Browse the corpus

Cardiovascular Medicine Testing The ECG shows LV hypertrophy and left atrial enlargement. Deeply inverted, symmetric T waves in leads V, to V6 are present in the apical hypertrophic form of the disease (mimics ischemia). Echocardiography demonstrates the degree and distribution of hypertrophy and the degree of LVOT obstruction and mitral regurgitation. 48-Hour ambulatory ECG monitoring is performed. to evaluate for arrhythmias. Treatment Patients with HCM should avoid competitive sports and intense isometric exercise. B-Blockers are first-line agents for patients with an EF >50%, dyspnea, and/or chest pain. Calcium channel blockers (verapamil or diltiazem) may be substituted for p-blockers. Disopyramide may be added if significant symptoms related to LVOT obstruction remain. ACE inhibitors are used only ifsystolic dysfunction is present. Anticoagulate all patients with AF regardless of CHATDST-VASc score. Surgery or septal ablation is indicated for patients with an outflow tract gradient of >50 mm Hg and continuing slrnptoms despite maximal drug therapy. patients with previous sudden cardiac death or sustained VT should receive an ICD for secondary prevention. DOI{'T BE TRICKED . Avoid vasodilating p-blockers (carvedilol, labetalol, and nebivolol). . Electrophysiologic studies are not useful in predicting sudden cardiac death. . Do not prescribe digoxin, vasodilators, or diuretics, which increase LV outflow obstruction, for patients with HCM. Screening All first degree relatives of patients with HCM should undergo ECG and echocardiography plus genetic counseling (if sarcomeric mutation is identified in index case). Genetic testing may disclose genotype positive persons who do not express clinical fea- tures of HCM, and ongoing screening is recommended because of the possibility of disease expression at any age. In the absence of a documented genetic mutation in the proband, ongoing screening of first-degree relatives is not indicated. Hypeilrophic Grdiomyopathy: Ihe ECG shows ST-segment depression and deeply inveted T waves (arorvs) in the precordial leads, consistent with marked apical hypertrophy. 11

Endocrinology and Metabolism Look for symptoms of posterior pituitary dysfunction: o polydipsia, polyuria, and nocturia (DI secondary to ADH deficiency) Testing Pituitary hormone deficiency is confirmed by documenting target-organ hormone deficiency and a corresponding low or "normal" serum pituitary hormone level. Stimulation testing may be needed to document hypopituitarism. STUDY TABIE: Key Hormone Tests for Pituitary Hormone Deficiency Pituitary Hormone Peripheral Hormone lnitial Test(s) ConfirmatoryTest ACTH Cortisol Simultaneous 8 arr,l ACTH, cortisol ACTH stimulation test LH and FSH Testosterone or estradiol Simultaneous LH, FSH, B au total testosterone (ma le), estradiol (female) TSH Thyroxine, triiodothyronine Simultaneous TSH, free (or total) thyroxine GH IGF-1 IGF-1 GHRH-arginine lnsulin tolerance Glucagon stimulation Ghrelin agonist stimulation GHRH = growth hormone releasing hormone. After documenting pituitary hormone deficiency, select dedicated pituitary MRI. DOil'T BE TRICKED . It is not necessary to measure serum FSH/LH levels in women who have normal menstrual cycles. Treatment Patients with panhypopituitarism require daily thyroxine and cortisol replacement. Androgen replacement is appropriate for men with hypogonadism, and estrogen replacement is used for premenopausal women with hypogonadism. GH replacement is rarely indicated. DON'T BE TRICKED . Thyroxine dosing for central hypothyroidism is based on serum free To rather than TSH levels. . To replacement is indicated only after hypoadrenalism has been ruled out or treated.

