Dermatology USMLE Practice Questions
Skin disorders and clinical dermatology.
5 free dermatology practice questions
Pick an answer and check it. After each question you get the same explanation StepGenie students see: the stem decoded clue by clue, the reasoning chain with its infographic, why every wrong option is wrong, and the trap the question was built around. Step 1 questions test mechanism; Step 2 CK questions ask for the next step.
A 52-year-old woman with type 2 diabetes mellitus presents with a 2-day history of painful blisters on her forearms and dyspareunia. She takes metformin and glyburide. Physical examination shows multiple flaccid bullae on the volar surfaces of the forearms and erosions involving the buccal, gingival, and vulvar mucosa. Gentle stroking of the perilesional skin on the forearm causes epidermal separation. Which of the following is the most likely diagnosis?
Correct answer · B
Pemphigus vulgaris
Decoding the stem
Step-by-step reasoning
Step 1 of 5
Flaccid bullae and erosions indicate an intraepidermal blistering disease rather than a tense, subepidermal blister (like bullous pemphigoid).
Step 2 of 5
Widespread mucosal involvement (buccal, gingival, vulvar) is highly characteristic of pemphigus vulgaris and uncommon in most other bullous disorders.
Step 3 of 5
A positive Nikolsky sign (epidermal separation with gentle rubbing) reflects loss of keratinocyte cohesion (acantholysis) in the epidermis.
Step 4 of 5
In pemphigus vulgaris, IgG autoantibodies target desmoglein 3 (and often 1) in desmosomes, causing suprabasal clefting and acantholysis.
Step 5 of 5
Adult age, painful flaccid bullae, prominent mucosal erosions, and Nikolsky positivity together best match pemphigus vulgaris, not the alternative diagnoses.
Why not the others?
A. Staphylococcal scalded skin syndrome
This option implies a toxin-mediated split in the superficial epidermis in infants/children with fever and systemic illness, BUT this patient is a stable middle-aged adult with chronic mucosal erosions, which is not typical for SSSS.
C. Behcet disease
This option implies a vasculitis with recurrent painful oral and genital ulcers plus uveitis, BUT Behcet does not produce flaccid bullae or a positive Nikolsky sign, and skin lesions are typically pustules or erythema nodosum-like, not bullous.
D. Lichen planus
This option implies pruritic, purple, polygonal, planar papules/plaques often on wrists and with Wickham striae, BUT lichen planus does not cause flaccid bullae or widespread erosive mucosal disease with a positive Nikolsky sign.
E. Dermatitis herpetiformis
This option implies intensely pruritic grouped vesicles on extensor surfaces associated with celiac disease, BUT lesions are small, tense vesicles, usually without painful mucosal erosions or a positive Nikolsky sign.
F. Toxic epidermal necrolysis
This option implies a severe drug reaction with diffuse epidermal necrosis, systemic toxicity, and involvement of large body surface areas, BUT the vignette shows localized forearm bullae without systemic illness or medication trigger typical for TEN.
G. Bullous pemphigoid
This option implies tense bullae in elderly patients with negative Nikolsky sign and rare mucosal involvement, BUT this patient has flaccid bullae, extensive mucosal erosions, and a positive Nikolsky sign, pointing away from bullous pemphigoid.
Exam trap
Flaccid bullae with Nikolsky positivity may push you toward other epidermal-splitting disorders (SSSS, TEN), but mucosal involvement in a middle-aged adult is the key discriminator for pemphigus vulgaris.
The bottom line
Pemphigus vulgaris: autoantibodies against desmoglein cause suprabasal acantholysis, flaccid bullae, mucosal erosions, and positive Nikolsky sign.
A 60-year-old man presents with a 3-month history of a slowly enlarging, painless lesion on his lower lip. He has type 2 diabetes mellitus treated with metformin, has smoked 1 pack of cigarettes daily for 35 years, and has worked in construction for the past 33 years. One year ago, he developed a painful rash near his upper lip that resolved completely with acyclovir. Physical examination reveals a 0.5 × 0.5-cm nontender ulcer with everted edges on the midline of the lower lip. The erythematous base bleeds on palpation. Numerous nevi of varying sizes are present over the body. There is no palpable cervical lymphadenopathy. Which of the following is the most likely diagnosis?
Correct answer · A
Squamous cell carcinoma
Decoding the stem
Step-by-step reasoning
- 1
Chronic lesion (>weeks to months) that is slowly enlarging and painless suggests a neoplastic process rather than an acute inflammatory or infectious lesion.
- 2
Location on the lower lip (a sun-exposed mucocutaneous junction) is a classic site for squamous cell carcinoma, especially in older individuals.
- 3
Risk factors: long history of smoking and likely chronic UV exposure from construction work both strongly predispose to squamous cell carcinoma of the lip.
