Free USMLE Step 2 CK Dermatology and Allergy practice questions

This patient has tinea versicolor (pityriasis versicolor), an overgrowth of Malassezia, a lipophilic yeast that normally lives on the skin. Heat, humidity and heavy sweating favor it, so it flares in summer in young adults with oily upper trunks. The lesions are scaly oval macules that coalesce on the chest, back and shoulders; Malassezia produces dicarboxylic acids (including azelaic acid) that inhibit melanocytes, so the affected skin fails to tan and stands out as pale after sun exposure. Scraping elicits fine scale, and the KOH preparation shows the classic "spaghetti and meatballs" pattern of short hyphae and round yeast.

Limited disease is treated with a topical antifungal: selenium sulfide lotion or shampoo, or ketoconazole shampoo or cream, applied to the affected area for a short course and then used intermittently (for example monthly in summer) because recurrence is common. Oral fluconazole or itraconazole is reserved for extensive or refractory disease; oral ketoconazole is no longer used because of hepatotoxicity. Patients should be told that the yeast is cleared within weeks but the pigment returns only over months, which is not treatment failure.

A. Oral terbinafine reaches high levels in keratin and works well for dermatophytes, but it is ineffective against Malassezia when given orally. C. Oral griseofulvin is a dermatophyte drug used mainly for tinea capitis and has no role in tinea versicolor. D. Topical hydrocortisone treats inflammation (for example pityriasis alba or seborrheic dermatitis) and would not clear the yeast. E. Topical tacrolimus is used for vitiligo and atopic dermatitis on the face; this patient's lesions are scaly, KOH-positive and hypopigmented rather than depigmented, so vitiligo therapy would not help.

This woman has hot tub folliculitis, caused by Pseudomonas aeruginosa proliferating in poorly chlorinated, warm water of hot tubs, whirlpools and some pools. The clues are onset 1 to 2 days after exposure, itchy or tender follicular papules and pustules that cluster in areas under the swimsuit, where contaminated water was held against the skin, and similar lesions in others who used the same tub. Mild malaise, low-grade temperature, otitis externa, mastitis or tender lymph nodes can accompany it.

In healthy people the infection is self-limited: lesions resolve on their own within about 1 to 2 weeks, usually without scarring, although post-inflammatory hyperpigmentation can persist in darker skin. Management is reassurance, symptomatic care (antihistamines, warm compresses, or topical acetic acid soaks), and avoiding the source until the water is properly treated; the owner should be informed. An oral fluoroquinolone such as ciprofloxacin is reserved for immunocompromised patients or unusually severe, persistent or systemic disease.

A. Pseudomonas bacteremia is a risk in neutropenic or otherwise immunocompromised hosts, not in a healthy adult with superficial folliculitis. C. Progression to furuncles and carbuncles is typical of deeper Staphylococcus aureus infection, not Pseudomonas folliculitis. D. Recurrence occurs only with re-exposure to contaminated water; chronic, persistent truncal folliculitis would suggest Malassezia or staphylococcal disease instead. E. Superficial bacterial folliculitis does not destroy follicles; scarring alopecia belongs to deep, chronic processes such as folliculitis decalvans or dissecting cellulitis of the scalp.

Nocturnal itch, burrows in the finger webs and wrists, papules at the waist and umbilicus, itching household members, and a mite on scraping confirm scabies (Sarcoptes scabiei). The mite spreads through prolonged skin-to-skin contact, so treatment must cover the patient and all close and household contacts at the same time, whether or not they have symptoms, to prevent ping-pong reinfection. Permethrin 5% cream is first-line: it is applied from the neck down (including the scalp and face in young children), under the nails and in skin folds, washed off after 8 to 14 hours, and repeated in 1 to 2 weeks. Permethrin is safe for children 2 months and older, so it suits her son. Bedding, towels, and clothing used in the prior 3 days should be machine washed in hot water and dried on high heat, or sealed in a bag for at least 72 hours. Patients should know that itching often persists for 2 to 4 weeks after successful treatment as a hypersensitivity reaction and does not by itself mean treatment failure.