Treatment Patients with panhypopituitarism require daily thyroxine and cortisol replacement. Androgen replacement is appropriate for men with hypogonadism, and estrogen replacement is used for premenopausal women with hypogonadism. GH replacement is rarely indicated. DON'T BE TRICKED . Thyroxine dosing for central hypothyroidism is based on serum free To rather than TSH levels. . To replacement is indicated only after hypoadrenalism has been ruled out or treated. TESTYOURSELF A 65-year-old man was diagnosed with SCLC 20 years ago and received chemotherapy and chest and cranial irradiation. Physical examination shows hypotension, tachycardia, and small testes. Serum sodium is 123 mEq/L. ANSWER: For diagnosis, choose hypopituitarism. For management, select immediate replacement with stress doses of hydrocor- tisone followed by confirmatory testing. Pituitary Adenomas Diagnosis Pituitary adenomas are benign tumors that originate from one of the different anterior pituitary cell ffpes. They are classified based on size as microadenomas (<rO mm) or macroadenomas (>10 mm). 55

General lnternal Medicine Testing Consider the appropriate indications for the following diagnostic tests: . Orthostatic blood pressure measurements: Done in all patients immediately after standing and again in 3 minutes. . ECG: Done in all cases. The finding of an arrhythmia and conduction block may establish the diagnosis, but a normal ECG does not rule out a cardiac cause. r Echocardiography: Obtain only if structural heart disease is suspected. r Ambulatory ECG recording: Indicated if cardiac arrhythmia is suspected or the cause is unclear. The choice of the recording device is determined by the frequency of the patient's symptoms (see Cardiovascular Medicine, Palpitations and Syncope). . Stress testing: Indicated for patients with exercise-associated syncope or those with significant risks for ischemic heart disease. o Carotid sinus massage: For suspected carotid sinus syncope or for unexplained syncope in those aged >60 years. . Tilt table testing: Most commonly used in patients with recurrent vasovagal syncope or if delayed orthostatic hypotension is suspected. . Electrophysiologic testing: Rarely helpful and almost always the incorrect answer. DO]I'I BE TRICKED o Do not order carotid vascular studies to diagnose cause of syncope. . Do not order brain imaging, cardiac enzymes, or EEG to evaluate syncope. Treatment Treatment of structural cardiac disease and arrhythmias is covered in the Cardiovascular Medicine section. Leg crossing, squatting, or handgrip maneuvers may be beneficial for vasovagal syncope with a prolonged prodrome. For recurrent neurocar- diogenic syncope, choose p-blockers. For hypovolemia or orthostatic syncope, eliminate o- and p-blockers, diuretics, and anticholinergic agents, if possible. Increase fluid and sodium intake, and consider compression stockings. As a last resort, add mineralocorticoids and a-adreneqgic receptor agonists. TESTYOURSETF An lS-year-old woman fainted while standing in line to purchase concert tickets. She felt 'woozy" and became pale and sweaty before fainting. Friends observed jerking motions of her face and fingers. ANSWER: For diagnosis, choose vasovagal syncope. Chronic Noncancer Pain Diagnosis Psychological screening for depression, anxiety, and somatization is an important adjunct to a thorough history and physical examination.

TESTYOURSETF An lS-year-old woman fainted while standing in line to purchase concert tickets. She felt 'woozy" and became pale and sweaty before fainting. Friends observed jerking motions of her face and fingers. ANSWER: For diagnosis, choose vasovagal syncope. Chronic Noncancer Pain Diagnosis Psychological screening for depression, anxiety, and somatization is an important adjunct to a thorough history and physical examination. Treatment Evidence-based nondrug treatment most commonly includes: o exercise o physical therapy . CBT 123

lnfectious Disease . Ieukopeniaandthrombocl,topenia . presence of morulae (clumps of organisms in the cytoplasm of the appropriate leukocyte) Testing Select whole blood PCR for diagnosis of acute infection. Antibodies are negative in early disease. DOil'T BE TRICKED (*-. . HGA is transmitted by the same vector as Lyme disease and babesiosis, so double or triple infection is possible. Treatment H' 'i: "' , .:. IV or oral doxycycline is the treatment of choice for HME Human Granulocytic Ehrlirhiosis: HME (/eft) and HGA (rgh|; demonstration of and HGA. morulae recognized as clumps of organisms in the cytoplasm. Rocky Mountain Spotted Fever Diagnosis Rocky Mountain spotted f'ever is a tick borne rickettsial infection most prevalent in the southeastern and south central states. Look for a history of tick bite and recent travel to an endemic area; febrile illness in spring and summer months; and symptoms such as nausea, myalgia, dyspnea, cough, and headache. Also look for a macular rash starting on the ankles and wrists and often affecting the palms and soles of the feet; lesions spread centripetally and become petechial. DOI{'T BE TRICKED . The Rocky Mountain spotted fever rash may not be present until 3 days after onset of illness. Testing Thrombocytopenia and elevated aminotransferase levels are characteristic. Serologr is negative during acute infection Immunohistochemistry or PCR of a skin biopsy specimen allows diagnosis at the time of acute infection. Treatment Empiric treatment is often necessary. Select doxycycline. In patients who are pregnant, choose chloramphenicol. Nonresponse in 72 hours suggests an alternative diagnosis. Cystitis Prevention Screen for and treat asymptomatic bacteriuria only in patients who are'pregnant or are about to undergo an invasive urologic procedure. 231

