWC, Andrews CN, Armstrong D, et al. Clinical practice guidelines for and spastic motor disorders: current diagnosis and treatment. Curr the assessment of uninvestigated esophageal dysphagia. J Can Assoc Gastroenterol Rep. 2014;16(11):421. [PMID: 25376746] doi:10.1007/s11894- Gastroenterol. 2018;1:5-19. [PMID: 31294391] doi:10.1093/jcag/gwx008- 014-0421-1 Item 51 Answer: D Item 50 Answer: C Educational Objective: Diagnose hepatic sarcoidosis. Educational Objective: Evaluate progressive The most appropriate diagnostic test to perform next is upper esophageal dysphagia. endoscopy (Option D). Granulomatous inflammation of the The most appropriate diagnostic test to perform next is endos- liver can result in portal hypertension, even in the absence copy with biopsy (Option C). This patient has esophageal of hepatic fibrosis. Hepatic sarcoidosis is an idiopathic con- dysphagia in the setting of weight loss and history of gastro- dition that results in non-necrotizing granulomas. The organ esophageal reflux disease (GERD). Endoscopy should be per- most commonly affected by sarcoidosis is the lung, although formed to evaluate for malignancy. The most common initial the liver is also often affected. Most patients with hepatic presentation of esophageal carcinoma is dysphagia with solid sarcoidosis are asymptomatic; if symptoms do exist, they are 132

Answers and Critiques typically mild and may consist of pruritus or abdominal pain should be assessed in all patients, and resuscitative measures due to hepatic capsule stretch. It is unclear whether immu- must be initiated with the goal of hemodynamic stabilization nosuppressive therapy affects the clinical course of hepatic before endoscopy. Adequate intravenous access, usually with sarcoidosis, and treatment is usually not initiated unless two large-bore peripheral intravenous catheters (minimum symptoms are severe or markers of liver inflammation are 18-gauge), should be established. Hemoglobin levels should significantly abnormal. Conditions such as tuberculosis, be measured in all patients. Intravenous proton pump inhib- fungal infections, brucellosis, Q fever, Hodgkin lymphoma, itor therapy should be initiated before endoscopy in patients and drug toxicity can also cause granulomatous lesions in with nonvariceal UGIB. Upper endoscopy is the diagnostic test the liver, and steps should be undertaken to exclude these of choice to evaluate UGIB and peptic ulcer disease. Patients conditions before a diagnosis of sarcoidosis is accepted. The with UGIB should undergo upper endoscopy within 24 hours presence of skin or chest imaging findings typical of sar- of admission following hemodynamic resuscitation; those coidosis also supports the diagnosis of hepatic sarcoidosis. with rapid bleeding or suspected of having variceal hemor- Hepatic sarcoidosis rarely results in liver failure, but portal rhage should have the procedure more emergently (within wn cH hypertension is common. Therefore, upper endoscopy to 12 hours). Endoscopy can determine the cause of bleeding s

typically mild and may consist of pruritus or abdominal pain should be assessed in all patients, and resuscitative measures due to hepatic capsule stretch. It is unclear whether immu- must be initiated with the goal of hemodynamic stabilization nosuppressive therapy affects the clinical course of hepatic before endoscopy. Adequate intravenous access, usually with sarcoidosis, and treatment is usually not initiated unless two large-bore peripheral intravenous catheters (minimum symptoms are severe or markers of liver inflammation are 18-gauge), should be established. Hemoglobin levels should significantly abnormal. Conditions such as tuberculosis, be measured in all patients. Intravenous proton pump inhib- fungal infections, brucellosis, Q fever, Hodgkin lymphoma, itor therapy should be initiated before endoscopy in patients and drug toxicity can also cause granulomatous lesions in with nonvariceal UGIB. Upper endoscopy is the diagnostic test the liver, and steps should be undertaken to exclude these of choice to evaluate UGIB and peptic ulcer disease. Patients conditions before a diagnosis of sarcoidosis is accepted. The with UGIB should undergo upper endoscopy within 24 hours presence of skin or chest imaging findings typical of sar- of admission following hemodynamic resuscitation; those coidosis also supports the diagnosis of hepatic sarcoidosis. with rapid bleeding or suspected of having variceal hemor- Hepatic sarcoidosis rarely results in liver failure, but portal rhage should have the procedure more emergently (within wn cH hypertension is common. Therefore, upper endoscopy to 12 hours). Endoscopy can determine the cause of bleeding s evaluate for esophageal varices is warranted, particularly in and helps to risk-stratify the patient. Lesions at high risk for = this patient with splenomegaly and thrombocytopenia. recurrent bleeding that require endoscopic treatment include = oO This patient’s abdominal ultrasound demonstrates a actively bleeding peptic ulcers, ulcers with nonbleeding visi- sc = mildly nodular liver, which can be seen in sarcoidosis. How- ble vessels, and ulcers with adherent clots. c

evaluate for esophageal varices is warranted, particularly in and helps to risk-stratify the patient. Lesions at high risk for = this patient with splenomegaly and thrombocytopenia. recurrent bleeding that require endoscopic treatment include = oO This patient’s abdominal ultrasound demonstrates a actively bleeding peptic ulcers, ulcers with nonbleeding visi- sc = mildly nodular liver, which can be seen in sarcoidosis. How- ble vessels, and ulcers with adherent clots. c ever, because liver biopsy specimens do not demonstrate Capsule endoscopy (Option A) is a first-line test to w theme o cirrhosis and ultrasound shows no masses, further imaging evaluate for a small-bowel source of bleeding in stable = with CT (Option A) is not necessary. patients after normal results on upper endoscopy and colo- wn : Hepatobiliary iminodiacetic acid scintigraphy (Option B) noscopy. This patient’s symptoms suggest that he has UGIB, <x

ever, because liver biopsy specimens do not demonstrate Capsule endoscopy (Option A) is a first-line test to w theme o cirrhosis and ultrasound shows no masses, further imaging evaluate for a small-bowel source of bleeding in stable = with CT (Option A) is not necessary. patients after normal results on upper endoscopy and colo- wn : Hepatobiliary iminodiacetic acid scintigraphy (Option B) noscopy. This patient’s symptoms suggest that he has UGIB, <x evaluates for pathology associated with gallbladder disease and he has not yet undergone endoscopy or colonoscopy. or for a bile leak. In a patient without colicky pain con- Therefore, capsule endoscopy would not be appropriate. cerning for gallbladder disease or a history of recent biliary Colonoscopy (Option B) is used to assess patients sus- interventions, this test would not be useful. pected of having lower gastrointestinal bleeding, which is Magnetic resonance cholangiopancreatography (MRCP) typically characterized by the sudden onset of hematochezia (Option C) can be useful if biliary stricture is a concern. (passage of fresh blood or clots from the colon). Colonoscopy Although this patient does have an elevated alkaline phos- would be indicated for this patient only if findings on upper phatase level, which can occur in the setting of biliary endoscopy are normal. strictures, his ultrasound does not demonstrate dilated bile If findings on upper endoscopy and colonoscopy are ducts. Therefore, MRCP is not indicated. negative and the patient continues to experience severe gas- trointestinal bleeding with hemodynamic instability, then CT angiography (Option C) would be appropriate. CT angiogra- e The organ most commonly affected by sarcoidosis is phy can detect active bleeding at a rate of 0.5 to 1 mL/min and the lung, although the liver is also often affected. can be used to localize and direct therapy with transcatheter e In addition to sarcoidosis, conditions such as tubercu- embolization by conventional mesenteric angiography. losis, fungal infections, brucellosis, Q fever, Hodgkin lymphoma and drug toxicity can also cause granu- e Upper endoscopy is the diagnostic test of choice to lomatous lesions in the liver. evaluate upper gastrointestinal bleeding and peptic ulcer disease. Bibliography Kumar M, Herrera JL. Sarcoidosis and the liver. Clin Liver Dis. 2019;23:331- e Patients with upper gastrointestinal bleeding should 343. [PMID: 30947880] doi:10.1016/j.cld.2018.12.012 undergo upper endoscopy within 24 hours of hospital admission following hemodynamic resuscitation. Item 52 Answer: D

evaluates for pathology associated with gallbladder disease and he has not yet undergone endoscopy or colonoscopy. or for a bile leak. In a patient without colicky pain con- Therefore, capsule endoscopy would not be appropriate. cerning for gallbladder disease or a history of recent biliary Colonoscopy (Option B) is used to assess patients sus- interventions, this test would not be useful. pected of having lower gastrointestinal bleeding, which is Magnetic resonance cholangiopancreatography (MRCP) typically characterized by the sudden onset of hematochezia (Option C) can be useful if biliary stricture is a concern. (passage of fresh blood or clots from the colon). Colonoscopy Although this patient does have an elevated alkaline phos- would be indicated for this patient only if findings on upper phatase level, which can occur in the setting of biliary endoscopy are normal. strictures, his ultrasound does not demonstrate dilated bile If findings on upper endoscopy and colonoscopy are ducts. Therefore, MRCP is not indicated. negative and the patient continues to experience severe gas- trointestinal bleeding with hemodynamic instability, then CT angiography (Option C) would be appropriate. CT angiogra- e The organ most commonly affected by sarcoidosis is phy can detect active bleeding at a rate of 0.5 to 1 mL/min and the lung, although the liver is also often affected. can be used to localize and direct therapy with transcatheter e In addition to sarcoidosis, conditions such as tubercu- embolization by conventional mesenteric angiography. losis, fungal infections, brucellosis, Q fever, Hodgkin lymphoma and drug toxicity can also cause granu- e Upper endoscopy is the diagnostic test of choice to lomatous lesions in the liver. evaluate upper gastrointestinal bleeding and peptic ulcer disease. Bibliography Kumar M, Herrera JL. Sarcoidosis and the liver. Clin Liver Dis. 2019;23:331- e Patients with upper gastrointestinal bleeding should 343. [PMID: 30947880] doi:10.1016/j.cld.2018.12.012 undergo upper endoscopy within 24 hours of hospital admission following hemodynamic resuscitation. Item 52 Answer: D Educational Objective: Diagnose upper Bibliography gastrointestinal bleeding. Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:1536. [PMID: 30910853] doi:10.1136/bmj.1536

Educational Objective: Diagnose upper Bibliography gastrointestinal bleeding. Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:1536. [PMID: 30910853] doi:10.1136/bmj.1536 After hemodynamic resuscitation, this patient should undergo upper endoscopy (Option D) for evaluation of suspected upper gastrointestinal bleeding (UGIB). Peptic ulcer disease Item 53 Answer: 8B is the most common cause of UGIB (50% of patients), with Educational Objective: Prevent recurrence of most gastroduodenal ulcers caused by Helicobacter pylori or NSAID-induced peptic ulcer disease. NSAID use. He has abdominal pain and melena in the context of ibuprofen use for osteoarthritis, which make peptic ulcer The most effective ulcer preventive strategy for this patient disease a likely cause of his symptoms. Hemodynamic status is celecoxib and omeprazole (Option B). This patient has 133

Answers and Critiques experienced bleeding, a complication of NSAID-related peptic and noncirrhotic causes (e.g., heart failure). The total protein ulcer disease. Although more than 85% of cases of NSAID- level can help differentiate cirrhotic ascites from cardiac asci- CONT. related peptic ulcers heal after 6 to 8 weeks of proton pump tes: The total protein level is low in cirrhotic ascites (<2.5 g/dL inhibitor (PPI) therapy and avoidance of NSAIDs, reintroduc- [25 g/L]}) and high in cardiac ascites (22.5 g/dL [25 g/L]). This ing NSAIDs risks ulcer recurrence. Prevention of ulcer recur- patient has elevated jugular venous pressure, a high SAAG, rence is therefore the most important long-term goal to reduce and high ascitic level of protein, suggesting a cardiac cause morbidity and mortality. If long-term NSAID use is necessary, of ascites. Therefore, echocardiography should be performed. potential treatment strategies include (1) an NSAID plus a The ascitic fluid cytologic finding is positive only in gastroprotective agent, such as a PPI; (2) an NSAID and an the setting of peritoneal carcinomatosis, and the sensitivity H,-blocker (Option A) or misoprostol; (3) a cyclooxygenase-2 approaches 94% if up to three samples are submitted from (COX-2)-selective NSAID in place of a nonselective NSAID; or three different paracenteses. In patients with peritoneal car- (4) a COX-2-selective NSAID plus a gastroprotective agent. A cinomatosis, the SAAG is low and the total protein is high; > systematic review and meta-analysis of 82 clinical trials total- therefore, ascitic fluid cytology (Option A) is not indicated = 7.) ing more than 125,000 participants found the combination of for this patient. = a COX-2-selective NSAID plus a PPI provided the best gastro- The measurement of ascitic triglyceride level (Option B) @ = n intestinal protection from ulcer recurrence and ulcer compli- is helpful in the diagnosis of chylous ascites. Chylous ascites gy = cations. Topical NSAIDs, such as diclofenac, are available by may be the result of portal hypertension (high SAAG) or a prescription for arthritis and pose a lower risk for systemic lymphatic obstruction (low SAAG) and high total protein (a) = adverse effects than oral NSAIDs. They may be preferred for level. In this patient with hemochromatosis and findings of =. patients at high risk for toxicity from oral NSAIDs and/or for jugular venous distention on examination, echocardiogra- 2 = patients age 75 years and older. However, topical NSAIDs are phy is much more likely to establish the diagnosis than is Oo n often expensive. The use of a topical NSAID in this patient measurement of ascitic triglyceride levels. would be impractical considering his widespread pain. This The American Association for the Study of Liver Disease review also showed that a COX-2-selective NSAID alone, a recommends liver biopsy (Option D) for specific clinical nonselective NSAID plus a PPI, and a nonselective NSAID plus situations, including diagnostic evaluation of focal or dif- misoprostol were more effective than a nonselective NSAID fuse lesions on imaging studies, parenchymal liver diseases, alone at reducing risk for ulcers and ulcer complications but chronically elevated liver test results of unknown cause, were not as effective as a COX-2-selective NSAID and a PPI. fever of unknown origin, and therapeutic planning and The use of nonselective NSAIDs with misoprostol staging of parenchymal liver diseases. Liver biopsy is of little (Option C) was associated with higher risk for adverse use in a patient with known cirrhosis and clinical evidence events and adverse event-related withdrawals compared of portal hypertension. with nonselective NSAIDs alone. Switching from one nonselective NSAID (ibuprofen) to another nonselective NSAID (naproxen) (Option D) e The differential diagnosis for ascitic fluid with a high

experienced bleeding, a complication of NSAID-related peptic and noncirrhotic causes (e.g., heart failure). The total protein ulcer disease. Although more than 85% of cases of NSAID- level can help differentiate cirrhotic ascites from cardiac asci- CONT. related peptic ulcers heal after 6 to 8 weeks of proton pump tes: The total protein level is low in cirrhotic ascites (<2.5 g/dL inhibitor (PPI) therapy and avoidance of NSAIDs, reintroduc- [25 g/L]}) and high in cardiac ascites (22.5 g/dL [25 g/L]). This ing NSAIDs risks ulcer recurrence. Prevention of ulcer recur- patient has elevated jugular venous pressure, a high SAAG, rence is therefore the most important long-term goal to reduce and high ascitic level of protein, suggesting a cardiac cause morbidity and mortality. If long-term NSAID use is necessary, of ascites. Therefore, echocardiography should be performed. potential treatment strategies include (1) an NSAID plus a The ascitic fluid cytologic finding is positive only in gastroprotective agent, such as a PPI; (2) an NSAID and an the setting of peritoneal carcinomatosis, and the sensitivity H,-blocker (Option A) or misoprostol; (3) a cyclooxygenase-2 approaches 94% if up to three samples are submitted from (COX-2)-selective NSAID in place of a nonselective NSAID; or three different paracenteses. In patients with peritoneal car- (4) a COX-2-selective NSAID plus a gastroprotective agent. A cinomatosis, the SAAG is low and the total protein is high; > systematic review and meta-analysis of 82 clinical trials total- therefore, ascitic fluid cytology (Option A) is not indicated = 7.) ing more than 125,000 participants found the combination of for this patient. = a COX-2-selective NSAID plus a PPI provided the best gastro- The measurement of ascitic triglyceride level (Option B) @ = n intestinal protection from ulcer recurrence and ulcer compli- is helpful in the diagnosis of chylous ascites. Chylous ascites gy = cations. Topical NSAIDs, such as diclofenac, are available by may be the result of portal hypertension (high SAAG) or a prescription for arthritis and pose a lower risk for systemic lymphatic obstruction (low SAAG) and high total protein (a) = adverse effects than oral NSAIDs. They may be preferred for level. In this patient with hemochromatosis and findings of =. patients at high risk for toxicity from oral NSAIDs and/or for jugular venous distention on examination, echocardiogra- 2 = patients age 75 years and older. However, topical NSAIDs are phy is much more likely to establish the diagnosis than is Oo n often expensive. The use of a topical NSAID in this patient measurement of ascitic triglyceride levels. would be impractical considering his widespread pain. This The American Association for the Study of Liver Disease review also showed that a COX-2-selective NSAID alone, a recommends liver biopsy (Option D) for specific clinical nonselective NSAID plus a PPI, and a nonselective NSAID plus situations, including diagnostic evaluation of focal or dif- misoprostol were more effective than a nonselective NSAID fuse lesions on imaging studies, parenchymal liver diseases, alone at reducing risk for ulcers and ulcer complications but chronically elevated liver test results of unknown cause, were not as effective as a COX-2-selective NSAID and a PPI. fever of unknown origin, and therapeutic planning and The use of nonselective NSAIDs with misoprostol staging of parenchymal liver diseases. Liver biopsy is of little (Option C) was associated with higher risk for adverse use in a patient with known cirrhosis and clinical evidence events and adverse event-related withdrawals compared of portal hypertension. with nonselective NSAIDs alone. Switching from one nonselective NSAID (ibuprofen) to another nonselective NSAID (naproxen) (Option D) e The differential diagnosis for ascitic fluid with a high does not lower the risk for ulcer recurrence or ulcer com- serum-ascites albumin gradient includes cirrhosis plications. and noncirrhotic causes (e.g., heart failure).

experienced bleeding, a complication of NSAID-related peptic and noncirrhotic causes (e.g., heart failure). The total protein ulcer disease. Although more than 85% of cases of NSAID- level can help differentiate cirrhotic ascites from cardiac asci- CONT. related peptic ulcers heal after 6 to 8 weeks of proton pump tes: The total protein level is low in cirrhotic ascites (<2.5 g/dL inhibitor (PPI) therapy and avoidance of NSAIDs, reintroduc- [25 g/L]}) and high in cardiac ascites (22.5 g/dL [25 g/L]). This ing NSAIDs risks ulcer recurrence. Prevention of ulcer recur- patient has elevated jugular venous pressure, a high SAAG, rence is therefore the most important long-term goal to reduce and high ascitic level of protein, suggesting a cardiac cause morbidity and mortality. If long-term NSAID use is necessary, of ascites. Therefore, echocardiography should be performed. potential treatment strategies include (1) an NSAID plus a The ascitic fluid cytologic finding is positive only in gastroprotective agent, such as a PPI; (2) an NSAID and an the setting of peritoneal carcinomatosis, and the sensitivity H,-blocker (Option A) or misoprostol; (3) a cyclooxygenase-2 approaches 94% if up to three samples are submitted from (COX-2)-selective NSAID in place of a nonselective NSAID; or three different paracenteses. In patients with peritoneal car- (4) a COX-2-selective NSAID plus a gastroprotective agent. A cinomatosis, the SAAG is low and the total protein is high; > systematic review and meta-analysis of 82 clinical trials total- therefore, ascitic fluid cytology (Option A) is not indicated = 7.) ing more than 125,000 participants found the combination of for this patient. = a COX-2-selective NSAID plus a PPI provided the best gastro- The measurement of ascitic triglyceride level (Option B) @ = n intestinal protection from ulcer recurrence and ulcer compli- is helpful in the diagnosis of chylous ascites. Chylous ascites gy = cations. Topical NSAIDs, such as diclofenac, are available by may be the result of portal hypertension (high SAAG) or a prescription for arthritis and pose a lower risk for systemic lymphatic obstruction (low SAAG) and high total protein (a) = adverse effects than oral NSAIDs. They may be preferred for level. In this patient with hemochromatosis and findings of =. patients at high risk for toxicity from oral NSAIDs and/or for jugular venous distention on examination, echocardiogra- 2 = patients age 75 years and older. However, topical NSAIDs are phy is much more likely to establish the diagnosis than is Oo n often expensive. The use of a topical NSAID in this patient measurement of ascitic triglyceride levels. would be impractical considering his widespread pain. This The American Association for the Study of Liver Disease review also showed that a COX-2-selective NSAID alone, a recommends liver biopsy (Option D) for specific clinical nonselective NSAID plus a PPI, and a nonselective NSAID plus situations, including diagnostic evaluation of focal or dif- misoprostol were more effective than a nonselective NSAID fuse lesions on imaging studies, parenchymal liver diseases, alone at reducing risk for ulcers and ulcer complications but chronically elevated liver test results of unknown cause, were not as effective as a COX-2-selective NSAID and a PPI. fever of unknown origin, and therapeutic planning and The use of nonselective NSAIDs with misoprostol staging of parenchymal liver diseases. Liver biopsy is of little (Option C) was associated with higher risk for adverse use in a patient with known cirrhosis and clinical evidence events and adverse event-related withdrawals compared of portal hypertension. with nonselective NSAIDs alone. Switching from one nonselective NSAID (ibuprofen) to another nonselective NSAID (naproxen) (Option D) e The differential diagnosis for ascitic fluid with a high does not lower the risk for ulcer recurrence or ulcer com- serum-ascites albumin gradient includes cirrhosis plications. and noncirrhotic causes (e.g., heart failure). e The total protein level is low in cirrhotic ascites

does not lower the risk for ulcer recurrence or ulcer com- serum-ascites albumin gradient includes cirrhosis plications. and noncirrhotic causes (e.g., heart failure). e The total protein level is low in cirrhotic ascites (<2.5 g/dL [25 g/L]) and high in cardiac ascites ¢ The combination of a cyclooxygenase-2-selective (22.5 g/dL [25 g/L]). NSAID plus a proton pump inhibitor provides the best gastrointestinal protection from ulcer recurrence and Bibliography ulcer complications. Runyon BA; AASLD. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult Bibliography patients with ascites due to cirrhosis 2012. Hepatology. 2013;57:1651-3. [PMID: 23463403] doi:10.1002/hep.26359 Yuan JQ, Tsoi KK, Yang M, et al. Systematic review with network meta- analysis: comparative effectiveness and safety of strategies for preventing NSAID-associated gastrointestinal toxicity. Aliment Pharmacol Ther. 2016;43:1262-75. [PMID: 27121479] doi:10.1111/apt.13642 Item 55 Answer: B

(<2.5 g/dL [25 g/L]) and high in cardiac ascites ¢ The combination of a cyclooxygenase-2-selective (22.5 g/dL [25 g/L]). NSAID plus a proton pump inhibitor provides the best gastrointestinal protection from ulcer recurrence and Bibliography ulcer complications. Runyon BA; AASLD. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult Bibliography patients with ascites due to cirrhosis 2012. Hepatology. 2013;57:1651-3. [PMID: 23463403] doi:10.1002/hep.26359 Yuan JQ, Tsoi KK, Yang M, et al. Systematic review with network meta- analysis: comparative effectiveness and safety of strategies for preventing NSAID-associated gastrointestinal toxicity. Aliment Pharmacol Ther. 2016;43:1262-75. [PMID: 27121479] doi:10.1111/apt.13642 Item 55 Answer: B Educational Objective: Diagnose drug-induced Item 54 Answer: C liver injury. Educational Objective: Evaluate cause of ascites. The most likely diagnosis is drug-induced liver injury (Option The most appropriate management is echocardiography B). Elevations in alkaline phosphatase and serum total biliru- (Option C). Ascites in a patient with liver disease is most likely bin levels and proportionally lesser elevations of aminotrans- to be due to cirrhosis. Portal hypertensive ascites is defined as a ferase levels indicate cholestatic hepatitis, the most common serum-ascites albumin gradient (SAAG) greater than or equal cause of which is drug-induced cholestasis. Drug-induced to 1.1 (calculated as serum albumin - ascites albumin). The liver injury can result from exposure to prescription differential diagnosis for high-SAAG ascites includes cirrhosis and nonprescription drugs as well as herbal and dietary

Educational Objective: Diagnose drug-induced Item 54 Answer: C liver injury. Educational Objective: Evaluate cause of ascites. The most likely diagnosis is drug-induced liver injury (Option The most appropriate management is echocardiography B). Elevations in alkaline phosphatase and serum total biliru- (Option C). Ascites in a patient with liver disease is most likely bin levels and proportionally lesser elevations of aminotrans- to be due to cirrhosis. Portal hypertensive ascites is defined as a ferase levels indicate cholestatic hepatitis, the most common serum-ascites albumin gradient (SAAG) greater than or equal cause of which is drug-induced cholestasis. Drug-induced to 1.1 (calculated as serum albumin - ascites albumin). The liver injury can result from exposure to prescription differential diagnosis for high-SAAG ascites includes cirrhosis and nonprescription drugs as well as herbal and dietary 134

Answers and Critiques supplements, even if the exposure occurred 6 months before the upper throat, the soft palate elevates, the epiglottis protects symptom onset. The likely source of this patient’s cholestasis the trachea, the tongue moves backward, and the pharyngeal CONT. is the amoxicillin-clavulanate she received for diverticulitis. wall moves forward), and esophageal phase (bolus enters the Antibiotics (particularly amoxicillin-clavulanate) and anti- esophagus with relaxation of the upper esophageal sphincter). epileptic medications (phenytoin and valproate) are among When the first two phases fail to position a bolus in the throat the most common medications associated with drug-induced for entry into the esophagus, choking, coughing, and nasal liver injury, representing 60% of cases. Liver injury typically regurgitation of solids and liquids may occur. These symptoms resolves after discontinuation of the offending drug; reso- pose a risk for aspiration pneumonia. Other presenting symp- lution of liver injury supports the diagnosis. Jaundice that toms may include hoarseness (resulting from laryngeal nerve occurs with cholestatic drug reactions can take months to damage) and dysarthria (from weakness of the soft palate resolve. Treatment of drug-induced liver disease is largely or pharyngeal constrictors), both suggesting an underlying supportive, with removal of the offending agent. Liver trans- neurologic disorder. Indeed, oropharyngeal dysphagia may be plantation can be considered in patients who have evidence of an early symptom or presenting sign of neurologic disorders, wn cH liver failure (i.e., those for whom liver injury is associated with such as Parkinson disease and stroke. It is important to recog- 3

supplements, even if the exposure occurred 6 months before the upper throat, the soft palate elevates, the epiglottis protects symptom onset. The likely source of this patient’s cholestasis the trachea, the tongue moves backward, and the pharyngeal CONT. is the amoxicillin-clavulanate she received for diverticulitis. wall moves forward), and esophageal phase (bolus enters the Antibiotics (particularly amoxicillin-clavulanate) and anti- esophagus with relaxation of the upper esophageal sphincter). epileptic medications (phenytoin and valproate) are among When the first two phases fail to position a bolus in the throat the most common medications associated with drug-induced for entry into the esophagus, choking, coughing, and nasal liver injury, representing 60% of cases. Liver injury typically regurgitation of solids and liquids may occur. These symptoms resolves after discontinuation of the offending drug; reso- pose a risk for aspiration pneumonia. Other presenting symp- lution of liver injury supports the diagnosis. Jaundice that toms may include hoarseness (resulting from laryngeal nerve occurs with cholestatic drug reactions can take months to damage) and dysarthria (from weakness of the soft palate resolve. Treatment of drug-induced liver disease is largely or pharyngeal constrictors), both suggesting an underlying supportive, with removal of the offending agent. Liver trans- neurologic disorder. Indeed, oropharyngeal dysphagia may be plantation can be considered in patients who have evidence of an early symptom or presenting sign of neurologic disorders, wn cH liver failure (i.e., those for whom liver injury is associated with such as Parkinson disease and stroke. It is important to recog- 3 encephalopathy and coagulopathy). nize oropharyngeal dysphagia by history because the initial = Autoimmune hepatitis (Option A) presents predomi- recommended study is a modified barium swallow (with a 7 oO nantly as a hepatocellular injury. The presentation of auto- range of liquid and solid consistencies) and videofluoroscopy. 3 & immune hepatitis can vary from asymptomatic elevation Endoscopy and esophageal manometry have a limited role c of aminotransferase levels to extrahepatic symptoms, such in the evaluation of oropharyngeal dysphagia. Management w =

encephalopathy and coagulopathy). nize oropharyngeal dysphagia by history because the initial = Autoimmune hepatitis (Option A) presents predomi- recommended study is a modified barium swallow (with a 7 oO nantly as a hepatocellular injury. The presentation of auto- range of liquid and solid consistencies) and videofluoroscopy. 3 & immune hepatitis can vary from asymptomatic elevation Endoscopy and esophageal manometry have a limited role c of aminotransferase levels to extrahepatic symptoms, such in the evaluation of oropharyngeal dysphagia. Management w = o as myalgia and malaise, to acute liver failure. This patient’s consists of dietary changes and a swallowing exercise program. = cholestatic liver injury pattern is not consistent with auto- Patients with achalasia (Option A) often have dysphagia wn & immune hepatitis. with solids and liquids, along with nonacidic oral regurgi- =

o as myalgia and malaise, to acute liver failure. This patient’s consists of dietary changes and a swallowing exercise program. = cholestatic liver injury pattern is not consistent with auto- Patients with achalasia (Option A) often have dysphagia wn & immune hepatitis. with solids and liquids, along with nonacidic oral regurgi- = Hepatitis A virus (Option C) is transmitted by the fecal- tation of undigested food. Choking and aspiration are often oral route. International travel is a risk factor. A prodrome of late-stage symptoms that may occur after long-standing malaise, nausea, vomiting, fever, and right-upper-quadrant regurgitation and other dysphagia symptoms. This patient discomfort is followed by development of jaundice and a does not have any regurgitation and can swallow soft foods, hepatocellular pattern of injury. Despite this patient’s inter- making achalasia an unlikely diagnosis. national travel, her illness is not compatible with hepatitis A Incarcerated paraesophageal hernia (Option B) is often virus infection because the incubation period for this infec- associated with pain and typically presents with solid dys- tion is 15 to 50 days. phagia before liquid dysphagia. This patient has no chest Primary biliary cholangitis (Option D) is an unlikely pain and is experiencing liquid dysphagia; thus, incarcerated cause of subacute cholestatic liver injury in this 73-year-old paraesophageal hernia is an unlikely diagnosis. patient. Most patients are diagnosed between the fourth and This patient is unlikely to have a mechanical obstruction, fifth decades of life and either present with pruritus or have such as a peptic stricture (Option D), because he has more incidentally discovered elevated alkaline phosphatase level. trouble swallowing liquids than solids. In addition, a peptic stricture is often more chronic, with gradual worsening.