A. Treating only the patient leaves infested family members to reinfect her. B. Oral ivermectin (two doses 1 to 2 weeks apart) is an effective alternative, but treating her alone has the same flaw, and ivermectin is not recommended for children who weigh less than 15 kg. D. A topical steroid may ease itching but does not kill mites. E. Lindane is no longer recommended as first-line therapy because of neurotoxicity and seizures, and it is contraindicated in young children.

The triad of adult-onset asthma, chronic rhinosinusitis with nasal polyps, and respiratory reactions to aspirin or other NSAIDs defines aspirin-exacerbated respiratory disease (AERD). Bilateral pale, glistening, insensate grapelike masses are nasal polyps, the anosmia and progressive congestion fit chronic rhinosinusitis with polyps, and eosinophilia is typical. Reactions begin 30 to 120 minutes after ingestion with bronchospasm, rhinorrhea, nasal congestion, and conjunctival injection. The reaction is not allergic: inhibition of COX-1 lowers protective prostaglandin E2 and shunts arachidonic acid toward cysteinyl leukotrienes, so it occurs with every COX-1 inhibitor regardless of chemical class. Patients should avoid aspirin and nonselective NSAIDs; acetaminophen at moderate doses and COX-2 selective drugs such as celecoxib are usually tolerated. Leukotriene modifiers, intranasal glucocorticoids, sinus surgery, aspirin desensitization after surgery, and biologics (such as dupilumab) are used for control.

B. IgE-mediated anaphylaxis is drug specific and typically causes urticaria, angioedema, or hypotension; reactions to two structurally unrelated NSAIDs with isolated respiratory symptoms point to COX-1 inhibition instead. C. Allergic bronchopulmonary aspergillosis causes poorly controlled asthma with very high IgE, fleeting infiltrates, and central bronchiectasis, but not NSAID reactions. D. Eosinophilic granulomatosis with polyangiitis can include asthma, polyps, and eosinophilia, but it requires vasculitic features (neuropathy, purpura, cardiac or renal disease) and eosinophilia is usually higher than 1500/mm³. E. Cystic fibrosis causes nasal polyps but would present in childhood with bronchiectasis and pancreatic insufficiency, not NSAID sensitivity.

Recurrent, nonpruritic swelling without urticaria, attacks of abdominal pain that mimic a surgical abdomen, triggers such as estrogen and dental trauma, onset in adolescence, an affected parent, and no response to antihistamines or glucocorticoids point to hereditary angioedema (HAE). HAE is an autosomal dominant deficiency (type 1) or dysfunction (type 2) of C1 esterase inhibitor. Unchecked kallikrein generates bradykinin, which causes the swelling, while unregulated C1 continuously cleaves C4. The best initial screening test is a serum C4 level, which is low in almost all patients both during and between attacks. A low C4 is followed by C1-INH antigenic level and functional assay to confirm and classify the disease. Management includes stopping the estrogen-containing contraceptive, on-demand therapy (C1-INH concentrate, icatibant, or ecallantide), and long-term or preprocedure prophylaxis.

B. Serum tryptase is elevated in mast cell-mediated reactions such as anaphylaxis and mastocytosis; it is normal in bradykinin-mediated angioedema and would not be informative between attacks. C. Total IgE is nonspecific and does not evaluate a bradykinin pathway disorder. D. CH50 screens for deficiencies of classical pathway components, such as C2 or terminal components that predispose to Neisseria infections; it is less specific and less sensitive than C4 for HAE. E. Antinuclear antibodies would be sought for lupus, which this patient does not have; the swelling pattern without hives, rash, or arthritis does not suggest autoimmune disease.