lnfectious Disease Testing Pearls about RPR and VDRL tests: . often negative in primary infection o positive in high titers in secondary syphilis . lower titers are seen in latent and tertian'infection Confirm positive nontreponemal test (RPR or VDRL) with specific treponemal test (fluo rescent treponemal antibody absorption test [FTA ABS], Treponema pallidum particle agglutir.ration ITPPAJ assay, T. pallidunt enzyme immunoassay [TP EIA]). Alternatively, use a "reverse" strategy, starting with a positive specific treponemal test and confirm with a nontreponemal test. If RPR or VDRL are negative. confirm or exclude infection r,r,ith a second specific treponemal test. Nontreponemal tests should decrease in titer after treatment (but will rise again in the setting of reinfection); the FTA ABS will remain positive indeflnitely. Test all p:rtients for HIV inlection. Perform a CSF examination for patients with primary or secondary syphilis with any neurologic sign or symptom. Diagnose neurosyphilis u,hen any one of the follort,ir.rg is present . CSF lymphocytes >s/pl. . elevated CSF protein o positive CSF VDRL test Syphilis: Primary syphilis is characterized by a clean'based, nonpainful genital ulcer (chancre). Treatment . 'l reat primary secondary or early latent syphilis with one dose of lM benzathine penicillin. . 'freat late latent or asymptomatic syphilis of unknown duration rt,ith three r,r,e.ekly doses of benzathine penicillin. Doxycycline and tetracy'cline are alternatives for syphilis not involving the CNS ir.r penicillin allergic. nonpregnant patients. DON'T BE TRICKED . Pregnant patients who are allergic to penicillin must be ,fxdfriea&a*;I': desensitized and treated with penicillin. . The Jarisch Herxheimer reaction is an acute febrile illness occurring within 24 hours of treatment for any stage of syphilis and is not an allergic reaction to penicillin. Seondary Syphilis: Pink to reddish brown macules and papu les on the palms are tharacteristir of secondary syphilis. 242

tnfectious Disease Testing The diagnosis is established by immunofluorescent monoclonal antibody stain or silver stain examination of induced sputum or a bronchoscopic sample showing characteristic cysts. DOil'T BE TRICKED . The most common cause of a pneumothorax in a patient with AIDS is P. jirouecii pneumonia. . P. jirouecii pneumonia may occur in patients not infected with HIV, typically in association with immunosuppressant drug therapy. Treatment Select 3 weeks of treatment with: . high-dose trimethoprim-sulfamethoxazole o glucocorticoids within 72 hours for A-a >35 mm Hg or arterial Po2<7O mm Hg TESTYOURSELF A 45 year old man with HIV and a CD4 cell count of 100/pL has had 3 weeks of dry cough and progressive dyspnea on exertion, now present at rest. On examination, his temperature is 38.3 'C (100.9 "F) and Po, is 67 mm Hg breathing ambient air. His chest x-ray shows diffuse bilateral infiltrates. ANSWER: For diagnosis, choose presumed P jirouecii pneumonia; for management, choose empiric treatment with IV trimethoprim- sulfamethoxazole and glucocorticoids. Mycobacterium avium Complex I nfection Diagnosis Disseminated MAC infection develops in patients with HIV who have CD4 cell counts <50/pL and are not receiving MAC prophy- laxis. The clinical presentation often consists of fever, night sweats, weight loss, and GI symptoms. Treatment Treatment for MAC infection usually consists of azithromycin with ethambutol and either rifampin or rifabutin. Toxoplasmosis Diagnosis and Testing Immunocompetent persons with primary infection are usually asymptomatic, but latent infection may persist, and reactivation of the infection is a risk if the person becomes immunocompromised. Look for: . encephalitis, chorioretinitis, or pneumonitis in immunocompromised patients . any focal neurologic syndrome, acute or subacute . mononucleosis like syndrome 255