Hepatitis A virus (Option C) is transmitted by the fecal- tation of undigested food. Choking and aspiration are often oral route. International travel is a risk factor. A prodrome of late-stage symptoms that may occur after long-standing malaise, nausea, vomiting, fever, and right-upper-quadrant regurgitation and other dysphagia symptoms. This patient discomfort is followed by development of jaundice and a does not have any regurgitation and can swallow soft foods, hepatocellular pattern of injury. Despite this patient’s inter- making achalasia an unlikely diagnosis. national travel, her illness is not compatible with hepatitis A Incarcerated paraesophageal hernia (Option B) is often virus infection because the incubation period for this infec- associated with pain and typically presents with solid dys- tion is 15 to 50 days. phagia before liquid dysphagia. This patient has no chest Primary biliary cholangitis (Option D) is an unlikely pain and is experiencing liquid dysphagia; thus, incarcerated cause of subacute cholestatic liver injury in this 73-year-old paraesophageal hernia is an unlikely diagnosis. patient. Most patients are diagnosed between the fourth and This patient is unlikely to have a mechanical obstruction, fifth decades of life and either present with pruritus or have such as a peptic stricture (Option D), because he has more incidentally discovered elevated alkaline phosphatase level. trouble swallowing liquids than solids. In addition, a peptic stricture is often more chronic, with gradual worsening. e Drug-induced liver disease can result from exposure to prescription and nonprescription drugs as well as e¢ Common symptoms of oropharyngeal dysphagia herbal and dietary supplements, even if the exposure include choking, coughing, and nasal regurgitation of occurred 6 months before symptom onset. solids and liquids.

e Drug-induced liver disease can result from exposure to prescription and nonprescription drugs as well as e¢ Common symptoms of oropharyngeal dysphagia herbal and dietary supplements, even if the exposure include choking, coughing, and nasal regurgitation of occurred 6 months before symptom onset. solids and liquids. ¢ The most common cause of cholestatic hepatitis is e The initial evaluation of oropharyngeal dysphagia is a drug-induced liver injury. modified barium swallow (with a range of liquid and solid consistencies) and videofluoroscopy. Bibliography Zhang J, Venkat D. Frequent offenders and patterns of injury. Clin Liver Dis. Bibliography 2020;24:37-48. [PMID: 31753249] doi:10.1016/j.cld.2019.09.002 Simons JA. Swallowing dysfunctions in Parkinson’s disease. Int Rev Neurobiol. 2017;134:1207-1238. [PMID: 28805570] doi:10.1016/bs.irn. 2017.05.026 Item 56 Answer: C Educational Objective: Diagnose oropharyngeal Item 57 Answer: D dysphagia. Educational Objective: Treat hepatic failure with liver transplantation. The most likely diagnosis is oropharyngeal dysphagia (Option C), also called transfer dysphagia. Swallowing has three The most appropriate management is referral for liver trans- phases: oral phase (food bolus forms and transfers to the back plantation (Option D). Referral for liver transplantation is of the throat), pharyngeal phase (bolus is safely positioned in indicated in patients whose MELD-Na (Model for End-Stage 135

Liver Disease-sodium) score is 15 or greater and in those with 2018 guidelines suggest that all adults should be screened findings of decompensated disease, such as ascites, jaundice, for HCV with an HCV antibody test. In patients positive for hepatocellular carcinoma, hepatorenal syndrome, variceal HCV antibody, a positive HCV RNA result indicates active hemorrhage, spontaneous bacterial peritonitis, and hepatic infection. Acute hepatitis C virus infection refers to the first encephalopathy. Although the MELD-Na score is used to 6 months after initial infection. Because there is a 20% to 50% prioritize patients on the liver transplant list, patients with chance that infection will spontaneously resolve during this symptoms of hepatic decompensation should be referred to period, monitoring HCV RNA for at least 12 to 16 weeks before a liver transplant center for consideration of transplantation. starting treatment is often recommended. All patients with Symptoms of liver decompensation herald a high risk for clin- chronic HCV infection should be treated regardless of fibrosis ical worsening and a 2-year mortality rate of 50%. The aver- stage, except those who have a short life expectancy, such as age 1- and 5-year survival rates after liver transplantation are this patient with metastatic pancreatic cancer. Because this 92% and 75% to 85%, respectively. Therefore, this patient with patient will not benefit from treatment, it is most appropriate > advancing symptoms of liver decompensation should be con- to provide no further testing or treatment. = 7) sidered for liver transplantation, regardless of the MELD-Na Patients may request specific diagnostic or therapeutic = score. interventions that may be inappropriate. Examples include @ = wn Patients with active hepatitis C virus infection can be requests for antibiotic therapy for a suspected viral infec- <3) = considered for antiviral therapy, although the use of pro- tion (Option A) and aggressive chemotherapy in a debil- t= tease inhibitors (Option A) in patients with decompen- itated patient with cancer. Although the physician needs oO on sated cirrhosis has been associated with worsening liver to respect patient autonomy, this duty must be weighed = failure. These medications should not be used in patients against the potential harms of inappropriate interven- 2 i= with advancing symptoms of liver dysfunction. Patients with tions, possible secondary effects (e.g., antimicrobial resis- @o wn decompensated cirrhosis should see a hepatologist before tance caused by inappropriate antibiotic prescribing), and treatment and be considered for liver transplantation. responsible stewardship of medical resources. When there The development of hepatic encephalopathy should is no evidence that the desired diagnostic or therapeutic prompt an evaluation for potential reversible causes. Infec- intervention will provide clinical benefit, physicians are not tions, gastrointestinal bleeding, volume depletion, and med- obligated to provide the service. Because this patient has a ications with sedating properties are common precipitants limited life expectancy, she should not be offered treatment of hepatic encephalopathy and, if present, should be treated for HCV. promptly. The initiation of lactulose therapy is appropriate The first step in the diagnosis of chronic HCV infec- in this setting, but the initiation of rifaximin (Option B) may tion is HCV antibody testing and, if the result is posi- be limited by cost. Rifaximin does not necessarily need to be tive, HCV RNA quantification. Patients with positive HCV added at this time unless lactulose alone does not adequately antibody and RNA test results have active infection, and control symptoms. a genotype test should be performed to guide selection Dietary protein intake was previously thought to be a of antiviral therapy. Because this patient will not bene- potential precipitant for hepatic encephalopathy, but this idea fit from treatment, additional testing (Option B) is not has been refuted. Even patients with hepatic encephalopathy indicated. should not be given a protein-restricted diet (Option C). All patients infected with HCV should be tested for hep- atitis B virus (HBV) and HIV infections (Option C) because of the potential shared routes of transmission. HBV reacti- e Findings of hepatic decompensation include ascites, vation can be seen during treatment of HCV infection with jaundice, hepatocellular carcinoma, hepatorenal syn- direct-acting antiviral therapy. This testing is not necessary drome, variceal hemorrhage, spontaneous bacterial in this patient with a limited life expectancy. peritonitis, and hepatic encephalopathy.

Liver Disease-sodium) score is 15 or greater and in those with 2018 guidelines suggest that all adults should be screened findings of decompensated disease, such as ascites, jaundice, for HCV with an HCV antibody test. In patients positive for hepatocellular carcinoma, hepatorenal syndrome, variceal HCV antibody, a positive HCV RNA result indicates active hemorrhage, spontaneous bacterial peritonitis, and hepatic infection. Acute hepatitis C virus infection refers to the first encephalopathy. Although the MELD-Na score is used to 6 months after initial infection. Because there is a 20% to 50% prioritize patients on the liver transplant list, patients with chance that infection will spontaneously resolve during this symptoms of hepatic decompensation should be referred to period, monitoring HCV RNA for at least 12 to 16 weeks before a liver transplant center for consideration of transplantation. starting treatment is often recommended. All patients with Symptoms of liver decompensation herald a high risk for clin- chronic HCV infection should be treated regardless of fibrosis ical worsening and a 2-year mortality rate of 50%. The aver- stage, except those who have a short life expectancy, such as age 1- and 5-year survival rates after liver transplantation are this patient with metastatic pancreatic cancer. Because this 92% and 75% to 85%, respectively. Therefore, this patient with patient will not benefit from treatment, it is most appropriate > advancing symptoms of liver decompensation should be con- to provide no further testing or treatment. = 7) sidered for liver transplantation, regardless of the MELD-Na Patients may request specific diagnostic or therapeutic = score. interventions that may be inappropriate. Examples include @ = wn Patients with active hepatitis C virus infection can be requests for antibiotic therapy for a suspected viral infec- <3) = considered for antiviral therapy, although the use of pro- tion (Option A) and aggressive chemotherapy in a debil- t= tease inhibitors (Option A) in patients with decompen- itated patient with cancer. Although the physician needs oO on sated cirrhosis has been associated with worsening liver to respect patient autonomy, this duty must be weighed = failure. These medications should not be used in patients against the potential harms of inappropriate interven- 2 i= with advancing symptoms of liver dysfunction. Patients with tions, possible secondary effects (e.g., antimicrobial resis- @o wn decompensated cirrhosis should see a hepatologist before tance caused by inappropriate antibiotic prescribing), and treatment and be considered for liver transplantation. responsible stewardship of medical resources. When there The development of hepatic encephalopathy should is no evidence that the desired diagnostic or therapeutic prompt an evaluation for potential reversible causes. Infec- intervention will provide clinical benefit, physicians are not tions, gastrointestinal bleeding, volume depletion, and med- obligated to provide the service. Because this patient has a ications with sedating properties are common precipitants limited life expectancy, she should not be offered treatment of hepatic encephalopathy and, if present, should be treated for HCV. promptly. The initiation of lactulose therapy is appropriate The first step in the diagnosis of chronic HCV infec- in this setting, but the initiation of rifaximin (Option B) may tion is HCV antibody testing and, if the result is posi- be limited by cost. Rifaximin does not necessarily need to be tive, HCV RNA quantification. Patients with positive HCV added at this time unless lactulose alone does not adequately antibody and RNA test results have active infection, and control symptoms. a genotype test should be performed to guide selection Dietary protein intake was previously thought to be a of antiviral therapy. Because this patient will not bene- potential precipitant for hepatic encephalopathy, but this idea fit from treatment, additional testing (Option B) is not has been refuted. Even patients with hepatic encephalopathy indicated. should not be given a protein-restricted diet (Option C). All patients infected with HCV should be tested for hep- atitis B virus (HBV) and HIV infections (Option C) because of the potential shared routes of transmission. HBV reacti- e Findings of hepatic decompensation include ascites, vation can be seen during treatment of HCV infection with jaundice, hepatocellular carcinoma, hepatorenal syn- direct-acting antiviral therapy. This testing is not necessary drome, variceal hemorrhage, spontaneous bacterial in this patient with a limited life expectancy. peritonitis, and hepatic encephalopathy. e Patients with findings of hepatic decompensation e All patients with chronic hepatitis C virus infection should be referred for consideration of liver trans- should be offered treatment regardless of fibrosis plantation. stage, except those who have a short life expectancy.

e Patients with findings of hepatic decompensation e All patients with chronic hepatitis C virus infection should be referred for consideration of liver trans- should be offered treatment regardless of fibrosis plantation. stage, except those who have a short life expectancy. Bibliography e When there is no evidence that the patient’s requested Ge PS, Runyon BA. Treatment of patients with cirrhosis. N EnglJ Med. 2016; diagnostic or therapeutic intervention will provide 375:767-77. [PMID: 27557303] doi:10.1056/NEJMra1504367 clinical benefit, physicians are not obligated to provide the service. ltem 58 Answer: D Educational Objective: Manage hepatitis C virus infec- Bibliography tion in a patient with short life expectancy. AASLD-IDSA HCV Guidance Panel. Hepatitis C guidance 2018 update: AASLD-IDSA recommendations for testing, managing, and treating hep- The most appropriate management is no further hepatitis C atitis C virus infection. Clin Infect Dis. 2018;67:1477-1492. [PMID: virus (HCV)-related testing or treatment (Option D). The 30215672] doi:10.1093/cid/ciy585 136

Item 59 Answer: B Item 60 Answer: D Educational Objective: Diagnose medication-related Educational Objective: Diagnose small-bowel bleeding. diarrhea. The most appropriate diagnostic test to perform next is video The most appropriate management is discontinuation of ibu- capsule endoscopy (Option D). The type of lesion responsi- profen (Option B). The evaluation of chronic diarrhea starts ble for small bowel bleeding depends on patient age but not with a history and physical examination, followed by selec- sex or ethnicity. Patients younger than 40 years are likely to tive diagnostic testing that includes laboratory analyses and have small-bowel bleeding due to inflammatory bowel disease, imaging, depending on the differential diagnosis. Many drugs Dieulafoy lesions, neoplasia, Meckel diverticulum, or a polyp- can cause diarrhea, and it can be difficult to identify a drug- osis syndrome. Patients older than 40 years are likely to have related cause of diarrhea in patients taking multiple medica- bleeding due to angiodysplasia, Dieulafoy lesions, neoplasia, or tions. The temporal relationship between starting a drug and NSAID-related ulcers. If a bleeding source is not identified on diarrhea onset can be helpful when present but is not always initial endoscopy and colonoscopy, second-look upper endo- wn e obvious. A reasonable strategy is to discontinue a potential scopy or colonoscopy should be performed if the initial studies =} culprit drug, if possible, and assess the effect on the patient’s were of low quality. Push enteroscopy may be pursued in lieu = symptoms. This patient’s history is notable for regular use of endoscopy to visualize the distal duodenum and proximal ‘= cs) of ibuprofen, an NSAID implicated in chronic diarrhea. The jejunum. Repeat colonoscopy should include intubation of the | mechanism by which ibuprofen causes diarrhea is uncertain, terminal ileum. This patient is suspected of having small-bowel = c but this effect sometimes occurs in the context of microscopic bleeding as the source of his iron deficiency anemia, given the n ev colitis. Discontinuing ibuprofen may lead to resolution of his lack of a source on high-quality upper endoscopy and colo- o

Item 59 Answer: B Item 60 Answer: D Educational Objective: Diagnose medication-related Educational Objective: Diagnose small-bowel bleeding. diarrhea. The most appropriate diagnostic test to perform next is video The most appropriate management is discontinuation of ibu- capsule endoscopy (Option D). The type of lesion responsi- profen (Option B). The evaluation of chronic diarrhea starts ble for small bowel bleeding depends on patient age but not with a history and physical examination, followed by selec- sex or ethnicity. Patients younger than 40 years are likely to tive diagnostic testing that includes laboratory analyses and have small-bowel bleeding due to inflammatory bowel disease, imaging, depending on the differential diagnosis. Many drugs Dieulafoy lesions, neoplasia, Meckel diverticulum, or a polyp- can cause diarrhea, and it can be difficult to identify a drug- osis syndrome. Patients older than 40 years are likely to have related cause of diarrhea in patients taking multiple medica- bleeding due to angiodysplasia, Dieulafoy lesions, neoplasia, or tions. The temporal relationship between starting a drug and NSAID-related ulcers. If a bleeding source is not identified on diarrhea onset can be helpful when present but is not always initial endoscopy and colonoscopy, second-look upper endo- wn e obvious. A reasonable strategy is to discontinue a potential scopy or colonoscopy should be performed if the initial studies =} culprit drug, if possible, and assess the effect on the patient’s were of low quality. Push enteroscopy may be pursued in lieu = symptoms. This patient’s history is notable for regular use of endoscopy to visualize the distal duodenum and proximal ‘= cs) of ibuprofen, an NSAID implicated in chronic diarrhea. The jejunum. Repeat colonoscopy should include intubation of the | mechanism by which ibuprofen causes diarrhea is uncertain, terminal ileum. This patient is suspected of having small-bowel = c but this effect sometimes occurs in the context of microscopic bleeding as the source of his iron deficiency anemia, given the n ev colitis. Discontinuing ibuprofen may lead to resolution of his lack of a source on high-quality upper endoscopy and colo- o symptoms, obviating the need for further evaluation. = noscopy. This bleeding can be further characterized as occult wn © Colonoscopy (Option A) is used selectively in the diagnos- given the absence of overt signs of gastrointestinal bleeding, =< tic evaluation of chronic diarrhea and is indicated for patients including melena and hematochezia. Video capsule endoscopy who have rectal bleeding, are age 50 years or older, have alarm noninvasively evaluates the entire small bowel. This test uses symptoms (e.g., weight loss), or have suspected Crohn disease a nondigestible wireless capsule camera that is swallowed or or ulcerative colitis. This patient’s lack of alarm symptoms placed endoscopically. Capsule endoscopy allows noninvasive and normal fecal calprotectin level make Crohn disease and evaluation of the entire small bowel in 79% to 90% of patients, ulcerative colitis less likely. His diarrhea may be due to NSAID- with a diagnostic yield of 38% to 83% in patients suspected of induced microscopic colitis, which can be diagnosed via colonos- having small-bowel bleeding. The American College of Gas- copy with biopsies; however, this diagnosis can be determined troenterology has recommended it as a first-line procedure for by discontinuing ibuprofen and monitoring his symptoms. further evaluation of the small bowel after upper and lower Tissue transglutaminase IgA levels are elevated in gastrointestinal sources of occult gastrointestinal bleeding have celiac disease, which is another cause of chronic diarrhea. been excluded. Alternatively, in uncomplicated asymptomatic Although measuring this antibody (Option C) is generally patients with iron deficiency anemia and negative bidirectional indicated in patients with chronic diarrhea, its diagnostic endoscopy, a trial of initial iron supplementation over the rou- utility is reduced in the setting of a gluten-free diet. If the tine use of video capsule endoscopy is conditionally suggested symptoms do not improve with withdrawal of ibuprofen, by the American Gastroenterological Association. the patient can discontinue the gluten-free diet and, after an CT angiography (Option A) and tagged red cell scin- appropriate interval, be tested for celiac disease. tigraphy (technetium-99m-labeled red cell scintigraphy) Video capsule endoscopy (Option D) allows visualiza- (Option C) require active bleeding to be effective in iden- tion of the small intestine. Capsule endoscopy can be of value tifying a source for small-bowel bleeding (bleeding rates of for diagnosing Crohn disease isolated to the small intestine; 0.3 mL/min for CT angiography and 0.1-0.2 mL/min for this cause of chronic diarrhea is less likely in this patient tagged red cell scintigraphy). This patient has no signs of given his normal fecal calprotectin level. NSAID-induced active bleeding; therefore, neither CT angiography nor a enteropathy, characterized by inflammation and ulcers in tagged red cell scintigraphy would be effective in identifying the small intestine, can also be diagnosed via video capsule a bleeding source in the small bowel. endoscopy, but discontinuing ibuprofen may lead to symp- Barium examinations of the small bowel (Option B) tom resolution without the need for this procedure. have demonstrated a low yield (only 3% to 17%) in identify- ing a source of suspected small-bowel bleeding and are no longer recommended for this purpose. ¢ Many drugs can cause chronic diarrhea; discontinuing a potential culprit drug may relieve symptoms and obviate the need for further diagnostic testing. ¢ For evaluating stable patients suspected of having

symptoms, obviating the need for further evaluation. = noscopy. This bleeding can be further characterized as occult wn © Colonoscopy (Option A) is used selectively in the diagnos- given the absence of overt signs of gastrointestinal bleeding, =< tic evaluation of chronic diarrhea and is indicated for patients including melena and hematochezia. Video capsule endoscopy who have rectal bleeding, are age 50 years or older, have alarm noninvasively evaluates the entire small bowel. This test uses symptoms (e.g., weight loss), or have suspected Crohn disease a nondigestible wireless capsule camera that is swallowed or or ulcerative colitis. This patient’s lack of alarm symptoms placed endoscopically. Capsule endoscopy allows noninvasive and normal fecal calprotectin level make Crohn disease and evaluation of the entire small bowel in 79% to 90% of patients, ulcerative colitis less likely. His diarrhea may be due to NSAID- with a diagnostic yield of 38% to 83% in patients suspected of induced microscopic colitis, which can be diagnosed via colonos- having small-bowel bleeding. The American College of Gas- copy with biopsies; however, this diagnosis can be determined troenterology has recommended it as a first-line procedure for by discontinuing ibuprofen and monitoring his symptoms. further evaluation of the small bowel after upper and lower Tissue transglutaminase IgA levels are elevated in gastrointestinal sources of occult gastrointestinal bleeding have celiac disease, which is another cause of chronic diarrhea. been excluded. Alternatively, in uncomplicated asymptomatic Although measuring this antibody (Option C) is generally patients with iron deficiency anemia and negative bidirectional indicated in patients with chronic diarrhea, its diagnostic endoscopy, a trial of initial iron supplementation over the rou- utility is reduced in the setting of a gluten-free diet. If the tine use of video capsule endoscopy is conditionally suggested symptoms do not improve with withdrawal of ibuprofen, by the American Gastroenterological Association. the patient can discontinue the gluten-free diet and, after an CT angiography (Option A) and tagged red cell scin- appropriate interval, be tested for celiac disease. tigraphy (technetium-99m-labeled red cell scintigraphy) Video capsule endoscopy (Option D) allows visualiza- (Option C) require active bleeding to be effective in iden- tion of the small intestine. Capsule endoscopy can be of value tifying a source for small-bowel bleeding (bleeding rates of for diagnosing Crohn disease isolated to the small intestine; 0.3 mL/min for CT angiography and 0.1-0.2 mL/min for this cause of chronic diarrhea is less likely in this patient tagged red cell scintigraphy). This patient has no signs of given his normal fecal calprotectin level. NSAID-induced active bleeding; therefore, neither CT angiography nor a enteropathy, characterized by inflammation and ulcers in tagged red cell scintigraphy would be effective in identifying the small intestine, can also be diagnosed via video capsule a bleeding source in the small bowel. endoscopy, but discontinuing ibuprofen may lead to symp- Barium examinations of the small bowel (Option B) tom resolution without the need for this procedure. have demonstrated a low yield (only 3% to 17%) in identify- ing a source of suspected small-bowel bleeding and are no longer recommended for this purpose. ¢ Many drugs can cause chronic diarrhea; discontinuing a potential culprit drug may relieve symptoms and obviate the need for further diagnostic testing. ¢ For evaluating stable patients suspected of having Bibliography small-bowel bleeding, video capsule endoscopy is the

symptoms, obviating the need for further evaluation. = noscopy. This bleeding can be further characterized as occult wn © Colonoscopy (Option A) is used selectively in the diagnos- given the absence of overt signs of gastrointestinal bleeding, =< tic evaluation of chronic diarrhea and is indicated for patients including melena and hematochezia. Video capsule endoscopy who have rectal bleeding, are age 50 years or older, have alarm noninvasively evaluates the entire small bowel. This test uses symptoms (e.g., weight loss), or have suspected Crohn disease a nondigestible wireless capsule camera that is swallowed or or ulcerative colitis. This patient’s lack of alarm symptoms placed endoscopically. Capsule endoscopy allows noninvasive and normal fecal calprotectin level make Crohn disease and evaluation of the entire small bowel in 79% to 90% of patients, ulcerative colitis less likely. His diarrhea may be due to NSAID- with a diagnostic yield of 38% to 83% in patients suspected of induced microscopic colitis, which can be diagnosed via colonos- having small-bowel bleeding. The American College of Gas- copy with biopsies; however, this diagnosis can be determined troenterology has recommended it as a first-line procedure for by discontinuing ibuprofen and monitoring his symptoms. further evaluation of the small bowel after upper and lower Tissue transglutaminase IgA levels are elevated in gastrointestinal sources of occult gastrointestinal bleeding have celiac disease, which is another cause of chronic diarrhea. been excluded. Alternatively, in uncomplicated asymptomatic Although measuring this antibody (Option C) is generally patients with iron deficiency anemia and negative bidirectional indicated in patients with chronic diarrhea, its diagnostic endoscopy, a trial of initial iron supplementation over the rou- utility is reduced in the setting of a gluten-free diet. If the tine use of video capsule endoscopy is conditionally suggested symptoms do not improve with withdrawal of ibuprofen, by the American Gastroenterological Association. the patient can discontinue the gluten-free diet and, after an CT angiography (Option A) and tagged red cell scin- appropriate interval, be tested for celiac disease. tigraphy (technetium-99m-labeled red cell scintigraphy) Video capsule endoscopy (Option D) allows visualiza- (Option C) require active bleeding to be effective in iden- tion of the small intestine. Capsule endoscopy can be of value tifying a source for small-bowel bleeding (bleeding rates of for diagnosing Crohn disease isolated to the small intestine; 0.3 mL/min for CT angiography and 0.1-0.2 mL/min for this cause of chronic diarrhea is less likely in this patient tagged red cell scintigraphy). This patient has no signs of given his normal fecal calprotectin level. NSAID-induced active bleeding; therefore, neither CT angiography nor a enteropathy, characterized by inflammation and ulcers in tagged red cell scintigraphy would be effective in identifying the small intestine, can also be diagnosed via video capsule a bleeding source in the small bowel. endoscopy, but discontinuing ibuprofen may lead to symp- Barium examinations of the small bowel (Option B) tom resolution without the need for this procedure. have demonstrated a low yield (only 3% to 17%) in identify- ing a source of suspected small-bowel bleeding and are no longer recommended for this purpose. ¢ Many drugs can cause chronic diarrhea; discontinuing a potential culprit drug may relieve symptoms and obviate the need for further diagnostic testing. ¢ For evaluating stable patients suspected of having Bibliography small-bowel bleeding, video capsule endoscopy is the Schiller LR, Pardi DS, Sellin JH. Chronic diarrhea: diagnosis and manage- preferred test after nondiagnostic upper endoscopy ment. Clin Gastroenterol Hepatol. 2017;15:182-193.e3. [PMID: 27496381] and colonoscopy. doi:10.1016 /j.cgh.2016.07.028

Schiller LR, Pardi DS, Sellin JH. Chronic diarrhea: diagnosis and manage- preferred test after nondiagnostic upper endoscopy ment. Clin Gastroenterol Hepatol. 2017;15:182-193.e3. [PMID: 27496381] and colonoscopy. doi:10.1016 /j.cgh.2016.07.028 137

Bibliography Ko CW, Siddique SM, Patel A, et al. AGA clinical practice guidelines on the gastrointestinal evaluation of iron deficiency anemia. Gastroenterology. ¢ Before initiation of anti-tumor necrosis factor agents, 2020;159:1085-1094. [PMID: 32810434] doi:10.1053/j.gastro.2020.06.046 patients should undergo testing for latent tuberculosis and hepatitis B virus infection. Item 61 Answer: B - Educational Objective: Treat moderate to severe Bibliography relapsed ulcerative colitis. Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: ulcerative colitis in adults. Am J Gastroenterol. 2019;114:384-413. [PMID: The most appropriate treatment is combination therapy 30840605] doi:10.14309/ajg.0000000000000152 with azathioprine and infliximab (Option B). This patient has recurrent symptoms of ulcerative colitis on tapering of Item 62 Answer: A glucocorticoids. Although glucocorticoids induce remission > Educational Objective: Identify the proper surveillance in moderate to severe flares of ulcerative colitis, they should = interval following removal of a large tubular adenoma. w not be used to maintain remission. Azathioprine and the = o anti-tumor necrosis factor (anti-TNF) agents infliximab and The appropriate surveillance interval for a patient with an = w golimumab induce and maintain remission in moderate to 11-mm tubular adenoma polyp is 3 years (Option A). A 3-year oy = severe ulcerative colitis. Combination therapy with inflix- colonoscopy interval is appropriate for patients with larger Qa. imab and azathioprine is more efficacious than monother- adenomas (210 mm), 5 to 10 tubular adenomas less than (2) ae apy with either agent alone in achieving glucocorticoid-free 10 mm, adenomas with tubulovillous or villous histology, or = 2 remission and mucosal healing. Before initiation of anti-TNF adenomas with high-grade dysplasia. A 3- to 5-year interval i] oO agents, patients should undergo testing for latent tuberculosis is appropriate for three or four tubular adenomas less than wr because of an increased risk for reactivation of tuberculosis 10 mm. Between 20% and 53% of adults older than age during therapy. If latent tuberculosis is present, treatment 50 years have premalignant adenomas of the colon detected with isoniazid should be administered for at least 2 months on screening, and 3% to 8% of the adenomas have advanced before initiation of anti-TNF therapy. Patients should also be histologic features. Because adenomas are an intermediary assessed for chronic hepatitis B virus infection before starting step in the progression from normal colonic mucosa to colon anti-TNF therapy and receive treatment if needed. cancer, identification and management of polyps are critical. Thiopurines (azathioprine and mercaptopurine) are The progression of adenoma to carcinoma takes approxi- immunomodulators used as glucocorticoid-sparing agents mately 8 to 10 years. Adenomas with any degree of villous in ulcerative colitis. They have a slow onset of action histology or high-grade dysplasia have greater malignant (2-3 months), and patients require a tapering glucocorticoid potential. Risk is also substantially increased in polyps 10 mm regimen to bridge the interval until the thiopurines take or larger. effect. Thiopurines are no more effective than placebo in A 7- to 10-year colonoscopy interval (Option B) is inducing short-term symptomatic remission and should appropriate for patients with one or two small (<10 mm) not be used in this manner. Given the slow onset of action, tubular adenomas. This interval is not recommended for this beginning azathioprine alone (Option A) is inappropriate. patient with an 11-mm tubular adenoma. For patients with Certolizumab (Option C), an anti-TNF agent, treats more than 10 adenomas found on a single examination, a moderate to severe Crohn disease resistant to glucocorticoids genetic cause of disease should be investigated and colonos- or immunomodulators. This agent has no role in treatment copy should be repeated in 1 year. of ulcerative colitis. Fecal-based testing with DNA (Option C) and fecal occult Multimatrix budesonide (Option D) is a colonic deliv- blood testing (Option D) are options for cancer screening rec- ery system of budesonide that allows directed therapy ommended for asymptomatic persons at average risk for col- throughout the colon with fewer glucocorticoid systemic orectal cancer. These screening strategies are not recommended adverse effects. It is effective in inducing remission in mild for surveillance in patients at increased risk for colorectal can- to moderate ulcerative colitis unresponsive to 5-aminosalic- cer or in whom polyps have been identified on colonoscopy. ylate. However, because multimatrix budesonide is effective only in inducing remission, it would be inappropriate for this patient, who requires an induction and a maintenance e A 3-year colonoscopy interval is appropriate for agent. In addition, he is already receiving a glucocorticoid patients with larger adenomas (210 mm), 5 to 10 and is steroid dependent. tubular adenomas less than 10 mm, adenomas with tubulovillous or villous histology, or adenomas with high-grade dysplasia; a 3- to 5-year interval is appropri- e¢ Combination therapy with infliximab and azathio- ate for three or four tubular adenomas less than 10 mm. prine is more efficacious than monotherapy with either agent alone in achieving glucocorticoid-free e A7- to 10-year colonoscopy interval is appropriate for

Bibliography Ko CW, Siddique SM, Patel A, et al. AGA clinical practice guidelines on the gastrointestinal evaluation of iron deficiency anemia. Gastroenterology. ¢ Before initiation of anti-tumor necrosis factor agents, 2020;159:1085-1094. [PMID: 32810434] doi:10.1053/j.gastro.2020.06.046 patients should undergo testing for latent tuberculosis and hepatitis B virus infection. Item 61 Answer: B - Educational Objective: Treat moderate to severe Bibliography relapsed ulcerative colitis. Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: ulcerative colitis in adults. Am J Gastroenterol. 2019;114:384-413. [PMID: The most appropriate treatment is combination therapy 30840605] doi:10.14309/ajg.0000000000000152 with azathioprine and infliximab (Option B). This patient has recurrent symptoms of ulcerative colitis on tapering of Item 62 Answer: A glucocorticoids. Although glucocorticoids induce remission > Educational Objective: Identify the proper surveillance in moderate to severe flares of ulcerative colitis, they should = interval following removal of a large tubular adenoma. w not be used to maintain remission. Azathioprine and the = o anti-tumor necrosis factor (anti-TNF) agents infliximab and The appropriate surveillance interval for a patient with an = w golimumab induce and maintain remission in moderate to 11-mm tubular adenoma polyp is 3 years (Option A). A 3-year oy = severe ulcerative colitis. Combination therapy with inflix- colonoscopy interval is appropriate for patients with larger Qa. imab and azathioprine is more efficacious than monother- adenomas (210 mm), 5 to 10 tubular adenomas less than (2) ae apy with either agent alone in achieving glucocorticoid-free 10 mm, adenomas with tubulovillous or villous histology, or = 2 remission and mucosal healing. Before initiation of anti-TNF adenomas with high-grade dysplasia. A 3- to 5-year interval i] oO agents, patients should undergo testing for latent tuberculosis is appropriate for three or four tubular adenomas less than wr because of an increased risk for reactivation of tuberculosis 10 mm. Between 20% and 53% of adults older than age during therapy. If latent tuberculosis is present, treatment 50 years have premalignant adenomas of the colon detected with isoniazid should be administered for at least 2 months on screening, and 3% to 8% of the adenomas have advanced before initiation of anti-TNF therapy. Patients should also be histologic features. Because adenomas are an intermediary assessed for chronic hepatitis B virus infection before starting step in the progression from normal colonic mucosa to colon anti-TNF therapy and receive treatment if needed. cancer, identification and management of polyps are critical. Thiopurines (azathioprine and mercaptopurine) are The progression of adenoma to carcinoma takes approxi- immunomodulators used as glucocorticoid-sparing agents mately 8 to 10 years. Adenomas with any degree of villous in ulcerative colitis. They have a slow onset of action histology or high-grade dysplasia have greater malignant (2-3 months), and patients require a tapering glucocorticoid potential. Risk is also substantially increased in polyps 10 mm regimen to bridge the interval until the thiopurines take or larger. effect. Thiopurines are no more effective than placebo in A 7- to 10-year colonoscopy interval (Option B) is inducing short-term symptomatic remission and should appropriate for patients with one or two small (<10 mm) not be used in this manner. Given the slow onset of action, tubular adenomas. This interval is not recommended for this beginning azathioprine alone (Option A) is inappropriate. patient with an 11-mm tubular adenoma. For patients with Certolizumab (Option C), an anti-TNF agent, treats more than 10 adenomas found on a single examination, a moderate to severe Crohn disease resistant to glucocorticoids genetic cause of disease should be investigated and colonos- or immunomodulators. This agent has no role in treatment copy should be repeated in 1 year. of ulcerative colitis. Fecal-based testing with DNA (Option C) and fecal occult Multimatrix budesonide (Option D) is a colonic deliv- blood testing (Option D) are options for cancer screening rec- ery system of budesonide that allows directed therapy ommended for asymptomatic persons at average risk for col- throughout the colon with fewer glucocorticoid systemic orectal cancer. These screening strategies are not recommended adverse effects. It is effective in inducing remission in mild for surveillance in patients at increased risk for colorectal can- to moderate ulcerative colitis unresponsive to 5-aminosalic- cer or in whom polyps have been identified on colonoscopy. ylate. However, because multimatrix budesonide is effective only in inducing remission, it would be inappropriate for this patient, who requires an induction and a maintenance e A 3-year colonoscopy interval is appropriate for agent. In addition, he is already receiving a glucocorticoid patients with larger adenomas (210 mm), 5 to 10 and is steroid dependent. tubular adenomas less than 10 mm, adenomas with tubulovillous or villous histology, or adenomas with high-grade dysplasia; a 3- to 5-year interval is appropri- e¢ Combination therapy with infliximab and azathio- ate for three or four tubular adenomas less than 10 mm. prine is more efficacious than monotherapy with either agent alone in achieving glucocorticoid-free e A7- to 10-year colonoscopy interval is appropriate for remission and mucosal healing in ulcerative colitis. patients with one or two small (<10 mm) tubular ade- (Continued) nomas.

