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Walk the Even Hospital Database by book and chapter — the raw source passages that ground Ask, DDx, and the rest.
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Hair follicles and their keratinized product, hair, are skin appendages present on nearly every part of the body. Areas of the body typically devoid of hair include the palmar and plantar surfaces, lips, and urogenital orifices. Sex hormones influence the distribution, texture, and color of hair. Hair follicles and hair are both multifunctional. Hair follicles generate hair and help to provide epithelial stem cells used for wound repair. Besides the cosmetic concerns of hair color, growth, and distribution, hair plays a vital role in thermoregulation, tactile sensation, and ultraviolet (UV) radiation protection. Diseases of hair follicles and hair are an important concern to the general population and have been an active topic of research in recent years.
Knowledge of hair follicle structure and the hair cycle is vital in the understanding of hair disorders.[10] There are three distinct phases of the hair cycle: anagen, catagen, and telogen. The anagen phase is the growth phase, which lasts for a period of roughly 2 to 7 years, depending on the individual. The length of this period determines hair length. The anagen phase begins in the dermal papilla which provides vital blood supply and nutrition for the growing hair. Hair grows at a rate of 1 centimeter per month. The catagen phase marks a transitional period from growth to rest periods. The hair detaches from its blood supply during the catagen phase, which usually lasts about 2 weeks. The final or resting phase, the telogen phase, reflects a period of relative quiescence lasting up to 4 months. The telogen phase results in hair shedding.
Knowledge of hair follicle structure and the hair cycle is vital in the understanding of hair disorders.[10] There are three distinct phases of the hair cycle: anagen, catagen, and telogen. The anagen phase is the growth phase, which lasts for a period of roughly 2 to 7 years, depending on the individual. The length of this period determines hair length. The anagen phase begins in the dermal papilla which provides vital blood supply and nutrition for the growing hair. Hair grows at a rate of 1 centimeter per month. The catagen phase marks a transitional period from growth to rest periods. The hair detaches from its blood supply during the catagen phase, which usually lasts about 2 weeks. The final or resting phase, the telogen phase, reflects a period of relative quiescence lasting up to 4 months. The telogen phase results in hair shedding. Alopecia has many variants that are categorized as scarring and non-scarring.[11] Telogen effluvium is usually a self-limiting disorder of hair loss caused by periods of increased stress in which excessive amounts of hairs (roughly 25% to 50%) prematurely enter the telogen phase simultaneously. The resultant hair loss occurs 2 or 4 months after an inciting event.[12] Anagen effluvium is a similar disorder that is most commonly due to chemotherapy agents.[13] Alopecia areata results from the autoimmune destruction of hair follicles. The actions of androgens, specifically dihydrotestosterone (DHT), in androgenic alopecia cause hair follicle miniaturization, shortening of the anagen phase, and hair loss occurs. Physicians distinguish alopecia, telogen effluvium, and trichotillomania on history and physical exam using observation and the hair pull test. Trichotillomania is a repetitive, impulsive hair-pulling disorder that results in visibly broken hair strands in various areas of the body. Some patients may also eat the hair they pull, which can lead to gastrointestinal complaints.[14] Traction alopecia is another behavioral variant due to tightly pulled hairstyles as seen in gymnasts. Lupus is a systemic disease that may cause either scarring (i.e., discoid lupus) or non-scarring forms of alopecia. A thorough history and physical is required to detect less common causes of alopecia, such as syphilis. Secondary syphilis classically causes "moth-eaten" alopecia.[15] Tinea capitis is an important consideration in pediatric populations as a fungal invasion of the hair shaft results in patches of hair loss.[16]
Alopecia has many variants that are categorized as scarring and non-scarring.[11] Telogen effluvium is usually a self-limiting disorder of hair loss caused by periods of increased stress in which excessive amounts of hairs (roughly 25% to 50%) prematurely enter the telogen phase simultaneously. The resultant hair loss occurs 2 or 4 months after an inciting event.[12] Anagen effluvium is a similar disorder that is most commonly due to chemotherapy agents.[13] Alopecia areata results from the autoimmune destruction of hair follicles. The actions of androgens, specifically dihydrotestosterone (DHT), in androgenic alopecia cause hair follicle miniaturization, shortening of the anagen phase, and hair loss occurs. Physicians distinguish alopecia, telogen effluvium, and trichotillomania on history and physical exam using observation and the hair pull test. Trichotillomania is a repetitive, impulsive hair-pulling disorder that results in visibly broken hair strands in various areas of the body. Some patients may also eat the hair they pull, which can lead to gastrointestinal complaints.[14] Traction alopecia is another behavioral variant due to tightly pulled hairstyles as seen in gymnasts. Lupus is a systemic disease that may cause either scarring (i.e., discoid lupus) or non-scarring forms of alopecia. A thorough history and physical is required to detect less common causes of alopecia, such as syphilis. Secondary syphilis classically causes "moth-eaten" alopecia.[15] Tinea capitis is an important consideration in pediatric populations as a fungal invasion of the hair shaft results in patches of hair loss.[16] Abnormal keratinization causing increased cohesiveness of keratinocytes within the pilosebaceous unit is implicated in both acne vulgaris and keratosis pilaris. Specifically, follicular hyperkeratinization leads to the obstruction of the pilosebaceous unit in acne vulgaris and of hair follicles in keratosis pilaris. Please note there are other important mechanisms involved in the pathogenesis of acne vulgaris. Folliculitis is the inflammation of hair follicles usually secondary to bacterial or fungal infection. Hidradenitis suppurativa is another inflammatory condition involving occlusion of the hair follicle in apocrine-rich areas of the body (e.g., axilla, groin).