lnfectious Disease STUDY TABLE: Differential Diagnosis of CerebralToxoplasmosis in lmmunocompromised Patients Diagnosis Characteristics Lymphoma (primary CNS, Often a solitary lesion is located in the periventricular or periependymal area or in the corpus B-cell lymphoma) callosum Neither clinical nor neuroradiologic findings reliably distinguish lymphoma from toxoplasmosis Brain biopsy is diagnostic Progressive mu ltifocal Dementia is often the presenting symptom leu koencep ha lopathy Typically nonenhancing, hypodense white matter lesions without mass effect. CD4 cell counts are usually <50/pL, and PCR of CSF may show JC virus Brain biopsy is diagnostic Select IgG serologic testing in patients with suspected toxoplasmosis and brain MRI for neurologic signs and symptoms. Typical findings on imaging include multiple ring.enhancing lesions. Treatment Select empiric treatment with sulfadiazine, pyrimethamine, and folic acid in patients with multiple ring enhancing lesions, positive Toxoplasma gondii serologic test results (lgG), and immune suppres- sion (CD4 cell count <200/gL). Biopsy lesions that f'ail to respond to 2 weeks of empiric therapy. lntraterebral foxoplasmosis: MRI showing a single ring enhancing brain lesion associated with edema consistent with toxoplasmosis. Most patients with AIDS and cerebral toxoplasmosis have multiple ring'enhancing brain lesions. lnfluenza Virus : Prevention See General Internal Medicine, Screening and Prevention. For institutional outbreaks, vaccinate staffmembers and residents not already immunized and give chemoprophylaxis with zanamivir or oseltamivir for at least 2 weeks fbllowing immunization.

lnfluenza Virus : Prevention See General Internal Medicine, Screening and Prevention. For institutional outbreaks, vaccinate staffmembers and residents not already immunized and give chemoprophylaxis with zanamivir or oseltamivir for at least 2 weeks fbllowing immunization. DO]II,T BE TRICKED . Do not administer live attenuated influenza vaccine to persons who have close contact with immunocompromised patients. I l '| . Diagnosis and Testing During November through April, look for acute onset of high fever. headache, fatigue, nonproductive cough, sore throat, nasal congestion, rhinorrhea, and myalgia. PCR is preferred to rapid antigen testing in patients for whom results would influence management (e.g., initiating antiviral treatment, performing other diagnostic testing, or inpatient infection control measures). During times of inf'luenza activig, test fbr influenza at hospital admission in all patients with acute respiratory infection and in patients with acute worsening of chronic cardiopulmonary disease. In these cases, treatment decisions should not be delayed pending confirmatory results. The most common complications of influenza are primary influenza pneumonia and secondary bacterial pneumon ia (St re pto cocc us p ne umoniae, Staphy I ococcus o u reus). 256

I lnfectious Disease I Treatment I i In addition to standard precautions in hospitalized patients, droplet precautions should be used for all patients with suspected t influenza. Treat all hospitalized patients with confirmed infection and outpatients at high risk for severe disease. Select I baloxavir, zanamivir, or oseltamivir, which are active against influenza A and B. peramivir is available for IV administration. I fusk factors for severe disease: . immunosuppression (highest risk) . chronic pulmonary disease (highest risk) I r age >64 years . pregnancy (or delivery within 2 weeks) I o diabetes . significant cardiovascular, kidney, liver, or hematologic disease . BMI >40 DON'T BE TRIGKED . Do not administer amantadine or rimantadine to prevent or treat influenza virus because of the high rate of resistance. o Zanamivir (inhaled) has been associated with bronchospasm and is contraindicated in patients with pulmonary or cardiovascular disease. : : TESTYOURSETF A 68-year-old woman with diabetes is admitted to the hospital in November with the acute onset of fever, chills, nonproductive cough, and fatigue. Her 6-year-old granddaughter has had similar symptoms for 3 days. ANSWER: For diagnosis, choose influenza; obtain PCR confirmatory test; for treatment, select immediate initiation of oseltamivir, I baloxavir, or zanamivir. I I t I I t Primary Varicella lnfection I I Patients present with a febrile pruritic vesicular rash (lesions in various stages of development) affecting the skin and mucocu L I I taneous surfaces. t I I tI Testing I I Varicella can be diagnosed clinically by the typical vesicular rash and confirmed with VZV PCR testing. i I t