Bibliography Ko CW, Siddique SM, Patel A, et al. AGA clinical practice guidelines on the gastrointestinal evaluation of iron deficiency anemia. Gastroenterology. ¢ Before initiation of anti-tumor necrosis factor agents, 2020;159:1085-1094. [PMID: 32810434] doi:10.1053/j.gastro.2020.06.046 patients should undergo testing for latent tuberculosis and hepatitis B virus infection. Item 61 Answer: B - Educational Objective: Treat moderate to severe Bibliography relapsed ulcerative colitis. Rubin DT, Ananthakrishnan AN, Siegel CA, et al. ACG clinical guideline: ulcerative colitis in adults. Am J Gastroenterol. 2019;114:384-413. [PMID: The most appropriate treatment is combination therapy 30840605] doi:10.14309/ajg.0000000000000152 with azathioprine and infliximab (Option B). This patient has recurrent symptoms of ulcerative colitis on tapering of Item 62 Answer: A glucocorticoids. Although glucocorticoids induce remission > Educational Objective: Identify the proper surveillance in moderate to severe flares of ulcerative colitis, they should = interval following removal of a large tubular adenoma. w not be used to maintain remission. Azathioprine and the = o anti-tumor necrosis factor (anti-TNF) agents infliximab and The appropriate surveillance interval for a patient with an = w golimumab induce and maintain remission in moderate to 11-mm tubular adenoma polyp is 3 years (Option A). A 3-year oy = severe ulcerative colitis. Combination therapy with inflix- colonoscopy interval is appropriate for patients with larger Qa. imab and azathioprine is more efficacious than monother- adenomas (210 mm), 5 to 10 tubular adenomas less than (2) ae apy with either agent alone in achieving glucocorticoid-free 10 mm, adenomas with tubulovillous or villous histology, or = 2 remission and mucosal healing. Before initiation of anti-TNF adenomas with high-grade dysplasia. A 3- to 5-year interval i] oO agents, patients should undergo testing for latent tuberculosis is appropriate for three or four tubular adenomas less than wr because of an increased risk for reactivation of tuberculosis 10 mm. Between 20% and 53% of adults older than age during therapy. If latent tuberculosis is present, treatment 50 years have premalignant adenomas of the colon detected with isoniazid should be administered for at least 2 months on screening, and 3% to 8% of the adenomas have advanced before initiation of anti-TNF therapy. Patients should also be histologic features. Because adenomas are an intermediary assessed for chronic hepatitis B virus infection before starting step in the progression from normal colonic mucosa to colon anti-TNF therapy and receive treatment if needed. cancer, identification and management of polyps are critical. Thiopurines (azathioprine and mercaptopurine) are The progression of adenoma to carcinoma takes approxi- immunomodulators used as glucocorticoid-sparing agents mately 8 to 10 years. Adenomas with any degree of villous in ulcerative colitis. They have a slow onset of action histology or high-grade dysplasia have greater malignant (2-3 months), and patients require a tapering glucocorticoid potential. Risk is also substantially increased in polyps 10 mm regimen to bridge the interval until the thiopurines take or larger. effect. Thiopurines are no more effective than placebo in A 7- to 10-year colonoscopy interval (Option B) is inducing short-term symptomatic remission and should appropriate for patients with one or two small (<10 mm) not be used in this manner. Given the slow onset of action, tubular adenomas. This interval is not recommended for this beginning azathioprine alone (Option A) is inappropriate. patient with an 11-mm tubular adenoma. For patients with Certolizumab (Option C), an anti-TNF agent, treats more than 10 adenomas found on a single examination, a moderate to severe Crohn disease resistant to glucocorticoids genetic cause of disease should be investigated and colonos- or immunomodulators. This agent has no role in treatment copy should be repeated in 1 year. of ulcerative colitis. Fecal-based testing with DNA (Option C) and fecal occult Multimatrix budesonide (Option D) is a colonic deliv- blood testing (Option D) are options for cancer screening rec- ery system of budesonide that allows directed therapy ommended for asymptomatic persons at average risk for col- throughout the colon with fewer glucocorticoid systemic orectal cancer. These screening strategies are not recommended adverse effects. It is effective in inducing remission in mild for surveillance in patients at increased risk for colorectal can- to moderate ulcerative colitis unresponsive to 5-aminosalic- cer or in whom polyps have been identified on colonoscopy. ylate. However, because multimatrix budesonide is effective only in inducing remission, it would be inappropriate for this patient, who requires an induction and a maintenance e A 3-year colonoscopy interval is appropriate for agent. In addition, he is already receiving a glucocorticoid patients with larger adenomas (210 mm), 5 to 10 and is steroid dependent. tubular adenomas less than 10 mm, adenomas with tubulovillous or villous histology, or adenomas with high-grade dysplasia; a 3- to 5-year interval is appropri- e¢ Combination therapy with infliximab and azathio- ate for three or four tubular adenomas less than 10 mm. prine is more efficacious than monotherapy with either agent alone in achieving glucocorticoid-free e A7- to 10-year colonoscopy interval is appropriate for remission and mucosal healing in ulcerative colitis. patients with one or two small (<10 mm) tubular ade- (Continued) nomas. 138

Answers and Critiques Bibliography intervals, whereas this patient’s pain occurs daily. Therefore, Gupta S, Lieberman D, Anderson JC, et al. Recommendations for follow-up ultrasonography would not be appropriate for this patient. after colonoscopy and polypectomy: a consensus update by the US Multi- Society Task Force on Colorectal Cancer. Am J Gastroenterol. 2020;115:415-434. [PMID: 32039982] doi:10.14309/ajg.00000000000 00544 ¢ The diagnosis of chronic mesenteric ischemia requires exclusion of alternative causes of postprandial abdominal pain and weight loss, along with compati- Item 63 Answer: B ble imaging findings. Educational Objective: Diagnose chronic mesenteric ¢ CT or magnetic resonance angiography findings sug- ischemia. gesting chronic mesenteric ischemia include severe The most appropriate diagnostic test to perform next is CT stenosis (>70%) of two of the three mesenteric arteries. mesenteric angiography (Option B). Chronic mesenteric ische- mia (CMI) is an uncommon condition most often resulting Bibliography w @ from atherosclerotic narrowing of the mesenteric arteries. Kolkman JJ, Geelkerken RH. Diagnosis and treatment of chronic mesenteric =

Bibliography intervals, whereas this patient’s pain occurs daily. Therefore, Gupta S, Lieberman D, Anderson JC, et al. Recommendations for follow-up ultrasonography would not be appropriate for this patient. after colonoscopy and polypectomy: a consensus update by the US Multi- Society Task Force on Colorectal Cancer. Am J Gastroenterol. 2020;115:415-434. [PMID: 32039982] doi:10.14309/ajg.00000000000 00544 ¢ The diagnosis of chronic mesenteric ischemia requires exclusion of alternative causes of postprandial abdominal pain and weight loss, along with compati- Item 63 Answer: B ble imaging findings. Educational Objective: Diagnose chronic mesenteric ¢ CT or magnetic resonance angiography findings sug- ischemia. gesting chronic mesenteric ischemia include severe The most appropriate diagnostic test to perform next is CT stenosis (>70%) of two of the three mesenteric arteries. mesenteric angiography (Option B). Chronic mesenteric ische- mia (CMI) is an uncommon condition most often resulting Bibliography w @ from atherosclerotic narrowing of the mesenteric arteries. Kolkman JJ, Geelkerken RH. Diagnosis and treatment of chronic mesenteric = The classic symptom triad of CMI is postprandial abdominal ischemia: an update. Best Pract Res Clin Gastroenterol. 2017:31:49-57. = [PMID: 28395788] doi:10.1016/j.bpg.2017.01.003 i pain, sitophobia (fear of eating), and weight loss, but this set 1S) of symptoms is seen in only 30% of patients with CMI. In cs < the setting of recurrent postprandial abdominal pain, CMI ltem 64 Answer: A cs

The classic symptom triad of CMI is postprandial abdominal ischemia: an update. Best Pract Res Clin Gastroenterol. 2017:31:49-57. = [PMID: 28395788] doi:10.1016/j.bpg.2017.01.003 i pain, sitophobia (fear of eating), and weight loss, but this set 1S) of symptoms is seen in only 30% of patients with CMI. In cs < the setting of recurrent postprandial abdominal pain, CMI ltem 64 Answer: A cs should be suspected. Pain begins approximately 30 minutes n how Educational Objective: Manage dual aspirin and i) after food ingestion as the fixed narrowing of the mesenteric anticoagulant therapy during lower gastrointestinal = 7) arteries prevents blood flow from increasing and meeting = bleeding. the increased functional demand of the small bowel, with <=

should be suspected. Pain begins approximately 30 minutes n how Educational Objective: Manage dual aspirin and i) after food ingestion as the fixed narrowing of the mesenteric anticoagulant therapy during lower gastrointestinal = 7) arteries prevents blood flow from increasing and meeting = bleeding. the increased functional demand of the small bowel, with <= resultant ischemia. The diagnosis of CMI requires exclusion of The most appropriate management of antiplatelet and antico- alternative causes of postprandial abdominal pain and weight agulant therapy in this patient is to hold apixaban (Option A). loss, along with compatible imaging findings. CT or mag- This patient most likely developed postpolypectomy bleeding netic resonance angiography findings suggesting CMI include that was exacerbated by aspirin and apixaban use. Because severe stenosis (>70%) of two of the three mesenteric arteries. he has hemodynamically significant lower gastrointestinal Ifthe patient has compatible symptoms and suggestive angio- bleeding, the initial steps are intravascular resuscitation and graphic findings, and alternative explanations for postpran- withholding apixaban. The duration of the anticoagulant dial abdominal pain have been excluded, then the diagnosis effect of the direct oral anticoagulants (DOACs), including of CMI is secure. In patients with symptoms suggestive of apixaban, is limited because of their relatively short half-life. CMI, CT mesenteric angiography is the recommended ini- In most cases of lower gastrointestinal bleeding, simply hold- tial diagnostic imaging test because it allows for rapid and ing the DOAC is sufficient. accurate assessment of the mesenteric vasculature. Duplex Andexanet is a recombinant modified factor Xa pro ultrasonography of the mesenteric vessels is a reasonable tein used to reverse the anticoagulant effects of apixaban screening modality to detect high-grade stenosis of the celiac and rivaroxaban in patients with life-threatening or uncon and superior mesenteric arteries for patients being evaluated trolled bleeding. Its use has been associated with serious in an outpatient setting. and life-threatening events, including myocardial infarction, Capsule endoscopy (Option A) can visualize the small stroke, cardiac arrest, and sudden death. For life-threatening intestine and is often used in the evaluation of small-bowel bleeding related to Xa inhibitors, such as apixaban, the bleeding. However, this patient’s symptoms suggest ische- American Society of Hematology suggests stopping the oral mic pain rather than bleeding, so capsule endoscopy will direct Xa inhibitor and considering treatment with four provide no diagnostic value. factor prothrombin complex concentrates or andexanet alfa A gastric emptying study (Option C) helps assess for (Options B, D). Because of the lack of comparative data, a gastroparesis as a cause of postprandial symptoms. Gast- preferred strategy cannot be identified. This patient does not roparesis entails delayed gastric emptying without mechan- have life-threatening uncontrolled bleeding (as indicated by ical obstruction and with the cardinal symptoms of nausea, the response to intravenous resuscitation) and therefore does vomiting, early satiety, aand postprandial upper abdominal not need apixaban reversal therapy. pain. For this patient, however, the presence of atheroscle- For secondary prevention of cardiovascular disease, the rotic vascular disease, an abdominal bruit and absent nau- risk of interrupting aspirin therapy (Option C) is substantial. sea, early satiety, and risk factors for gastroparesis support Studies have shown that discontinuation of long-term low- CT mesenteric angiography as the next diagnostic step. dose aspirin therapy for secondary prevention is associated Ultrasonography of the gallbladder (Option D) would with a threefold increased risk for cardiovascular or cerebro be appropriate if biliary colic were suspected. Abdominal vascular events, with 70% of such events occurring within pain from biliary colic is episodic, severe, and steady and 7 to 10 days of discontinuation. The American College of is often located in the epigastrium or right upper quadrant, Gastroenterology and the British Society of Gastroenterology as in this patient. However, biliary pain recurs at different have recommended that to avoid thromboembolic events,

resultant ischemia. The diagnosis of CMI requires exclusion of The most appropriate management of antiplatelet and antico- alternative causes of postprandial abdominal pain and weight agulant therapy in this patient is to hold apixaban (Option A). loss, along with compatible imaging findings. CT or mag- This patient most likely developed postpolypectomy bleeding netic resonance angiography findings suggesting CMI include that was exacerbated by aspirin and apixaban use. Because severe stenosis (>70%) of two of the three mesenteric arteries. he has hemodynamically significant lower gastrointestinal Ifthe patient has compatible symptoms and suggestive angio- bleeding, the initial steps are intravascular resuscitation and graphic findings, and alternative explanations for postpran- withholding apixaban. The duration of the anticoagulant dial abdominal pain have been excluded, then the diagnosis effect of the direct oral anticoagulants (DOACs), including of CMI is secure. In patients with symptoms suggestive of apixaban, is limited because of their relatively short half-life. CMI, CT mesenteric angiography is the recommended ini- In most cases of lower gastrointestinal bleeding, simply hold- tial diagnostic imaging test because it allows for rapid and ing the DOAC is sufficient. accurate assessment of the mesenteric vasculature. Duplex Andexanet is a recombinant modified factor Xa pro ultrasonography of the mesenteric vessels is a reasonable tein used to reverse the anticoagulant effects of apixaban screening modality to detect high-grade stenosis of the celiac and rivaroxaban in patients with life-threatening or uncon and superior mesenteric arteries for patients being evaluated trolled bleeding. Its use has been associated with serious in an outpatient setting. and life-threatening events, including myocardial infarction, Capsule endoscopy (Option A) can visualize the small stroke, cardiac arrest, and sudden death. For life-threatening intestine and is often used in the evaluation of small-bowel bleeding related to Xa inhibitors, such as apixaban, the bleeding. However, this patient’s symptoms suggest ische- American Society of Hematology suggests stopping the oral mic pain rather than bleeding, so capsule endoscopy will direct Xa inhibitor and considering treatment with four provide no diagnostic value. factor prothrombin complex concentrates or andexanet alfa A gastric emptying study (Option C) helps assess for (Options B, D). Because of the lack of comparative data, a gastroparesis as a cause of postprandial symptoms. Gast- preferred strategy cannot be identified. This patient does not roparesis entails delayed gastric emptying without mechan- have life-threatening uncontrolled bleeding (as indicated by ical obstruction and with the cardinal symptoms of nausea, the response to intravenous resuscitation) and therefore does vomiting, early satiety, aand postprandial upper abdominal not need apixaban reversal therapy. pain. For this patient, however, the presence of atheroscle- For secondary prevention of cardiovascular disease, the rotic vascular disease, an abdominal bruit and absent nau- risk of interrupting aspirin therapy (Option C) is substantial. sea, early satiety, and risk factors for gastroparesis support Studies have shown that discontinuation of long-term low- CT mesenteric angiography as the next diagnostic step. dose aspirin therapy for secondary prevention is associated Ultrasonography of the gallbladder (Option D) would with a threefold increased risk for cardiovascular or cerebro be appropriate if biliary colic were suspected. Abdominal vascular events, with 70% of such events occurring within pain from biliary colic is episodic, severe, and steady and 7 to 10 days of discontinuation. The American College of is often located in the epigastrium or right upper quadrant, Gastroenterology and the British Society of Gastroenterology as in this patient. However, biliary pain recurs at different have recommended that to avoid thromboembolic events, 139

Answers and Critiques aspirin for secondary prophylaxis in patients with estab- therapy is prescribed for secondary prevention of athero- lished cardiovascular disease should not be discontinued sclerotic cardiovascular disease and should be continued CONT. in patients with lower gastrointestinal bleeding. If aspirin uninterrupted. If discontinuation of aspirin is necessary is discontinued, it should be restarted as soon as possible in these cases, it should be reinstated as soon as possible following hemostasis. following hemostasis.

aspirin for secondary prophylaxis in patients with estab- therapy is prescribed for secondary prevention of athero- lished cardiovascular disease should not be discontinued sclerotic cardiovascular disease and should be continued CONT. in patients with lower gastrointestinal bleeding. If aspirin uninterrupted. If discontinuation of aspirin is necessary is discontinued, it should be restarted as soon as possible in these cases, it should be reinstated as soon as possible following hemostasis. following hemostasis. ¢ The duration of the anticoagulant effect of the direct e In hemodynamically stable patients without evidence oral anticoagulants (DOACs) is limited because of of rapid lower gastrointestinal bleeding, colonoscopy their short half-life; in most cases of gastrointestinal is the first test of choice. bleeding, simply holding the DOAC is sufficient. e Although nuclear studies may be able to detect lower gastrointestinal bleeding, precise anatomic location is > Bibliography inferior to that provided by first-line diagnostic tests, = Oakland K, Chadwick G, East JE, et al. Diagnosis and management of acute wn such as colonoscopy, CT angiography, and conventional = lower gastrointestinal bleeding: guidelines from the British Society of © Gastroenterology. Gut. 2019;68:776-789. [PMID: 30792244] doi:10.1136/ angiography. = wn gutjnl-2018-317807 gy = Bibliography a. a Strate LL, Gralnek IM. ACG clinical guideline: management of patients with PAG acute lower gastrointestinal bleeding. Am J Gastroenterol. 2016;111: Item 65 Answer: A a 459-74. [PMID: 26925883] doi:10.1038/ajg.2016.41 2 f Educational Objective: Evaluate lower gastrointestinal @o bleeding in a hemodynamically stable patient. wn Item 66 Answer: B The most appropriate next diagnostic test is colonoscopy Educational Objective: Treat moderate to severe Crohn (Option A). This patient likely has lower gastrointestinal disease. bleeding. She has no signs of active bleeding and is hemo- dynamically stable. Given her age, comorbid conditions, and The most appropriate treatment is starting infliximab (Option significant decrease in hemoglobin, observation and urgent B), an anti-tumor necrosis factor (anti-TNF) agent. The patient colonoscopy are warranted. Colonoscopy should be per- presented with a flare of severe ileocolonic Crohn disease. formed within 24 hours of presentation after adequate colon She has required several courses of glucocorticoid treatment preparation, which may include rapid preparation. Colonos- because maintenance therapy with azathioprine, an immuno- copy identifies a source of lower gastrointestinal bleeding in modulator, failed. The anti-TNF agents infliximab, adalim two thirds of patients. umab, and certolizumab treat moderate to severe Crohn There is no need for CT angiography (CTA) (Option B) disease that is resistant to glucocorticoids or immunomod- or tagged red cell scintigraphy (technetium-99m-labeled red ulators. Combination therapy with infliximab and azathio cell scintigraphy) (Option C) to detect and localize a site for prine is more efficacious than monotherapy with either agent active bleeding. CTA is the initial diagnostic test in patients alone in achieving glucocorticoid-free remission and mucosal who are hemodynamically unstable or have rapid ongoing healing. Before initiation of anti-TNF agents, patients should bleeding, followed by immediate upper endoscopy if CTA undergo testing for latent tuberculosis because of an increased does not reveal a source of bleeding. Because this patient is risk for reactivation of tuberculosis during therapy. If latent hemodynamically stable and does not have active bleeding, tuberculosis is present, treatment with isoniazid should be CTA would not be appropriate. Although tagged red cell administered for at least 2 months before initiation of anti scintigraphy can detect bleeding rates as low as 0.1 mL/min, TNF therapy. Patients should also be assessed for chronic its usefulness in acute lower gastrointestinal bleeding is hepatitis B virus infection before starting anti-TNF therapy debated. Sensitivity of nuclear studies for the detection of a and receive treatment if needed. lower gastrointestinal bleeding site varies from 60% to 93%. Various formulations of oral and intravenous gluco- Although nuclear studies may be able to detect lower gas- corticoids are commonly used to treat mild to severe flares trointestinal bleeding, precise anatomic location is inferior of Crohn disease. Although they are effective in inducing to that provided by first-line diagnostic tests. Tagged red cell remission, they are not effective for maintenance therapy scintigraphy may be considered when results of first-line and have significant adverse effects. Controlled-release oral tests, such as CTA, angiography, or colonoscopy, are negative. budesonide (Option A) is a glucocorticoid that is effective in Although this patient takes aspirin, her presentation of inducing remission in mild to moderate ileocolonic Crohn multiple maroon stools does not suggest upper gastrointesti- disease. This patient has severe ileocolonic disease, how- nal bleeding. Furthermore, she is receiving long-term gastric ever, which will likely lead to failure of induction with oral protective therapy with omeprazole, further reducing the risk budesonide. for upper gastrointestinal bleeding. If colonoscopy results fail Thiopurines (azathioprine and 6-mercaptopurine) to reveal a cause of bleeding, upper endoscopy (Option D) are immunomodulators used as glucocorticoid-sparing can be considered as a secondary test. This patient’s aspirin agents in Crohn disease. They have a slow onset of action

¢ The duration of the anticoagulant effect of the direct e In hemodynamically stable patients without evidence oral anticoagulants (DOACs) is limited because of of rapid lower gastrointestinal bleeding, colonoscopy their short half-life; in most cases of gastrointestinal is the first test of choice. bleeding, simply holding the DOAC is sufficient. e Although nuclear studies may be able to detect lower gastrointestinal bleeding, precise anatomic location is > Bibliography inferior to that provided by first-line diagnostic tests, = Oakland K, Chadwick G, East JE, et al. Diagnosis and management of acute wn such as colonoscopy, CT angiography, and conventional = lower gastrointestinal bleeding: guidelines from the British Society of © Gastroenterology. Gut. 2019;68:776-789. [PMID: 30792244] doi:10.1136/ angiography. = wn gutjnl-2018-317807 gy = Bibliography a. a Strate LL, Gralnek IM. ACG clinical guideline: management of patients with PAG acute lower gastrointestinal bleeding. Am J Gastroenterol. 2016;111: Item 65 Answer: A a 459-74. [PMID: 26925883] doi:10.1038/ajg.2016.41 2 f Educational Objective: Evaluate lower gastrointestinal @o bleeding in a hemodynamically stable patient. wn Item 66 Answer: B The most appropriate next diagnostic test is colonoscopy Educational Objective: Treat moderate to severe Crohn (Option A). This patient likely has lower gastrointestinal disease. bleeding. She has no signs of active bleeding and is hemo- dynamically stable. Given her age, comorbid conditions, and The most appropriate treatment is starting infliximab (Option significant decrease in hemoglobin, observation and urgent B), an anti-tumor necrosis factor (anti-TNF) agent. The patient colonoscopy are warranted. Colonoscopy should be per- presented with a flare of severe ileocolonic Crohn disease. formed within 24 hours of presentation after adequate colon She has required several courses of glucocorticoid treatment preparation, which may include rapid preparation. Colonos- because maintenance therapy with azathioprine, an immuno- copy identifies a source of lower gastrointestinal bleeding in modulator, failed. The anti-TNF agents infliximab, adalim two thirds of patients. umab, and certolizumab treat moderate to severe Crohn There is no need for CT angiography (CTA) (Option B) disease that is resistant to glucocorticoids or immunomod- or tagged red cell scintigraphy (technetium-99m-labeled red ulators. Combination therapy with infliximab and azathio cell scintigraphy) (Option C) to detect and localize a site for prine is more efficacious than monotherapy with either agent active bleeding. CTA is the initial diagnostic test in patients alone in achieving glucocorticoid-free remission and mucosal who are hemodynamically unstable or have rapid ongoing healing. Before initiation of anti-TNF agents, patients should bleeding, followed by immediate upper endoscopy if CTA undergo testing for latent tuberculosis because of an increased does not reveal a source of bleeding. Because this patient is risk for reactivation of tuberculosis during therapy. If latent hemodynamically stable and does not have active bleeding, tuberculosis is present, treatment with isoniazid should be CTA would not be appropriate. Although tagged red cell administered for at least 2 months before initiation of anti scintigraphy can detect bleeding rates as low as 0.1 mL/min, TNF therapy. Patients should also be assessed for chronic its usefulness in acute lower gastrointestinal bleeding is hepatitis B virus infection before starting anti-TNF therapy debated. Sensitivity of nuclear studies for the detection of a and receive treatment if needed. lower gastrointestinal bleeding site varies from 60% to 93%. Various formulations of oral and intravenous gluco- Although nuclear studies may be able to detect lower gas- corticoids are commonly used to treat mild to severe flares trointestinal bleeding, precise anatomic location is inferior of Crohn disease. Although they are effective in inducing to that provided by first-line diagnostic tests. Tagged red cell remission, they are not effective for maintenance therapy scintigraphy may be considered when results of first-line and have significant adverse effects. Controlled-release oral tests, such as CTA, angiography, or colonoscopy, are negative. budesonide (Option A) is a glucocorticoid that is effective in Although this patient takes aspirin, her presentation of inducing remission in mild to moderate ileocolonic Crohn multiple maroon stools does not suggest upper gastrointesti- disease. This patient has severe ileocolonic disease, how- nal bleeding. Furthermore, she is receiving long-term gastric ever, which will likely lead to failure of induction with oral protective therapy with omeprazole, further reducing the risk budesonide. for upper gastrointestinal bleeding. If colonoscopy results fail Thiopurines (azathioprine and 6-mercaptopurine) to reveal a cause of bleeding, upper endoscopy (Option D) are immunomodulators used as glucocorticoid-sparing can be considered as a secondary test. This patient’s aspirin agents in Crohn disease. They have a slow onset of action 140

; _Answers and Critiques (2-3 months), and patients require a tapering glucocor for improvement in symptoms may be reasonable in patients ticoid regimen to bridge the interval until the thiopu with a high probability of SIBO. CONT. rine takes effect. Azathioprine and 6-mercaptopurine are Eluxadoline (Option A), a mixed «- and p-opioid equivalent immunomodulators, and changing from one to receptor agonist and 6-opioid receptor antagonist, decreases the other (Option C) would have no benefit in this patient. the frequency of bowel contractions and treats diarrhea- Although several formulations of 5-aminosalicylates predominant irritable bowel syndrome. This patient’s age deliver the drug to the small bowel, they are not efficacious at symptom onset and lack of abdominal pain, as well as in small-bowel Crohn disease. Sulfasalazine (Option D) the presence of a risk factor for SIBO, make irritable bowel is effective for treating symptoms of colonic Crohn dis syndrome a less likely diagnosis. ease that is mild to moderately active and can be used as Stool should be tested for Clostridioides difficile toxin treatment for this patient population. Given its lack of (Option C) in patients with suspected C. difficile colitis, usu- efficacy in small-bowel Crohn disease and this patient's ally in the setting of antecedent antibiotic use. This patient’s severe colonic disease, initiating sulfasalazine would not steatorrhea in the absence of risk factors for C. difficile infec- wn ao be appropriate. tion makes this diagnosis unlikely. =

(2-3 months), and patients require a tapering glucocor for improvement in symptoms may be reasonable in patients ticoid regimen to bridge the interval until the thiopu with a high probability of SIBO. CONT. rine takes effect. Azathioprine and 6-mercaptopurine are Eluxadoline (Option A), a mixed «- and p-opioid equivalent immunomodulators, and changing from one to receptor agonist and 6-opioid receptor antagonist, decreases the other (Option C) would have no benefit in this patient. the frequency of bowel contractions and treats diarrhea- Although several formulations of 5-aminosalicylates predominant irritable bowel syndrome. This patient’s age deliver the drug to the small bowel, they are not efficacious at symptom onset and lack of abdominal pain, as well as in small-bowel Crohn disease. Sulfasalazine (Option D) the presence of a risk factor for SIBO, make irritable bowel is effective for treating symptoms of colonic Crohn dis syndrome a less likely diagnosis. ease that is mild to moderately active and can be used as Stool should be tested for Clostridioides difficile toxin treatment for this patient population. Given its lack of (Option C) in patients with suspected C. difficile colitis, usu- efficacy in small-bowel Crohn disease and this patient's ally in the setting of antecedent antibiotic use. This patient’s severe colonic disease, initiating sulfasalazine would not steatorrhea in the absence of risk factors for C. difficile infec- wn ao be appropriate. tion makes this diagnosis unlikely. = Upper endoscopy with duodenal biopsy (Option D) is = = indicated in the setting of chronic diarrhea when serologic YY e An anti-tumor necrosis factor agent is most likely to results suggest celiac disease. In this patient, the normal tis- cs i= induce and maintain remission of moderate to severe sue transglutaminase IgA level makes celiac disease unlikely. cs

Upper endoscopy with duodenal biopsy (Option D) is = = indicated in the setting of chronic diarrhea when serologic YY e An anti-tumor necrosis factor agent is most likely to results suggest celiac disease. In this patient, the normal tis- cs i= induce and maintain remission of moderate to severe sue transglutaminase IgA level makes celiac disease unlikely. cs ileocolonic Crohn disease resistant to glucocorticoids wn a ao or immunomodulators. 3 ¢ Causes of fat malabsorption include pancreatic w ¢ Combination therapy with an anti-tumor necrosis i dysfunction, infections (e.g., giardiasis and Whipple <= factor and an immunomodulator is more efficacious disease), celiac disease, tropical sprue, and small than monotherapy with either agent alone in achiev- intestinal bacterial overgrowth. ing glucocorticoid-free remission and mucosal heal- ing in moderate to severe Crohn disease. ¢ Small intestinal bacterial overgrowth can be diagnosed in the appropriate clinical context with both typical

ileocolonic Crohn disease resistant to glucocorticoids wn a ao or immunomodulators. 3 ¢ Causes of fat malabsorption include pancreatic w ¢ Combination therapy with an anti-tumor necrosis i dysfunction, infections (e.g., giardiasis and Whipple <= factor and an immunomodulator is more efficacious disease), celiac disease, tropical sprue, and small than monotherapy with either agent alone in achiev- intestinal bacterial overgrowth. ing glucocorticoid-free remission and mucosal heal- ing in moderate to severe Crohn disease. ¢ Small intestinal bacterial overgrowth can be diagnosed in the appropriate clinical context with both typical Bibliography symptoms (abdominal discomfort, flatulence, bloating, Lichtenstein GR, Loftus EV, Isaacs KL, et al. ACG clinical guideline: manage- and diarrhea) and a positive result on a glucose breath ment of Crohn’s disease in adults. Am J Gastroenterol. 2018;113:481-517. test. [PMID: 29610508] doi:10.1038/ajg.2018.27

Bibliography symptoms (abdominal discomfort, flatulence, bloating, Lichtenstein GR, Loftus EV, Isaacs KL, et al. ACG clinical guideline: manage- and diarrhea) and a positive result on a glucose breath ment of Crohn’s disease in adults. Am J Gastroenterol. 2018;113:481-517. test. [PMID: 29610508] doi:10.1038/ajg.2018.27 Bibliography Item 67 Answer: B Rezaie A, Buresi M, Lembo A, et al. Hydrogen and methane-based breath testing in gastrointestinal disorders: the North American consensus. Am Educational Objective: Diagnose small intestinal J Gastroenterol. 2017;112:775-784. [PMID: 28323273] doi:10.1038/ajg. bacterial overgrowth. 2017.46

Bibliography Item 67 Answer: B Rezaie A, Buresi M, Lembo A, et al. Hydrogen and methane-based breath testing in gastrointestinal disorders: the North American consensus. Am Educational Objective: Diagnose small intestinal J Gastroenterol. 2017;112:775-784. [PMID: 28323273] doi:10.1038/ajg. bacterial overgrowth. 2017.46 The appropriate management is a glucose breath test (Option B). The patient’s 5-month history of diarrhea, characterized Item 68 Answer: 8B as bowel movements containing oil droplets and necessitat- Educational Objective: Manage low-risk upper ing multiple flushes, is consistent with steatorrhea. Causes of gastrointestinal bleeding. fat malabsorption include pancreatic dysfunction, infections (e.g., giardiasis and Whipple disease), celiac disease, tropical The most appropriate management for this patient with upper sprue, and small intestinal bacterial overgrowth (SIBO). SIBO gastrointestinal bleeding due to a low-risk duodenal ulcer is is caused by various conditions, including impaired motility, a once-daily oral proton pump inhibitor (PPI), initiation of strictures (e.g., in Crohn disease), or blind loops (e.g., small- oral intake of food, and early planning for hospital discharge bowel diverticula). The patient’s jejunal diverticulum is a (Option B). In patients with bleeding peptic ulcer disease, blind loop and a key risk factor for SIBO. The pathogenesis of factors that increase the risk for recurrent bleeding and death steatorrhea in SIBO is thought to be due to the deconjugation include tachycardia, hypotension, age older than 60 years, of bile salts by excessive intraluminal bacteria, interfering hemoglobin level less than 7 g/dL (70 g/L) (8 g/dL [80 g/L] in with formation of micelles that are necessary for fat absorp- patients with cardiovascular disease), and comorbid illness. tion. SIBO can be diagnosed in the appropriate clinical context This young patient is otherwise healthy, has a hemoglobin with both typical symptoms (abdominal discomfort, flatu- level above 7 g/dL (70 g/L), and is hemodynamically stable. lence, bloating, and diarrhea) and a confirmatory test, such as Upper endoscopy for risk stratification revealed a clean-based a glucose breath test, in which exhaled hydrogen and meth- ulcer, which is a predictor of low risk for recurrent hemor ane (byproducts of bacterial metabolism of ingested glucose) rhage. The other lesion at low risk for rebleeding includes an are measured after glucose administration. Glucose breath ulcer with a pigmented spot. These low-risk lesions do not tests are approximately 80% sensitive but only 40% specific for require endoscopic therapy. Patients with peptic ulcer disease diagnosing SIBO. Empiric antibiotic therapy with monitoring and low-risk stigmata can start oral feeding within 24 hours

The appropriate management is a glucose breath test (Option B). The patient’s 5-month history of diarrhea, characterized Item 68 Answer: 8B as bowel movements containing oil droplets and necessitat- Educational Objective: Manage low-risk upper ing multiple flushes, is consistent with steatorrhea. Causes of gastrointestinal bleeding. fat malabsorption include pancreatic dysfunction, infections (e.g., giardiasis and Whipple disease), celiac disease, tropical The most appropriate management for this patient with upper sprue, and small intestinal bacterial overgrowth (SIBO). SIBO gastrointestinal bleeding due to a low-risk duodenal ulcer is is caused by various conditions, including impaired motility, a once-daily oral proton pump inhibitor (PPI), initiation of strictures (e.g., in Crohn disease), or blind loops (e.g., small- oral intake of food, and early planning for hospital discharge bowel diverticula). The patient’s jejunal diverticulum is a (Option B). In patients with bleeding peptic ulcer disease, blind loop and a key risk factor for SIBO. The pathogenesis of factors that increase the risk for recurrent bleeding and death steatorrhea in SIBO is thought to be due to the deconjugation include tachycardia, hypotension, age older than 60 years, of bile salts by excessive intraluminal bacteria, interfering hemoglobin level less than 7 g/dL (70 g/L) (8 g/dL [80 g/L] in with formation of micelles that are necessary for fat absorp- patients with cardiovascular disease), and comorbid illness. tion. SIBO can be diagnosed in the appropriate clinical context This young patient is otherwise healthy, has a hemoglobin with both typical symptoms (abdominal discomfort, flatu- level above 7 g/dL (70 g/L), and is hemodynamically stable. lence, bloating, and diarrhea) and a confirmatory test, such as Upper endoscopy for risk stratification revealed a clean-based a glucose breath test, in which exhaled hydrogen and meth- ulcer, which is a predictor of low risk for recurrent hemor ane (byproducts of bacterial metabolism of ingested glucose) rhage. The other lesion at low risk for rebleeding includes an are measured after glucose administration. Glucose breath ulcer with a pigmented spot. These low-risk lesions do not tests are approximately 80% sensitive but only 40% specific for require endoscopic therapy. Patients with peptic ulcer disease diagnosing SIBO. Empiric antibiotic therapy with monitoring and low-risk stigmata can start oral feeding within 24 hours 141