- 4
Physical exam description of an ulcer with everted edges and a base that bleeds on palpation is characteristic of malignant ulcers (SCC) rather than benign conditions.
- 5
Absence of cervical lymphadenopathy suggests early/local disease but does not rule out SCC; it only informs staging, not diagnosis.
- 6
Taken together—chronic, nonhealing, everted, friable ulcer on sun‑exposed lower lip in an older smoker—most consistent with squamous cell carcinoma.
Why not the others?
B. Basal cell carcinoma
This option implies basal cell carcinoma, which typically presents as a pearly papule with telangiectasias and rolled borders, often on the upper lip or other sun-exposed facial skin, BUT this patient has an ulcer with everted edges that bleeds, and SCC is far more common on the lower lip.
C. Aphthous stomatitis
This option implies aphthous ulcers (canker sores), which are painful, shallow, gray ulcers with erythematous rim on nonkeratinized oral mucosa, BUT this lesion is painless, chronic (3 months), has everted edges, and occurs on the lower lip vermilion, all favoring malignancy.
D. Psoriasis
This option implies psoriasis, which causes well-demarcated, erythematous plaques with silvery scale on extensor surfaces and scalp, BUT this patient has a single lip ulcer with everted edges and bleeding, not scaly plaques.
E. Seborrheic keratosis
This option implies seborrheic keratosis, presenting as well-circumscribed, “stuck-on,” waxy, pigmented papules on trunk or face, BUT the patient has an ulcerative, friable lesion on the lip, not a pigmented, stuck-on papule.
F. Cold sore
This option implies herpes labialis (HSV-1), which causes painful, grouped vesicles on an erythematous base that crust and resolve in days, often recurrent in the same region, BUT this lesion is painless, a chronic ulcer with everted edges, and does not match the vesicular pattern or rapid resolution of a cold sore.
G. Melanoma
This option implies melanoma, which typically presents as an evolving pigmented lesion following ABCDE criteria, BUT this patient has a nonpigmented, ulcerative lesion of the lip, with no mention of color change or irregular pigment.
H. Actinic keratosis
This option implies actinic keratosis, a precursor to SCC that presents as rough, scaly erythematous patches or plaques on sun-exposed skin, BUT here the lesion is already an ulcer with everted edges and bleeding, more consistent with invasive SCC than a premalignant scaly patch.
Exam trap
The prior history of a painful rash that resolved with acyclovir may tempt you to pick cold sore, but the current lesion is chronic, painless, and ulcerative with malignant features, pointing to squamous cell carcinoma instead.
The bottom line
Squamous cell carcinoma of the lower lip from chronic sun and tobacco exposure presents as a nonhealing, everted, friable ulcer in an older smoker.
A 31-year-old man presents with a 2-day history of blistering skin lesions and dark-colored urine. His symptoms began shortly after returning from a 4-day vacation in Florida, where he spent significant time outdoors. He reports having had two similar episodes of blistering over the past 3 years, each resolving spontaneously over several weeks. Physical examination reveals vesicles and bullae on the face and the dorsal surfaces of the hands and forearms. This patient’s condition is most likely due to a defect in which of the following enzymes?
Correct answer · D
Uroporphyrinogen III decarboxylase
Decoding the stem
Step-by-step reasoning
Step 1 of 5
Patient has recurrent photosensitive blistering on sun-exposed areas (face, dorsum of hands/forearms) plus dark urine → think cutaneous porphyria.
Step 2 of 5
Porphyrias are due to defects in heme synthesis enzymes leading to accumulation of porphyrin intermediates that absorb light and damage skin.
Step 3 of 5
Blistering photosensitivity without severe abdominal pain or neuro symptoms points specifically to porphyria cutanea tarda, the most common porphyria.
Step 4 of 5
Porphyria cutanea tarda is caused by deficiency of uroporphyrinogen decarboxylase, leading to accumulation of uroporphyrin in skin and urine.
Step 5 of 5
Uroporphyrin causes tea-colored (dark) urine and sun-exposed blistering → matches this patient’s presentation exactly, so the defective enzyme is uroporphyrinogen III decarboxylase.
Why not the others?
A. Aminolevulinic acid dehydratase
This option implies ALA dehydratase deficiency or lead poisoning, which cause abdominal pain, neuro issues, and anemia, BUT not chronic photosensitive blistering on sun-exposed skin.
B. Uroporphyrinogen III synthase
This option implies congenital erythropoietic porphyria, which presents in infancy with severe photosensitivity, hemolytic anemia, and red-brown teeth, BUT this adult has mild, episodic blistering without hemolysis.
C. Porphobilinogen deaminase
This option implies acute intermittent porphyria, which causes painful abdomen, psychiatric symptoms, peripheral neuropathy, and dark urine, BUT it does not cause blistering or photosensitive skin lesions.