t Primary Varicella lnfection I I Patients present with a febrile pruritic vesicular rash (lesions in various stages of development) affecting the skin and mucocu L I I taneous surfaces. t I I tI Testing I I Varicella can be diagnosed clinically by the typical vesicular rash and confirmed with VZV PCR testing. i I t Epstein-Barr Virus Diagnosis EBV is the primary agent of infectious mononucleosis and is associated with the development of B-cell lymphoma, T-cell lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. Another EBV manifestation is oral hairy leukoplakia that characteristically affects the lateral portions of the tongue as white corrugated painless plaques. Oral hairy leukoplakia is most commonly associated with underlying HIV infection. 257

lnfectious Disease Typical symptoms in patients with acute infectious mononucleosis include: o severe fatigue, headache, and sore throat . fever associated with posterior cervical lymphadenopathy . splenomegaly o reactive lymphocytosis Consider EBV infection in all patients with aseptic meningitis or encephalitis, hepatitis, hemoly'tic anemia' and thromborytopenia' DON'T BETRICKED . The morbilliform rash appearing in patients with infectious mononucleosis following the administration of ampicillin is not an allergic reaction; patients can subsequently use ampicillin without rash recurrence' Testing Select a Monospot test (heterophile antibody test), which is specific but not very sensitive early in disease' If the Monospot test is negative, repeat in 2 weeks or select EBV serologr. Infectious mononucleosis syndrome may also be caused by CMV or HIV infection; it is often not possible to make a clinical diagnosis, and serologic testing is necessary. STUDY TABLE: Epstein-Barr Virus Serology Condition Antibody Acute primary infection Elevated VCA lgM, VCA lgG, and EA lgG Low or undetectable EBNA-1 lgG Past infection Undetectable VCA lgM and EA lgG Elevated VCA lgG and EBNA-1 lgG EA = early antigen; EBNA = Epstein'Barr nuclear antigen; VCA = viral capsid antigen. Treatment Supportive care is typically sufficient. Select glucocorticoids only ifairway obstruction or another life-threatening condition, such as hemoly-tic anemia, is present. DON'T BE TRICKED . Do not prescribe antiviral drugs for treatment of infectious mononucleosis TEST YOURSELF An l8-year-old female soccer player has malaise, anorexia, and a sore throat for 3 days. She has exudative pharyngitis, tender ante- rior and posterior cervical lymph nodes, and fullness in her left upper abdominal quadrant. Leukoclte count is 8500/pL with moderate atypical lymphocytes. ANSWER: For diagnosis, choose infectious mononucleosis. For management, select contact sport avoidance because of the risk of splenic rupture in the setting of splenomegaly. 258

Nephrology Glomerular Filtration Rate At high levels of GFR, small changes in the serum creatinine may reflect large changes in GFR. At low levels of GFR, large changes in the serum creatinine reflect relatively smaller changes in GFR. Serum cystatin C is an alternative marker of GFR less influenced than serum creatinine by age, sex, muscle mass, and body weight; it is more sensitive than serum creatinine in identi8zing milder decrements in kidney function. i Conditions that decrease kidney perfusion and urine flow, such as hypovolemia or HE, are associated with increased resorption of urine urea nitrogen in the proximal tubules, resulting in a disproportionate increase in the BUN creatinine ratio, typically to 20:1 or higher. DON'T BE TRICKED i I I . A reduction or loss of muscle mass because of advanced age, liver failure, or malnutrition may cause a disproportionately I low serum creatinine concentration, which results in overestimation of the GFR. I o When the MDRD study equation is used to estimate GFR, higher levels of GFR are reported only as >60 ml/min 11.73 m2, I but this does not guarantee an absence ofstructural kidney disease. I t I I L Urinalysis L I Proteinuria t Albumin is the only protein that is detected on dipstick urinalysis. t I I Protein detected by urine dipstick should always be quantified with either a 24 hour urine collection or protein-creatinine or albumin creatinine ratio on random urine samples. t The albumin-creatinine ratio measures only albumin in the urine and is used to evaluate diabetic kidney disease: S . 30 to 300 mg/g defines moderately increased albuminuria. . >300 mg/g defines seuerelg increased albuminuria. A protein-creatinine ratio can be used to measure proteinuria (abnormal protein creatinine ratio defined as >150 mg/g). Proteinuria is a marker of renal parenchymal and glomerular disease and an independent predictor of progressive kidney disease, cardiovascular disease, and peripheral vascular disease.