Answers and Critiques of endoscopy, receive once-daily oral PPI therapy, and be dis- cystic neoplasms, are thought to have malignant potential, but charged from the hospital. NSAIDs should be discontinued in many never become malignant. Non-mucin-producing cysts, CONT. patients with NSAID-induced bleeding peptic ulcer disease. such as a serous cystadenoma, have no malignant potential If there is no effective alternative to NSAIDs, a selective cyclo- and can often be identified by their characteristic imaging oxygenase-2 inhibitor plus a once-daily PPI should be used. features. These cysts require no further evaluation unless Intravenous PPI therapy and hospital observation for symptomatic. 72 hours (Option A) would be appropriate for patients with For patients in whom the diagnosis is unclear, endo- high-risk lesions. Lesions at high risk for recurrent bleed- scopic ultrasonography and fine-needle aspiration (Option ing that require endoscopic treatment include actively A) can be performed for cytology, measurement of carci- bleeding peptic ulcers, ulcers with nonbleeding visible noembryonic antigen level, and DNA analysis. vessels, and ulcers with adherent clots. An adherent clot In the absence of high-risk features (e.g., main pan- should be irrigated with the intention of removing the creatic duct dilation, cysts 3 cm or larger, change in the P= clot; if clot removal is successful, the underlying stigmata main duct diameter with distal parenchymal atrophy, and =] wn is addressed. In this patient, intravenous PPI therapy plus association with a solid mass), patients with mucinous cysts = hospital observation for 72 hours is not an appropriate may undergo MRI surveillance (Option B), the frequency @o = wn management strategy given the low risk for rebleeding depending on many factors, including cyst size. 3) = from a clean-based ulcer. Surgical resection (Option C) of high-risk cysts is the 2. Once-daily oral PPI, no feeding, and hospital observa- only treatment option. In addition to the high-risk features (‘s) =f tion for 72 hours (Option C) is insufficient therapy for high- just described, cysts in patients presenting with obstructive =e risk lesions and is unnecessary in patients with low-risk jaundice are also high risk. Surgical resection is recom- 2 i= lesions. mended for nearly all mucinous neoplasms and main-duct Oo wn If bleeding recurs, endoscopic therapy should be intraductal papillary mucinous neoplasms if the patient is an repeated, but routine second-look endoscopy (Option D) is appropriate surgical candidate. Mucinous cystic neoplasms not recommended. occur almost exclusively in women in their fifth to seventh decades of life and are almost always located in the body or tail of the pancreas. These neoplasms have moderate malig- e NSAIDs should be discontinued in patients with nant potential. Intraductal papillary mucinous neoplasms NSAID-induced bleeding peptic ulcer disease; if treat- (IPMNs) are equally prevalent in men and women, usually ment must be continued, a selective cyclooxygenase-2 appearing in their fifth to seventh decades of life. Branch- inhibitor plus a once-daily proton pump inhibitor duct IPMNs are characterized by cystic structures that may should be used. appear throughout the pancreas. Imaging characteristics of main duct IPMNs include main pancreatic duct dilation e Patients with peptic ulcer disease and low risk for and parenchymal atrophy. These neoplasms have variable rebleeding (clean-based ulcer, ulcers with pigmented malignant potential. spots) can start oral feeding within 24 hours of endo- scopy, receive once-daily oral proton pump inhibitor

of endoscopy, receive once-daily oral PPI therapy, and be dis- cystic neoplasms, are thought to have malignant potential, but charged from the hospital. NSAIDs should be discontinued in many never become malignant. Non-mucin-producing cysts, CONT. patients with NSAID-induced bleeding peptic ulcer disease. such as a serous cystadenoma, have no malignant potential If there is no effective alternative to NSAIDs, a selective cyclo- and can often be identified by their characteristic imaging oxygenase-2 inhibitor plus a once-daily PPI should be used. features. These cysts require no further evaluation unless Intravenous PPI therapy and hospital observation for symptomatic. 72 hours (Option A) would be appropriate for patients with For patients in whom the diagnosis is unclear, endo- high-risk lesions. Lesions at high risk for recurrent bleed- scopic ultrasonography and fine-needle aspiration (Option ing that require endoscopic treatment include actively A) can be performed for cytology, measurement of carci- bleeding peptic ulcers, ulcers with nonbleeding visible noembryonic antigen level, and DNA analysis. vessels, and ulcers with adherent clots. An adherent clot In the absence of high-risk features (e.g., main pan- should be irrigated with the intention of removing the creatic duct dilation, cysts 3 cm or larger, change in the P= clot; if clot removal is successful, the underlying stigmata main duct diameter with distal parenchymal atrophy, and =] wn is addressed. In this patient, intravenous PPI therapy plus association with a solid mass), patients with mucinous cysts = hospital observation for 72 hours is not an appropriate may undergo MRI surveillance (Option B), the frequency @o = wn management strategy given the low risk for rebleeding depending on many factors, including cyst size. 3) = from a clean-based ulcer. Surgical resection (Option C) of high-risk cysts is the 2. Once-daily oral PPI, no feeding, and hospital observa- only treatment option. In addition to the high-risk features (‘s) =f tion for 72 hours (Option C) is insufficient therapy for high- just described, cysts in patients presenting with obstructive =e risk lesions and is unnecessary in patients with low-risk jaundice are also high risk. Surgical resection is recom- 2 i= lesions. mended for nearly all mucinous neoplasms and main-duct Oo wn If bleeding recurs, endoscopic therapy should be intraductal papillary mucinous neoplasms if the patient is an repeated, but routine second-look endoscopy (Option D) is appropriate surgical candidate. Mucinous cystic neoplasms not recommended. occur almost exclusively in women in their fifth to seventh decades of life and are almost always located in the body or tail of the pancreas. These neoplasms have moderate malig- e NSAIDs should be discontinued in patients with nant potential. Intraductal papillary mucinous neoplasms NSAID-induced bleeding peptic ulcer disease; if treat- (IPMNs) are equally prevalent in men and women, usually ment must be continued, a selective cyclooxygenase-2 appearing in their fifth to seventh decades of life. Branch- inhibitor plus a once-daily proton pump inhibitor duct IPMNs are characterized by cystic structures that may should be used. appear throughout the pancreas. Imaging characteristics of main duct IPMNs include main pancreatic duct dilation e Patients with peptic ulcer disease and low risk for and parenchymal atrophy. These neoplasms have variable rebleeding (clean-based ulcer, ulcers with pigmented malignant potential. spots) can start oral feeding within 24 hours of endo- scopy, receive once-daily oral proton pump inhibitor therapy, and be discharged from the hospital. e¢ Mucin-producing cysts, including intraductal papillary mucinous neoplasms and mucinous cystic Bibliography neoplasms, are thought to have malignant potential. Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:1536. [PMID: 30910853] doi:10.1136/bmj.1536 ¢ Non-mucin-producing cysts, such as a serous cystad- enoma, have no malignant potential.

therapy, and be discharged from the hospital. e¢ Mucin-producing cysts, including intraductal papillary mucinous neoplasms and mucinous cystic Bibliography neoplasms, are thought to have malignant potential. Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:1536. [PMID: 30910853] doi:10.1136/bmj.1536 ¢ Non-mucin-producing cysts, such as a serous cystad- enoma, have no malignant potential. Item 69 Answer: D Bibliography Elta GH, Enestvedt BK, Sauer BG, et al. ACG clinical guideline: diagnosis and Educational Objective: Manage a serous cystadenoma. management of pancreatic cysts. Am J Gastroenterol. 2018;113:464-479. [PMID: 29485131] doi:10.1038/ajg.2018.14 The most appropriate management for the patient’s serous cystadenoma is no further evaluation or intervention (Option D). Characteristic findings of serous cystadenomas include Item 70 Answer: D multicystic, lobulated structures (sometimes described as a Educational Objective: Diagnose Helicobacter pylori “bunch of grapes”), which may have a central fibrosis scar infection. or calcification. Pancreatic cysts are being detected more fre- quently because of increased use of imaging and improved The most appropriate management for this young patient imaging techniques; these cysts may be found in 15% of indi- with uninvestigated dyspepsia is stool antigen testing for viduals undergoing abdominal imaging. Cystic neoplasms Helicobacter pylori (Option D). In the management of dys- of the pancreas are subcategorized as mucin-producing and pepsia, benefits and costs favor a test-and-treat strategy for non-mucin-producing cysts. Mucin-producing cysts, includ- H. pylori infection. Patients who test positive for H. pylori ing intraductal papillary mucinous neoplasms and mucinous should receive eradication therapy. Patients negative for

Item 69 Answer: D Bibliography Elta GH, Enestvedt BK, Sauer BG, et al. ACG clinical guideline: diagnosis and Educational Objective: Manage a serous cystadenoma. management of pancreatic cysts. Am J Gastroenterol. 2018;113:464-479. [PMID: 29485131] doi:10.1038/ajg.2018.14 The most appropriate management for the patient’s serous cystadenoma is no further evaluation or intervention (Option D). Characteristic findings of serous cystadenomas include Item 70 Answer: D multicystic, lobulated structures (sometimes described as a Educational Objective: Diagnose Helicobacter pylori “bunch of grapes”), which may have a central fibrosis scar infection. or calcification. Pancreatic cysts are being detected more fre- quently because of increased use of imaging and improved The most appropriate management for this young patient imaging techniques; these cysts may be found in 15% of indi- with uninvestigated dyspepsia is stool antigen testing for viduals undergoing abdominal imaging. Cystic neoplasms Helicobacter pylori (Option D). In the management of dys- of the pancreas are subcategorized as mucin-producing and pepsia, benefits and costs favor a test-and-treat strategy for non-mucin-producing cysts. Mucin-producing cysts, includ- H. pylori infection. Patients who test positive for H. pylori ing intraductal papillary mucinous neoplasms and mucinous should receive eradication therapy. Patients negative for 142

Answers and Critiques H. pylori on noninvasive testing are treated with empiric tumor (9%), lung (7%-17%), and pancreatic (11%-36%). The proton pump inhibitor (PPI) therapy. Appropriate noninvasive multiple melanotic macules present on this patient’s lips are testing for H. pylori includes a monoclonal stool antigen test not seen in other familial polyposis syndromes. It is important or aC urea breath test. to recognize that people without PJS may also have melanotic If H. pylori test results are negative or H. pylori erad- macules, most commonly on the lower lip, but macules may ication fails to relieve the dyspepsia, an empiric trial of a also be found on the gingiva, buccal mucosa, or tongue or daily PPI (Option B) should be followed for 4 weeks. Patients within the genital mucosa. Solitary lesions are the rule, but whose symptoms are not alleviated with PPI therapy should multiple lesions suggest PJS. undergo further evaluation with upper endoscopy. Adenomatous polyposis syndromes (Option A) include Serologic testing (Option C), which does not discrimi- familial adenomatous polyposis, which is caused by muta- nate between past and active H. pylori infection, should be tions in the APC gene, as well as MUTYH-associated pol- avoided. Particularly in low-prevalence populations, such as yposis, caused by bi-allelic loss of MUTYH. Mutations in this patient, the test has a low accuracy for identifying active polymerase proofreading genes POLE and POLD1 are rare wn v infection. A positive serologic test result may lead to unnec- but are also associated with adenomatous polyposis. These 3 essary treatment in a substantial number of patients because latter syndromes have features of both Lynch syndrome and = of its high false-positive rates. familial adenomatous polyposis. The dermatologic findings = oO This patient is young and has no alarm features for observed in this patient are not seen in adenomatous polyp- sc < malignancy, such as anemia, family history of gastrointes- osis syndromes. © tinal cancer, or melena; therefore, further invasive testing Mutations in the tumor suppressor PTEN gene cause nr real o with upper endoscopy (Option E) is not indicated at this PTEN hamartoma syndrome (also known as Cowden syn- = time. For the same reasons, CT (Option A) would be of low drome) (Option B) and are associated with a lifetime risk for wn = yield and would not warrant the cost or radiation exposure. colorectal cancer of 9% to 16%. Patients with this syndrome <x

H. pylori on noninvasive testing are treated with empiric tumor (9%), lung (7%-17%), and pancreatic (11%-36%). The proton pump inhibitor (PPI) therapy. Appropriate noninvasive multiple melanotic macules present on this patient’s lips are testing for H. pylori includes a monoclonal stool antigen test not seen in other familial polyposis syndromes. It is important or aC urea breath test. to recognize that people without PJS may also have melanotic If H. pylori test results are negative or H. pylori erad- macules, most commonly on the lower lip, but macules may ication fails to relieve the dyspepsia, an empiric trial of a also be found on the gingiva, buccal mucosa, or tongue or daily PPI (Option B) should be followed for 4 weeks. Patients within the genital mucosa. Solitary lesions are the rule, but whose symptoms are not alleviated with PPI therapy should multiple lesions suggest PJS. undergo further evaluation with upper endoscopy. Adenomatous polyposis syndromes (Option A) include Serologic testing (Option C), which does not discrimi- familial adenomatous polyposis, which is caused by muta- nate between past and active H. pylori infection, should be tions in the APC gene, as well as MUTYH-associated pol- avoided. Particularly in low-prevalence populations, such as yposis, caused by bi-allelic loss of MUTYH. Mutations in this patient, the test has a low accuracy for identifying active polymerase proofreading genes POLE and POLD1 are rare wn v infection. A positive serologic test result may lead to unnec- but are also associated with adenomatous polyposis. These 3 essary treatment in a substantial number of patients because latter syndromes have features of both Lynch syndrome and = of its high false-positive rates. familial adenomatous polyposis. The dermatologic findings = oO This patient is young and has no alarm features for observed in this patient are not seen in adenomatous polyp- sc < malignancy, such as anemia, family history of gastrointes- osis syndromes. © tinal cancer, or melena; therefore, further invasive testing Mutations in the tumor suppressor PTEN gene cause nr real o with upper endoscopy (Option E) is not indicated at this PTEN hamartoma syndrome (also known as Cowden syn- = time. For the same reasons, CT (Option A) would be of low drome) (Option B) and are associated with a lifetime risk for wn = yield and would not warrant the cost or radiation exposure. colorectal cancer of 9% to 16%. Patients with this syndrome <x exhibit macrocephaly, facial trichilemmomas, lipomas, and oral papillomas as well as hamartomatous polyps. ¢ For patients with dyspepsia, a “test and treat” strategy Juvenile polyposis syndrome (Option C) is caused by for Helicobacter pylori infection is recommended. mutations in SMAD4 and BMPRIA. Patients often present

exhibit macrocephaly, facial trichilemmomas, lipomas, and oral papillomas as well as hamartomatous polyps. ¢ For patients with dyspepsia, a “test and treat” strategy Juvenile polyposis syndrome (Option C) is caused by for Helicobacter pylori infection is recommended. mutations in SMAD4 and BMPRIA. Patients often present e Ina person from an area with a low prevalence of with rectal bleeding in their teens or early twenties. Eval- Helicobacter pylori, a positive serologic result is likely uation can reveal multiple juvenile polyps (>5 polyps) in a false positive and should be followed by a stool anti- the colon (98%), stomach (14%), and small bowel (14%). It gen test or a 8C urea breath test. is important to differentiate juvenile polyposis syndrome from sporadic juvenile polyps, which may be seen in 1% of Bibliography children and are not considered syndromic.

a false positive and should be followed by a stool anti- the colon (98%), stomach (14%), and small bowel (14%). It gen test or a 8C urea breath test. is important to differentiate juvenile polyposis syndrome from sporadic juvenile polyps, which may be seen in 1% of Bibliography children and are not considered syndromic. Moayyedi P, Lacy BE, Andrews CN, et al. ACG and CAG clinical guideline: management of dyspepsia. AmJ Gastroenterol. 2017;112:988-1013. [PMID: 28631728] doi:10.1038/ajg.2017.154 ¢ The diagnosis of Peutz-Jeghers syndrome (PJS) is based on the presence of two of the following three criteria: two or more PJS-type hamartomatous polyps Item 71 Answer: D in the gastrointestinal tract; multiple melanotic Educational Objective: Diagnose Peutz-Jeghers macules in the mouth, buccal mucosa, nose, eyes, syndrome. genitalia, or fingers; and family history of PJS. This patient likely has Peutz-Jeghers syndrome (PJS) (Option D), which is caused by mutations in the STK11 (LKB1) gene. Bibliography PJS is a hamartomatous polyposis syndrome, and PJS-type Kidambi TD, Kohli DR, Samadder NJ, et al. Hereditary polyposis syndromes. Curr Treat Options Gastroenterol. 2019;17:650-665. [PMID: 31705372] polyps are found primarily in the small bowel as well as the doi:10.1007/s11938-019-00251-4 stomach and colon. Small-bowel hamartomas develop at a young age (average age, 18.5 years), and patients may present with rectal bleeding (most commonly), bowel obstruction, Item 72 Answer: D and intussusception. A clinical diagnosis of PJS may be made Educational Objective: Manage fundic gland polyps. when two of the following three criteria are met: two or more PJS-type hamartomatous polyps in the gastrointestinal The patient does not require follow-up upper endoscopy tract; typical mucocutaneous hyperpigmentation (melanotic (Option D). Fundic gland polyps are the most common macules) in the mouth, buccal mucosa, nose, eyes, genitalia, benign epithelial gastric polyp incidentally found on upper or fingers; and family history of PJS. Patients with PJS have endoscopy. These polyps are typically asymptomatic, smaller increased lifetime risk for multiple malignancies: colorectal than 1 cm, and located in the gastric fundus and/or gastric (39%), gastric (29%), small bowel (13%), breast (32%-54%), body; they can be solitary but are more often multiple. They ovarian/sex cord tumor with annular tubules (21%), cervical/ can be sporadic or can result from long-term proton pump adenoma malignum (1%), uterine (9%), testicular/Sertoli cell inhibitor (PPI) use (©12 months). Dysplasia is exceedingly

Moayyedi P, Lacy BE, Andrews CN, et al. ACG and CAG clinical guideline: management of dyspepsia. AmJ Gastroenterol. 2017;112:988-1013. [PMID: 28631728] doi:10.1038/ajg.2017.154 ¢ The diagnosis of Peutz-Jeghers syndrome (PJS) is based on the presence of two of the following three criteria: two or more PJS-type hamartomatous polyps Item 71 Answer: D in the gastrointestinal tract; multiple melanotic Educational Objective: Diagnose Peutz-Jeghers macules in the mouth, buccal mucosa, nose, eyes, syndrome. genitalia, or fingers; and family history of PJS. This patient likely has Peutz-Jeghers syndrome (PJS) (Option D), which is caused by mutations in the STK11 (LKB1) gene. Bibliography PJS is a hamartomatous polyposis syndrome, and PJS-type Kidambi TD, Kohli DR, Samadder NJ, et al. Hereditary polyposis syndromes. Curr Treat Options Gastroenterol. 2019;17:650-665. [PMID: 31705372] polyps are found primarily in the small bowel as well as the doi:10.1007/s11938-019-00251-4 stomach and colon. Small-bowel hamartomas develop at a young age (average age, 18.5 years), and patients may present with rectal bleeding (most commonly), bowel obstruction, Item 72 Answer: D and intussusception. A clinical diagnosis of PJS may be made Educational Objective: Manage fundic gland polyps. when two of the following three criteria are met: two or more PJS-type hamartomatous polyps in the gastrointestinal The patient does not require follow-up upper endoscopy tract; typical mucocutaneous hyperpigmentation (melanotic (Option D). Fundic gland polyps are the most common macules) in the mouth, buccal mucosa, nose, eyes, genitalia, benign epithelial gastric polyp incidentally found on upper or fingers; and family history of PJS. Patients with PJS have endoscopy. These polyps are typically asymptomatic, smaller increased lifetime risk for multiple malignancies: colorectal than 1 cm, and located in the gastric fundus and/or gastric (39%), gastric (29%), small bowel (13%), breast (32%-54%), body; they can be solitary but are more often multiple. They ovarian/sex cord tumor with annular tubules (21%), cervical/ can be sporadic or can result from long-term proton pump adenoma malignum (1%), uterine (9%), testicular/Sertoli cell inhibitor (PPI) use (©12 months). Dysplasia is exceedingly 143

rare; sporadic fundic gland polyps progressing to cancer have recommended routine surveillance for gastric ulcers. Instead, not been reported. In fact, dysplastic changes typically affect the decision to perform surveillance endoscopy for a gastric only polyps larger than 1 cm. Some polyp characteristics can ulcer should be individualized. Surveillance with endoscopy raise concern: symptomatic polyps, polyps larger than 1 cm, is not necessary in patients with a low risk for gastric cancer, polyps in the gastric antrum, or polyps with an abnormal such as this patient, who was taking an NSAID and had endo appearance. In these patients, the polyp should be completely scopic findings suggesting a typical NSAID-associated gastric resected rather than being biopsied. Polyps later found to con- ulcer, unremarkable biopsy specimens from the ulcer, and tain dysplasia on biopsy are also of concern, and repeat upper symptom resolution with appropriate medical therapy. endoscopy should be promptly performed to completely Surveillance endoscopy may be considered in gastric remove these polyps. If fundic gland polyps are histologically ulcers that appear suspicious for malignancy, ulcers that confirmed and no dysplasia or concern for syndrornic polyps were not biopsied at the time of index endoscopy, or ulcers is present (as in this patient), no further endoscopic follow-up with an unclear cause. Features of the ulcer that raise sus- > is needed. picion for malignancy include a dirty ulcer base, a raised 5 wn Universal recommendations for surveillance when dys- ulcer border, and/or irregular ulcer margins. Ulcers larger = plasia is found are lacking, although expert opinion suggests than 3 cm should also be followed endoscopically given their © a wn that initial surveillance upper endoscopy be pursued at 1 year increased risk for complications, including rebleeding, pen- Py (Option A), with the interval of subsequent upper endosco- etration, and/or perforation. Surveillance endoscopy may =] 2. pies to be determined by findings, given the polyps’ slow rate be considered in patients who remain symptomatic despite a) = of growth, such as over 3 to 5 years (Option B). Repeat upper an appropriate course (8-12 weeks) of antisecretory therapy =f endoscopy should be considered at an even shorter interval, with a proton pump inhibitor (Options A, B). 2 =| such as 6 months for polyps with high-grade dysplasia. Fun- Refractory ulcers (those failing to heal despite 8-12 weeks © wn dic gland polyps can be syndromic in association with the of antisecretory therapy) should be considered for surveil- familial adenomatous polyposis syndrome. In this setting, lance endoscopy (Option C) until healing is documented or dysplasia is common (present in 25% to more than 50% of until the cause is defined, such as surreptitious NSAID use, polyps). The finding of a carpet of fundic gland polyps (>50 high-gastrin states, or ischemia. polyps) in a young patient, especially one not taking a PPI, and/or the presence of dysplasia should raise suspicion for familial adenomatous polyposis and prompt further evalu- e Routine repeat upper endoscopy for gastric ulcer is not

rare; sporadic fundic gland polyps progressing to cancer have recommended routine surveillance for gastric ulcers. Instead, not been reported. In fact, dysplastic changes typically affect the decision to perform surveillance endoscopy for a gastric only polyps larger than 1 cm. Some polyp characteristics can ulcer should be individualized. Surveillance with endoscopy raise concern: symptomatic polyps, polyps larger than 1 cm, is not necessary in patients with a low risk for gastric cancer, polyps in the gastric antrum, or polyps with an abnormal such as this patient, who was taking an NSAID and had endo appearance. In these patients, the polyp should be completely scopic findings suggesting a typical NSAID-associated gastric resected rather than being biopsied. Polyps later found to con- ulcer, unremarkable biopsy specimens from the ulcer, and tain dysplasia on biopsy are also of concern, and repeat upper symptom resolution with appropriate medical therapy. endoscopy should be promptly performed to completely Surveillance endoscopy may be considered in gastric remove these polyps. If fundic gland polyps are histologically ulcers that appear suspicious for malignancy, ulcers that confirmed and no dysplasia or concern for syndrornic polyps were not biopsied at the time of index endoscopy, or ulcers is present (as in this patient), no further endoscopic follow-up with an unclear cause. Features of the ulcer that raise sus- > is needed. picion for malignancy include a dirty ulcer base, a raised 5 wn Universal recommendations for surveillance when dys- ulcer border, and/or irregular ulcer margins. Ulcers larger = plasia is found are lacking, although expert opinion suggests than 3 cm should also be followed endoscopically given their © a wn that initial surveillance upper endoscopy be pursued at 1 year increased risk for complications, including rebleeding, pen- Py (Option A), with the interval of subsequent upper endosco- etration, and/or perforation. Surveillance endoscopy may =] 2. pies to be determined by findings, given the polyps’ slow rate be considered in patients who remain symptomatic despite a) = of growth, such as over 3 to 5 years (Option B). Repeat upper an appropriate course (8-12 weeks) of antisecretory therapy =f endoscopy should be considered at an even shorter interval, with a proton pump inhibitor (Options A, B). 2 =| such as 6 months for polyps with high-grade dysplasia. Fun- Refractory ulcers (those failing to heal despite 8-12 weeks © wn dic gland polyps can be syndromic in association with the of antisecretory therapy) should be considered for surveil- familial adenomatous polyposis syndrome. In this setting, lance endoscopy (Option C) until healing is documented or dysplasia is common (present in 25% to more than 50% of until the cause is defined, such as surreptitious NSAID use, polyps). The finding of a carpet of fundic gland polyps (>50 high-gastrin states, or ischemia. polyps) in a young patient, especially one not taking a PPI, and/or the presence of dysplasia should raise suspicion for familial adenomatous polyposis and prompt further evalu- e Routine repeat upper endoscopy for gastric ulcer is not ation with a colonoscopy. In the setting of PPI-induced spo- recommended.

rare; sporadic fundic gland polyps progressing to cancer have recommended routine surveillance for gastric ulcers. Instead, not been reported. In fact, dysplastic changes typically affect the decision to perform surveillance endoscopy for a gastric only polyps larger than 1 cm. Some polyp characteristics can ulcer should be individualized. Surveillance with endoscopy raise concern: symptomatic polyps, polyps larger than 1 cm, is not necessary in patients with a low risk for gastric cancer, polyps in the gastric antrum, or polyps with an abnormal such as this patient, who was taking an NSAID and had endo appearance. In these patients, the polyp should be completely scopic findings suggesting a typical NSAID-associated gastric resected rather than being biopsied. Polyps later found to con- ulcer, unremarkable biopsy specimens from the ulcer, and tain dysplasia on biopsy are also of concern, and repeat upper symptom resolution with appropriate medical therapy. endoscopy should be promptly performed to completely Surveillance endoscopy may be considered in gastric remove these polyps. If fundic gland polyps are histologically ulcers that appear suspicious for malignancy, ulcers that confirmed and no dysplasia or concern for syndrornic polyps were not biopsied at the time of index endoscopy, or ulcers is present (as in this patient), no further endoscopic follow-up with an unclear cause. Features of the ulcer that raise sus- > is needed. picion for malignancy include a dirty ulcer base, a raised 5 wn Universal recommendations for surveillance when dys- ulcer border, and/or irregular ulcer margins. Ulcers larger = plasia is found are lacking, although expert opinion suggests than 3 cm should also be followed endoscopically given their © a wn that initial surveillance upper endoscopy be pursued at 1 year increased risk for complications, including rebleeding, pen- Py (Option A), with the interval of subsequent upper endosco- etration, and/or perforation. Surveillance endoscopy may =] 2. pies to be determined by findings, given the polyps’ slow rate be considered in patients who remain symptomatic despite a) = of growth, such as over 3 to 5 years (Option B). Repeat upper an appropriate course (8-12 weeks) of antisecretory therapy =f endoscopy should be considered at an even shorter interval, with a proton pump inhibitor (Options A, B). 2 =| such as 6 months for polyps with high-grade dysplasia. Fun- Refractory ulcers (those failing to heal despite 8-12 weeks © wn dic gland polyps can be syndromic in association with the of antisecretory therapy) should be considered for surveil- familial adenomatous polyposis syndrome. In this setting, lance endoscopy (Option C) until healing is documented or dysplasia is common (present in 25% to more than 50% of until the cause is defined, such as surreptitious NSAID use, polyps). The finding of a carpet of fundic gland polyps (>50 high-gastrin states, or ischemia. polyps) in a young patient, especially one not taking a PPI, and/or the presence of dysplasia should raise suspicion for familial adenomatous polyposis and prompt further evalu- e Routine repeat upper endoscopy for gastric ulcer is not ation with a colonoscopy. In the setting of PPI-induced spo- recommended. radic fundic gland polyps with no strong indication for PPI e Repeat upper endoscopy for gastric ulcer is reasonable use, discontinuation of PPI should be discussed, although for ulcers that appear suspicious for malignancy, the data are mixed on whether PPI-associated sporadic fun- ulcers that were not biopsied originally, ulcers with dic gland polyps regress after PPI discontinuation. an unclear cause, or continued symptoms despite Repeat endoscopy in 10 years (Option C) is not recom- adequate therapy. mended for any gastric polyp setting.

radic fundic gland polyps with no strong indication for PPI e Repeat upper endoscopy for gastric ulcer is reasonable use, discontinuation of PPI should be discussed, although for ulcers that appear suspicious for malignancy, the data are mixed on whether PPI-associated sporadic fun- ulcers that were not biopsied originally, ulcers with dic gland polyps regress after PPI discontinuation. an unclear cause, or continued symptoms despite Repeat endoscopy in 10 years (Option C) is not recom- adequate therapy. mended for any gastric polyp setting. Bibliography Banerjee S, Cash BD, Dominitz JA, et al; ASGE Standards of Practice e Fundic gland polyps are the most common benign Committee. The role of endoscopy in the management of patients with epithelial gastric polyp and require no endoscopic peptic ulcer disease. Gastrointest Endosc. 2010;71:663-8. [PMID: 20363407] doi:10.1016/j.gie.2009.11.026 follow-up. Bibliography Item 74 Answer: A Cheesman AR, Greenwald DA, Shah SC. Current management of benign epithelial gastric polyps. Curr Treat Options Gastroenterol. 2017;15: Educational Objective: Treat acute cholecystitis with 676-690. [PMID: 28975540] doi:10.1007/s11938-017-0159-6 early surgery.

