DDx: Common Dermatologic Disorders

Question 1

Ddx: Skin Infections (Bacterial)

Answer 1

Cellulitis

Erysipelas

Folliculitis

Furuncles

Impetigo

Ecthymia

Question 2

Cellulitis

Answer 2

A rapidly spreading deep subcutaneous dermis-based infection most often caused by S. aureus or group A streptococci.

Hx: Risk factors for lower extremity cellulitis include eczema, tinea pedis, onychomycosis, skin trauma (including insect bites, drug injection), chronic leg ulcers, long-standing diabetes mellitus, and edema. Risk factors for MRSA infection include recent close contact with persons having a similar infection, recent antibiotic use, recent hospitalization, hemodialysis, injection drug use, diabetes, and previous MRSA colonization or infection.

Px: Characterized by a well-demarcated area of warmth, swelling, tenderness, and erythema. possibly accompanied by lymphatic streaking or fever and chills.

Tx: Cellulitis without Purulence: Probable β-hemolytic streptococci or MSSA; MRSA unlikely.

Oral : Dicloxacillin, Cephalexin, Clindamycin

Intravenous: Oxacillin, Nafcillin, Cefazolin, Clindamycin

Cellulitis with Purulence: Probable MRSA; risk factors for MRSAc; failure to respond to non-MRSA therapy:

Oral: Trimethoprim–sulfamethoxazole, Clindamycin, Doxycycline, Minocycline, Linezolid

Intravenous: Vancomycin, Linezolid, Daptomycin

$ Cephalexin

$ Dicloxacillin

$ Doxycycline

$ Trimethoprim–sulfamethoxazole

$$ Clindamycin

$$ Minocycline

$$$ Linezolid

Question 3

Erysipelas

Answer 3

A superficial skin infection involving the upper dermis and superficial lymphatics.

Px: It is usually erythematous in appearance (“St. Anthony’s fire”) with well-demarcated borders and is almost always caused by group A streptococci.

Tx: Treatment is usually a β-lactam antibiotic (eg, penicillin or amoxicillin).

Question 4

Folliculitis

Answer 4

A pustular skin infection in the hair follicle. Causes include S. aureus and, less frequently, group A streptococci.

Px: Typically affects the beard, pubic area, axillae, and thighs.

Tx: Folliculitis often is effectively treated with local application of heat and a topical antibiotic (mupirocin, chlorhexidine cleanser).

“Hot tub folliculitis” infection is generally caused by Pseudomonas aeruginosa
or Pseudomonas cepacia. The condition is usually self-limited, and therefore reassurance is all that is necessary. Antibiotic therapy is only indicated in recalcitrant
cases, or if patients are symptomatic.

Question 5

Furuncles (boils/skin abscess)

Answer 5

Tender, pus-containing nodules that commonly appear on the neck or in the axillae or groin but may occur at any skin site

Boil: infection of the hair follicle that extends into the dermis and subcutaneous tissues

Abscess: Pus collections in the dermis and deeper tissues

Hx: Nearly always are caused by S. aureus.

Dx: Cultures from purulent material can distinguish MRSA from methicillin-susceptible S. aureus (MSSA) and can guide treatment.

Tx: Warm compresses to facilitate drainage may be adequate therapy for small furuncles. Incision and drainage (I & D) is required for larger furuncles and all abscesses. Incision and drainage may be adequate therapy for skin abscesses, and systemic antibiotics are not routinely required. However, they may be indicated if the patient is febrile or immunocompromised, has diabetes, or is at risk for MRSA or if there is a surrounding cellulitis

Question 6

Impetigo

Answer 6

A superficial infection of the skin (epidermis) characterized by a group of yellowish, crusted pustules. caused by staphylococci (staph aureus) or streptococci.

Hx: Predisposing factors include poor hygiene, neglected minor trauma, and eczema.

Tx: Limited disease usually can be treated effectively with topical mupirocin or bacitracin; more extensive disease can be treated with a cephalosporin, penicillinase-resistant penicillin, or β-lactam-β-lactamase inhibitor.

Question 7

Ecthyma

Answer 7

An ulcerative form of impetigo usually caused by streptococci or staphylococci.

Px: The classic findings are superficial, saucer-shaped ulcers with overlying crusts, typically on the legs or feet.

Tx: Effective treatment consists of cleansing with an antibacterial wash followed by topical mupirocin plus oral cephalexin, dicloxacillin, or clindamycin. If MRSA is suspected or there is β-lactam allergy, one should consider other options.