Blistering, fragility, and milia on the sun-exposed dorsal hands, facial hypertrichosis, and urine that fluoresces coral pink are diagnostic of porphyria cutanea tarda (PCT), the most common porphyria. Reduced hepatic uroporphyrinogen decarboxylase (UROD) activity lets uroporphyrins accumulate and photosensitize the skin. Clinical disease is unmasked by factors that increase hepatic iron and oxidative stress: alcohol, estrogen, hepatitis C, HIV, smoking, and iron overload, here from HFE hemochromatosis. After removing triggers, the two effective treatments are phlebotomy and low-dose hydroxychloroquine. Serial phlebotomy (about 450 mL every 1 to 2 weeks, guided by hemoglobin, to a ferritin near the low end of normal) is the clear choice for her: her hemoglobin is normal, her iron stores are markedly elevated, and her hemochromatosis independently requires iron removal to prevent liver, heart, and pancreatic damage. Low-dose hydroxychloroquine is also less effective in C282Y homozygotes. Remission typically follows within months.

A. Intravenous hemin treats acute neurovisceral attacks of acute intermittent porphyria; PCT has no such attacks, and hemin adds iron. C. Beta-carotene is used for the burning photosensitivity of erythropoietic protoporphyria, not the blistering of PCT. D. Hydroxychloroquine at standard antimalarial doses mobilizes porphyrins too quickly and can cause acute hepatotoxicity in PCT; only low doses (100 mg twice weekly) are used, and they are a second choice in hemochromatosis. E. Corticosteroids have no role, because PCT is a metabolic photosensitivity rather than an inflammatory or autoimmune blistering disease.

This woman has papulopustular rosacea: central facial erythema with telangiectasias, inflammatory papules and pustules, flushing triggered by heat, alcohol and sun, and, crucially, no comedones, which separates it from acne. Her skin is sensitive (burning with benzoyl peroxide), which is typical. Topical corticosteroids briefly reduce redness but then worsen rosacea and can cause steroid-induced rosacea-like dermatitis, so the hydrocortisone must be stopped (a short rebound flare may follow).

First-line therapy for mild to moderate papulopustular disease is a topical agent: ivermectin 1% cream, metronidazole or azelaic acid; ivermectin, which also targets Demodex mites, has the strongest efficacy data. Oral doxycycline (often a 40-mg modified-release, sub-antimicrobial dose) is added for more extensive papulopustular disease or ocular involvement. Gentle skin care, daily broad-spectrum sunscreen and avoiding her known triggers are part of every plan. Persistent background erythema can be treated with topical brimonidine or oxymetazoline, and telangiectasias with vascular laser.

A. Topical clobetasol is a superpotent corticosteroid; any topical steroid worsens rosacea, and a superpotent one on the face would also cause atrophy and telangiectasias. B. Topical tretinoin is a first-line acne drug that targets comedones; she has none, and retinoids irritate rosacea-prone skin. D. Oral isotretinoin is first-line for severe nodulocystic acne and is used off label only for severe, treatment-refractory rosacea, not as initial therapy for mild disease, given its teratogenicity and toxicity. E. Oral prednisone has no role and would provoke a worse steroid-induced flare.

She has aspirin-exacerbated respiratory disease (AERD): asthma, chronic rhinosinusitis with nasal polyps and anosmia, and respiratory reactions to aspirin and ibuprofen. The reaction results from COX-1 inhibition, which removes PGE2 restraint and shunts arachidonic acid toward cysteinyl leukotrienes; it is not IgE mediated, and every COX-1 inhibitor cross-reacts. When aspirin is needed for coronary disease, especially for dual antiplatelet therapy after a drug-eluting stent, the recommended approach is aspirin desensitization: graded oral doses given under monitoring (commonly in a rapid protocol in the cardiac unit), after which tolerance persists only with uninterrupted daily aspirin. A lapse of more than about 48 hours can restore sensitivity. Her well-controlled asthma (FEV1 above 70%) makes her a suitable candidate, and desensitization can be performed before or soon after the procedure.

A is wrong because single antiplatelet therapy with a P2Y12 inhibitor alone is not standard after an acute coronary syndrome with a new stent when aspirin can be made tolerable. B is wrong because celecoxib, although usually tolerated in AERD, has no meaningful antiplatelet effect and cannot substitute for aspirin. C is wrong because leukotriene modifiers can soften reactions during desensitization, but no premedication allows a full aspirin dose to be given safely without a graded protocol. E is wrong because the reaction is not IgE mediated, so skin testing has no predictive value.