Bibliography Item 74 Answer: A Cheesman AR, Greenwald DA, Shah SC. Current management of benign epithelial gastric polyps. Curr Treat Options Gastroenterol. 2017;15: Educational Objective: Treat acute cholecystitis with 676-690. [PMID: 28975540] doi:10.1007/s11938-017-0159-6 early surgery. The most appropriate treatment is cholecystectomy before hospital discharge (Option A). This patient has acute cho- Item 73 Answer: D lecystitis. This condition is associated with severe right Educational Objective: Manage gastric ulcer upper-quadrant or epigastric pain lasting longer than 6 hours, surveillance. accompanied by fever and tenderness in the right upper The most appropriate next step in management is no further quadrant. A positive Murphy sign (inspiratory arrest during surveillance—no follow-up endoscopy is needed (Option D). right-upper-quadrant palpation) may be seen on physical Surveillance endoscopy is based on the concern that some examination. Laboratory studies may show leukocytosis. gastric cancers present as gastric ulcers that initially appear Results of liver chemistries are not usually abnormal in acute endoscopically and histologically benign. However, this cholecystitis unless choledocholithiasis is present. Acute rationale is of limited clinical use and is not cost-effective. cholecystitis can be diagnosed by ultrasonography showing As such, no U.S. or Canadian gastroenterology society has gallbladder wall thickening and/or edema and a sonographic 144

Answers and Critiques Murphy sign, elicited with compression of the right upper is a common manifestation of cirrhosis and results from abdomen with the ultrasound probe. Treatment includes insufficient liver function and portosystemic shunting. Man- Nr analgesia, intravenous antibiotics with gram-negative and ifestations include behavioral, cognitive, and motor abnor- anaerobic coverage, and cholecystectomy before hospital malities. Severity ranges from mild changes of psychomotor discharge. slowing to frank coma. Hepatic encephalopathy indicates Cholecystectomy during the initial hospitalization is decompensation of liver disease and signals worsening associated with improved clinical outcomes and lower costs liver function. Immediate management centers on identi- compared with delayed cholecystectomy (Option B). fying precipitating factors and administering medications, Emergency surgery (Option C) is necessary for suspected such as lactulose, that decrease absorption of toxins, such as gallbladder perforation or emphysematous cholecystitis ammonia, from the colon. Common precipitants of hepatic (infection of gallbladder wall with gas-forming organisms, encephalopathy include infections; gastrointestinal bleed- such as Clostridium perfringens). These conditions can be ing; exposure to toxins, such as alcohol; and medications fatal if not treated urgently. The previous good health of with sedating properties, such as benzodiazepines and opiate wn <5) the patient and her clinical stability argue against these rare analgesics. Use of these medications in patients presenting S sz diagnoses, and emergency cholecystectomy is not necessary with hepatic encephalopathy must be discontinued. Identifi- = in this patient. cation of culprit drug exposures may involve a careful review = ss) Endoscopic retrograde cholangiopancreatography of mediations with family members, including medications <3 (ERCP) (Option D) would be indicated if choledocholithi- = that were prescribed by other clinicians or that were not co asis (stones in the bile ducts) or cholangitis (infection of prescribed but are being used by the patient, such as opioids wn cad

Murphy sign, elicited with compression of the right upper is a common manifestation of cirrhosis and results from abdomen with the ultrasound probe. Treatment includes insufficient liver function and portosystemic shunting. Man- Nr analgesia, intravenous antibiotics with gram-negative and ifestations include behavioral, cognitive, and motor abnor- anaerobic coverage, and cholecystectomy before hospital malities. Severity ranges from mild changes of psychomotor discharge. slowing to frank coma. Hepatic encephalopathy indicates Cholecystectomy during the initial hospitalization is decompensation of liver disease and signals worsening associated with improved clinical outcomes and lower costs liver function. Immediate management centers on identi- compared with delayed cholecystectomy (Option B). fying precipitating factors and administering medications, Emergency surgery (Option C) is necessary for suspected such as lactulose, that decrease absorption of toxins, such as gallbladder perforation or emphysematous cholecystitis ammonia, from the colon. Common precipitants of hepatic (infection of gallbladder wall with gas-forming organisms, encephalopathy include infections; gastrointestinal bleed- such as Clostridium perfringens). These conditions can be ing; exposure to toxins, such as alcohol; and medications fatal if not treated urgently. The previous good health of with sedating properties, such as benzodiazepines and opiate wn <5) the patient and her clinical stability argue against these rare analgesics. Use of these medications in patients presenting S sz diagnoses, and emergency cholecystectomy is not necessary with hepatic encephalopathy must be discontinued. Identifi- = in this patient. cation of culprit drug exposures may involve a careful review = ss) Endoscopic retrograde cholangiopancreatography of mediations with family members, including medications <3 (ERCP) (Option D) would be indicated if choledocholithi- = that were prescribed by other clinicians or that were not co asis (stones in the bile ducts) or cholangitis (infection of prescribed but are being used by the patient, such as opioids wn cad the bile ducts) were present. Common duct stones can be ® or benzodiazepines. = visualized on transabdominal ultrasonography, but in the CT of the head (Option A) with or without contrast 4) = absence of visualization, an elevated serum bilirubin level does not typically contribute diagnostic information. How- 4

the bile ducts) were present. Common duct stones can be ® or benzodiazepines. = visualized on transabdominal ultrasonography, but in the CT of the head (Option A) with or without contrast 4) = absence of visualization, an elevated serum bilirubin level does not typically contribute diagnostic information. How- 4 and dilated common duct on ultrasonography make the ever, the risk for intracerebral hemorrhage is increased diagnosis likely. Cholangitis is suggested by fever, jaundice, in this patient group, and the symptoms may be indis- and right-upper-quadrant abdominal pain. Cholangitis is tinguishable; therefore, brain imaging may be part of the potentially life-threatening; identified common bile duct diagnostic workup based on clinical suspicion. However, stones should be removed urgently with ERCP, after which this patient has a history of anxiety and alcoholism, and a elective cholecystectomy should be performed during the careful review of medications and exposure to other toxins, initial hospitalization. This patient's laboratory and imaging such as alcohol or opioids, is the appropriate next step in findings do not suggest choledocholithiasis or cholangitis. his evaluation. In patients who are not good candidates for cholecys- Electroencephalography (Option B) to evaluate for sub tectomy and do not respond to antibiotics, a percutaneous clinical seizure activity is also unlikely to yield diagnostic cholecystostomy tube or endoscopic drainage (Option E) can findings. It is typically reserved for evaluation of patients be considered. This patient is otherwise healthy and is a good without evidence of common precipitants. candidate for surgery. Minimal manifestations of hepatic encephalopathy can be detected on neuropsychiatric testing (Option D). “Minimal” defines the disease as having no clinical signs ¢ Acute cholecystitis can be diagnosed by ultrasonogra- of encephalopathy, such as confusion or asterixis. Neuro- phy showing gallbladder wall thickening and/or psychiatric testing is of value because it can help predict edema and a positive Murphy sign elicited during the development of overt hepatic encephalopathy, indicate ultrasonography. poor quality of life and reduced socioeconomic potential, ¢ Treatment of acute cholecystitis includes analgesia, and help counsel patients and caregivers about the disease. intravenous antibiotics with gram-negative and Neuropsychiatric testing will be of no value in this patient

and dilated common duct on ultrasonography make the ever, the risk for intracerebral hemorrhage is increased diagnosis likely. Cholangitis is suggested by fever, jaundice, in this patient group, and the symptoms may be indis- and right-upper-quadrant abdominal pain. Cholangitis is tinguishable; therefore, brain imaging may be part of the potentially life-threatening; identified common bile duct diagnostic workup based on clinical suspicion. However, stones should be removed urgently with ERCP, after which this patient has a history of anxiety and alcoholism, and a elective cholecystectomy should be performed during the careful review of medications and exposure to other toxins, initial hospitalization. This patient's laboratory and imaging such as alcohol or opioids, is the appropriate next step in findings do not suggest choledocholithiasis or cholangitis. his evaluation. In patients who are not good candidates for cholecys- Electroencephalography (Option B) to evaluate for sub tectomy and do not respond to antibiotics, a percutaneous clinical seizure activity is also unlikely to yield diagnostic cholecystostomy tube or endoscopic drainage (Option E) can findings. It is typically reserved for evaluation of patients be considered. This patient is otherwise healthy and is a good without evidence of common precipitants. candidate for surgery. Minimal manifestations of hepatic encephalopathy can be detected on neuropsychiatric testing (Option D). “Minimal” defines the disease as having no clinical signs ¢ Acute cholecystitis can be diagnosed by ultrasonogra- of encephalopathy, such as confusion or asterixis. Neuro- phy showing gallbladder wall thickening and/or psychiatric testing is of value because it can help predict edema and a positive Murphy sign elicited during the development of overt hepatic encephalopathy, indicate ultrasonography. poor quality of life and reduced socioeconomic potential, ¢ Treatment of acute cholecystitis includes analgesia, and help counsel patients and caregivers about the disease. intravenous antibiotics with gram-negative and Neuropsychiatric testing will be of no value in this patient anaerobic coverage, and cholecystectomy before with overt encephalopathy.

and dilated common duct on ultrasonography make the ever, the risk for intracerebral hemorrhage is increased diagnosis likely. Cholangitis is suggested by fever, jaundice, in this patient group, and the symptoms may be indis- and right-upper-quadrant abdominal pain. Cholangitis is tinguishable; therefore, brain imaging may be part of the potentially life-threatening; identified common bile duct diagnostic workup based on clinical suspicion. However, stones should be removed urgently with ERCP, after which this patient has a history of anxiety and alcoholism, and a elective cholecystectomy should be performed during the careful review of medications and exposure to other toxins, initial hospitalization. This patient's laboratory and imaging such as alcohol or opioids, is the appropriate next step in findings do not suggest choledocholithiasis or cholangitis. his evaluation. In patients who are not good candidates for cholecys- Electroencephalography (Option B) to evaluate for sub tectomy and do not respond to antibiotics, a percutaneous clinical seizure activity is also unlikely to yield diagnostic cholecystostomy tube or endoscopic drainage (Option E) can findings. It is typically reserved for evaluation of patients be considered. This patient is otherwise healthy and is a good without evidence of common precipitants. candidate for surgery. Minimal manifestations of hepatic encephalopathy can be detected on neuropsychiatric testing (Option D). “Minimal” defines the disease as having no clinical signs ¢ Acute cholecystitis can be diagnosed by ultrasonogra- of encephalopathy, such as confusion or asterixis. Neuro- phy showing gallbladder wall thickening and/or psychiatric testing is of value because it can help predict edema and a positive Murphy sign elicited during the development of overt hepatic encephalopathy, indicate ultrasonography. poor quality of life and reduced socioeconomic potential, ¢ Treatment of acute cholecystitis includes analgesia, and help counsel patients and caregivers about the disease. intravenous antibiotics with gram-negative and Neuropsychiatric testing will be of no value in this patient anaerobic coverage, and cholecystectomy before with overt encephalopathy. hospital discharge.

and dilated common duct on ultrasonography make the ever, the risk for intracerebral hemorrhage is increased diagnosis likely. Cholangitis is suggested by fever, jaundice, in this patient group, and the symptoms may be indis- and right-upper-quadrant abdominal pain. Cholangitis is tinguishable; therefore, brain imaging may be part of the potentially life-threatening; identified common bile duct diagnostic workup based on clinical suspicion. However, stones should be removed urgently with ERCP, after which this patient has a history of anxiety and alcoholism, and a elective cholecystectomy should be performed during the careful review of medications and exposure to other toxins, initial hospitalization. This patient's laboratory and imaging such as alcohol or opioids, is the appropriate next step in findings do not suggest choledocholithiasis or cholangitis. his evaluation. In patients who are not good candidates for cholecys- Electroencephalography (Option B) to evaluate for sub tectomy and do not respond to antibiotics, a percutaneous clinical seizure activity is also unlikely to yield diagnostic cholecystostomy tube or endoscopic drainage (Option E) can findings. It is typically reserved for evaluation of patients be considered. This patient is otherwise healthy and is a good without evidence of common precipitants. candidate for surgery. Minimal manifestations of hepatic encephalopathy can be detected on neuropsychiatric testing (Option D). “Minimal” defines the disease as having no clinical signs ¢ Acute cholecystitis can be diagnosed by ultrasonogra- of encephalopathy, such as confusion or asterixis. Neuro- phy showing gallbladder wall thickening and/or psychiatric testing is of value because it can help predict edema and a positive Murphy sign elicited during the development of overt hepatic encephalopathy, indicate ultrasonography. poor quality of life and reduced socioeconomic potential, ¢ Treatment of acute cholecystitis includes analgesia, and help counsel patients and caregivers about the disease. intravenous antibiotics with gram-negative and Neuropsychiatric testing will be of no value in this patient anaerobic coverage, and cholecystectomy before with overt encephalopathy. hospital discharge. ¢ The first step in the evaluation of hepatic encephalo- Bibliography pathy is the identification of precipitating factors. Bagla P, Sarria JC, Riall TS. Management of acute cholecystitis. Curr Opin Infect Dis. 2016;29(5):508-513. [PMID: 27429137] doi:10.1097/QCO. ¢ Common precipitants of hepatic encephalopathy 0000000000000297 include infections, gastrointestinal bleeding, alcohol, and medications with sedating properties, such as Item 75 Answer: C benzodiazepines and opioids.

¢ The first step in the evaluation of hepatic encephalo- Bibliography pathy is the identification of precipitating factors. Bagla P, Sarria JC, Riall TS. Management of acute cholecystitis. Curr Opin Infect Dis. 2016;29(5):508-513. [PMID: 27429137] doi:10.1097/QCO. ¢ Common precipitants of hepatic encephalopathy 0000000000000297 include infections, gastrointestinal bleeding, alcohol, and medications with sedating properties, such as Item 75 Answer: C benzodiazepines and opioids. Educational Objective: Evaluate hepatic encephalopa- thy with a medication review. Bibliography Yanny B, Winters A, Boutros S, et al. Hepatic encephalopathy challenges, The most appropriate next step in evaluation is medication burden, and diagnostic and therapeutic approach. Clin Liver Dis. review and reconciliation (Option C). Hepatic encephalopathy 2019;23:607-623. [PMID: 31563214] doi:10.1016/j.cld.2019.07.001 145

Item 76 Answer: D Item 77 Answer: D Educational Objective: Perform endoscopic follow-up Educational Objective: Manage upper gastrointestinal for intestinal metaplasia. bleeding in a patient taking anticoagulant therapy for atrial fibrillation. The most appropriate next step in management is surveillance endoscopy (Option D). Gastric intestinal metaplasia (GIM) is a The most appropriate management is reinitiating warfarin premalignant condition; patients have up to a 10-fold increase within 7 days (Option D). This patient had significant upper in the risk for gastric cancer compared with the general pop- gastrointestinal hemorrhage related to peptic ulcer disease. He ulation. The risk for GIM and progression to gastric cancer is was appropriately initiated on an intravenous proton pump largely mediated by a history of Helicobacter pylori infection, inhibitor, anticoagulation with warfarin was withheld, and race and ethnicity, immigration status, age, family history, and endoscopic therapy was performed. In patients with significant other environmental factors, such as autoimmune metaplasia, bleeding and an INR less than 2.5, guidelines recommend not

Educational Objective: Perform endoscopic follow-up Educational Objective: Manage upper gastrointestinal for intestinal metaplasia. bleeding in a patient taking anticoagulant therapy for atrial fibrillation. The most appropriate next step in management is surveillance endoscopy (Option D). Gastric intestinal metaplasia (GIM) is a The most appropriate management is reinitiating warfarin premalignant condition; patients have up to a 10-fold increase within 7 days (Option D). This patient had significant upper in the risk for gastric cancer compared with the general pop- gastrointestinal hemorrhage related to peptic ulcer disease. He ulation. The risk for GIM and progression to gastric cancer is was appropriately initiated on an intravenous proton pump largely mediated by a history of Helicobacter pylori infection, inhibitor, anticoagulation with warfarin was withheld, and race and ethnicity, immigration status, age, family history, and endoscopic therapy was performed. In patients with significant other environmental factors, such as autoimmune metaplasia, bleeding and an INR less than 2.5, guidelines recommend not > infection with Epstein-Barr virus, high salt intake, consump- delaying endoscopy. Few prospective data are available to guide = optimal timing of resuming anticoagulation after gastrointesti w tion of pickled foods, and use of tobacco products. Although = gastric cancer is the fifth most commonly diagnosed can- nal bleeding. In general, if hemostasis is certain, anticoagulants Oo = wn cer worldwide and the third most deadly cancer worldwide should be restarted as soon as possible because the outcome of Qe (nearly 800,000 deaths annually), it is uncommon in North a thrombotic event is usually far worse than recurrent gastro = Qn America, with an estimated incidence of only 6 in 100,000. intestinal bleeding. Retrospective data suggest that resuming (=) anticoagulation (warfarin or direct oral anticoagulants) within Given the low risk for gastric cancer in the United States, =- =. routine use of endoscopic surveillance is not recommended the first week minimizes risk for 90-day thrombosis, without 2 £ for GIM. Surveillance should therefore be tailored to the increasing risk for 90-day recurrent gastrointestinal bleeding. @o ~” characteristics of GIM in addition to family history, ethnicity, In patients with atrial fibrillation for whom warfarin was race, and immigration status. Risk factors for gastric cancer discontinued, re-anticoagulation with low-molecular-weight include the presence of incomplete or extensive GIM; having a heparin or unfractionated heparin (Option A) should be con first-degree relative with gastric cancer; being African Ameri- sidered within 48 hours in patients at high thrombotic risk, can, Asian, and Hispanic; and/or being first- or second-gener- such as those with a mechanical prosthetic heart valve in the ation immigrants from high-incidence areas, including South mitral position, atrial fibrillation with prosthetic heart valve, America, Central America, Mexico, Caribbean nations, East or mitral stenosis. This patient has no indication for heparin Asia, Southeast Asia, post-Soviet states, Iran, and Turkey. bridging before reinitiation of warfarin therapy. Individuals with higher risk should be considered for surveil- Resuming anticoagulation after 30 days would be asso lance endoscopy based on shared decision-making in which ciated with increased risk for thrombosis and death without the patient puts a high value on the possible increased risk a significant increase in risk for recurrent gastrointestinal for gastric cancer and a low value on the risks associated with bleeding. Therefore, permanently discontinuing warfarin repeat endoscopy. The optimal interval for surveillance endo- (Option B) or delaying reinitiation of warfarin beyond 7 days scopy remains unknown; however, indirect data suggest a (Option C) would not be appropriate. 3- to 5-year interval for endoscopy. There is no evidence that long-term treatment with proton pump inhibitors promotes the development of GIM; e Ina patient with gastrointestinal bleeding, resuming

> infection with Epstein-Barr virus, high salt intake, consump- delaying endoscopy. Few prospective data are available to guide = optimal timing of resuming anticoagulation after gastrointesti w tion of pickled foods, and use of tobacco products. Although = gastric cancer is the fifth most commonly diagnosed can- nal bleeding. In general, if hemostasis is certain, anticoagulants Oo = wn cer worldwide and the third most deadly cancer worldwide should be restarted as soon as possible because the outcome of Qe (nearly 800,000 deaths annually), it is uncommon in North a thrombotic event is usually far worse than recurrent gastro = Qn America, with an estimated incidence of only 6 in 100,000. intestinal bleeding. Retrospective data suggest that resuming (=) anticoagulation (warfarin or direct oral anticoagulants) within Given the low risk for gastric cancer in the United States, =- =. routine use of endoscopic surveillance is not recommended the first week minimizes risk for 90-day thrombosis, without 2 £ for GIM. Surveillance should therefore be tailored to the increasing risk for 90-day recurrent gastrointestinal bleeding. @o ~” characteristics of GIM in addition to family history, ethnicity, In patients with atrial fibrillation for whom warfarin was race, and immigration status. Risk factors for gastric cancer discontinued, re-anticoagulation with low-molecular-weight include the presence of incomplete or extensive GIM; having a heparin or unfractionated heparin (Option A) should be con first-degree relative with gastric cancer; being African Ameri- sidered within 48 hours in patients at high thrombotic risk, can, Asian, and Hispanic; and/or being first- or second-gener- such as those with a mechanical prosthetic heart valve in the ation immigrants from high-incidence areas, including South mitral position, atrial fibrillation with prosthetic heart valve, America, Central America, Mexico, Caribbean nations, East or mitral stenosis. This patient has no indication for heparin Asia, Southeast Asia, post-Soviet states, Iran, and Turkey. bridging before reinitiation of warfarin therapy. Individuals with higher risk should be considered for surveil- Resuming anticoagulation after 30 days would be asso lance endoscopy based on shared decision-making in which ciated with increased risk for thrombosis and death without the patient puts a high value on the possible increased risk a significant increase in risk for recurrent gastrointestinal for gastric cancer and a low value on the risks associated with bleeding. Therefore, permanently discontinuing warfarin repeat endoscopy. The optimal interval for surveillance endo- (Option B) or delaying reinitiation of warfarin beyond 7 days scopy remains unknown; however, indirect data suggest a (Option C) would not be appropriate. 3- to 5-year interval for endoscopy. There is no evidence that long-term treatment with proton pump inhibitors promotes the development of GIM; e Ina patient with gastrointestinal bleeding, resuming therefore, omeprazole does not need to be discontinued anticoagulation within the first week after discontin-

> infection with Epstein-Barr virus, high salt intake, consump- delaying endoscopy. Few prospective data are available to guide = optimal timing of resuming anticoagulation after gastrointesti w tion of pickled foods, and use of tobacco products. Although = gastric cancer is the fifth most commonly diagnosed can- nal bleeding. In general, if hemostasis is certain, anticoagulants Oo = wn cer worldwide and the third most deadly cancer worldwide should be restarted as soon as possible because the outcome of Qe (nearly 800,000 deaths annually), it is uncommon in North a thrombotic event is usually far worse than recurrent gastro = Qn America, with an estimated incidence of only 6 in 100,000. intestinal bleeding. Retrospective data suggest that resuming (=) anticoagulation (warfarin or direct oral anticoagulants) within Given the low risk for gastric cancer in the United States, =- =. routine use of endoscopic surveillance is not recommended the first week minimizes risk for 90-day thrombosis, without 2 £ for GIM. Surveillance should therefore be tailored to the increasing risk for 90-day recurrent gastrointestinal bleeding. @o ~” characteristics of GIM in addition to family history, ethnicity, In patients with atrial fibrillation for whom warfarin was race, and immigration status. Risk factors for gastric cancer discontinued, re-anticoagulation with low-molecular-weight include the presence of incomplete or extensive GIM; having a heparin or unfractionated heparin (Option A) should be con first-degree relative with gastric cancer; being African Ameri- sidered within 48 hours in patients at high thrombotic risk, can, Asian, and Hispanic; and/or being first- or second-gener- such as those with a mechanical prosthetic heart valve in the ation immigrants from high-incidence areas, including South mitral position, atrial fibrillation with prosthetic heart valve, America, Central America, Mexico, Caribbean nations, East or mitral stenosis. This patient has no indication for heparin Asia, Southeast Asia, post-Soviet states, Iran, and Turkey. bridging before reinitiation of warfarin therapy. Individuals with higher risk should be considered for surveil- Resuming anticoagulation after 30 days would be asso lance endoscopy based on shared decision-making in which ciated with increased risk for thrombosis and death without the patient puts a high value on the possible increased risk a significant increase in risk for recurrent gastrointestinal for gastric cancer and a low value on the risks associated with bleeding. Therefore, permanently discontinuing warfarin repeat endoscopy. The optimal interval for surveillance endo- (Option B) or delaying reinitiation of warfarin beyond 7 days scopy remains unknown; however, indirect data suggest a (Option C) would not be appropriate. 3- to 5-year interval for endoscopy. There is no evidence that long-term treatment with proton pump inhibitors promotes the development of GIM; e Ina patient with gastrointestinal bleeding, resuming therefore, omeprazole does not need to be discontinued anticoagulation within the first week after discontin- (Option A). uation minimizes risk for 90-day thrombosis, without

> infection with Epstein-Barr virus, high salt intake, consump- delaying endoscopy. Few prospective data are available to guide = optimal timing of resuming anticoagulation after gastrointesti w tion of pickled foods, and use of tobacco products. Although = gastric cancer is the fifth most commonly diagnosed can- nal bleeding. In general, if hemostasis is certain, anticoagulants Oo = wn cer worldwide and the third most deadly cancer worldwide should be restarted as soon as possible because the outcome of Qe (nearly 800,000 deaths annually), it is uncommon in North a thrombotic event is usually far worse than recurrent gastro = Qn America, with an estimated incidence of only 6 in 100,000. intestinal bleeding. Retrospective data suggest that resuming (=) anticoagulation (warfarin or direct oral anticoagulants) within Given the low risk for gastric cancer in the United States, =- =. routine use of endoscopic surveillance is not recommended the first week minimizes risk for 90-day thrombosis, without 2 £ for GIM. Surveillance should therefore be tailored to the increasing risk for 90-day recurrent gastrointestinal bleeding. @o ~” characteristics of GIM in addition to family history, ethnicity, In patients with atrial fibrillation for whom warfarin was race, and immigration status. Risk factors for gastric cancer discontinued, re-anticoagulation with low-molecular-weight include the presence of incomplete or extensive GIM; having a heparin or unfractionated heparin (Option A) should be con first-degree relative with gastric cancer; being African Ameri- sidered within 48 hours in patients at high thrombotic risk, can, Asian, and Hispanic; and/or being first- or second-gener- such as those with a mechanical prosthetic heart valve in the ation immigrants from high-incidence areas, including South mitral position, atrial fibrillation with prosthetic heart valve, America, Central America, Mexico, Caribbean nations, East or mitral stenosis. This patient has no indication for heparin Asia, Southeast Asia, post-Soviet states, Iran, and Turkey. bridging before reinitiation of warfarin therapy. Individuals with higher risk should be considered for surveil- Resuming anticoagulation after 30 days would be asso lance endoscopy based on shared decision-making in which ciated with increased risk for thrombosis and death without the patient puts a high value on the possible increased risk a significant increase in risk for recurrent gastrointestinal for gastric cancer and a low value on the risks associated with bleeding. Therefore, permanently discontinuing warfarin repeat endoscopy. The optimal interval for surveillance endo- (Option B) or delaying reinitiation of warfarin beyond 7 days scopy remains unknown; however, indirect data suggest a (Option C) would not be appropriate. 3- to 5-year interval for endoscopy. There is no evidence that long-term treatment with proton pump inhibitors promotes the development of GIM; e Ina patient with gastrointestinal bleeding, resuming therefore, omeprazole does not need to be discontinued anticoagulation within the first week after discontin- (Option A). uation minimizes risk for 90-day thrombosis, without Studies of antioxidant therapy with ascorbic acid increasing risk for 90-day recurrent gastrointestinal (Option B) and B-carotene have not consistently demon- bleeding. strated a benefit in patients with GIM; therefore, this treat- ment cannot be routinely recommended. Bibliography No randomized controlled trials have demonstrated that Acosta RD, Abraham NS, Chandrasekhara V, et al; ASGE Standards of Practice Committee. The management of antithrombotic agents for chemoprophylaxis with aspirin (Option C) or NSAIDs decreases patients undergoing GI endoscopy. Gastrointest Endosc. 2016;83:3-16. the risk for gastric cancer or progression of GIM. Some evidence [PMID: 26621548] doi:10.1016/j.gie.2015.09.035 of benefit has been described in observational studies.

Studies of antioxidant therapy with ascorbic acid increasing risk for 90-day recurrent gastrointestinal (Option B) and B-carotene have not consistently demon- bleeding. strated a benefit in patients with GIM; therefore, this treat- ment cannot be routinely recommended. Bibliography No randomized controlled trials have demonstrated that Acosta RD, Abraham NS, Chandrasekhara V, et al; ASGE Standards of Practice Committee. The management of antithrombotic agents for chemoprophylaxis with aspirin (Option C) or NSAIDs decreases patients undergoing GI endoscopy. Gastrointest Endosc. 2016;83:3-16. the risk for gastric cancer or progression of GIM. Some evidence [PMID: 26621548] doi:10.1016/j.gie.2015.09.035 of benefit has been described in observational studies. Item 78 Answer: E e Gastric intestinal metaplasia is a premalignant condi- Educational Objective: Manage asymptomatic tion; patients have up to a 10-fold increased risk for gallstones. gastric cancer compared with the general population. The most appropriate management is clinical observation (Option E). Gallstones are asymptomatic in most patients. Bibliography Symptomatic gallstone disease manifests as colicky pain Gupta S, Li D, El Serag HB, et al. AGA clinical practice guidelines on manage- resulting from stimulation of the gallbladder in the presence of ment of gastric intestinal metaplasia. Gastroenterology. 2020;158:693-702. [PMID: 31816298] doi:10.1053/j.gastro.2019.12.003 an obstructive cystic duct from gallstones or sludge. This pain 146

Answers and Critiques is typically of relatively acute onset, is fairly severe and steady, mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the and is located in the right upper quadrant or epigastrium. epithelial cell adhesion molecule gene (EPCAM). Risks for col- Pain may radiate to the right scapula and can be associated orectal cancer vary by gene mutation but range from approx- with nausea, vomiting, and diaphoresis, lasting 30 minutes to imately 50% to 80% lifetime risk. Individuals with Lynch 6 hours. This symptom complex may be precipitated by eating syndrome are at increased risk for colorectal and endometrial a fatty meal, which causes gallbladder contraction. Patients cancers (most common), as well as other cancers, including with unrelenting right-upper-quadrant or epigastric pain, tumors of the stomach and small bowel. The Amsterdam bothersome early satiety, or postprandial fullness generally do II criteria are specific but not sensitive for the diagnosis of not have biliary colic. Asymptomatic gallstones are commonly Lynch syndrome. This patient’s family fulfills the Amsterdam discovered when patients undergo abdominal imaging (CT or II criteria for Lynch syndrome, which states that a diagnosis is ultrasonography) for unrelated reasons. Incidental gallstones warranted if all of the following criteria are met: do not typically cause symptoms, and prophylactic chole- e Three or more family members have a Lynch syndrome- cystectomy is generally not recommended. wn associated cancer. @ Cholecystectomy (Option A) is indicated in asymptom- 3 e Two or more successive generations are affected. — atic patients at high risk for gallbladder cancer, including ¢ One of the cancers was diagnosed before age 50 years. - patients with gallstones larger than 3 cm, porcelain (calci- oO e One affected family member is a first-degree relative of fied) gallbladder, or gallbladder polyps larger than 1 cm in a) the other two affected family members. e size. This patient does not have these risk factors. © ¢ Familial adenomatous polyposis has been ruled out. wn Endoscopic retrograde cholangiopancreatography em e Tumors have been verified pathologically. o (ERCP) (Option B) would be indicated for choledocholithiasis FS a) (stones present in the bile ducts) or cholangitis (infection of Online prediction models, such as the PREdiction & the biliary tree). Choledocholithiasis can often be visualized Model for gene Mutation5 (PREMM,), can also help predict =

is typically of relatively acute onset, is fairly severe and steady, mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the and is located in the right upper quadrant or epigastrium. epithelial cell adhesion molecule gene (EPCAM). Risks for col- Pain may radiate to the right scapula and can be associated orectal cancer vary by gene mutation but range from approx- with nausea, vomiting, and diaphoresis, lasting 30 minutes to imately 50% to 80% lifetime risk. Individuals with Lynch 6 hours. This symptom complex may be precipitated by eating syndrome are at increased risk for colorectal and endometrial a fatty meal, which causes gallbladder contraction. Patients cancers (most common), as well as other cancers, including with unrelenting right-upper-quadrant or epigastric pain, tumors of the stomach and small bowel. The Amsterdam bothersome early satiety, or postprandial fullness generally do II criteria are specific but not sensitive for the diagnosis of not have biliary colic. Asymptomatic gallstones are commonly Lynch syndrome. This patient’s family fulfills the Amsterdam discovered when patients undergo abdominal imaging (CT or II criteria for Lynch syndrome, which states that a diagnosis is ultrasonography) for unrelated reasons. Incidental gallstones warranted if all of the following criteria are met: do not typically cause symptoms, and prophylactic chole- e Three or more family members have a Lynch syndrome- cystectomy is generally not recommended. wn associated cancer. @ Cholecystectomy (Option A) is indicated in asymptom- 3 e Two or more successive generations are affected. — atic patients at high risk for gallbladder cancer, including ¢ One of the cancers was diagnosed before age 50 years. - patients with gallstones larger than 3 cm, porcelain (calci- oO e One affected family member is a first-degree relative of fied) gallbladder, or gallbladder polyps larger than 1 cm in a) the other two affected family members. e size. This patient does not have these risk factors. © ¢ Familial adenomatous polyposis has been ruled out. wn Endoscopic retrograde cholangiopancreatography em e Tumors have been verified pathologically. o (ERCP) (Option B) would be indicated for choledocholithiasis FS a) (stones present in the bile ducts) or cholangitis (infection of Online prediction models, such as the PREdiction & the biliary tree). Choledocholithiasis can often be visualized Model for gene Mutation5 (PREMM,), can also help predict = on transabdominal ultrasonography or is suggested by an risk for Lynch syndrome or other hereditary gastrointestinal elevated serum bilirubin level and dilated common duct on cancer syndromes. ultrasonography. Acute cholangitis is characterized by fever, Screening for colorectal cancer in patients with Lynch jaundice, and right-upper-quadrant pain. This patient’s clini- syndrome should begin between ages 20 and 25 years, or 2 to cal findings do not suggest choledocholithiasis or cholangitis. 5 years before the earliest cancer diagnosis in the family. The In patients who have indeterminate findings suggesting recommended screening modality is colonoscopy, which a common bile duct stone, magnetic resonance cholan- should be repeated every 1 to 2 years. Patients with Lynch syn- giopancreatography (MRCP) (Option C) or endoscopic ultra- drome are also at increased risk for stomach and small-bowel sonography may be performed as a less invasive diagnostic cancers. Upper endoscopy may be considered around age 30 to alternative to ERCP. There is no role for MRCP or endoscopic 35 years and should be repeated every 2 to 5 years. This patient ultrasonography, however, in the evaluation of a patient with should therefore undergo both upper endoscopy and colonos- asymptomatic gallstones without risk factors for gallbladder copy, with careful inspection of the distal duodenum and ter- cancer or suspected choledocholithiasis. minal ileum. Helicobacter pylori testing should be performed Ursodeoxycholic acid (Option D) can be considered at least once, and H. pylori should be eradicated if found. for dissolving cholesterol stones in patients with biliary Fecal DNA testing (Option A) and a fecal immunochem- colic who cannot tolerate surgery. This agent has no role in ical test (Option B) are acceptable colorectal cancer screen- patients with low-risk, asymptomatic gallstones. ing strategies for average-risk patients but are not sufficiently sensitive for a high-risk patient who requires both colorectal and stomach/small-intestine cancer screening. e Incidental gallstones do not typically cause symptoms, Routine wireless capsule endoscopy (Option D) is not and prophylactic cholecystectomy and other treatments recommended unless the patient has iron deficiency anemia are generally not recommended. in the absence of an obvious source of bleeding following upper endoscopy and colonoscopy. Bibliography Ibrahim M, Sarvepalli S, Morris-Stiff G, et al. Gallstones: watch and wait, or intervene? Cleve Clin J Med. 2018;85:323-331. [PMID: 29634468] doi:10. 3949/ccjm.85a.17035 e Lynch syndrome is caused by germline mutations in the mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the epithelial cell adhesion molecule gene (EPCAM).

