113+ Free Dermatology Board Practice Questions

Explanation: Pemphigus vulgaris (PV) is an autoimmune blistering disease characterized by flaccid bullae and mucosal erosions. The mucosal-dominant form of PV is characterized by autoantibodies directed primarily against Desmoglein 3 (Dsg3). When both mucosal and cutaneous lesions are present (mucocutaneous PV), autoantibodies against both Desmoglein 1 (Dsg1) and Desmoglein 3 are found. Dsg3 is heavily expressed in mucosal epithelium throughout all layers, whereas Dsg1 expression is minimal in mucosa, explaining why anti-Dsg3 antibodies cause mucosal blistering.

Explanation: Bullous pemphigoid is a subepidermal autoimmune blistering disease. Direct immunofluorescence (DIF) of perilesional skin characteristically shows linear deposition of IgG and C3 along the basement membrane zone (BMZ). The autoantibodies target BP180 (type XVII collagen) and BP230, which are components of the hemidesmosome.

Explanation: Interleukin-23 (IL-23) is a heterodimeric cytokine composed of a unique p19 subunit and a p40 subunit. Interleukin-12 (IL-12) is composed of a unique p35 subunit and the same p40 subunit. Selective IL-23 inhibitors (e.g., guselkumab, risankizumab, tildrakizumab) target the p19 subunit of IL-23, leaving the p40 subunit (and thus IL-12) unaffected. Older agents like ustekinumab bind the p40 subunit, blocking both IL-12 and IL-23.

Explanation: Anti-MDA5 (melanoma differentiation-associated gene 5, also known as anti-CADM-140) autoantibody is strongly associated with clinically amyopathic dermatomyositis (CADM), characteristic cutaneous features (ulcerative Gottron's papules, palmar macules, painful oral ulcers), and a high risk of rapidly progressive interstitial lung disease (RP-ILD), which carries a high mortality rate and requires aggressive immunosuppressive therapy.

Explanation: Subacute cutaneous lupus erythematosus (SCLE) is strongly associated with anti-Ro/SSA antibodies (positive in >80% of cases). Drug-induced SCLE is a well-recognized entity, and hydrochlorothiazide is the most classic and frequently reported culprit medication. Other common triggers include terbinafine, calcium channel blockers, and TNF-alpha inhibitors. Unlike drug-induced systemic lupus (which is associated with anti-histone antibodies), drug-induced SCLE patients have anti-Ro/SSA antibodies and present with classic annular or psoriasiform lesions.

Explanation: The clinical description of a rapidly expanding painful ulcer with a violaceous, undermined border is diagnostic of Pyoderma Gangrenosum (PG). Approximately 50% of PG cases are associated with an underlying systemic disease, most commonly Inflammatory Bowel Disease (IBD: Crohn's disease or Ulcerative Colitis), followed by rheumatoid arthritis and hematologic malignancies (e.g., AML, IgA monoclonal gammopathy). The development of PG lesions at sites of minor trauma (like a scratch or needle stick) is called pathergy.

Explanation: Sweet syndrome (acute febrile neutrophilic dermatosis) presents with fever, leukocytosis, painful erythematous plaques ('juicy' due to marked papillary dermal edema), and a dense neutrophilic dermal infiltrate without vasculitis. Malignancy-associated Sweet syndrome occurs in about 20% of cases and is most commonly associated with hematologic malignancies, especially Acute Myeloid Leukemia (AML) and myelodysplastic syndrome (MDS).

Explanation: The clinical features (pruritic, purple, polygonal, planar papules with Wickham's striae) and histopathological findings (band-like interface lymphocytic infiltrate, saw-tooth epidermal hyperplasia) are diagnostic of Lichen Planus (LP). There is a significant, well-established association between lichen planus (particularly oral and erosive subtypes) and chronic Hepatitis C virus (HCV) infection. Screening for HCV is recommended for patients diagnosed with lichen planus.

Explanation: Erythema nodosum (EN) is the most common form of panniculitis. It classically presents as tender, erythematous nodules on the anterior shins. Histopathologically, EN is the prototype of septal panniculitis without vasculitis. The presence of Miescher's radial granulomas (small nodular collections of histiocytes around a central cleft) is highly characteristic of EN. It is often reactive to streptococcal infections, sarcoidosis, inflammatory bowel disease, or drugs (e.g., oral contraceptives).

Explanation: Porphyria cutanea tarda (PCT) is caused by a deficiency of the enzyme uroporphyrinogen decarboxylase (UROD). It presents with subepidermal blistering and skin fragility on sun-exposed areas (especially the dorsum of hands), milia, scarring, hypertrichosis of the face, and hyperpigmentation. PCT can be familial or acquired (sporadic), and is strongly triggered by iron overload, alcohol consumption, estrogens, and chronic Hepatitis C virus (HCV) infection.