Question 8

Ecthymia Gangrenosum

Answer 8

Ecthyma gangrenosum is an ulcerative infection involving the dermis usually caused by Pseudomonas aeruginosa.

Hx: It is usually seen in immunocompromised patients and may indicate pseudomonal sepsis.

Px: Classic findings are ulcers with a central gray-black eschar and erythematous halo, typically on the legs or feet.

Tx: Initial therapy usually involves an antipseudomonal penicillin plus an aminoglycoside.

Question 9

FUNGAL

Question 10

Tinea capitis

Answer 10

Caused by T. tonaurans

Tx: Systemic therapy is necessary for a cure,

Griseofulvin is considered the treatment of choice in the United States, and should be used for 4 to 8 weeks.

Terbinafine, itraconazole, fluconazole, and ketoconazole can also be used. If fluconazole were to be used, the treatment duration would only be for 3 to 4 weeks.

Topical ketoconazole shampoo or selenium sulfide lotion may kill spores on the hair.

Question 11

Tinea corporis (“ringworm”)

Answer 11

Scaly patch with central clearing and an active border of erythema, papules, and vesicles. Tinea is more erythematous than BCC and usually has a larger area of central clearing.

Most commonly caused by Trichophyton rubrum

Question 12

Tinea cruris

Answer 12

Caused by T mentagrophytes

Occurs in the groin

Question 13

Ddx: Common rashes

Answer 13

Erythema multiforme (EM)

Question 14

Acne

Answer 14

The true cause is multifactorial, but familial factors are involved. The key factors are follicular keratinization, angrogens, and Propionibacterium acnes. In acne, the kertatinization pattern in the pilosebaceous unit changes, and keratin becomes more dense, blocking the secretion of sebum. The keratin plugs are called “comedones.”

Hx: Contributory factors to acne include certain medications, emotional stress, and occlusion and pressure on the skin, such as by leaning the face on the hands (acne mechanica).

Acne is not caused by dirt, chocolate, greasy foods or the presence or absence of any foods in the diet.

Tx: Initial management of comedonal acne without a significant inflammatory component includes:

Topical retinoids with the addition of

Organic acid preparations (eg, salicylic, azelaic, or glycolic acid) if initial therapy fails.

Benzoyl peroxide, a widely used antibacterial agent, is another option for patients with comedonal acne, although it is preferred for inflammatory acne. Some patients with comedonal acne will develop inflammatory features, and benzoyl peroxide can be added at that time.

Topical antibiotics (eg, erythromycin, clindamycin) is used in most patients with moderate or moderate-to-severe inflammatory acne require .

Oral isotretinoin is indicated for nodular acne, severe acne, or moderate recalcitrant acne. 🕷

Oral antibiotics (eg, tetracyclines) are reserved for patients with severe or nodular acne and for moderate inflammatory acne unresponsive to topical antibiotics. Oral antibiotics are also considered in patients with widespread inflammatory acne (eg, back, upper arms) that makes topical therapy impractical.

In addition, since both tetracycline and isotretinoin cause pseudotumor cerebri, the two medications should never be used together.

Question 15

Acute urticaria (hives)

Answer 15

Tx:

An H1-blocking nonsedating antihistamine (e.g., cetirizine [Zyrtec]), which will stop the likely allergic cause of her urticaria.

A short course of systemic glucocorticoids may also be helpful for patients with widespread or highly symptomatic involvement. In persistent cases, an H2-blocking antihistamine is sometimes added, although the effectiveness of doing so has not been established.

Topical corticosteroids can occasionally provide additional relief for symptomatic urticarial lesions

❗Concerning features: wheezing; stridor; and lip, tongue, or eyelid swelling; dyspnea, difficulty clearing secretions, or hemodynamic instability

Tx: Administration of epinephrine would be indicated.

Question 16

Atopic Dermatitis (eczema)

Answer 16

The rash may look like rough, red plaques with some flaking that can affect the face, neck, upper trunk, and behind the knees. The flexural surfaces are often involved. Pruritus may be severe.

Most patients have the onset of eczema in childhood, and onset after the age of 30 is very
uncommon.

Question 17

Basal cell carcinomas (BCCs)

Answer 17

Basal cell carcinomas (BCCs) most commonly appear as pearly telangiectatic papules. because the most important risk factors for the development of BCCs are fair skin and sun exposure (the same risk factors as for AKs), the two often occur in the same area.