E. Aminolevulinic acid synthase
This option implies the rate-limiting step of heme synthesis; defects more often cause sideroblastic anemia, BUT do not produce the classic photosensitive blistering and dark urine pattern seen here.
Exam trap
Sun exposure and blisters may tempt recall of autoimmune blistering (e.g., pemphigus/bullous pemphigoid). The dark urine and recurrent episodes instead point to a porphyria—specifically porphyria cutanea tarda due to uroporphyrinogen decarboxylase deficiency.
The bottom line
Porphyria cutanea tarda from uroporphyrinogen decarboxylase deficiency → photosensitive blistering on sun-exposed skin and dark urine due to uroporphyrin accumulation.
A 35-year-old man is brought to the emergency department after a kitchen grease fire splashes boiling oil onto his torso and extremities. He is alert and speaking clearly. Temperature is 37.6°C (99.7°F), blood pressure is 127/82 mm Hg, pulse is 120/min initially and decreases to 80/min after IV opioids, respirations are 12/min, and oxygen saturation is 98% on room air. Examination reveals stiff, dry, leathery, nonblanching burns that circumferentially encircle both upper extremities; the hands are tense, cool, and pale with capillary refill >4 seconds and markedly diminished distal pulses detectable only by Doppler. The anterior chest and abdomen are covered by similar inelastic burns, and there are tender blistered patches on the shins. After a 1-L bolus of lactated Ringer’s, a Foley catheter drains 10 mL of urine in the first hour. What is the best next step in management?
Correct answer · B
Additional fluids and escharotomy
Decoding the stem
Step-by-step reasoning
- 1
Circumferential, stiff, leathery, nonblanching burns of the arms and torso indicate full-thickness (third-degree) burns forming a rigid eschar.
- 2
The inelastic eschar cannot expand with underlying tissue edema after burns, so it compresses vessels and soft tissue within the limb.
- 3
Tense, cool, pale hands with markedly delayed capillary refill and Doppler-only pulses indicate severe distal ischemia/impending compartment syndrome from this compression.
- 4
Major burns also cause capillary leak and hypovolemia; oliguria (10 mL/hr) after only 1 L fluid indicates inadequate resuscitation, so more IV fluids are needed.
- 5
To reverse limb ischemia caused by eschar, you must perform an escharotomy, which releases the constricting burned tissue and restores perfusion.
- 6
Therefore, the best next step is additional IV fluids for burn resuscitation plus escharotomy of circumferential extremity burns.
Why not the others?
C. Additional fluids and continuous observation
This option implies no decompression. It recognizes hypovolemia but ignores clear signs of limb ischemia/compartment syndrome (cool, pale hands, delayed cap refill, Doppler pulses only), which requires escharotomy, not just observation.
D. Escharotomy without additional fluids
This implies addressing only mechanical compression. However, the patient has severe hypovolemia (oliguria after burns) that must be corrected with additional fluids; escharotomy alone would not address shock risk.
E. Moist dressings and outpatient observation
This option implies minor superficial burns suitable for outpatient care. But the patient has extensive full-thickness circumferential burns with vascular compromise and oliguria, requiring ICU-level care, fluids, and escharotomy, not outpatient dressings.
A. Additional fluids and fasciotomy
This implies deep compartment syndrome from muscle/fascial swelling. In early post-burn limb ischemia with a tight eschar, the problem is the inelastic eschar, so escharotomy, not fasciotomy, is indicated unless deep compartment pressures remain elevated after escharotomy.
Exam trap
Students often confuse escharotomy with fasciotomy in ischemic limbs. Here, ischemia is from a tight burn eschar, not deep muscle swelling, so escharotomy is required along with proper burn fluid resuscitation.
The bottom line
Circumferential full-thickness burns cause vascular compromise and compartment syndrome; treat with aggressive IV fluids plus escharotomy to restore distal perfusion.
A 62-year-old man with poorly controlled type 2 diabetes mellitus presents with a 1-week history of an oozing ulcer on the dorsum of his left foot. He admits to poor adherence to his diabetes medications. Examination reveals a purulent, draining ulcer with surrounding erythema. Pinprick sensation is decreased bilaterally up to the mid-tibia. Wound culture grows beta-hemolytic, coagulase-positive cocci in clusters. Which of the following virulence factors is most likely produced by this organism?
Correct answer · A
Protein A
Decoding the stem
Step-by-step reasoning
Step 1 of 6
Foot ulcer with purulent drainage and erythema in a poorly controlled diabetic → likely soft tissue infection by common skin flora.
Step 2 of 6
Culture shows beta-hemolytic, coagulase-positive cocci in clusters → this combination is pathognomonic for Staphylococcus aureus.
Step 3 of 6
To answer a virulence-factor question, first firmly identify the organism, then recall its key immune evasion tools.