I Protein detected by urine dipstick should always be quantified with either a 24 hour urine collection or protein-creatinine or albumin creatinine ratio on random urine samples. t The albumin-creatinine ratio measures only albumin in the urine and is used to evaluate diabetic kidney disease: S . 30 to 300 mg/g defines moderately increased albuminuria. . >300 mg/g defines seuerelg increased albuminuria. A protein-creatinine ratio can be used to measure proteinuria (abnormal protein creatinine ratio defined as >150 mg/g). Proteinuria is a marker of renal parenchymal and glomerular disease and an independent predictor of progressive kidney disease, cardiovascular disease, and peripheral vascular disease. DO]I'T BE TRICKED . Dipstick urinalysis does not detect immunoglobulin light chains associated with multiple myeloma. . Because moderately increased albuminuria may go undetected by dipstick, direct quantification using a random (spot) protein-creatinine ratio or albumin-creatinine ratio is required when screening patients at high risk. o Positional (orthostatic) proteinuria, a benign cause of isolated proteinuria, is diagnosed by obtaining split daytime (standing) and nighttime (supine) urine collections. 2s9

Neurology Testing Noncontrast CT establishes the diagnosis of SAH in >90% of patients. Cerebral angiography identifies the aneurysm and determines man- agement. Other causes of abrupt severe headache include arterial dis section and venous sinus thrombosis, both of which may be detected with vascular imaging, pituitary apoplexy, reversible cerebral vasocon striction syndrome, and ICH. DOil'T BE TRICKED . If the CT scan is normal, always select CSF examination to look for erythrocytes or xanthochromia. Treatment The three main neurologic complications for a patient with SAH are rebleeding, delayed brain ischemia from vasospasm, and hydrocepha- lus. To manage these complications, do the following: o Treat ruptured aneurysms with surgical clipping or endovascular coiling within 48 to 72 hours. . Maintain BP <140/80 mm Hg to prevent rebleeding. r Select oral nimodipine for 21 days to prevent vasospasm and improve neurologic outcomes. Any change in mental status should prompt emergency CT to evaluate for repeat bleeding and for signs of hydrocephalus, which is treated with ventricular drainage. Screening transcranial ultrasonography or CTA is used to detect cerebral vasospasm. Subhyaloid Hemorrhage: Bleeding under the vitreous membrane (sub' hyaloid hemonhage) is a finding associated with SAH. TEST YOURSELF A 44 year-old woman comes to the emergency department reporting "the worst headache of my life." She has meningismus but no focal neurologic findings. CT scan is normal. ANSWER: For diagnosis, choose SAH. For management, select CSF examination. I ntracerebral Hemorrhage Diagnosis The most common risk factor for ICH is hypertension. Other risk factors include amyloid angiopathy (primarily in older adult patients with lobar hemorrhage), coagulopathy, vascular malformations, and the use of cocaine or alcohol. ICH cannot be reliably distinguished from ischemic stroke by clinical criteria alone. CT without contrast establishes the diagnosis.