on transabdominal ultrasonography or is suggested by an risk for Lynch syndrome or other hereditary gastrointestinal elevated serum bilirubin level and dilated common duct on cancer syndromes. ultrasonography. Acute cholangitis is characterized by fever, Screening for colorectal cancer in patients with Lynch jaundice, and right-upper-quadrant pain. This patient’s clini- syndrome should begin between ages 20 and 25 years, or 2 to cal findings do not suggest choledocholithiasis or cholangitis. 5 years before the earliest cancer diagnosis in the family. The In patients who have indeterminate findings suggesting recommended screening modality is colonoscopy, which a common bile duct stone, magnetic resonance cholan- should be repeated every 1 to 2 years. Patients with Lynch syn- giopancreatography (MRCP) (Option C) or endoscopic ultra- drome are also at increased risk for stomach and small-bowel sonography may be performed as a less invasive diagnostic cancers. Upper endoscopy may be considered around age 30 to alternative to ERCP. There is no role for MRCP or endoscopic 35 years and should be repeated every 2 to 5 years. This patient ultrasonography, however, in the evaluation of a patient with should therefore undergo both upper endoscopy and colonos- asymptomatic gallstones without risk factors for gallbladder copy, with careful inspection of the distal duodenum and ter- cancer or suspected choledocholithiasis. minal ileum. Helicobacter pylori testing should be performed Ursodeoxycholic acid (Option D) can be considered at least once, and H. pylori should be eradicated if found. for dissolving cholesterol stones in patients with biliary Fecal DNA testing (Option A) and a fecal immunochem- colic who cannot tolerate surgery. This agent has no role in ical test (Option B) are acceptable colorectal cancer screen- patients with low-risk, asymptomatic gallstones. ing strategies for average-risk patients but are not sufficiently sensitive for a high-risk patient who requires both colorectal and stomach/small-intestine cancer screening. e Incidental gallstones do not typically cause symptoms, Routine wireless capsule endoscopy (Option D) is not and prophylactic cholecystectomy and other treatments recommended unless the patient has iron deficiency anemia are generally not recommended. in the absence of an obvious source of bleeding following upper endoscopy and colonoscopy. Bibliography Ibrahim M, Sarvepalli S, Morris-Stiff G, et al. Gallstones: watch and wait, or intervene? Cleve Clin J Med. 2018;85:323-331. [PMID: 29634468] doi:10. 3949/ccjm.85a.17035 e Lynch syndrome is caused by germline mutations in the mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the epithelial cell adhesion molecule gene (EPCAM). Item 79 Answer: C e Patients with Lynch syndrome should be screened for

on transabdominal ultrasonography or is suggested by an risk for Lynch syndrome or other hereditary gastrointestinal elevated serum bilirubin level and dilated common duct on cancer syndromes. ultrasonography. Acute cholangitis is characterized by fever, Screening for colorectal cancer in patients with Lynch jaundice, and right-upper-quadrant pain. This patient’s clini- syndrome should begin between ages 20 and 25 years, or 2 to cal findings do not suggest choledocholithiasis or cholangitis. 5 years before the earliest cancer diagnosis in the family. The In patients who have indeterminate findings suggesting recommended screening modality is colonoscopy, which a common bile duct stone, magnetic resonance cholan- should be repeated every 1 to 2 years. Patients with Lynch syn- giopancreatography (MRCP) (Option C) or endoscopic ultra- drome are also at increased risk for stomach and small-bowel sonography may be performed as a less invasive diagnostic cancers. Upper endoscopy may be considered around age 30 to alternative to ERCP. There is no role for MRCP or endoscopic 35 years and should be repeated every 2 to 5 years. This patient ultrasonography, however, in the evaluation of a patient with should therefore undergo both upper endoscopy and colonos- asymptomatic gallstones without risk factors for gallbladder copy, with careful inspection of the distal duodenum and ter- cancer or suspected choledocholithiasis. minal ileum. Helicobacter pylori testing should be performed Ursodeoxycholic acid (Option D) can be considered at least once, and H. pylori should be eradicated if found. for dissolving cholesterol stones in patients with biliary Fecal DNA testing (Option A) and a fecal immunochem- colic who cannot tolerate surgery. This agent has no role in ical test (Option B) are acceptable colorectal cancer screen- patients with low-risk, asymptomatic gallstones. ing strategies for average-risk patients but are not sufficiently sensitive for a high-risk patient who requires both colorectal and stomach/small-intestine cancer screening. e Incidental gallstones do not typically cause symptoms, Routine wireless capsule endoscopy (Option D) is not and prophylactic cholecystectomy and other treatments recommended unless the patient has iron deficiency anemia are generally not recommended. in the absence of an obvious source of bleeding following upper endoscopy and colonoscopy. Bibliography Ibrahim M, Sarvepalli S, Morris-Stiff G, et al. Gallstones: watch and wait, or intervene? Cleve Clin J Med. 2018;85:323-331. [PMID: 29634468] doi:10. 3949/ccjm.85a.17035 e Lynch syndrome is caused by germline mutations in the mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the epithelial cell adhesion molecule gene (EPCAM). Item 79 Answer: C e Patients with Lynch syndrome should be screened for Educational Objective: Identify the proper screening colon cancer with colonoscopy beginning at ages 20

on transabdominal ultrasonography or is suggested by an risk for Lynch syndrome or other hereditary gastrointestinal elevated serum bilirubin level and dilated common duct on cancer syndromes. ultrasonography. Acute cholangitis is characterized by fever, Screening for colorectal cancer in patients with Lynch jaundice, and right-upper-quadrant pain. This patient’s clini- syndrome should begin between ages 20 and 25 years, or 2 to cal findings do not suggest choledocholithiasis or cholangitis. 5 years before the earliest cancer diagnosis in the family. The In patients who have indeterminate findings suggesting recommended screening modality is colonoscopy, which a common bile duct stone, magnetic resonance cholan- should be repeated every 1 to 2 years. Patients with Lynch syn- giopancreatography (MRCP) (Option C) or endoscopic ultra- drome are also at increased risk for stomach and small-bowel sonography may be performed as a less invasive diagnostic cancers. Upper endoscopy may be considered around age 30 to alternative to ERCP. There is no role for MRCP or endoscopic 35 years and should be repeated every 2 to 5 years. This patient ultrasonography, however, in the evaluation of a patient with should therefore undergo both upper endoscopy and colonos- asymptomatic gallstones without risk factors for gallbladder copy, with careful inspection of the distal duodenum and ter- cancer or suspected choledocholithiasis. minal ileum. Helicobacter pylori testing should be performed Ursodeoxycholic acid (Option D) can be considered at least once, and H. pylori should be eradicated if found. for dissolving cholesterol stones in patients with biliary Fecal DNA testing (Option A) and a fecal immunochem- colic who cannot tolerate surgery. This agent has no role in ical test (Option B) are acceptable colorectal cancer screen- patients with low-risk, asymptomatic gallstones. ing strategies for average-risk patients but are not sufficiently sensitive for a high-risk patient who requires both colorectal and stomach/small-intestine cancer screening. e Incidental gallstones do not typically cause symptoms, Routine wireless capsule endoscopy (Option D) is not and prophylactic cholecystectomy and other treatments recommended unless the patient has iron deficiency anemia are generally not recommended. in the absence of an obvious source of bleeding following upper endoscopy and colonoscopy. Bibliography Ibrahim M, Sarvepalli S, Morris-Stiff G, et al. Gallstones: watch and wait, or intervene? Cleve Clin J Med. 2018;85:323-331. [PMID: 29634468] doi:10. 3949/ccjm.85a.17035 e Lynch syndrome is caused by germline mutations in the mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the epithelial cell adhesion molecule gene (EPCAM). Item 79 Answer: C e Patients with Lynch syndrome should be screened for Educational Objective: Identify the proper screening colon cancer with colonoscopy beginning at ages 20 strategy for Lynch syndrome. to 25 years (or 2-5 years before the earliest cancer diagnosis in the family) and screened for stomach and The most appropriate screening strategy is upper endo- small-bowel cancers with upper endoscopy beginning scopy and colonoscopy (Option C). This patient has Lynch at age 30 to 35 years. syndrome, which is caused by germline mutations in the

strategy for Lynch syndrome. to 25 years (or 2-5 years before the earliest cancer diagnosis in the family) and screened for stomach and The most appropriate screening strategy is upper endo- small-bowel cancers with upper endoscopy beginning scopy and colonoscopy (Option C). This patient has Lynch at age 30 to 35 years. syndrome, which is caused by germline mutations in the 147

Answers and Critiques Bibliography Sinicrope FA. Lynch syndrome-associated colorectal cancer. N Engl J Med. 2018;379:764-773. [PMID: 30134129] doi:10.1056/NEJMcp1714533 e Patients with cirrhosis and portal hypertension who present with dyspnea on exertion should be suspected of having portopulmonary hypertension; echocardi- Item 80 Answer: B ography is the initial screening test. Educational Objective: Evaluate dyspnea in a patient with cirrhosis. Bibliography Cartin-Ceba R, Krowka MJ. Pulmonary complications of portal hyperten- The most appropriate diagnostic test to perform next is echo- sion. Clin Liver Dis. 2019;23:683-711. [PMID: 31563218] doi:10.1016/j. cardiography (Option B). Patients with cirrhosis and por- cld.2019.06.003

Bibliography Sinicrope FA. Lynch syndrome-associated colorectal cancer. N Engl J Med. 2018;379:764-773. [PMID: 30134129] doi:10.1056/NEJMcp1714533 e Patients with cirrhosis and portal hypertension who present with dyspnea on exertion should be suspected of having portopulmonary hypertension; echocardi- Item 80 Answer: B ography is the initial screening test. Educational Objective: Evaluate dyspnea in a patient with cirrhosis. Bibliography Cartin-Ceba R, Krowka MJ. Pulmonary complications of portal hyperten- The most appropriate diagnostic test to perform next is echo- sion. Clin Liver Dis. 2019;23:683-711. [PMID: 31563218] doi:10.1016/j. cardiography (Option B). Patients with cirrhosis and por- cld.2019.06.003 tal hypertension are at risk for hepatopulmonary syndrome and portopulmonary hypertension. In hepatopulmonary Item 81 Answer: C > syndrome, the pulmonary vasculature becomes dilated, = Educational Objective: Manage nocturnal wn resulting in right-to-left shunting of blood and hypoxemia. = Patients may present with characteristic findings of orthode- gastroesophageal reflux disease with lifestyle @ = modifications. ~n oxia (worsening oxygen saturation while upright) and platyp- 3¥) = nea (worsening sense of dyspnea when upright). Dyspnea The most appropriate additional management in this patient a. a on exertion suggests possible portopulmonary hypertension, with nocturnal gastroesophageal reflux disease (GERD) is to = wherein increases in pulmonary arterial pressure cause high recommend lifestyle modifications (Option C). Weight loss and =a 2 right-sided heart pressures. This condition is less common tobacco smoking cessation should be recommended to patients = than hepatopulmonary syndrome but carries a high mortal- @o with GERD who are obese and smoke, respectively. Patients 72) ity rate. Echocardiography is the best initial diagnostic test with nocturnal GERD should avoid late-evening meals by eat- in a patient with suspected pulmonary hypertension. If the ing at least 3 hours before bedtime and should elevate the head echocardiogram shows high right-side pressures, potential of the bed. Avoidance of large meals and fatty foods that stay in causes of pulmonary hypertension should be evaluated before the stomach for longer periods is also helpful if adherence can portopulmonary hypertension is selected as the diagnosis. be maintained. Drastic changes in the diet are not generally In this patient with normal pulmonary examination and recommended because they are difficult to maintain. However, normal chest radiographs, CT of the chest (Option A) is not if a trigger is identified, such as alcohol, it is reasonable to rec- likely to be helpful. If pulmonary hypertension is confirmed, ommend elimination of that trigger from the diet. pulmonary function testing and high-resolution CT of the chest Although some patients require dosage escalation to might be useful if interstitial lung disease is a consideration. twice-daily proton pump inhibitor (PPI) therapy (Option The diagnosis of hepatopulmonary syndrome should A), directed lifestyle modifications should first be attempted be suspected in patients with portal hypertension who have for the patient’s weekend symptoms, which are related to symptoms of dyspnea and evidence of hypoxia. Findings large late-night meals. Her symptoms are otherwise con- of intrapulmonary shunting with contrast administration, trolled with the existing drug regimen. Dosage escalation such as agitated saline during echocardiography (Option C), may be appropriate if a trial of lifestyle modifications is not confirm the diagnosis. This patient’s symptoms and findings successful. are not compatible with hepatopulmonary syndrome, and Surgical treatments for GERD include laparoscopic echocardiography with agitated saline is not indicated. fundoplication (Option B). However, surgery is infre- Progressive exertional dyspnea is the most common quently required; indications include failure of optimal symptom of chronic thromboembolic pulmonary hyperten- PPI therapy with documented evidence of ongoing acid sion (CTEPH). CTEPH remains an underrecognized cause of reflux, desire to stop medication, and intolerable medi- pulmonary hypertension and requires a high index of suspi- cation side effects. These indications do not apply to this cion. Ventilation-perfusion scanning (Option D) is the most patient. sensitive indicator of CTEPH and should be performed in all Most patients with GERD have normal findings on patients for whom the diagnosis is suspected. However, the upper endoscopy (Option D). Upper endoscopy is war- diagnosis of pulmonary hypertension should be confirmed ranted in patients reporting dysphagia, weight loss, first, and the initial diagnostic study for pulmonary hyper- hematemesis, or failure to respond to treatment. Lifestyle tension is echocardiography. modifications should be introduced before upper endos- copy. Wireless esophageal pH testing (Option E) can quantify e Features of hepatopulmonary syndrome include orth- acid exposure in the esophagus, confirm adequacy of acid odeoxia (worsening oxygen saturation while upright) suppression therapy, and differentiate between acid and and platypnea (worsening sense of dyspnea when nonacid reflux. Because the patient has classic symptoms upright); echocardiography with contrast can confirm of GERD that are generally well controlled with a PPI and the diagnosis. ae (Continued) weekend symptoms that should be amenable to lifestyle modifications, wireless pH testing is unnecessary.

tal hypertension are at risk for hepatopulmonary syndrome and portopulmonary hypertension. In hepatopulmonary Item 81 Answer: C > syndrome, the pulmonary vasculature becomes dilated, = Educational Objective: Manage nocturnal wn resulting in right-to-left shunting of blood and hypoxemia. = Patients may present with characteristic findings of orthode- gastroesophageal reflux disease with lifestyle @ = modifications. ~n oxia (worsening oxygen saturation while upright) and platyp- 3¥) = nea (worsening sense of dyspnea when upright). Dyspnea The most appropriate additional management in this patient a. a on exertion suggests possible portopulmonary hypertension, with nocturnal gastroesophageal reflux disease (GERD) is to = wherein increases in pulmonary arterial pressure cause high recommend lifestyle modifications (Option C). Weight loss and =a 2 right-sided heart pressures. This condition is less common tobacco smoking cessation should be recommended to patients = than hepatopulmonary syndrome but carries a high mortal- @o with GERD who are obese and smoke, respectively. Patients 72) ity rate. Echocardiography is the best initial diagnostic test with nocturnal GERD should avoid late-evening meals by eat- in a patient with suspected pulmonary hypertension. If the ing at least 3 hours before bedtime and should elevate the head echocardiogram shows high right-side pressures, potential of the bed. Avoidance of large meals and fatty foods that stay in causes of pulmonary hypertension should be evaluated before the stomach for longer periods is also helpful if adherence can portopulmonary hypertension is selected as the diagnosis. be maintained. Drastic changes in the diet are not generally In this patient with normal pulmonary examination and recommended because they are difficult to maintain. However, normal chest radiographs, CT of the chest (Option A) is not if a trigger is identified, such as alcohol, it is reasonable to rec- likely to be helpful. If pulmonary hypertension is confirmed, ommend elimination of that trigger from the diet. pulmonary function testing and high-resolution CT of the chest Although some patients require dosage escalation to might be useful if interstitial lung disease is a consideration. twice-daily proton pump inhibitor (PPI) therapy (Option The diagnosis of hepatopulmonary syndrome should A), directed lifestyle modifications should first be attempted be suspected in patients with portal hypertension who have for the patient’s weekend symptoms, which are related to symptoms of dyspnea and evidence of hypoxia. Findings large late-night meals. Her symptoms are otherwise con- of intrapulmonary shunting with contrast administration, trolled with the existing drug regimen. Dosage escalation such as agitated saline during echocardiography (Option C), may be appropriate if a trial of lifestyle modifications is not confirm the diagnosis. This patient’s symptoms and findings successful. are not compatible with hepatopulmonary syndrome, and Surgical treatments for GERD include laparoscopic echocardiography with agitated saline is not indicated. fundoplication (Option B). However, surgery is infre- Progressive exertional dyspnea is the most common quently required; indications include failure of optimal symptom of chronic thromboembolic pulmonary hyperten- PPI therapy with documented evidence of ongoing acid sion (CTEPH). CTEPH remains an underrecognized cause of reflux, desire to stop medication, and intolerable medi- pulmonary hypertension and requires a high index of suspi- cation side effects. These indications do not apply to this cion. Ventilation-perfusion scanning (Option D) is the most patient. sensitive indicator of CTEPH and should be performed in all Most patients with GERD have normal findings on patients for whom the diagnosis is suspected. However, the upper endoscopy (Option D). Upper endoscopy is war- diagnosis of pulmonary hypertension should be confirmed ranted in patients reporting dysphagia, weight loss, first, and the initial diagnostic study for pulmonary hyper- hematemesis, or failure to respond to treatment. Lifestyle tension is echocardiography. modifications should be introduced before upper endos- copy. Wireless esophageal pH testing (Option E) can quantify e Features of hepatopulmonary syndrome include orth- acid exposure in the esophagus, confirm adequacy of acid odeoxia (worsening oxygen saturation while upright) suppression therapy, and differentiate between acid and and platypnea (worsening sense of dyspnea when nonacid reflux. Because the patient has classic symptoms upright); echocardiography with contrast can confirm of GERD that are generally well controlled with a PPI and the diagnosis. ae (Continued) weekend symptoms that should be amenable to lifestyle modifications, wireless pH testing is unnecessary. 148

Answers and Critiques in patients with cirrhosis. If analgesics are required, low-dose acetaminophen, up to 2000 mg/d, is generally ¢ Weight loss and tobacco smoking cessation should safe and well tolerated in patients with advanced liver be recommended to patients with gastroesophageal dysfunction. reflux disease who are obese and smoke, respec- tively. e Patients with nocturnal gastroesophageal reflux dis- e Opioid analgesics can precipitate hepatic encephalop- ease should avoid late-evening meals by eating at least athy in patients with cirrhosis.

in patients with cirrhosis. If analgesics are required, low-dose acetaminophen, up to 2000 mg/d, is generally ¢ Weight loss and tobacco smoking cessation should safe and well tolerated in patients with advanced liver be recommended to patients with gastroesophageal dysfunction. reflux disease who are obese and smoke, respec- tively. e Patients with nocturnal gastroesophageal reflux dis- e Opioid analgesics can precipitate hepatic encephalop- ease should avoid late-evening meals by eating at least athy in patients with cirrhosis. 3 hours before bedtime and should elevate the head of e Management of chronic pain in patients with chronic the bed. liver disease should always include physical therapy because it will not exacerbate the manifestations of Bibliography chronic liver disease. wn Ness-Jensen E, Hveem K, El-Serag H, et al. Lifestyle intervention in gastroe- o sophageal reflux disease. Clin Gastroenterol Hepatol. 2016:14:175-82. s e1-3. [PMID: 25956834] doi:10.1016/j.cgh.2015.04.176 Bibliography A Klinge M, Coppler T, Liebschutz JM, et al. The assessment and management of pain in cirrhosis. Curr Hepatol Rep. 2018;17:42-51. [PMID: 29552453] + cs) doi:10.1007/s11901-018-0389-7 sc Item 82 Answer: D = c Educational Objective: Treat chronic pain in a patient w Item 83 Answer: D nal with cirrhosis. o

3 hours before bedtime and should elevate the head of e Management of chronic pain in patients with chronic the bed. liver disease should always include physical therapy because it will not exacerbate the manifestations of Bibliography chronic liver disease. wn Ness-Jensen E, Hveem K, El-Serag H, et al. Lifestyle intervention in gastroe- o sophageal reflux disease. Clin Gastroenterol Hepatol. 2016:14:175-82. s e1-3. [PMID: 25956834] doi:10.1016/j.cgh.2015.04.176 Bibliography A Klinge M, Coppler T, Liebschutz JM, et al. The assessment and management of pain in cirrhosis. Curr Hepatol Rep. 2018;17:42-51. [PMID: 29552453] + cs) doi:10.1007/s11901-018-0389-7 sc Item 82 Answer: D = c Educational Objective: Treat chronic pain in a patient w Item 83 Answer: D nal with cirrhosis. o Educational Objective: Treat acute cholangitis. = a) The most appropriate treatment is physical ther- SJ = apy (Option D). Patients with cirrhosis are at risk for The most appropriate treatment is urgent endoscopic ret- metabolic bone disease and osteoporosis. Bone densi- rograde cholangiopancreatography (ERCP) (Option D). This tometry is thus indicated in patients with cirrhosis to patient has acute cholangitis, an infection of the biliary screen for metabolic bone disease, and bone-fortifying tree that is heralded by the Charcot triad (fever, jaundice, therapy is indicated in patients found to have osteopo- and right-upper-quadrant pain). Cholangitis is potentially rosis. The management of chronic pain can be challeng- life-threatening; therapy should include immediate antimi ing in patients with chronic liver disease because the crobial therapy targeting Enterobacteriaceae in combination recognized adverse effects of analgesic medications can with urgent decompression of the biliary tree with endo- be exaggerated in these patients. Nonpharmacologic scopic sphincterotomy and stone extraction. Additionally, approaches to managing chronic pain should always be cholecystectomy should be performed during initial hospi- considered because they will not exacerbate the mani- talization or within 2 weeks to reduce the risk for subsequent festations of chronic liver disease. Therefore, physical complications. therapy should be considered initially in this patient pop- Surgical drainage of the biliary tree, either open or ulation. Other nonpharmacologic therapies, including laparoscopic (Option A), is reserved for patients with acute local injection therapies and behavioral therapy, may also cholecystitis who cannot undergo ERCP or in whom ERCP be beneficial. has failed. The surgical objectives are biliary decompression The serotonin norepinephrine reuptake inhibitor with choledocholithiasis removal. ERCP biliary drainage is duloxetine (Option A) is approved by the FDA to treat preferred over surgical drainage because of substantially chronic low back pain and may be useful in select patients. lower morbidity and mortality. However, duloxetine should be avoided in patients with Magnetic resonance cholangiopancreatography (Option hepatic dysfunction. Rare cases of hepatic failure (some B) is a valuable tool in evaluating the biliary and pancreatic leading to death) have been reported with use. Hepatitis ducts and may be indicated in the nonurgent evaluation of with abdominal pain, hepatomegaly, and elevated amino- suspected choledocholithiasis. In this case, however, the transferase levels with and without jaundice have all been patient has a life-threatening infection (acute cholangitis), observed. and urgent decompression of the biliary tree is indicated. NSAIDs, such as ibuprofen (Option B), inhibit the pro- There is no need for further imaging before intervention duction of renal prostaglandins and can exacerbate renal because the stone has already been identified on ultraso- dysfunction and worsen fluid retention in the setting of nography. cirrhosis. Therefore, NSAIDs should be avoided in patients Although cholecystectomy (Option C) is the treatment with cirrhosis, particularly those with renal impairment or of choice for acute cholecystitis, it has an ancillary role in ascites, such as this patient. the management of acute cholangitis. In acute cholangitis, Opioid analgesics (Option C) can precipitate hepatic stone location is typically within the common bile duct encephalopathy in patients with cirrhosis. Furthermore, rather than in the cystic duct (as in acute cholecystitis), and these agents can cause vasodilation and hypotension in cholecystectomy does not result in decompression of the patients with more advanced liver dysfunction. Therefore, biliary tree. After the stones are removed with ERCP, elective opioid analgesics should be avoided for pain management cholecystectomy should be performed during the initial

Educational Objective: Treat acute cholangitis. = a) The most appropriate treatment is physical ther- SJ = apy (Option D). Patients with cirrhosis are at risk for The most appropriate treatment is urgent endoscopic ret- metabolic bone disease and osteoporosis. Bone densi- rograde cholangiopancreatography (ERCP) (Option D). This tometry is thus indicated in patients with cirrhosis to patient has acute cholangitis, an infection of the biliary screen for metabolic bone disease, and bone-fortifying tree that is heralded by the Charcot triad (fever, jaundice, therapy is indicated in patients found to have osteopo- and right-upper-quadrant pain). Cholangitis is potentially rosis. The management of chronic pain can be challeng- life-threatening; therapy should include immediate antimi ing in patients with chronic liver disease because the crobial therapy targeting Enterobacteriaceae in combination recognized adverse effects of analgesic medications can with urgent decompression of the biliary tree with endo- be exaggerated in these patients. Nonpharmacologic scopic sphincterotomy and stone extraction. Additionally, approaches to managing chronic pain should always be cholecystectomy should be performed during initial hospi- considered because they will not exacerbate the mani- talization or within 2 weeks to reduce the risk for subsequent festations of chronic liver disease. Therefore, physical complications. therapy should be considered initially in this patient pop- Surgical drainage of the biliary tree, either open or ulation. Other nonpharmacologic therapies, including laparoscopic (Option A), is reserved for patients with acute local injection therapies and behavioral therapy, may also cholecystitis who cannot undergo ERCP or in whom ERCP be beneficial. has failed. The surgical objectives are biliary decompression The serotonin norepinephrine reuptake inhibitor with choledocholithiasis removal. ERCP biliary drainage is duloxetine (Option A) is approved by the FDA to treat preferred over surgical drainage because of substantially chronic low back pain and may be useful in select patients. lower morbidity and mortality. However, duloxetine should be avoided in patients with Magnetic resonance cholangiopancreatography (Option hepatic dysfunction. Rare cases of hepatic failure (some B) is a valuable tool in evaluating the biliary and pancreatic leading to death) have been reported with use. Hepatitis ducts and may be indicated in the nonurgent evaluation of with abdominal pain, hepatomegaly, and elevated amino- suspected choledocholithiasis. In this case, however, the transferase levels with and without jaundice have all been patient has a life-threatening infection (acute cholangitis), observed. and urgent decompression of the biliary tree is indicated. NSAIDs, such as ibuprofen (Option B), inhibit the pro- There is no need for further imaging before intervention duction of renal prostaglandins and can exacerbate renal because the stone has already been identified on ultraso- dysfunction and worsen fluid retention in the setting of nography. cirrhosis. Therefore, NSAIDs should be avoided in patients Although cholecystectomy (Option C) is the treatment with cirrhosis, particularly those with renal impairment or of choice for acute cholecystitis, it has an ancillary role in ascites, such as this patient. the management of acute cholangitis. In acute cholangitis, Opioid analgesics (Option C) can precipitate hepatic stone location is typically within the common bile duct encephalopathy in patients with cirrhosis. Furthermore, rather than in the cystic duct (as in acute cholecystitis), and these agents can cause vasodilation and hypotension in cholecystectomy does not result in decompression of the patients with more advanced liver dysfunction. Therefore, biliary tree. After the stones are removed with ERCP, elective opioid analgesics should be avoided for pain management cholecystectomy should be performed during the initial 149

Answers and Critiques hospital stay to reduce the risk for additional complications 1.5-cm polyp, follow-up ultrasonography would not be from gallstones. appropriate. CONT.

Answers and Critiques hospital stay to reduce the risk for additional complications 1.5-cm polyp, follow-up ultrasonography would not be from gallstones. appropriate. CONT. e Acute cholangitis is suggested by fever, jaundice, and ¢ Gallbladder polyp size greater than 1 cm is a risk fac- right-upper-quadrant pain. tor for malignancy; treatment for such polyps should be cholecystectomy. e The treatment of choice for acute cholangitis is antibi- otics and biliary drainage with endoscopic retrograde ¢ Gallbladder polyps associated with gallbladder stones cholangiopancreatography. or primary sclerosing cholangitis are more likely to be neoplastic regardless of the polyp size. Bibliography Buxbaum JL, Abbas Fehmi SM, Sultan S, et al; ASGE Standards of Practice Bibliography = Committee. ASGE guideline on the role of endoscopy in the evaluation Wiles R, Thoeni RF, Barbu ST, et al. Management and follow-up of gallblad- = and management of choledocholithiasis. Gastrointest Endosc. 2019: wn der polyps: joint guidelines between the European Society of 89:1075-1105.e15. [PMID: 30979521] doi:10.1016/j.gie.2018.10.001 = Gastrointestinal and Abdominal Radiology (ESGAR), European @o Association for Endoscopic Surgery and Other Interventional Techniques = n (EAES), International Society of Digestive Surgery-European Federation a (EFISDS) and European Society of Gastrointestinal Endoscopy (ESGE). = Item 84 Answer: A Eur Radiol. 2017:27:3856-3866. [PMID: 28185005] doi:10.1007/s00330- Qa. 017-4742-y (a) Educational Objective: Treat a large gallbladder polyp. me =. a The most appropriate management is cholecystectomy <= Oo (Option A). This patient has a gallbladder polyp. Incidental Item 85 Answer: D n findings, including gallbladder polyps, are usually seen on Educational Objective: Treat functional dyspepsia. 1% to 5% of gallbladder ultrasounds, as well as in resected gallbladders. Neoplastic adenomas are rare, representing The most appropriate next step in treatment is initiating a less than 0.5% of polyps. The best predictor of a malignant nortriptyline trial (Option D). This patient has functional dys- or premalignant lesion is size; polyps greater than 1 cm are pepsia, epigastric pain that lacks an identifiable cause. Symp- more likely to be neoplastic and should be treated with toms that may accompany epigastric pain include fullness, cholecystectomy if possible. Gallbladder polyps associated nausea, vomiting, bloating, heartburn, or alteration in bowel with gallbladder stones or primary sclerosing cholangitis habits; however, the epigastric pain must be the predominant are also more likely to be neoplastic. This patient has a symptom. A diagnosis of functional dyspepsia traditionally polyp larger than 1 cm and therefore should be offered requires normal findings on upper endoscopy or an upper cholecystectomy. gastrointestinal series. In patients with functional dyspepsia If common bile duct dilation had been present on ultra- for whom Helicobacter pyloriinfection is confirmed, eradica- sonography, two options could be considered: (1) endoscopic tion therapy should be pursued because it may relieve symp- retrograde cholangiopancreatography (ERCP) (Option B) for toms. Some evidence suggests that a subset of patients with patients with cholelithiasis and therefore a high likelihood functional dyspepsia are sensitive to acid; therefore, a proton of choledocholithiasis, and (2) magnetic resonance cholan- pump inhibitor (PPI) should be the initial therapy. However, giopancreatography for diagnostic evaluation if ultrasonog- pooled studies indicate that about 70% of patients with func- raphy findings are indeterminate. Urgent ERCP is indicated tional dyspepsia still have dyspeptic symptoms after a 2- to for acute cholangitis, signaled by fever, right-upper-quad- 8-week PPI trial. Tricyclic antidepressants (TCAs) are effective rant abdominal pain, and jaundice. This patient does not in the treatment of functional dyspepsia. Pooled results of have a dilated common bile duct or ascending cholangitis, three clinical trials involving 339 patients with this disor- and ERCP would not be appropriate. der demonstrated superiority of TCAs over placebo (number When cholecystitis is suspected and the ultrasound is needed to treat, 6). The adverse events of TCAs, such as con not conclusive, hepatobiliary iminodiacetic acid scanning stipation, dry mouth, urinary retention, and somnolence, with ejection fraction (Option C) may help determine gall- can be minimized by initiating TCA therapy at a low dosage bladder function in symptomatic patients without evidence (e.g., 10 mg once daily) and slowly titrating the dose by 10-mg of larger stones. However, the issue in this case is not the increments every several weeks. function of the gallbladder but rather the risk for neoplasm Selective serotonin reuptake inhibitors, such as citalo- of the gallbladder polyp. pram (Option A), have shown no superiority over placebo in Gallbladder polyps that are 5 mm or less may be the treatment of functional dyspepsia. monitored with repeat ultrasonography (Option D) in Studies directly comparing H, blockers vs PPIs for treat- 12 months. If they have increased in size, cholecystectomy ing functional dyspepsia have found no difference in treat- may be offered. Gallbladder polyps that are 6 to 9 mm may ment efficacy. Switching from omeprazole to famotidine be monitored with ultrasonography in 6 months and then (Option B) is unlikely to improve this patient’s symptoms. yearly thereafter. Cholecystectomy may also be offered if Although prokinetic agents, such as metoclopramide the polyp size has increased. Because this patient has a (Option C), may also help a small subset of patients with

e Acute cholangitis is suggested by fever, jaundice, and ¢ Gallbladder polyp size greater than 1 cm is a risk fac- right-upper-quadrant pain. tor for malignancy; treatment for such polyps should be cholecystectomy. e The treatment of choice for acute cholangitis is antibi- otics and biliary drainage with endoscopic retrograde ¢ Gallbladder polyps associated with gallbladder stones cholangiopancreatography. or primary sclerosing cholangitis are more likely to be neoplastic regardless of the polyp size. Bibliography Buxbaum JL, Abbas Fehmi SM, Sultan S, et al; ASGE Standards of Practice Bibliography = Committee. ASGE guideline on the role of endoscopy in the evaluation Wiles R, Thoeni RF, Barbu ST, et al. Management and follow-up of gallblad- = and management of choledocholithiasis. Gastrointest Endosc. 2019: wn der polyps: joint guidelines between the European Society of 89:1075-1105.e15. [PMID: 30979521] doi:10.1016/j.gie.2018.10.001 = Gastrointestinal and Abdominal Radiology (ESGAR), European @o Association for Endoscopic Surgery and Other Interventional Techniques = n (EAES), International Society of Digestive Surgery-European Federation a (EFISDS) and European Society of Gastrointestinal Endoscopy (ESGE). = Item 84 Answer: A Eur Radiol. 2017:27:3856-3866. [PMID: 28185005] doi:10.1007/s00330- Qa. 017-4742-y (a) Educational Objective: Treat a large gallbladder polyp. me =. a The most appropriate management is cholecystectomy <= Oo (Option A). This patient has a gallbladder polyp. Incidental Item 85 Answer: D n findings, including gallbladder polyps, are usually seen on Educational Objective: Treat functional dyspepsia. 1% to 5% of gallbladder ultrasounds, as well as in resected gallbladders. Neoplastic adenomas are rare, representing The most appropriate next step in treatment is initiating a less than 0.5% of polyps. The best predictor of a malignant nortriptyline trial (Option D). This patient has functional dys- or premalignant lesion is size; polyps greater than 1 cm are pepsia, epigastric pain that lacks an identifiable cause. Symp- more likely to be neoplastic and should be treated with toms that may accompany epigastric pain include fullness, cholecystectomy if possible. Gallbladder polyps associated nausea, vomiting, bloating, heartburn, or alteration in bowel with gallbladder stones or primary sclerosing cholangitis habits; however, the epigastric pain must be the predominant are also more likely to be neoplastic. This patient has a symptom. A diagnosis of functional dyspepsia traditionally polyp larger than 1 cm and therefore should be offered requires normal findings on upper endoscopy or an upper cholecystectomy. gastrointestinal series. In patients with functional dyspepsia If common bile duct dilation had been present on ultra- for whom Helicobacter pyloriinfection is confirmed, eradica- sonography, two options could be considered: (1) endoscopic tion therapy should be pursued because it may relieve symp- retrograde cholangiopancreatography (ERCP) (Option B) for toms. Some evidence suggests that a subset of patients with patients with cholelithiasis and therefore a high likelihood functional dyspepsia are sensitive to acid; therefore, a proton of choledocholithiasis, and (2) magnetic resonance cholan- pump inhibitor (PPI) should be the initial therapy. However, giopancreatography for diagnostic evaluation if ultrasonog- pooled studies indicate that about 70% of patients with func- raphy findings are indeterminate. Urgent ERCP is indicated tional dyspepsia still have dyspeptic symptoms after a 2- to for acute cholangitis, signaled by fever, right-upper-quad- 8-week PPI trial. Tricyclic antidepressants (TCAs) are effective rant abdominal pain, and jaundice. This patient does not in the treatment of functional dyspepsia. Pooled results of have a dilated common bile duct or ascending cholangitis, three clinical trials involving 339 patients with this disor- and ERCP would not be appropriate. der demonstrated superiority of TCAs over placebo (number When cholecystitis is suspected and the ultrasound is needed to treat, 6). The adverse events of TCAs, such as con not conclusive, hepatobiliary iminodiacetic acid scanning stipation, dry mouth, urinary retention, and somnolence, with ejection fraction (Option C) may help determine gall- can be minimized by initiating TCA therapy at a low dosage bladder function in symptomatic patients without evidence (e.g., 10 mg once daily) and slowly titrating the dose by 10-mg of larger stones. However, the issue in this case is not the increments every several weeks. function of the gallbladder but rather the risk for neoplasm Selective serotonin reuptake inhibitors, such as citalo- of the gallbladder polyp. pram (Option A), have shown no superiority over placebo in Gallbladder polyps that are 5 mm or less may be the treatment of functional dyspepsia. monitored with repeat ultrasonography (Option D) in Studies directly comparing H, blockers vs PPIs for treat- 12 months. If they have increased in size, cholecystectomy ing functional dyspepsia have found no difference in treat- may be offered. Gallbladder polyps that are 6 to 9 mm may ment efficacy. Switching from omeprazole to famotidine be monitored with ultrasonography in 6 months and then (Option B) is unlikely to improve this patient’s symptoms. yearly thereafter. Cholecystectomy may also be offered if Although prokinetic agents, such as metoclopramide the polyp size has increased. Because this patient has a (Option C), may also help a small subset of patients with 150