Question 18

Dermatofibromas

Answer 18

Dermatofibromas are firm, dermal nodules approximately 6 mm in diameter; the surface often is hyperpigmented (Plate 29 :). Dermatofibromas are most commonly seen on the legs of women but also occur on the trunk in both men and women. Excision is indicated only if the lesion is symptomatic, has changed, or bleeds.

Question 19

Erythema multiforme (EM)

Answer 19

erythema multiforme (EM), which is an acute, often recurrent mucocutaneous eruption that usually follows an acute infection, most frequently recurrent herpes simplex virus (HSV) infection. It may also be idiopathic or drug related. Most patients are between 20 and 40 years of age. Lesions range in size from several millimeters to several centimeters and consist of erythematous plaques with concentric rings of color. The dusky center may become necrotic and can form a discrete blister or eschar. Few to hundreds of lesions develop within several days and are most commonly located on the extensor surfaces of the extremities, particularly the hands and feet. Lesions occur less frequently on the face, trunk, and thighs. Mucosal lesions are present in up to 70% of patients and involve the cutaneous and mucosal lips, gingival sulcus, and the sides of the tongue. Mucosal lesions consist of painful erosions or, less commonly, intact bullae. The conjunctival, nasal, and genital mucosal surfaces can also be affected. Patients may have low-grade fever during an EM outbreak. Lesions usually last 1 to 2 weeks before healing; however, hyperpigmentation may persist. Recurrences are common, particularly in HSV-associated infection. Treatment of EM is primarily symptomatic. Systemic corticosteroids may provide symptomatic improvement but may be associated with complications. Antiviral therapy does not shorten the EM outbreak in HSV-associated infection, but continuous prophylactic antiviral therapy may help prevent further episodes. Treatment for bacterial infection-associated EM is appropriate for management of the specific active infection; however, there are no studies that demonstrate that treatment impacts the duration of the EM lesions. Antibiotic therapy is based on identification of an infectious cause. If EM is thought to be due to a new drug, the drug should be discontinued.

Question 20

Epidermoid inclusion cyst

Answer 20

The most common type of skin cyst is an epidermoid inclusion cyst. Usually present on the face, neck, or chest, this type of cyst is made up of epidermal cells that are present in the dermis. Patients usually note a nontender lump that may become painful if infected. In this case, treatment involves incision and drainage and removal of the cyst and cyst wall.

Question 21

Herpes zoster ophthalmicus (shingles)

Answer 21

Ophthalmic zoster, if not treated promptly, can lead to blindness. Shingles, which is reactivation of varicella-zoster virus, can occur any time after the primary varicella infection. It often begins with a prodrome of intense pain, and in more than 90% of patients, it is associated with pruritus, tingling, tenderness, or hyperesthesia. The cutaneous eruption typically involves a single dermatome and rarely crosses the midline. In a recent, prospective multicenter study, eye redness and rash in the supratrochlear nerve distribution had a statistically significant association with clinically relevant eye disease. One hundred percent of patients who developed moderate to severe eye disease presented with a red eye. Hutchinson sign (zoster eruption on the tip of the nose) was not predictive of clinically relevant eye disease. Clinical diagnosis is based on both history and physical examination. Testing by direct fluorescent-antibody testing or by polymerase chain reaction can confirm the diagnosis; however, decisions regarding antiviral therapy are often based on the history and physical examination rather than reliance on laboratory testing.

Question 22

Keratocanthoma

Answer 22

red, volcano-like nodules with a prominent central keratin plug. They are considered to be a subtype of well-differentiated squamous cell carcinoma. They grow rapidly and may reach a size of several centimeters within a few weeks. Classic keratoacanthomas eventually stabilize in size and may spontaneously regress without treatment.

Question 23

Lipoma

Answer 23

A lipoma is a group of fat cells encased in a thin fibrous capsule. These are typically softer and more pliable than cysts and can be single or multiple. Lipomas can be superficial or deep and usually do not need to be removed. However, if there is growth or pain, removal should be carried out.

Question 24

Nummular eczema

Answer 24

Round, well-demarcated, eczematous patches (1-10 cm) found on the extremities and trunk. Pruritus may be intense, which results in scratching. The scratch marks may be the best way to discriminate nummular eczema from superficial BCC. Onset is usually spontaneous with no inciting event.

Question 25

Peripheral Edema

Answer 25

Bilateral edema:

CHF (dyspnea, rales, or JVD) would necessitate a chest x-ray to rule in the diagnosis, followed by an echocardiogram.