I ntracerebral Hemorrhage Diagnosis The most common risk factor for ICH is hypertension. Other risk factors include amyloid angiopathy (primarily in older adult patients with lobar hemorrhage), coagulopathy, vascular malformations, and the use of cocaine or alcohol. ICH cannot be reliably distinguished from ischemic stroke by clinical criteria alone. CT without contrast establishes the diagnosis. Treatment Identiff and reverse anticoagulation. For warfarin-associated ICH, IV vitamin K lntracerebral Hemorrhage: CI scan of the brain shows a and 4f PCC should be given. For patients taking an oral direct Xa inhibitor, stop hemorrhage in the left basal ganglia. 297

Oncology Testing 'l'he initial diagnostic procedure is upper endoscopy. pEl c'l scans are used to identify the presence of regional and metastatic disease. DON'T BE TRICKED . Always obtain upper endoscopy and biopsy in a patient with "achalasia', to rule out gastric cancer Treatment Surgery is the primary treatment fbr locoregional disease. Survival is improved with chemotherapy or combined chemotherapy and radiation therapy. Up to 25'7, of gastric cancers overexpress the HER2 growth factor receptor. In these patients with metastatic clisease, add trastuzumab. Use antibiotic and PPI therapy lbr early stage MALT lymphoma of the stomach and evidence of Helicobacter pulori intection. Colorectal Cancer Screening Average risk: See General Internal Medicine chapter fbr USPSI'F recommended screening. High risk: The risk for colorectal cancer is elevated in inflammatory bowel disease; patients with pancolitis are at highest risk, whereas risk is negligible in patients with proctitis. Risk is also incre:rsed with longer duration oldisease and coexistent PSC. The following is a list of the most common hereditary syndromes Familial adenomatous polyposis is an autosomal dominant disorder that requires prophylactic colectomy. Gardner syndrome is a type of familial adenomatous polyposis with extraintestinal manif'estations, including osteomas, duo denal ampullary tumors, thyroid cancers, and medulloblastomas. Lynch syndrome is diagnosed if'a patient has an identified germline mutation in one or more mismatch repair genes. Lynch syndrome is an autosomal dominant disorder, and patients and family members should be offered genetic counseling and intense cancer surveillance. Lynch syndrome is also associated with an increased risk for extracolonic tumors, most com- monly endometrial.

Lynch syndrome is diagnosed if'a patient has an identified germline mutation in one or more mismatch repair genes. Lynch syndrome is an autosomal dominant disorder, and patients and family members should be offered genetic counseling and intense cancer surveillance. Lynch syndrome is also associated with an increased risk for extracolonic tumors, most com- monly endometrial. STUDY TABLE: Screening for Colorectal Cancer in lndividuals at Elevated Risk Risk Category Criteria Screening Recommendations (Age; Modality; lnterval) lncreased Family history of CRC: CRC diagnosed in FDR age <60 years Begin at age 40 years or 1 0 years earlier than age of youngest FDR at or >2 FDRs at any age diagnosis, whichever comes first; colonoscopy; repeat every 5 yearsu CRC diagnosed in FDR age >60 years Begin at age 40 years; any modality; repeat every 10 years" Personal history of CRC Perform at time of diagnosis; colonoscopy; repeat at 1 year, 3 years, and, if normal, every 5 years thereafter until risks outweigh benefit of continued screening Adult patients with cystic fibrosis Cystic Fibrosis Foundation recommends beginning CRC screening at age 40 years in individuals with cystic fibrosis, with continued rescreening every 5 years (Continued on the next page) 317