Answers and Critiques functional dyspepsia, a TCA trial should be pursued first Stool molecular testing (Option D), aimed at a broad given the potential side effects of prokinetic agents, such as range of clinically relevant pathogens, is preferred when dystonia and tardive dyskinesia, and stronger evidence of rapid results are clinically important or nonmolecular tests efficacy for TCAs. have not established a diagnosis. e In patients with functional dyspepsia who do not e Antimotility drugs, such as loperamide, can be used respond to an initial trial of a proton pump inhibitor, in patients with mild or moderate traveler’s nondysen- therapy with a tricyclic antidepressant should be teric diarrhea and as adjuvant therapy in patients initiated. treated with antibiotics.

e In patients with functional dyspepsia who do not e Antimotility drugs, such as loperamide, can be used respond to an initial trial of a proton pump inhibitor, in patients with mild or moderate traveler’s nondysen- therapy with a tricyclic antidepressant should be teric diarrhea and as adjuvant therapy in patients initiated. treated with antibiotics. e Antibiotics are not recommended for mild traveler’s Bibliography diarrhea. Moayyedi P, Lacy BE, Andrews CN, et al. ACG and CAG clinical guideline: wn o management of dyspepsia. Am J Gastroenterol. 2017;112:988-1013. =] [PMID: 28631728] doi:10.1038/ajg.2017.154 Bibliography = Riddle MS, Connor BA, Beeching NJ, et al. Guidelines for the prevention and <= treatment of travelers’ diarrhea: a graded expert panel report. J Travel cs) Med. 2017;24:S57-S74. [PMID: 28521004] doi:10.1093/jtm/tax026 sc Item 86 Answer: 8B = © Educational Objective: Manage mild, travel-related “

e Antibiotics are not recommended for mild traveler’s Bibliography diarrhea. Moayyedi P, Lacy BE, Andrews CN, et al. ACG and CAG clinical guideline: wn o management of dyspepsia. Am J Gastroenterol. 2017;112:988-1013. =] [PMID: 28631728] doi:10.1038/ajg.2017.154 Bibliography = Riddle MS, Connor BA, Beeching NJ, et al. Guidelines for the prevention and <= treatment of travelers’ diarrhea: a graded expert panel report. J Travel cs) Med. 2017;24:S57-S74. [PMID: 28521004] doi:10.1093/jtm/tax026 sc Item 86 Answer: 8B = © Educational Objective: Manage mild, travel-related “ diarrhea. Item 87 Answer: A thos o = Educational Objective: Treat Helicobacter pylori wn The most appropriate treatment is loperamide (Option B). eS infection persisting after initial therapy. = In the setting of recent travel, the most likely cause of acute diarrhea is infectious, with Escherichia coli being the most The most appropriate next step in management is a 14-day common agent. Viral (e.g., noroviruses) and protozoal (e.g., course of bismuth, tetracycline, metronidazole, and ome- Entamoeba histolytica, Giardia duodenalis) pathogens are prazole (Option A). This patient’s fecal antigen test confirms also possibilities. Traveler’s diarrhea usually occurs within persistent Helicobacter pylori infection despite a previous the first 2 weeks of travel and is usually self-limited, lasting course of eradication therapy. The most common factors about 4 days; however, life-threatening volume depletion or responsible for failure of eradication therapy are lack of severe colitis with systemic manifestations can occur. Some adherence to the treatment regimen or resistance of the H. travelers develop chronic diarrhea or a postinfective irritable pylori strain to the antibiotics. Other factors that decrease bowel syndrome. Fluid replacement is the mainstay of treat- efficacy of eradication therapy include smoking, diabetes, ment, preferably by the oral route, with solutions that contain and genetic factors affecting metabolism of proton pump water, salt, and sugar. Antimotility drugs such as loperamide inhibitors. As a result, eradication rates are less than 80% and diphenoxylate can be used in patients with mild or mod- for a treatment regimen consisting of clarithromycin, amox- erate traveler’s diarrhea and as adjuvant therapy in patients icillin, and a proton pump inhibitor (Option B), largely treated with antibiotics. Antimotility drugs should be avoided due to clarithromycin resistance of some H. pylori strains. in patients with dysentery (severe diarrhea and bloody stools). Antibiotic resistance also exists for metronidazole (Option C) Bismuth is another appropriate treatment for traveler’s diar- and levofloxacin, although metronidazole resistance can be thea because of its antimotility and antimicrobial effects. overcome with higher doses of metronidazole. Resistance Widespread use of antibiotics for traveler’s diarrhea has to amoxicillin is rare. Given the importance of antibiotic been associated with the acquisition of multidrug-resistant resistance for treatment efficacy, salvage therapy should not bacteria. Therefore, antimicrobials are recommended only include antibiotics that have been previously taken. There- for moderate or severe disease. Treatment with azithromy- fore, the combination of bismuth subcitrate or bismuth cin (preferred for travel to South Asia and Southeast Asia) subsalicylate along with metronidazole, tetracycline, and or a fluoroquinolone (Option A) (with increasing concern a proton pump inhibitor is the preferred salvage regimen for resistance and adverse reactions) is recommended for for H. pylori infection that has not responded to a previous moderate to severe traveler’s diarrhea. Rifaximin and rifa- eradication regimen containing clarithromycin. A 14-day mycin are minimally absorbed oral antibiotic alternatives. course of therapy (rather than a 10-day course) should be Neither rifaximin nor fluoroquinolone antibiotics are used used for persistent H. pylori infection. This four-drug reg- in patients with dysentery. imen can be challenging given the pill count, length of Stool culture (Option C) is not indicated in patients therapy, and potential for adverse effects. It is therefore with mild traveler’s diarrhea because it is typically a important to counsel patients about adhering to the regimen self-limited illness. This patient with a 2-day illness can and the potential for adverse effects. expect the diarrhea to improve in another 1 to 2 days. The fecal antigen test results are sufficiently accurate Microbiologic testing is recommended in returning travel- to confirm persistent infection, obviating the need for ers with severe or persistent symptoms or those for whom further testing (Option D). The test was done more than empiric therapy fails. 4 weeks after completion of eradication therapy (to reduce

diarrhea. Item 87 Answer: A thos o = Educational Objective: Treat Helicobacter pylori wn The most appropriate treatment is loperamide (Option B). eS infection persisting after initial therapy. = In the setting of recent travel, the most likely cause of acute diarrhea is infectious, with Escherichia coli being the most The most appropriate next step in management is a 14-day common agent. Viral (e.g., noroviruses) and protozoal (e.g., course of bismuth, tetracycline, metronidazole, and ome- Entamoeba histolytica, Giardia duodenalis) pathogens are prazole (Option A). This patient’s fecal antigen test confirms also possibilities. Traveler’s diarrhea usually occurs within persistent Helicobacter pylori infection despite a previous the first 2 weeks of travel and is usually self-limited, lasting course of eradication therapy. The most common factors about 4 days; however, life-threatening volume depletion or responsible for failure of eradication therapy are lack of severe colitis with systemic manifestations can occur. Some adherence to the treatment regimen or resistance of the H. travelers develop chronic diarrhea or a postinfective irritable pylori strain to the antibiotics. Other factors that decrease bowel syndrome. Fluid replacement is the mainstay of treat- efficacy of eradication therapy include smoking, diabetes, ment, preferably by the oral route, with solutions that contain and genetic factors affecting metabolism of proton pump water, salt, and sugar. Antimotility drugs such as loperamide inhibitors. As a result, eradication rates are less than 80% and diphenoxylate can be used in patients with mild or mod- for a treatment regimen consisting of clarithromycin, amox- erate traveler’s diarrhea and as adjuvant therapy in patients icillin, and a proton pump inhibitor (Option B), largely treated with antibiotics. Antimotility drugs should be avoided due to clarithromycin resistance of some H. pylori strains. in patients with dysentery (severe diarrhea and bloody stools). Antibiotic resistance also exists for metronidazole (Option C) Bismuth is another appropriate treatment for traveler’s diar- and levofloxacin, although metronidazole resistance can be thea because of its antimotility and antimicrobial effects. overcome with higher doses of metronidazole. Resistance Widespread use of antibiotics for traveler’s diarrhea has to amoxicillin is rare. Given the importance of antibiotic been associated with the acquisition of multidrug-resistant resistance for treatment efficacy, salvage therapy should not bacteria. Therefore, antimicrobials are recommended only include antibiotics that have been previously taken. There- for moderate or severe disease. Treatment with azithromy- fore, the combination of bismuth subcitrate or bismuth cin (preferred for travel to South Asia and Southeast Asia) subsalicylate along with metronidazole, tetracycline, and or a fluoroquinolone (Option A) (with increasing concern a proton pump inhibitor is the preferred salvage regimen for resistance and adverse reactions) is recommended for for H. pylori infection that has not responded to a previous moderate to severe traveler’s diarrhea. Rifaximin and rifa- eradication regimen containing clarithromycin. A 14-day mycin are minimally absorbed oral antibiotic alternatives. course of therapy (rather than a 10-day course) should be Neither rifaximin nor fluoroquinolone antibiotics are used used for persistent H. pylori infection. This four-drug reg- in patients with dysentery. imen can be challenging given the pill count, length of Stool culture (Option C) is not indicated in patients therapy, and potential for adverse effects. It is therefore with mild traveler’s diarrhea because it is typically a important to counsel patients about adhering to the regimen self-limited illness. This patient with a 2-day illness can and the potential for adverse effects. expect the diarrhea to improve in another 1 to 2 days. The fecal antigen test results are sufficiently accurate Microbiologic testing is recommended in returning travel- to confirm persistent infection, obviating the need for ers with severe or persistent symptoms or those for whom further testing (Option D). The test was done more than empiric therapy fails. 4 weeks after completion of eradication therapy (to reduce 151

Answers and Critiques false-negative results) and the result was positive; repeating once-daily oral PPI therapy, such as omeprazole (Option the test 1 month later is unnecessary. D), for 8 weeks. Following endoscopy, these patients can be In this asymptomatic patient, repeat upper endoscopy fed within 24 hours and discharged from the hospital. This (Option E) is unnecessary to obtain additional gastric biopsy patient has a high-risk ulcer; after 72 hours of intravenous specimens or to document interval healing of the duodenal PPI treatment, he will require treatment with PPI orally ulcers. twice daily for 2 weeks followed by once daily for an addi- tional 6 weeks.

false-negative results) and the result was positive; repeating once-daily oral PPI therapy, such as omeprazole (Option the test 1 month later is unnecessary. D), for 8 weeks. Following endoscopy, these patients can be In this asymptomatic patient, repeat upper endoscopy fed within 24 hours and discharged from the hospital. This (Option E) is unnecessary to obtain additional gastric biopsy patient has a high-risk ulcer; after 72 hours of intravenous specimens or to document interval healing of the duodenal PPI treatment, he will require treatment with PPI orally ulcers. twice daily for 2 weeks followed by once daily for an addi- tional 6 weeks. e Salvage therapy for Helicobacter pylori infection should not include antibiotics that have been previ- ¢ Patients with ulcers at high risk for rebleeding (active ously taken. bleeding, nonbleeding visible vessel, or adherent clot) should receive intravenous proton pump inhibitor ¢ The combination of bismuth subcitrate or bismuth > (PPI) therapy for 72 hours, followed by an oral PPI subsalicylate along with metronidazole, tetracycline, J twice daily for 8 weeks. wn and a proton pump inhibitor is the preferred salvage = @ regimen for Helicobacter pylori infection. ¢ Because of the higher costs associated with continu- = wa ous infusion, twice-daily intravenous PPI therapy is oo = Bibliography preferable given the similar clinical efficacy for upper 2. Chey WD, Leontiadis GI, Howden CW, et al. ACG clinical guideline: treat- gastrointestinal bleeding. oO = ment of Helicobacter pylori infection. Am J Gastroenterol. 2017;112: =. 212-239. [PMID: 28071659] doi:10.1038/ajg.2016.563 —2 Bibliography < oO Barkun AN, Almadi M, Kuipers EJ, et al. Management of nonvariceal upper wa gastrointestinal bleeding: guideline recommendations from the interna- Item 88 Answer: B tional consensus group. Ann Intern Med. 2019;171:805-822. [PMID: Educational Objective: Manage high-risk upper 31634917] doi:10.7326/M19-1795

e Salvage therapy for Helicobacter pylori infection should not include antibiotics that have been previ- ¢ Patients with ulcers at high risk for rebleeding (active ously taken. bleeding, nonbleeding visible vessel, or adherent clot) should receive intravenous proton pump inhibitor ¢ The combination of bismuth subcitrate or bismuth > (PPI) therapy for 72 hours, followed by an oral PPI subsalicylate along with metronidazole, tetracycline, J twice daily for 8 weeks. wn and a proton pump inhibitor is the preferred salvage = @ regimen for Helicobacter pylori infection. ¢ Because of the higher costs associated with continu- = wa ous infusion, twice-daily intravenous PPI therapy is oo = Bibliography preferable given the similar clinical efficacy for upper 2. Chey WD, Leontiadis GI, Howden CW, et al. ACG clinical guideline: treat- gastrointestinal bleeding. oO = ment of Helicobacter pylori infection. Am J Gastroenterol. 2017;112: =. 212-239. [PMID: 28071659] doi:10.1038/ajg.2016.563 —2 Bibliography < oO Barkun AN, Almadi M, Kuipers EJ, et al. Management of nonvariceal upper wa gastrointestinal bleeding: guideline recommendations from the interna- Item 88 Answer: B tional consensus group. Ann Intern Med. 2019;171:805-822. [PMID: Educational Objective: Manage high-risk upper 31634917] doi:10.7326/M19-1795 gastrointestinal bleeding.

e Salvage therapy for Helicobacter pylori infection should not include antibiotics that have been previ- ¢ Patients with ulcers at high risk for rebleeding (active ously taken. bleeding, nonbleeding visible vessel, or adherent clot) should receive intravenous proton pump inhibitor ¢ The combination of bismuth subcitrate or bismuth > (PPI) therapy for 72 hours, followed by an oral PPI subsalicylate along with metronidazole, tetracycline, J twice daily for 8 weeks. wn and a proton pump inhibitor is the preferred salvage = @ regimen for Helicobacter pylori infection. ¢ Because of the higher costs associated with continu- = wa ous infusion, twice-daily intravenous PPI therapy is oo = Bibliography preferable given the similar clinical efficacy for upper 2. Chey WD, Leontiadis GI, Howden CW, et al. ACG clinical guideline: treat- gastrointestinal bleeding. oO = ment of Helicobacter pylori infection. Am J Gastroenterol. 2017;112: =. 212-239. [PMID: 28071659] doi:10.1038/ajg.2016.563 —2 Bibliography < oO Barkun AN, Almadi M, Kuipers EJ, et al. Management of nonvariceal upper wa gastrointestinal bleeding: guideline recommendations from the interna- Item 88 Answer: B tional consensus group. Ann Intern Med. 2019;171:805-822. [PMID: Educational Objective: Manage high-risk upper 31634917] doi:10.7326/M19-1795 gastrointestinal bleeding. The most appropriate treatment is esomeprazole, a proton Item 89 Answer: C pump inhibitor (PPI), intravenously twice daily for 72 hours Educational Objective: Treat Candida esophagitis. (Option B). Upper endoscopy should be performed within 24 hours in patients with acute upper gastrointestinal bleed- The most appropriate treatment is oral fluconazole (Option ing (UGIB). In this patient, endoscopy revealed a nonbleed- C). This patient probably has Candida esophagitis given his ing visible vessel within the ulcer base, which is classified dysphagia with odynophagia, HIV infection with low CD4 as an ulcer with high risk for rebleeding. After endoscopy, count, and oral thrush. In patients with these clinical char- patients with UGIB and ulcers with high risk for rebleeding acteristics, the provisional clinical diagnosis can be made (active bleeding, nonbleeding visible vessel, or adherent clot) and empiric treatment begun. The most common causative should receive continuous-infusion PPI therapy for 72 hours species is Candida albicans, which is treated with oral flu- or a PPI intravenously twice daily for 72 hours and remain conazole. in the hospital during that time. Intravenous PPI therapy is Viral esophagitis, caused by herpes simplex virus (HSV) followed by an oral PPI twice daily for 2 weeks, followed by or cytomegalovirus, may also occur in immunocompro- once daily for an additional 6 weeks. The risk for rebleeding mised patients. HSV esophagitis is treated with acyclovir, in patients with high-risk ulcers that are successfully treated and cytomegalovirus is treated with ganciclovir (oral val- endoscopically is similar for patients who receive twice-daily ganciclovir is also an option). Viral esophagitis, however, is intravenous PPI and those who receive continuous PPI infu- typically associated more with odynophagia than with dys- sion. Because of the higher costs associated with continuous phagia. More important, the presence of oral thrush is highly infusion, twice-daily PPI is preferable given the similar clin- predictive of Candida esophagitis; therefore, treatment with ical efficacy. ganciclovir (Option A) or acyclovir is not indicated as initial Initiation of broad-spectrum antibiotics for 7 days is rec therapy. Endoscopy with biopsy is needed to confirm the ommended in all patients with cirrhosis and gastrointestinal diagnosis of viral esophagitis and should be performed if the bleeding even in the absence of ascites. This patient does not patient does not respond to empiric antifungal treatment. have cirrhosis; therefore, treatment with broad-spectrum Intravenous echinocandin therapy with caspofungin antibiotics (Option A) is not indicated. (Option B), micafungin, or anidulafungin may be used in Octreotide (Option C) is an analogue of somatostatin hospitalized patients with Candida esophagitis refractory that decreases splanchnic blood flow and lowers portal pres- to azole therapy. This patient does not have an indication for sure; it should be initiated before endoscopic evaluation and intravenous echinocandin therapy. continuously infused for 3 to 5 days after variceal hemor- Simultaneous infection with Candida and HSV neces- rhage. Octreotide is not routinely used in nonvariceal UGIB. sitating dual therapy with fluconazole and acyclovir (Option Patients with low-risk stigmata following recent UGIB D) would be unusual. The most likely diagnosis is Candida (i.e., flat pigmented spot, clean-based ulcer) should receive esophagitis, and empiric treatment with fluconazole alone

The most appropriate treatment is esomeprazole, a proton Item 89 Answer: C pump inhibitor (PPI), intravenously twice daily for 72 hours Educational Objective: Treat Candida esophagitis. (Option B). Upper endoscopy should be performed within 24 hours in patients with acute upper gastrointestinal bleed- The most appropriate treatment is oral fluconazole (Option ing (UGIB). In this patient, endoscopy revealed a nonbleed- C). This patient probably has Candida esophagitis given his ing visible vessel within the ulcer base, which is classified dysphagia with odynophagia, HIV infection with low CD4 as an ulcer with high risk for rebleeding. After endoscopy, count, and oral thrush. In patients with these clinical char- patients with UGIB and ulcers with high risk for rebleeding acteristics, the provisional clinical diagnosis can be made (active bleeding, nonbleeding visible vessel, or adherent clot) and empiric treatment begun. The most common causative should receive continuous-infusion PPI therapy for 72 hours species is Candida albicans, which is treated with oral flu- or a PPI intravenously twice daily for 72 hours and remain conazole. in the hospital during that time. Intravenous PPI therapy is Viral esophagitis, caused by herpes simplex virus (HSV) followed by an oral PPI twice daily for 2 weeks, followed by or cytomegalovirus, may also occur in immunocompro- once daily for an additional 6 weeks. The risk for rebleeding mised patients. HSV esophagitis is treated with acyclovir, in patients with high-risk ulcers that are successfully treated and cytomegalovirus is treated with ganciclovir (oral val- endoscopically is similar for patients who receive twice-daily ganciclovir is also an option). Viral esophagitis, however, is intravenous PPI and those who receive continuous PPI infu- typically associated more with odynophagia than with dys- sion. Because of the higher costs associated with continuous phagia. More important, the presence of oral thrush is highly infusion, twice-daily PPI is preferable given the similar clin- predictive of Candida esophagitis; therefore, treatment with ical efficacy. ganciclovir (Option A) or acyclovir is not indicated as initial Initiation of broad-spectrum antibiotics for 7 days is rec therapy. Endoscopy with biopsy is needed to confirm the ommended in all patients with cirrhosis and gastrointestinal diagnosis of viral esophagitis and should be performed if the bleeding even in the absence of ascites. This patient does not patient does not respond to empiric antifungal treatment. have cirrhosis; therefore, treatment with broad-spectrum Intravenous echinocandin therapy with caspofungin antibiotics (Option A) is not indicated. (Option B), micafungin, or anidulafungin may be used in Octreotide (Option C) is an analogue of somatostatin hospitalized patients with Candida esophagitis refractory that decreases splanchnic blood flow and lowers portal pres- to azole therapy. This patient does not have an indication for sure; it should be initiated before endoscopic evaluation and intravenous echinocandin therapy. continuously infused for 3 to 5 days after variceal hemor- Simultaneous infection with Candida and HSV neces- rhage. Octreotide is not routinely used in nonvariceal UGIB. sitating dual therapy with fluconazole and acyclovir (Option Patients with low-risk stigmata following recent UGIB D) would be unusual. The most likely diagnosis is Candida (i.e., flat pigmented spot, clean-based ulcer) should receive esophagitis, and empiric treatment with fluconazole alone 152

Answers and Critiques is preferred. If viral esophagitis is suspected, endoscopy preferred over shorter solid-emptying studies or sole liquid- and biopsy are required for diagnosis and to direct therapy, emptying studies because those methods are less sensitive. rather than empiric antifungal and antiviral therapy. The most reliable parameter to document a delayed gas- If symptoms are atypical or do not respond to treat- tric emptying is the percentage of retained gastric contents ment, endoscopy with biopsy or cytologic brushings (Option 4 hours after meal consumption. E) may be performed to confirm the diagnosis and evaluate Medical therapy for gastroparesis—erythromycin for other causes of dysphagia. However, the presence of (Option A) or metoclopramide (Option B)—should not be oral thrush is highly predictive of Candida esophagitis in initiated until the diagnosis is confirmed. immunocompromised patients presenting with dysphagia An upper gastrointestinal barium series (Option D) and odynophagia. Infectious esophagitis can more rarely can exclude mechanical obstruction and other structural be caused by other viral, bacterial, and parasitic pathogens, abnormalities of the upper gastrointestinal tract, but this including Lactobacillus species, B-hemolytic streptococci, confirmation has already been accomplished with upper Cryptosporidium species, Pneumocystis jirovecii, Mycobac- endoscopy. A barium series cannot objectively assess gastric wn a terium avium complex, and Mycobacterium tuberculosis. emptying. 3

is preferred. If viral esophagitis is suspected, endoscopy preferred over shorter solid-emptying studies or sole liquid- and biopsy are required for diagnosis and to direct therapy, emptying studies because those methods are less sensitive. rather than empiric antifungal and antiviral therapy. The most reliable parameter to document a delayed gas- If symptoms are atypical or do not respond to treat- tric emptying is the percentage of retained gastric contents ment, endoscopy with biopsy or cytologic brushings (Option 4 hours after meal consumption. E) may be performed to confirm the diagnosis and evaluate Medical therapy for gastroparesis—erythromycin for other causes of dysphagia. However, the presence of (Option A) or metoclopramide (Option B)—should not be oral thrush is highly predictive of Candida esophagitis in initiated until the diagnosis is confirmed. immunocompromised patients presenting with dysphagia An upper gastrointestinal barium series (Option D) and odynophagia. Infectious esophagitis can more rarely can exclude mechanical obstruction and other structural be caused by other viral, bacterial, and parasitic pathogens, abnormalities of the upper gastrointestinal tract, but this including Lactobacillus species, B-hemolytic streptococci, confirmation has already been accomplished with upper Cryptosporidium species, Pneumocystis jirovecii, Mycobac- endoscopy. A barium series cannot objectively assess gastric wn a terium avium complex, and Mycobacterium tuberculosis. emptying. 3 Although poor glycemic control is known to further = delay gastric emptying, there is no value in repeating upper 7 rw) e Candida esophagitis can be diagnosed clinically in endoscopy after better control of this patient’s diabetes sc = patients with dysphagia and odynophagia, immuno- (Option E) to reassess for retained food. 6 suppression, and findings of oral thrush. nn i o ¢ Candida esophagitis can be treated with oral flucona- = e The diagnostic criteria for gastroparesis include a wn zole. < combination of compatible symptoms, absence of 4 gastric outlet obstruction or ulceration, and an Bibliography objectively measured delay in gastric emptying. Hoversten P, Kamboj AK, Katzka DA. Infections of the esophagus: an update on risk factors, diagnosis, and management. Dis Esophagus. 2018;31. e Tests to document delayed gastric emptying include [PMID: 30295751] doi:10.1093/dote/doy094 scintigraphy, wireless motility capsule, and breath testing; scintigraphy of a solid-phase meal is preferred. Item 90 Answer: C Educational Objective: Evaluate suspected Bibliography Camilleri M, Parkman HP, Shafi MA, et al; American College of gastroparesis. Gastroenterology. Clinical guideline: management of gastroparesis. Am J Gastroenterol. 2013;108:18-37; quiz 38. [PMID: 23147521] doi:10.1038/ The most appropriate next step in management is 4-hour ajg.2012.373 gastric scintigraphy (Option C). This patient’s presentation strongly suggests—but is not diagnostic of—diabetic gastropa- resis. Her upper gastrointestinal symptoms and the retained Item 91 Answer: B food on upper endoscopy indicate delayed gastric emptying. Educational Objective: Treat microscopic colitis. However, definitive diagnosis of gastroparesis requires objec- tively demonstrating a delay in gastric emptying. American The most appropriate management is discontinuation of ibu- College of Gastroenterology guidelines state that the diagnosis profen (Option B). The histologic finding of marked intraep- of gastroparesis must be based on the combination of symp- ithelial lymphocytosis in the context of a normal-appear- toms of gastroparesis, absence of gastric outlet obstruction ing colon is compatible with lymphocytic colitis, a form of or ulceration, and a delay in gastric emptying. Objective evi- microscopic colitis. This form of inflammatory bowel disease dence of delayed gastric emptying is important because other comes in two predominant forms: lymphocytic colitis and conditions, such as accelerated gastric emptying, functional collagenous colitis. The condition mostly affects middle-aged dyspepsia, Helicobacter pylori infection, and peptic ulcer women and is characterized by abrupt or gradual onset of disease, can present with similar symptoms. This patient watery diarrhea that has a relapsing-remitting course over reports many gastroparesis symptoms, which can include months to years, sometimes accompanied by weight loss early satiety, postprandial fullness, nausea, vomiting, bloat- and abdominal pain. Microscopic colitis can be idiopathic, ing, and/or upper abdominal pain. Her upper endoscopy but medications, including NSAIDs, proton pump inhibitors, excluded a mechanical obstruction of the stomach and H. and selective serotonin reuptake inhibitors, have been asso- pylori gastritis. To document a delay in gastric emptying, fur- ciated with its development. Management of microscopic ther testing must be performed. The three tests used are scin- colitis starts with discontinuation of potentially causative tigraphy, wireless motility capsule, and breath testing using %C- medications, in this case ibuprofen. This patient could be labeled Spirulina platensis. Of these tests, scintigraphy of a advised to substitute acetaminophen or, if that drug is not solid-phase meal is considered the standard for diagnosis of effective, a trial of topical NSAIDs; gastrointestinal toxicity gastroparesis because it quantifies the emptying of a phys- is much lower with topical NSAIDs because of reduced sys- iologic caloric meal. The 4-hour solid-emptying study is temic absorption.

Although poor glycemic control is known to further = delay gastric emptying, there is no value in repeating upper 7 rw) e Candida esophagitis can be diagnosed clinically in endoscopy after better control of this patient’s diabetes sc = patients with dysphagia and odynophagia, immuno- (Option E) to reassess for retained food. 6 suppression, and findings of oral thrush. nn i o ¢ Candida esophagitis can be treated with oral flucona- = e The diagnostic criteria for gastroparesis include a wn zole. < combination of compatible symptoms, absence of 4 gastric outlet obstruction or ulceration, and an Bibliography objectively measured delay in gastric emptying. Hoversten P, Kamboj AK, Katzka DA. Infections of the esophagus: an update on risk factors, diagnosis, and management. Dis Esophagus. 2018;31. e Tests to document delayed gastric emptying include [PMID: 30295751] doi:10.1093/dote/doy094 scintigraphy, wireless motility capsule, and breath testing; scintigraphy of a solid-phase meal is preferred. Item 90 Answer: C Educational Objective: Evaluate suspected Bibliography Camilleri M, Parkman HP, Shafi MA, et al; American College of gastroparesis. Gastroenterology. Clinical guideline: management of gastroparesis. Am J Gastroenterol. 2013;108:18-37; quiz 38. [PMID: 23147521] doi:10.1038/ The most appropriate next step in management is 4-hour ajg.2012.373 gastric scintigraphy (Option C). This patient’s presentation strongly suggests—but is not diagnostic of—diabetic gastropa- resis. Her upper gastrointestinal symptoms and the retained Item 91 Answer: B food on upper endoscopy indicate delayed gastric emptying. Educational Objective: Treat microscopic colitis. However, definitive diagnosis of gastroparesis requires objec- tively demonstrating a delay in gastric emptying. American The most appropriate management is discontinuation of ibu- College of Gastroenterology guidelines state that the diagnosis profen (Option B). The histologic finding of marked intraep- of gastroparesis must be based on the combination of symp- ithelial lymphocytosis in the context of a normal-appear- toms of gastroparesis, absence of gastric outlet obstruction ing colon is compatible with lymphocytic colitis, a form of or ulceration, and a delay in gastric emptying. Objective evi- microscopic colitis. This form of inflammatory bowel disease dence of delayed gastric emptying is important because other comes in two predominant forms: lymphocytic colitis and conditions, such as accelerated gastric emptying, functional collagenous colitis. The condition mostly affects middle-aged dyspepsia, Helicobacter pylori infection, and peptic ulcer women and is characterized by abrupt or gradual onset of disease, can present with similar symptoms. This patient watery diarrhea that has a relapsing-remitting course over reports many gastroparesis symptoms, which can include months to years, sometimes accompanied by weight loss early satiety, postprandial fullness, nausea, vomiting, bloat- and abdominal pain. Microscopic colitis can be idiopathic, ing, and/or upper abdominal pain. Her upper endoscopy but medications, including NSAIDs, proton pump inhibitors, excluded a mechanical obstruction of the stomach and H. and selective serotonin reuptake inhibitors, have been asso- pylori gastritis. To document a delay in gastric emptying, fur- ciated with its development. Management of microscopic ther testing must be performed. The three tests used are scin- colitis starts with discontinuation of potentially causative tigraphy, wireless motility capsule, and breath testing using %C- medications, in this case ibuprofen. This patient could be labeled Spirulina platensis. Of these tests, scintigraphy of a advised to substitute acetaminophen or, if that drug is not solid-phase meal is considered the standard for diagnosis of effective, a trial of topical NSAIDs; gastrointestinal toxicity gastroparesis because it quantifies the emptying of a phys- is much lower with topical NSAIDs because of reduced sys- iologic caloric meal. The 4-hour solid-emptying study is temic absorption. 153

Answers and Critiques Fecal calprotectin (Option A) can be of diagnostic utility symptoms despite strict adherence to this diet. Such patients in evaluating chronic diarrhea; an elevated level suggests may respond to dapsone (Option A). Before initiation of dap- colonic inflammation and warrants further investigation, sone therapy, it is necessary to check for glucose-6-phos- such as colonoscopy. However, fecal calprotectin is not of phate dehydrogenase deficiency because individuals with this diagnostic value in this case, for which colonoscopy has condition can develop hemolytic anemia when exposed to already established a diagnosis of microscopic colitis. this medication. Methemoglobinemia, agranulocytosis, and Oral budesonide (Option C), a glucocorticoid with a dapsone hypersensitivity reaction are additional adverse extensive first-pass metabolism by the liver, is effective in effects. If the patient exhibits normal glucose-6-phosphate the treatment of microscopic colitis. However, it is reserved dehydrogenase activity, dapsone can be initiated. for patients whose symptoms do not improve after other Topical glucocorticoids, such as hydrocortisone (Option measures, such as cessation of associated medications (in B), can be helpful as an adjuvant treatment for pruritus in this case ibuprofen) or symptomatic treatment with lop- patients with dermatitis herpetiformis, but they are ineffec- S eramide. tive as monotherapy in inducing remission. When topical = wn Oral prednisone (Option D) can be used as induction glucocorticoids are used, they should be administered along = therapy in patients with other forms of inflammatory bowel with dapsone and a gluten-free diet. Systemic glucocor- o disease (ulcerative colitis and Crohn disease), but these diag- ?