Liver Failure: Ascities; Dx: Liver function studies are needed. If these are absent, the clinician should check an urinalysis. If the sediment is abnormal, nephritic syndrome or acute tubular necrosis (ATN) is the likely diagnosis.

Medications: Antihypertensives (ACE), such as calcium channel blockers are well known to cause this, but direct vasodilators, β-blockers, centrally acting agents, and antisympathetics also can cause edema. Of the diabetic medications, insulin sensitizers, such as rosiglitazone often cause edema. Hormones, corticosteroids, and NSAIDs also cause problems.

Unilateral Edema:

Angioedema

Hereditary:

Dx: C4 level and C1 esterase

Drug-induced:

Urticaria

Chronic spontaneous Hx:

Question 26

Pityriasis rosea

Answer 26

A self-limited papulosquamous eruption. The classic history includes a single herald patch (an oval, slightly raised plaque with scale) followed in the next 1 to 2 weeks with a more generalized eruption. It will spontaneously resolve in 6 to
12 weeks, and recurrences are uncommon. The treatment is symptomatic, and includes antihistamines or corticosteroids to relieve itch.

Question 27

Pyoderma gangrenosum

Answer 27

Pyoderma gangrenosum is an ulcerative skin condition typically associated with an underlying systemic condition, such as inflammatory bowel disease, rheumatoid arthritis, spondyloarthritis, or a hematologic disease or malignancy (most commonly acute myelogenous leukemia). Lesions often are multiple and tend to appear on the lower extremities. They begin as tender papules, pustules, or vesicles that spontaneously ulcerate and progress to painful ulcers with a purulent base and undermined, ragged, violaceous borders.

Question 28

Psoriasis

Answer 28

A chronic skin condition in young adults. In the early phase, the sharply demarcated erythematous plaques with slight scale may resemble superficial BCC.

As the psoriatic area matures, a silvery-white scale develops that has characteristic pinpoint bleeding when removed,

Plaques are symmetrically distributed and usually occur on scalp, extensor surfaces (elbows, knees and back).

Tx: For localized skin rashes, topical corticosteroids are appropriate therapeutic agent. Topical pimecrolimus is effective for inverse psoriasis (located on the perianal and genital regions) or on the face and ear canals, but is generally not used for lesions on the
trunk or extremities.

Question 29

Rosacea

Answer 29

In stage I, there is persistent erythema, generally with telangiectasia formation. Stage II is characterized by the addition of papules and tiny pustules. In stage III, the erythema is deep and persistent, the telangiectases are dense, and there may be a solid appearing edema of the central part of the face due to sebaceous hyperplasia and lymphedema (rhinophyma and metophyma).

Tx: Management may include topical or oral therapies. Topical metronidazole, clindamyacin, and sodium sulfacetamide can work, but oral antibiotics are more effective than topical treatments.

Minocycline or doxycycline are very effective first-line therapies.

Topical steroids are NOT generally effective.

Question 30

Seborrheic keratoses

Answer 30

Seborrheic keratoses are common benign, painless neoplasms that present as brown to black, well-demarcated papules with a waxy surface and a “stuck-on” appearance (Plate 28 :). Seborrheic keratoses are more common in older patients. Treatment is not indicated unless the growths are inflamed, irritated, or pruritic.

Question 31

Stevens-Johnson syndrome (SJS) and TEN

Answer 31

Stevens-Johnson syndrome (SJS) and TEN are severe, idiosyncratic reactions that lead to sloughing of the epidermis. The two syndromes are differentiated by the degree of epidermal detachment, with SJS defined as involvement of ≤ 10% of body surface area and TEN involving at least 30% of body surface area; intermediate degrees of body surface area involvement are considered to be overlap syndromes (SJS/TEN). Both typically begins with a prodrome that may include fatigue, malaise, fever, sore throat, or a burning sensation in the eyes 1 to 3 days before skin lesions appear.

Skin findings may be characterized by flat, purpuric, targetoid lesions that coalesce into patches, or there may be diffuse, tender erythema without identifiable individual lesions. The involved epidermis blisters and sloughs, leaving behind denuded dermis, and a positive Nikolsky sign (lateral pressure on nonblistered skin leads to denudation) is usually present. Skin pain is prominent. Two or more mucosal surfaces, such as the eyes, nasopharynx, mouth, and genitals, are involved in more than 80% of cases. SJS/TEN is most commonly caused by medications; antiepileptic agents, nonsteroidal anti-inflammatory drugs, antibiotics, pantoprazole, sertraline, tramadol, and allopurinol are the most frequently implicated drugs. The reaction most commonly occurs within 4 and 28 days of exposure. The diagnosis is often made clinically, but a biopsy can be confirmatory. Treatment requires discontinuation of the suspected causative medication and is otherwise supportive.