Oncology Testing After discovery of a testicular mass, select scrotal ultrasonography. Select inguinal orchiectomy for histopathologic examina tion. Other studies include chest x-ray; CT of the abdomen and pelvis; and measurement of the B-hCG, LDH, and AFp levels. . An elevated serum AFP level always indicates the tumor has a nonseminomatous component. o hCG may be present in seminomatous or nonseminomatous tumors. Any testicular cancer that has a nonseminomatous component based on histologic examination or the presence of an elevated serum AFP level is treated as a nonseminoma. DOil'T BETRICI(ED . Do not select testicular biopsy Treatment Select semen cryopreservation for men before they undergo therapy for testicular cancer. Inguinal orchiectomy is the initial step in treatment for all testicular tumors. Additional treatment modalities are determined by tumor histologz and clinical stage. Seminoma . Observation following orchiectomy is an option in low-risk, early-stage seminomas (stage I disease). When treatment is selected, one to tvvo cycles ofcarboplatin chemotherapy are offered. . Cisplatin-based chemotherapy or radiation therapy is recommended for patients with retroperitoneal lymph node metastases. . Chemotherapy (cisplatin based) is recommended for extensive lymph node involvement or higher stage disease. PET scan/CT can be used to determine whether postchemotherapy residual masses require resection. Residual masses that are PET scan-positive are resected. Nonseminoma . Following orchiectomy, localized disease (stage I) can be managed with active surveillance, one cycle of cisplatin-based chemotherapy, or retroperitoneal lymph node dissection. . Cisplatin-based chemotherapy is indicated for patients with positive lymph nodes or persistent tumor marker elevation, even for those with normal imaging studies. . For patients with advanced disease or bulky retroperitoneal lymphadenopathy identified on CT, cisplatin-based chemo- therapy is recommended. . Any residual masses after chemotherapy are resected. Follow-up Men treated with chemotherapy are at long-term risk for cardiovascular disease, metabolic syndrome, pulmonary toxicity, hypogonadism, infertility, CKD, and neurotoxicity. The risk for a second solid tumor is also increased.

Nonseminoma . Following orchiectomy, localized disease (stage I) can be managed with active surveillance, one cycle of cisplatin-based chemotherapy, or retroperitoneal lymph node dissection. . Cisplatin-based chemotherapy is indicated for patients with positive lymph nodes or persistent tumor marker elevation, even for those with normal imaging studies. . For patients with advanced disease or bulky retroperitoneal lymphadenopathy identified on CT, cisplatin-based chemo- therapy is recommended. . Any residual masses after chemotherapy are resected. Follow-up Men treated with chemotherapy are at long-term risk for cardiovascular disease, metabolic syndrome, pulmonary toxicity, hypogonadism, infertility, CKD, and neurotoxicity. The risk for a second solid tumor is also increased. TESTYOURSELF A 28-year-old man with nonseminoma testicular cancer is treated with orchiectomy and chemotherapy. Following chemotherapy, persistent retroperitoneal lymph nodes are noted on imaging studies. ANSWER: For management, select retroperitoneal lymph node resection. 325

Pulmonary and Critical Care Medicine . occupation and environmental exposure history (e.g., automobile mechanics, ship builders, and asbestos exposure) . connective tissue disorders review of symptoms . exposure to drugs and/or radiation Testing Desaturation >4?, with ambulation is consistent with a diffusion limitation. a hallmark of DPLD. Look for interstitial reticular or nodular infiltrates on chest x-ray; the [zpe and pattern of the infiltrate often correlate with underlying pathologz on lung biopsy. Look for restrictive or combined restrictive/obstructive findings on PFTs and low Dlco measurement. Obtain chest HRCT, even if chest x-ray is normal, if clinical suspicion is high. Look lbr presence of mediastinal andior hilar lymphadenopathy (sarcoidosis), pleural effusion (asbestos or connective tissue related DPLD), and pleural plaques (asbestosis). Testing for CRB ESR, ANA, RF, myositis panel, and anti CPP antibodies is recommended. DOil'T BE TRICKED . Patients with dyspnea for days or weeks (vs months) are more likely to have pneumonia or HF than DPLD. . Plain radiography may be normal in2o% of patients with early DPLD; continue evaluation if suspicion remains high' e Consider DPLD in patients with dyspnea and pulmonary crackles but no other findings of HF' Treatment (drug discon When possible, treatment is clirected toward the underlying cause (connective tissue disease), limiting exposure tinuation), and smoking cessation. The evidence lor glucocorticoid efficacy is weak' Acute Hypersensitivity Pneumonitis Diagnosis (e'g'' agricultural dusts' thermophilic fungi' bacteria) Hypersensitivity pneumonitis occurs through organic antigen exposure Fever, cough, and fatigue develop t2 hours later' Physical examination reveals inspiratory crackles' Testing and ground' disease' HRCT shows diffuse centrilobular micronodules Chest x ray may be normal or show diffuse micronodular glass opacities.

Testing and ground' disease' HRCT shows diffuse centrilobular micronodules Chest x ray may be normal or show diffuse micronodular glass opacities. Treatment 48 hours' Glucocorticoids are provided for severe symptoms' Antigen removal results in resolution of symptoms in 345