Step 4 of 6
S. aureus’s hallmark virulence factor is Protein A, located in its cell wall.
Step 5 of 6
Protein A binds the Fc portion of IgG, flipping antibodies so the Fc is not available for Fc receptor binding on phagocytes → impaired opsonization and phagocytosis.
Step 6 of 6
Thus, among the listed options, Protein A is the virulence factor most characteristic of this organism.
Why not the others?
B. P fimbriae
This option implies uropathogenic E. coli, which uses P fimbriae to adhere to uroepithelium causing pyelonephritis, BUT this patient has a skin/soft tissue infection with gram-positive cocci, not a UTI with gram-negative rods.
C. Exotoxin A
This option implies either Pseudomonas aeruginosa (EF-2 inhibitor causing tissue necrosis) or Streptococcus pyogenes (superantigen). Pseudomonas are gram-negative rods, NOT coagulase-positive cocci in clusters, and S. pyogenes are beta-hemolytic chains, not clusters.
D. Urease
This option implies organisms like Proteus, Helicobacter pylori, or Klebsiella, which split urea and predispose to struvite stones or gastric colonization, BUT the described organism is a gram-positive coccus (S. aureus), not a urease-positive gram-negative rod.
E. IgA protease
This option implies Neisseria, Streptococcus pneumoniae, or Haemophilus influenzae, which colonize mucosal surfaces and cleave IgA, BUT the infection here is a skin/soft tissue foot ulcer and the lab profile fits S. aureus, which uses Protein A instead.
F. M protein
This option implies Streptococcus pyogenes (Group A strep), which is beta-hemolytic but forms cocci in chains, not clusters, and is catalase-negative. Our culture is coagulase-positive cocci in clusters → S. aureus, not GAS.
G. Lethal factor
This option implies Bacillus anthracis (anthrax toxin: protective antigen, edema factor, lethal factor). Anthrax is a large gram-positive rod, often associated with animal or wool exposure, NOT coagulase-positive cocci in clusters from a diabetic foot ulcer.
Exam trap
Students may fixate on "diabetic foot" and think polymicrobial or Pseudomonas, but the stem hands you the microbiology (beta-hemolytic, coagulase-positive cocci in clusters) → Staph aureus, so you must then pick its classic virulence factor, Protein A, not a general toxin or a virulence factor from another commonly memorized pathogen.
The bottom line
Staphylococcus aureus (beta-hemolytic, coagulase-positive cocci in clusters) expresses Protein A, which binds Fc of IgG and prevents opsonization/phagocytosis.
Source: StepGenie question bank. Questions are written by StepGenie, not taken from NBME or USMLE materials, and are chosen for this page by how students actually performed on them (first-attempt accuracy on StepGenie). Selection last refreshed September 5, 2026.
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About Dermatology
Essential dermatology covering common rashes, skin infections, dermatologic manifestations of systemic disease, and skin cancers. Learn to recognize classic skin lesion patterns.
Key Topics Covered
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Dermatology — Frequently Asked Questions
How do you describe a skin lesion correctly on the USMLE?
Use the standard vocabulary, because the stem describes rather than shows. A macule is flat and under one centimetre and a patch is larger. A papule is raised and under one centimetre and a plaque is larger. A vesicle contains fluid and under one centimetre, and a bulla is larger. Getting the primary lesion right narrows the differential immediately.
What features suggest melanoma?
The ABCDE criteria: asymmetry, border irregularity, colour variation within the lesion, diameter greater than six millimetres, and evolution over time. Evolution is the most important, since any changing lesion warrants biopsy. Depth of invasion, measured as Breslow thickness, is the strongest prognostic factor, which is why excisional rather than shave biopsy is preferred.
How do you distinguish psoriasis from eczema?
Psoriasis produces well-demarcated plaques with thick silvery scale on extensor surfaces, scalp and the sacrum, with nail pitting and the Auspitz sign of pinpoint bleeding when the scale is removed. Eczema produces poorly demarcated, intensely itchy lesions on flexural surfaces, associates with asthma and allergic rhinitis, and commonly begins in childhood.
Which skin findings signal a dermatologic emergency?
Widespread skin sloughing with mucosal involvement and a positive Nikolsky sign suggests Stevens-Johnson syndrome or toxic epidermal necrolysis, usually drug-induced. Rapidly spreading pain out of proportion with crepitus or skin necrosis suggests necrotising fasciitis and needs surgical exploration. A purpuric non-blanching rash with fever suggests meningococcemia.
Are the dermatology practice questions on this page free?
Yes. The 5 questions above come from StepGenie's question bank and can be answered here without an account, with the full explanation shown after each one. From the link under the set you can try three more Dermatology questions in the dashboard preview, also without an account; a free account is what lets you choose the system and keep going.