Question 32

Verruca vulgaris (common wart)

Answer 32

Verruca vulgaris (common wart) is caused by infection with a human papillomavirus. Common warts generally appear as 5- to 10-mm, rough-surfaced, skin-colored papules. The diagnosis is based on the typical verrucous appearance of a papule or plaque noted on the hands or feet.

Tx: Spontaneous involution occurs in most patients within 3 years; thus, not treating cutaneous warts often is a reasonable option. Topical salicylic acid is the first-line therapy. Cryotherapy is used for warts that do not respond to initial topical management; cryotherapy should be avoided with subungual and periungual warts.

Question 33

BUGS

Question 34

Head lice

Answer 34

Erythematous popular rash and “nits” on the hair follicles.

The itching from lice generally begin approximately 2 to 3 weeks after infestation.

Tx: Treatment options include premethrin and lindane. The preferred treatment is permethrin 1%, permethrin 5% is a second option, and lindane 1% is a third option. If treatment failure occurs, a second-line medcation is 0.5% malathion lotion.

Question 35

Scabies

Answer 35

Sarcoptes scabiei burrow into intertriginous areas (skin touches skin), wrists, or areas where clothing is tight next to the skin (belt line, wrists).

Question 36

Chigger bites

Answer 36

Typically found in a linear pattern over wrists, ankles, and legs.

Question 37

Bedbugs

Answer 37

Typically infest unclothed areas—the neck, hands, and face.

Question 38

Fleas

Answer 38

Flea bites often occur in clusters, and are typically on the lower extremities.

Question 39

Cat bite

Answer 39

After a cat bite to the hand, hospitalization is indicated unless it is very superficial and does not appear to be infected.

Question 40

Ddx: Hep C-related Dermatologic conditions

Answer 40

Porphyria cutanea tarda (PCT)

Question 41

Lichen planus

Answer 41

Lichen planus is a mucocutaneous disorder of unclear etiology that also appears to have an association with hepatitis C, although it may also be found as an isolated disorder or in association with autoimmune disorders and some medications. The skin findings are a generalized rash that is characteristically polygonal, pruritic, papular, planar, purple, and with plaques (the six Ps).

Question 42

Porphyria cutanea tarda (PCT)

Answer 42

There is a very strong association of PCT with chronic hepatitis C infection, although why this relationship occurs is not known. PCT is the most common of the porphyrias worldwide. PCT is caused by a deficiency in uroporphyrinogen decarboxylase, an enzyme in the heme biosynthesis pathway. PCT may be acquired (type 1) and familial (type 2); 80% are of the acquired type, and the enzymatic defect is limited to the liver. Whereas this type develops most often in mid-adult life, type 2 develops in younger patients and represents a decrease in enzymatic activity in all tissues. Both types of PCT often require susceptibility factors such as alcohol, hepatitis C or HIV infection, iron overload (e.g., hemochromatosis), or estrogen use for clinical evidence of PCT to occur. Sunlight activates the large amounts of uroporphyrinogen that are deposited in the skin, leading to photosensitization and tissue damage. The result is a variety of cutaneous findings, which include blisters, erosions, hyperpigmentation, hypertrichosis, and sclerodermoid plaques. Involvement of the liver usually is seen with modest elevations of the hepatic transaminases. The diagnosis should be suspected in at-risk patients with consistent skin findings and with reddish-to-brown urine in natural light (and pink to red with fluorescence). Measurement of urinary porphyrins confirms the diagnosis. Treatment is by sunlight avoidance, phlebotomy, or hydroxychloroquine (which mobilizes accumulated porphyrins), and treatment of hepatitis C.

Question 43

Erythema nodosum

Answer 43

Erythema nodosum causes tender, reddish, palpable inflammatory nodules that typically occur on the anterior lower legs. It is a hypersensitivity immune reaction to infection or systemic inflammation and may be seen with hepatitis C. However, it is a nonspecific finding that may occur in a wide range of systemic diseases or with different medications.

Erythema nodosum is the result of a hypersensitivity immune reaction that may be secondary to drugs, infection (such as fungal or streptococcal), or systemic inflammation due to sarcoidosis, tuberculosis, lymphoma, or inflammatory bowel disease. At least 50% of cases are idiopathic. The condition usually is acute and self-limited, and treatment is supportive following treatment of any associated cause.