Fecal calprotectin (Option A) can be of diagnostic utility symptoms despite strict adherence to this diet. Such patients in evaluating chronic diarrhea; an elevated level suggests may respond to dapsone (Option A). Before initiation of dap- colonic inflammation and warrants further investigation, sone therapy, it is necessary to check for glucose-6-phos- such as colonoscopy. However, fecal calprotectin is not of phate dehydrogenase deficiency because individuals with this diagnostic value in this case, for which colonoscopy has condition can develop hemolytic anemia when exposed to already established a diagnosis of microscopic colitis. this medication. Methemoglobinemia, agranulocytosis, and Oral budesonide (Option C), a glucocorticoid with a dapsone hypersensitivity reaction are additional adverse extensive first-pass metabolism by the liver, is effective in effects. If the patient exhibits normal glucose-6-phosphate the treatment of microscopic colitis. However, it is reserved dehydrogenase activity, dapsone can be initiated. for patients whose symptoms do not improve after other Topical glucocorticoids, such as hydrocortisone (Option measures, such as cessation of associated medications (in B), can be helpful as an adjuvant treatment for pruritus in this case ibuprofen) or symptomatic treatment with lop- patients with dermatitis herpetiformis, but they are ineffec- S eramide. tive as monotherapy in inducing remission. When topical = wn Oral prednisone (Option D) can be used as induction glucocorticoids are used, they should be administered along = therapy in patients with other forms of inflammatory bowel with dapsone and a gluten-free diet. Systemic glucocor- o disease (ulcerative colitis and Crohn disease), but these diag- ? “ ticoids, such as prednisone, are usually ineffective in the oy noses are not supported by the patient’s lack of endoscopically treatment of dermatitis herpetiformis. =o a. visible colonic abnormalities, such as ulcers, edema, or ery- Hydroxychloroquine (Option C) is an immunomodulator (2) — thema. In addition, prednisone should not be used as first-line that is widely used in systemic lupus erythematosus (SLE) = treatment of microscopic colitis because of its adverse effects. and can be used as monotherapy to treat mild skin and joint ft = symptoms. A rare variant of acute cutaneous lupus presents © “nn with vesicles and bullae; invariably, however, these patients e Microscopic colitis can be idiopathic, but medications, have other systemic manifestations of SLE. Therefore, treat- including NSAIDs, proton pump inhibitors, and selec- ment with hydroxychloroquine is not indicated in this patient. tive serotonin reuptake inhibitors, have been associated with its development. e Dermatitis herpetiformis typically presents with e Treatment of microscopic colitis starts with discontinu- intensely pruritic papules and fragile vesicles that ation of potentially causative medications, symptomatic rapidly break, leaving tiny erosions, and is commonly treatment with loperamide, and possibly progression to associated with histologic and serologic evidence of oral budesonide. celiac disease.

“ ticoids, such as prednisone, are usually ineffective in the oy noses are not supported by the patient’s lack of endoscopically treatment of dermatitis herpetiformis. =o a. visible colonic abnormalities, such as ulcers, edema, or ery- Hydroxychloroquine (Option C) is an immunomodulator (2) — thema. In addition, prednisone should not be used as first-line that is widely used in systemic lupus erythematosus (SLE) = treatment of microscopic colitis because of its adverse effects. and can be used as monotherapy to treat mild skin and joint ft = symptoms. A rare variant of acute cutaneous lupus presents © “nn with vesicles and bullae; invariably, however, these patients e Microscopic colitis can be idiopathic, but medications, have other systemic manifestations of SLE. Therefore, treat- including NSAIDs, proton pump inhibitors, and selec- ment with hydroxychloroquine is not indicated in this patient. tive serotonin reuptake inhibitors, have been associated with its development. e Dermatitis herpetiformis typically presents with e Treatment of microscopic colitis starts with discontinu- intensely pruritic papules and fragile vesicles that ation of potentially causative medications, symptomatic rapidly break, leaving tiny erosions, and is commonly treatment with loperamide, and possibly progression to associated with histologic and serologic evidence of oral budesonide. celiac disease. Bibliography e Dermatitis herpetiformis responds rapidly to dapsone;

“ ticoids, such as prednisone, are usually ineffective in the oy noses are not supported by the patient’s lack of endoscopically treatment of dermatitis herpetiformis. =o a. visible colonic abnormalities, such as ulcers, edema, or ery- Hydroxychloroquine (Option C) is an immunomodulator (2) — thema. In addition, prednisone should not be used as first-line that is widely used in systemic lupus erythematosus (SLE) = treatment of microscopic colitis because of its adverse effects. and can be used as monotherapy to treat mild skin and joint ft = symptoms. A rare variant of acute cutaneous lupus presents © “nn with vesicles and bullae; invariably, however, these patients e Microscopic colitis can be idiopathic, but medications, have other systemic manifestations of SLE. Therefore, treat- including NSAIDs, proton pump inhibitors, and selec- ment with hydroxychloroquine is not indicated in this patient. tive serotonin reuptake inhibitors, have been associated with its development. e Dermatitis herpetiformis typically presents with e Treatment of microscopic colitis starts with discontinu- intensely pruritic papules and fragile vesicles that ation of potentially causative medications, symptomatic rapidly break, leaving tiny erosions, and is commonly treatment with loperamide, and possibly progression to associated with histologic and serologic evidence of oral budesonide. celiac disease. Bibliography e Dermatitis herpetiformis responds rapidly to dapsone; Pardi DS. Diagnosis and management of microscopic colitis. Am J testing for glucose-6-phosphate dehydrogenase defi- Gastroenterol. 2017;112:78-85. [PMID: 27897155] doi:10.1038/ajg.2016.477 ciency is required before initiation of therapy.

Pardi DS. Diagnosis and management of microscopic colitis. Am J testing for glucose-6-phosphate dehydrogenase defi- Gastroenterol. 2017;112:78-85. [PMID: 27897155] doi:10.1038/ajg.2016.477 ciency is required before initiation of therapy. Item 92 Answer: D Bibliography Collin P, Salmi TT, Hervonen K, et al. Dermatitis herpetiformis: a cutaneous Educational Objective: Manage dermatitis manifestation of coeliac disease. Ann Med. 2017;49:23-31. [PMID: herpetiformis. 27499257] doi:10.1080/07853890.2016.1222450

Item 92 Answer: D Bibliography Collin P, Salmi TT, Hervonen K, et al. Dermatitis herpetiformis: a cutaneous Educational Objective: Manage dermatitis manifestation of coeliac disease. Ann Med. 2017;49:23-31. [PMID: herpetiformis. 27499257] doi:10.1080/07853890.2016.1222450 The most appropriate management is measurement of glucose-6-phosphate dehydrogenase activity (Option D). This Item 93 Answer: D patient with a history of celiac disease has a chronic pruritic Educational Objective: Treat chronic pancreatitis with vesicular rash on the elbows and knees. Dermatitis herpeti- tobacco avoidance. formis is a neutrophilic dermatosis caused by IgA antibodies against tissue and epidermal transglutaminase. It typically The most appropriate additional treatment for pain is tobacco presents with intensely pruritic papules and fragile vesicles cessation (Option D). The patient has chronic pancreatitis. that rapidly break, leaving tiny erosions. A skin biopsy spec- Long-term tobacco use is an independent risk factor for acute imen will show numerous neutrophils stuffing the dermal and chronic pancreatitis, as well as pancreatic cancer. It is papillae, and a granular pattern of IgA deposition will be seen synergistic with alcohol in promoting morbidity related to on direct immunofluorescence. Most patients with derma- pancreatic disease. Initial therapy for chronic pancreatitis titis herpetiformis will have an underlying gluten-sensitive pain should entail lifestyle modification, including alcohol enteropathy. However, they are usually free of gastrointesti- and tobacco cessation, and simple analgesics. No direct evi- nal symptoms; only 20% of patients with celiac disease will dence addresses whether alcohol cessation alters the natural develop dermatitis herpetiformis. The distribution and mor- history of chronic pancreatitis pain. However, several case phology, in the context of a history of celiac disease, are com- series have suggested that discontinuing alcohol use improves patible with dermatitis herpetiformis. This condition is treated the pain in chronic pancreatitis but does not necessarily alter with a gluten-free diet, but patients may have continued the progression to endocrine or exocrine dysfunction. There

The most appropriate management is measurement of glucose-6-phosphate dehydrogenase activity (Option D). This Item 93 Answer: D patient with a history of celiac disease has a chronic pruritic Educational Objective: Treat chronic pancreatitis with vesicular rash on the elbows and knees. Dermatitis herpeti- tobacco avoidance. formis is a neutrophilic dermatosis caused by IgA antibodies against tissue and epidermal transglutaminase. It typically The most appropriate additional treatment for pain is tobacco presents with intensely pruritic papules and fragile vesicles cessation (Option D). The patient has chronic pancreatitis. that rapidly break, leaving tiny erosions. A skin biopsy spec- Long-term tobacco use is an independent risk factor for acute imen will show numerous neutrophils stuffing the dermal and chronic pancreatitis, as well as pancreatic cancer. It is papillae, and a granular pattern of IgA deposition will be seen synergistic with alcohol in promoting morbidity related to on direct immunofluorescence. Most patients with derma- pancreatic disease. Initial therapy for chronic pancreatitis titis herpetiformis will have an underlying gluten-sensitive pain should entail lifestyle modification, including alcohol enteropathy. However, they are usually free of gastrointesti- and tobacco cessation, and simple analgesics. No direct evi- nal symptoms; only 20% of patients with celiac disease will dence addresses whether alcohol cessation alters the natural develop dermatitis herpetiformis. The distribution and mor- history of chronic pancreatitis pain. However, several case phology, in the context of a history of celiac disease, are com- series have suggested that discontinuing alcohol use improves patible with dermatitis herpetiformis. This condition is treated the pain in chronic pancreatitis but does not necessarily alter with a gluten-free diet, but patients may have continued the progression to endocrine or exocrine dysfunction. There 154

Answers and Critiques is no direct evidence that smoking cessation is beneficial in decision to initiate low-dose aspirin in this population should improving the natural history of chronic pancreatitis. How- be individualized. The American College of Cardiology and ever, case series have shown a decrease in the amount of American Diabetes Association suggest that low-dose aspirin pancreatic calcification progression when smoking cessation might be considered for ASCVD primary prevention in adults occurs at the time of diagnosis of chronic pancreatitis. Both aged 40 to 70 years who are at higher ASCVD risk but not at alcohol and smoking cessation are strongly recommended increased bleeding risk. This patient recently experienced in the American College of Gastroenterology (ACG) guideline hemodynamically significant lower gastrointestinal bleeding on chronic pancreatitis. Amitriptyline and nortriptyline may from diverticulosis. Although this bleeding was successfully reduce pain from neuropathic conditions and therefore may treated, he is at considerable risk for recurrent bleeding from be useful in patients with chronic pancreatitis. ACG makes his diverticulosis. Case series demonstrate early rebleeding, no recommendation for or against these drug therapies in defined as before hospital discharge, in up to 16% of patients patients with chronic pancreatitis. and late rebleeding, defined as 30 or more days after discharge Opioids, such as oxycodone (Option A), should be (Option B), in up to 24% of patients. Reinitiation of an NSAID wn a avoided in the long-term management of chronic pancre- or aspirin further increases risk for rebleeding. This patient S

is no direct evidence that smoking cessation is beneficial in decision to initiate low-dose aspirin in this population should improving the natural history of chronic pancreatitis. How- be individualized. The American College of Cardiology and ever, case series have shown a decrease in the amount of American Diabetes Association suggest that low-dose aspirin pancreatic calcification progression when smoking cessation might be considered for ASCVD primary prevention in adults occurs at the time of diagnosis of chronic pancreatitis. Both aged 40 to 70 years who are at higher ASCVD risk but not at alcohol and smoking cessation are strongly recommended increased bleeding risk. This patient recently experienced in the American College of Gastroenterology (ACG) guideline hemodynamically significant lower gastrointestinal bleeding on chronic pancreatitis. Amitriptyline and nortriptyline may from diverticulosis. Although this bleeding was successfully reduce pain from neuropathic conditions and therefore may treated, he is at considerable risk for recurrent bleeding from be useful in patients with chronic pancreatitis. ACG makes his diverticulosis. Case series demonstrate early rebleeding, no recommendation for or against these drug therapies in defined as before hospital discharge, in up to 16% of patients patients with chronic pancreatitis. and late rebleeding, defined as 30 or more days after discharge Opioids, such as oxycodone (Option A), should be (Option B), in up to 24% of patients. Reinitiation of an NSAID wn a avoided in the long-term management of chronic pancre- or aspirin further increases risk for rebleeding. This patient S atitis. Although they may be helpful for analgesia in acute had been taking aspirin for primary prevention of ASCVD. = pancreatitis and during flares of chronic pancreatitis, they Although he does have several cardiovascular risk factors (age, a rs) may lead to hyperesthesia and opioid tolerance. The ACG hypertension, diabetes, dyslipidemia), the risk for recurrent sc = recommends that opiates may be considered to treat painful lower gastrointestinal bleeding is greater than the benefit of © chronic pancreatitis only in patients for whom all other rea- daily aspirin in preventing myocardial infarction or stroke. wn a o sonable therapeutic options have been exhausted. Therefore, he should not restart aspirin now (Option C). = A large systematic review found conflicting evidence for Guidelines on the management of lower gastrointestinal 2) = the efficacy of pancreatic enzyme replacement (Option B) bleeding recommend avoidance of aspirin for primary pre- =< in pain control; however, enzyme therapy may improve fat vention of cardiovascular events in most patients, particularly absorption. The ACG makes a conditional recommendation those with bleeding due to diverticulosis or angiodysplasia. not to use pancreatic enzyme supplements to improve pain However, after an episode of gastrointestinal bleeding, aspirin in chronic pancreatitis. for secondary prevention of ASCVD should not be routinely Patients with chronic pancreatitis often experience pain stopped. If aspirin is stopped, then it should be restarted as in the setting of pancreatic duct obstruction due to duct soon as hemostasis is achieved. stones and strictures. Although surgical approaches to pan- The addition of a proton pump inhibitor such as ome- creatic duct decompression (Option C) provide better long- prazole (Option D) may provide some protection from upper term pain relief than endoscopic approaches, they are rarely gastrointestinal bleeding, but it will not protect this patient first-line therapies; in addition, many surgeons operate only from recurrent lower gastrointestinal bleeding. In this after endoscopic approaches to pancreatic drainage have patient aspirin should be discontinued. been exhausted or unsuccessful. This patient does not have evidence of pancreatic duct obstruction. e After an episode of gastrointestinal bleeding, aspirin for primary prevention of atherosclerotic cardiovascu- e Alcohol and tobacco avoidance are strongly recom- lar disease should be discontinued. mended for patients with chronic pancreatitis. e After an episode of gastrointestinal bleeding, aspirin for secondary prevention of atherosclerotic cardiovas- Bibliography cular disease should not be routinely stopped; if aspi- Gardner TB, Adler DG, Forsmark CE, et al. ACG clinical guideline: chronic pancreatitis. Am J Gastroenterol. 2020;115:322-339. [PMID: 32022720] rin is stopped, then it should be restarted as soon as doi:10.14309/ajg.0000000000000535 hemostasis is achieved.

atitis. Although they may be helpful for analgesia in acute had been taking aspirin for primary prevention of ASCVD. = pancreatitis and during flares of chronic pancreatitis, they Although he does have several cardiovascular risk factors (age, a rs) may lead to hyperesthesia and opioid tolerance. The ACG hypertension, diabetes, dyslipidemia), the risk for recurrent sc = recommends that opiates may be considered to treat painful lower gastrointestinal bleeding is greater than the benefit of © chronic pancreatitis only in patients for whom all other rea- daily aspirin in preventing myocardial infarction or stroke. wn a o sonable therapeutic options have been exhausted. Therefore, he should not restart aspirin now (Option C). = A large systematic review found conflicting evidence for Guidelines on the management of lower gastrointestinal 2) = the efficacy of pancreatic enzyme replacement (Option B) bleeding recommend avoidance of aspirin for primary pre- =< in pain control; however, enzyme therapy may improve fat vention of cardiovascular events in most patients, particularly absorption. The ACG makes a conditional recommendation those with bleeding due to diverticulosis or angiodysplasia. not to use pancreatic enzyme supplements to improve pain However, after an episode of gastrointestinal bleeding, aspirin in chronic pancreatitis. for secondary prevention of ASCVD should not be routinely Patients with chronic pancreatitis often experience pain stopped. If aspirin is stopped, then it should be restarted as in the setting of pancreatic duct obstruction due to duct soon as hemostasis is achieved. stones and strictures. Although surgical approaches to pan- The addition of a proton pump inhibitor such as ome- creatic duct decompression (Option C) provide better long- prazole (Option D) may provide some protection from upper term pain relief than endoscopic approaches, they are rarely gastrointestinal bleeding, but it will not protect this patient first-line therapies; in addition, many surgeons operate only from recurrent lower gastrointestinal bleeding. In this after endoscopic approaches to pancreatic drainage have patient aspirin should be discontinued. been exhausted or unsuccessful. This patient does not have evidence of pancreatic duct obstruction. e After an episode of gastrointestinal bleeding, aspirin for primary prevention of atherosclerotic cardiovascu- e Alcohol and tobacco avoidance are strongly recom- lar disease should be discontinued. mended for patients with chronic pancreatitis. e After an episode of gastrointestinal bleeding, aspirin for secondary prevention of atherosclerotic cardiovas- Bibliography cular disease should not be routinely stopped; if aspi- Gardner TB, Adler DG, Forsmark CE, et al. ACG clinical guideline: chronic pancreatitis. Am J Gastroenterol. 2020;115:322-339. [PMID: 32022720] rin is stopped, then it should be restarted as soon as doi:10.14309/ajg.0000000000000535 hemostasis is achieved. Bibliography Item 94 Answer: A Oakland K, Chadwick G, East JE, et al. Diagnosis and management of acute lower gastrointestinal bleeding: guidelines from the British Society of Educational Objective: Manage aspirin therapy after Gastroenterology. Gut. 2019;68:776-789. [PMID: 30792244] doi:10.1136/ lower gastrointestinal bleeding. gutjnl-2018-317807

Bibliography Item 94 Answer: A Oakland K, Chadwick G, East JE, et al. Diagnosis and management of acute lower gastrointestinal bleeding: guidelines from the British Society of Educational Objective: Manage aspirin therapy after Gastroenterology. Gut. 2019;68:776-789. [PMID: 30792244] doi:10.1136/ lower gastrointestinal bleeding. gutjnl-2018-317807 The most appropriate management is to discontinue aspirin indefinitely (Option A). The U.S. Preventive Services Task Item 95 Answer: C Force recommends low-dose aspirin for the primary preven Educational Objective: Evaluate for possible celiac tion of atherosclerotic cardiovascular disease (ASCVD) and disease. colorectal cancer in adults aged 50 to 59 years with a 10-year ASCVD risk of 10% or higher who do not have an increased The most appropriate diagnostic test to perform next is repeat- risk for bleeding. In those aged 60 to 69 years, the benefits ing the tissue transglutaminase IgA test after resumption of of aspirin use for primary prevention are smaller and the a gluten-containing diet (Option C). The patient is mostly 155

asymptomatic and has normal physical examination and labo- reduced rates of gallstone-related complications compared ratory findings. However, her celiac disease status is uncertain with cholecystectomy 25 to 30 days after hospital discharge because she has been maintaining a gluten-free diet for the (Option D). The diagnosis of acute pancreatitis requires two past year without having been tested for celiac disease. Her of the following three criteria: (1) acute-onset abdominal pain clinical improvement after starting a gluten-free diet may be characteristic of pancreatitis (severe, persistent for hours to due to celiac disease or to nonceliac gluten sensitivity, a clinical days, and epigastric in location, often radiating to the back), syndrome of unknown pathophysiology. Because gluten-con- (2) serum lipase or amylase levels elevated at least three times taining foods can also contain nonabsorbable carbohydrates, the upper limit of normal, and (3) characteristic imaging find such as fructans, they can cause gastrointestinal symptoms ings. Because acute pancreatitis is most commonly caused due to osmotic mechanisms, as well as fermentation by colonic by biliary disorders, patients with acute pancreatitis should bacteria. By definition, celiac disease must first be excluded undergo transabdominal ultrasonography. Transabdominal before nonceliac gluten sensitivity is diagnosed. Although the ultrasonography is preferred over CT for detection of gallstones > tissue transglutaminase IgA level is normal, the patient’s glu- because it has a higher sensitivity for detection of gallstones, = wn ten-free diet reduces the sensitivity of this serologic test. Celiac avoids the risks associated with intravenous contrast, and is = disease testing should therefore be repeated while the patient more cost-effective. Imaging during this patient’s hospitaliza C3) =e wn is on a gluten-containing diet; gluten should be reintroduced tion revealed multiple small gallstones in the gallbladder. Her » daily, preferably for 1 to 3 months before testing. common bile duct is normal in size and without choledocho- | Q. Although Clostridioides difficile colitis can cause lithiasis; therefore, it is likely that a stone has passed through QO the common bile duct. Gallstone-induced acute pancreatitis =p chronic diarrhea, the response of the patient’s symptoms to Pep a gluten-free diet make this diagnosis less likely. Therefore, can be caused by obstruction of the pancreatic duct or the 2 f= testing for this pathogen (Option A) is not indicated. ampulla, causing bile to reflux back into the pancreatic duct. @o wa Most patients with celiac disease carry HLA-DQ2 or Endoscopic retrograde cholangiopancreatography HLA-DQ8 genetic susceptibility; however, these genes can (ERCP) (Option A) may be considered in the setting of be found in up to 40% of the general population. Therefore, ascending cholangitis with choledocholithiasis or if ongoing genetic testing (Option B) can rule out disease but not confirm biliary obstruction is confirmed. The presence of cholangitis it. Genetic markers for celiac disease are stable throughout life, is manifested by fever, jaundice, and right-upper-quadrant regardless of one’s diet, and repeating testing for them is not abdominal pain and, in severely ill patients, hypotension and useful. A positive result on a serologic test for celiac disease altered mental status. Cholangitis is potentially life-threaten requires upper endoscopy with biopsies (Option D) from the ing, and antibiotic therapy targeting gram-negative Entero duodenum to confirm the disease. If biopsy results suggesting bacteriaceae should be administered. Identified common celiac disease are obtained before serologic testing, confirma- bile duct stones should be removed urgently with ERCP, after tory serologic testing should be performed. Findings on upper which elective cholecystectomy should be performed during endoscopy and biopsy may be normal in a patient with celiac the initial hospitalization or within 2 weeks to reduce the disease who has adhered to a gluten-free diet for the past year. risk for complications. This patient does not have cholangi Therefore, the most appropriate management is resumption of tis, choledocholithiasis, or biliary obstruction. a gluten-containing diet and follow-up serologic.testing. Endoscopic ultrasonography (Option B) and magnetic resonance cholangiopancreatography (Option E) may be considered if ongoing biliary obstruction is suspected. This ¢ Serologic testing for celiac disease must occur while patient requires neither examination because she is clini the patient is on a gluten-containing diet. cally improving, her laboratory values are normal, and the e Genetic testing for celiac disease with HLA-DQ2 or bile duct on ultrasonography is of normal caliber. These

asymptomatic and has normal physical examination and labo- reduced rates of gallstone-related complications compared ratory findings. However, her celiac disease status is uncertain with cholecystectomy 25 to 30 days after hospital discharge because she has been maintaining a gluten-free diet for the (Option D). The diagnosis of acute pancreatitis requires two past year without having been tested for celiac disease. Her of the following three criteria: (1) acute-onset abdominal pain clinical improvement after starting a gluten-free diet may be characteristic of pancreatitis (severe, persistent for hours to due to celiac disease or to nonceliac gluten sensitivity, a clinical days, and epigastric in location, often radiating to the back), syndrome of unknown pathophysiology. Because gluten-con- (2) serum lipase or amylase levels elevated at least three times taining foods can also contain nonabsorbable carbohydrates, the upper limit of normal, and (3) characteristic imaging find such as fructans, they can cause gastrointestinal symptoms ings. Because acute pancreatitis is most commonly caused due to osmotic mechanisms, as well as fermentation by colonic by biliary disorders, patients with acute pancreatitis should bacteria. By definition, celiac disease must first be excluded undergo transabdominal ultrasonography. Transabdominal before nonceliac gluten sensitivity is diagnosed. Although the ultrasonography is preferred over CT for detection of gallstones > tissue transglutaminase IgA level is normal, the patient’s glu- because it has a higher sensitivity for detection of gallstones, = wn ten-free diet reduces the sensitivity of this serologic test. Celiac avoids the risks associated with intravenous contrast, and is = disease testing should therefore be repeated while the patient more cost-effective. Imaging during this patient’s hospitaliza C3) =e wn is on a gluten-containing diet; gluten should be reintroduced tion revealed multiple small gallstones in the gallbladder. Her » daily, preferably for 1 to 3 months before testing. common bile duct is normal in size and without choledocho- | Q. Although Clostridioides difficile colitis can cause lithiasis; therefore, it is likely that a stone has passed through QO the common bile duct. Gallstone-induced acute pancreatitis =p chronic diarrhea, the response of the patient’s symptoms to Pep a gluten-free diet make this diagnosis less likely. Therefore, can be caused by obstruction of the pancreatic duct or the 2 f= testing for this pathogen (Option A) is not indicated. ampulla, causing bile to reflux back into the pancreatic duct. @o wa Most patients with celiac disease carry HLA-DQ2 or Endoscopic retrograde cholangiopancreatography HLA-DQ8 genetic susceptibility; however, these genes can (ERCP) (Option A) may be considered in the setting of be found in up to 40% of the general population. Therefore, ascending cholangitis with choledocholithiasis or if ongoing genetic testing (Option B) can rule out disease but not confirm biliary obstruction is confirmed. The presence of cholangitis it. Genetic markers for celiac disease are stable throughout life, is manifested by fever, jaundice, and right-upper-quadrant regardless of one’s diet, and repeating testing for them is not abdominal pain and, in severely ill patients, hypotension and useful. A positive result on a serologic test for celiac disease altered mental status. Cholangitis is potentially life-threaten requires upper endoscopy with biopsies (Option D) from the ing, and antibiotic therapy targeting gram-negative Entero duodenum to confirm the disease. If biopsy results suggesting bacteriaceae should be administered. Identified common celiac disease are obtained before serologic testing, confirma- bile duct stones should be removed urgently with ERCP, after tory serologic testing should be performed. Findings on upper which elective cholecystectomy should be performed during endoscopy and biopsy may be normal in a patient with celiac the initial hospitalization or within 2 weeks to reduce the disease who has adhered to a gluten-free diet for the past year. risk for complications. This patient does not have cholangi Therefore, the most appropriate management is resumption of tis, choledocholithiasis, or biliary obstruction. a gluten-containing diet and follow-up serologic.testing. Endoscopic ultrasonography (Option B) and magnetic resonance cholangiopancreatography (Option E) may be considered if ongoing biliary obstruction is suspected. This ¢ Serologic testing for celiac disease must occur while patient requires neither examination because she is clini the patient is on a gluten-containing diet. cally improving, her laboratory values are normal, and the e Genetic testing for celiac disease with HLA-DQ2 or bile duct on ultrasonography is of normal caliber. These HLA-DQ8 can rule out celiac disease but not confirm it. findings suggest that biliary obstruction is unlikely.

asymptomatic and has normal physical examination and labo- reduced rates of gallstone-related complications compared ratory findings. However, her celiac disease status is uncertain with cholecystectomy 25 to 30 days after hospital discharge because she has been maintaining a gluten-free diet for the (Option D). The diagnosis of acute pancreatitis requires two past year without having been tested for celiac disease. Her of the following three criteria: (1) acute-onset abdominal pain clinical improvement after starting a gluten-free diet may be characteristic of pancreatitis (severe, persistent for hours to due to celiac disease or to nonceliac gluten sensitivity, a clinical days, and epigastric in location, often radiating to the back), syndrome of unknown pathophysiology. Because gluten-con- (2) serum lipase or amylase levels elevated at least three times taining foods can also contain nonabsorbable carbohydrates, the upper limit of normal, and (3) characteristic imaging find such as fructans, they can cause gastrointestinal symptoms ings. Because acute pancreatitis is most commonly caused due to osmotic mechanisms, as well as fermentation by colonic by biliary disorders, patients with acute pancreatitis should bacteria. By definition, celiac disease must first be excluded undergo transabdominal ultrasonography. Transabdominal before nonceliac gluten sensitivity is diagnosed. Although the ultrasonography is preferred over CT for detection of gallstones > tissue transglutaminase IgA level is normal, the patient’s glu- because it has a higher sensitivity for detection of gallstones, = wn ten-free diet reduces the sensitivity of this serologic test. Celiac avoids the risks associated with intravenous contrast, and is = disease testing should therefore be repeated while the patient more cost-effective. Imaging during this patient’s hospitaliza C3) =e wn is on a gluten-containing diet; gluten should be reintroduced tion revealed multiple small gallstones in the gallbladder. Her » daily, preferably for 1 to 3 months before testing. common bile duct is normal in size and without choledocho- | Q. Although Clostridioides difficile colitis can cause lithiasis; therefore, it is likely that a stone has passed through QO the common bile duct. Gallstone-induced acute pancreatitis =p chronic diarrhea, the response of the patient’s symptoms to Pep a gluten-free diet make this diagnosis less likely. Therefore, can be caused by obstruction of the pancreatic duct or the 2 f= testing for this pathogen (Option A) is not indicated. ampulla, causing bile to reflux back into the pancreatic duct. @o wa Most patients with celiac disease carry HLA-DQ2 or Endoscopic retrograde cholangiopancreatography HLA-DQ8 genetic susceptibility; however, these genes can (ERCP) (Option A) may be considered in the setting of be found in up to 40% of the general population. Therefore, ascending cholangitis with choledocholithiasis or if ongoing genetic testing (Option B) can rule out disease but not confirm biliary obstruction is confirmed. The presence of cholangitis it. Genetic markers for celiac disease are stable throughout life, is manifested by fever, jaundice, and right-upper-quadrant regardless of one’s diet, and repeating testing for them is not abdominal pain and, in severely ill patients, hypotension and useful. A positive result on a serologic test for celiac disease altered mental status. Cholangitis is potentially life-threaten requires upper endoscopy with biopsies (Option D) from the ing, and antibiotic therapy targeting gram-negative Entero duodenum to confirm the disease. If biopsy results suggesting bacteriaceae should be administered. Identified common celiac disease are obtained before serologic testing, confirma- bile duct stones should be removed urgently with ERCP, after tory serologic testing should be performed. Findings on upper which elective cholecystectomy should be performed during endoscopy and biopsy may be normal in a patient with celiac the initial hospitalization or within 2 weeks to reduce the disease who has adhered to a gluten-free diet for the past year. risk for complications. This patient does not have cholangi Therefore, the most appropriate management is resumption of tis, choledocholithiasis, or biliary obstruction. a gluten-containing diet and follow-up serologic.testing. Endoscopic ultrasonography (Option B) and magnetic resonance cholangiopancreatography (Option E) may be considered if ongoing biliary obstruction is suspected. This ¢ Serologic testing for celiac disease must occur while patient requires neither examination because she is clini the patient is on a gluten-containing diet. cally improving, her laboratory values are normal, and the e Genetic testing for celiac disease with HLA-DQ2 or bile duct on ultrasonography is of normal caliber. These HLA-DQ8 can rule out celiac disease but not confirm it. findings suggest that biliary obstruction is unlikely. Bibliography ¢ Acute pancreatitis is most commonly caused by biliary Husby S, Murray JA, Katzka DA. AGA clinical practice update on diagnosis and monitoring of celiac disease-changing utility of serology and histo- disorders, and patients should undergo transabdominal logic measures: expert review. Gastroenterology. 2019;156:885-889. ultrasonography for the detection of gallstones. [PMID: 30578783] doi:10.1053/j.gastro.2018.12.010 ¢ For patients with mild gallstone pancreatitis, same- admission cholecystectomy can reduce rates of gallstone- Item 96 Answer: C related complications compared with cholecystectomy 25 to 30 days after hospital discharge. Educational Objective: Treat gallstone pancreatitis with early cholecystectomy. Bibliography The most appropriate management is laparoscopic cholecys- Crockett SD, Wani S, Gardner TB, et al; American Gastroenterological tectomy before hospital discharge (Option C). A multicenter, Association Institute Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on initial manage- randomized, controlled trial showed that for patients with ment of acute pancreatitis. Gastroenterology. 2018;154:1096-1101. [PMID: mild gallstone pancreatitis, same-admission cholecystectomy 29409760] doi:10.1053/j.gastro.2018.01.032

Bibliography ¢ Acute pancreatitis is most commonly caused by biliary Husby S, Murray JA, Katzka DA. AGA clinical practice update on diagnosis and monitoring of celiac disease-changing utility of serology and histo- disorders, and patients should undergo transabdominal logic measures: expert review. Gastroenterology. 2019;156:885-889. ultrasonography for the detection of gallstones. [PMID: 30578783] doi:10.1053/j.gastro.2018.12.010 ¢ For patients with mild gallstone pancreatitis, same- admission cholecystectomy can reduce rates of gallstone- Item 96 Answer: C related complications compared with cholecystectomy 25 to 30 days after hospital discharge. Educational Objective: Treat gallstone pancreatitis with early cholecystectomy. Bibliography The most appropriate management is laparoscopic cholecys- Crockett SD, Wani S, Gardner TB, et al; American Gastroenterological tectomy before hospital discharge (Option C). A multicenter, Association Institute Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on initial manage- randomized, controlled trial showed that for patients with ment of acute pancreatitis. Gastroenterology. 2018;154:1096-1101. [PMID: mild gallstone pancreatitis, same-admission cholecystectomy 29409760] doi:10.1053/j.gastro.2018.01.032 156