Question 44

Cryoglobulinemia

Answer 44

Cryoglobulinemia, in which temperature-dependent circulating immune complexes are deposited in small- to medium-sized blood vessels, is also associated with hepatitis C infection. The most common clinical manifestations include cutaneous palpable purpura, which often involves the lower legs, may come in “crops,” and can leave areas of hyperpigmentation after resolution. Cryoglobulins may also involve the kidney (causing glomerulonephritis) and other organ systems (e.g., the central nervous system).

Question 45

Molluscum contagiosum

Answer 45

The lesion is due to an infection with a poxvirus transmitted through direct skin-to-skin contact. Lesions are common in children in a daycare or nursery school setting and are in that case not likely to be sexually transmitted. However, in adults and in the pubic region, they are sexually transmitted.

Although the lesions can be similar to those seen with basal cell cancers, the lack of telangiectasia is a diagnostic clue.

Tx: Most lesions will resolve spontaneously within months of appearance, but they can be treated with cryotherapy, cautery, or curettage.

Question 46

Ddx: Vascular Tumor

Answer 46

Cherry Angioma

Question 47

Pemphigus vulgaris (PV)

Answer 47

Including painful, flaccid bullae, mucosal erosions, and separation of epidermis from dermis by light friction (Nikolsky sign). The roof of the bullous lesions is fragile and rapidly desquamates, leaving raw ulcers. PV is an autoimmune disorder caused by antibodies directed against desmogleins 1 and 3, which are components of desmosomes normally involved in adherence between epidermal keratinocytes.

Light microscopy of a biopsy specimen from a lesion edge shows intraepithelial cleavage with detached keratinocytes (acantholysis). Because the attachment of keratinocytes to the basement membrane is mediated by hemidesmosomes (which are immunologically distinct from desmosomes), a single cell layer remains along the basement membrane with an appearance described as a “row of tombstones.” Immunofluorescence microscopy reveals IgG and C3 deposits in a netlike or “chicken wire” pattern. Serology for antibodies to desmoglein 1 and 3 can further support the diagnosis.

Question 48

Bullous pemphigoid

Answer 48

An autoimmune blistering disease that causes pruritic, tense bullae in the flexural surfaces, groin, and axilla. Mucosal lesions occur in only a minority of patients. Biopsy shows subepidermal cleavage, with linear IgG deposits at the basement membrane on immunofluorescence studies.

Question 49

ALLOPECIA

Question 50

Telogen effluvium (TE)

Answer 50

One of the most common causes of hair loss in adults. Hair follicles pass through 3 phases: growth phase (anagen; 90% of follicles), transformative phase (catagen; <1%), and rest/shedding phase (telogen; 10%). In TE, follicles undergo a widespread shift into the rest/shedding phase, with cessation of growth and subsequent shedding. It is often triggered by a stressful event, such as weight loss, pregnancy, major illness or surgery, or psychiatric trauma.

Question 51

Alopecia areata

Answer 51

An autoimmune disorder characterized by circumscribed patches of hair loss. Hair shafts show narrowing close to the surface and may be broken off.

Question 52

Androgenetic alopecia

Answer 52

Causes uneven hair loss in a characteristic pattern. Men have thinning at the frontotemporal hairline and vertex; women predominantly have thinning at the vertex and sides with preservation of the hairline.

Question 53

Trichotillomania

Answer 53

A behavioral disorder characterized by compulsive pulling of hair. It presents with irregular patches of hair loss and broken fibers, and typically affects the front and sides of the scalp, eyebrows, and eyelashes.

Question 54

INFLAMMATORY

Question 55

Hidradenitis suppurativa (HS, also known as acne inversa)

Answer 55

Most commonly occurs in intertriginous areas (eg, axilla; inguinal, perineal areas) but can occur in any hair-bearing skin. HS is due to chronic inflammatory occlusion of folliculopilosebaceous units, which prevents keratinocytes from properly shedding from the follicular epithelium. Risk factors include family history of HS, smoking, obesity, diabetes, and mechanical stress on the skin (eg, friction, pressure).

HS initially presents as solitary, painful, inflamed nodules that can last for several days to months. The nodules may regress or can progress to abscesses that open to the surface with purulent or serosanguineous drainage. Most patients have a chronic, relapsing course. Complications include sinus tracts, comedones, and scarring. Severe scarring can lead to dense, rope-like bands in the skin with strictures and lymphedema. The diagnosis of HS is usually made clinically without the need for biopsy or cultures.