Bullous disorders flashcards
11 high-yield MRCP Part 1 cards from the Intellect Medicos Dermatology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Pemphigus vulgaris autoantibodies target ______; bullous pemphigoid autoantibodies target BP180 and BP230 (hemidesmosomes).
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desmogleins 3 and 1 (desmosomes)
Why? Desmosome loss causes intraepidermal acantholysis (flaccid blisters, Nikolsky positive); hemidesmosome loss splits at the dermo-epidermal junction (tense subepidermal blisters, Nikolsky negative).
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Pemphigus vulgaris autoantibodies target desmogleins 3 and 1 (desmosomes); bullous pemphigoid autoantibodies target ______.
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BP180 and BP230 (hemidesmosomes)
Why? Desmosome loss causes intraepidermal acantholysis (flaccid blisters, Nikolsky positive); hemidesmosome loss splits at the dermo-epidermal junction (tense subepidermal blisters, Nikolsky negative).
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An 80-year-old woman has had weeks of intense itch and an urticarial rash, and now has large tense blisters on her limbs. Her mouth is spared and Nikolsky sign is negative. Which investigation confirms the diagnosis?
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Skin biopsy for histology (subepidermal blister, eosinophils) plus direct immunofluorescence (linear IgG and C3 along the basement membrane).
Why? This is bullous pemphigoid; biopsy with direct immunofluorescence is the gold standard.
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What is the first-line treatment for localised bullous pemphigoid?
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A very potent topical corticosteroid (e.g. clobetasol propionate); oral prednisolone if extensive or severe.
Why? Topical therapy controls disease while avoiding systemic steroid harm in frail elderly patients.
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What is the first-line treatment for pemphigus vulgaris?
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Systemic (oral) corticosteroids, combined with an adjuvant — rituximab (increasingly used first-line in moderate–severe disease) or azathioprine / mycophenolate mofetil.
Why? Pemphigus is life-threatening if untreated. It typically starts with painful oral erosions before flaccid skin blisters.
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Dermatitis herpetiformis: which drug gives rapid itch control, and what must be checked before starting it?
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Dapsone; check G6PD activity first because of the risk of haemolysis.
Why? Dapsone acts within days; direct immunofluorescence in DH shows granular IgA.
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Direct immunofluorescence in pemphigus vulgaris shows ______ deposition in a "fishnet" or "chicken-wire" pattern.
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intercellular IgG
Why? Gold-standard diagnosis of both pemphigus and pemphigoid is skin biopsy for histology plus direct immunofluorescence. Pemphigus histology shows suprabasal acantholysis ("row of tombstones").
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Against which autoantigen are the IgA antibodies of dermatitis herpetiformis directed?
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Epidermal transglutaminase (transglutaminase 3).
Why? Direct immunofluorescence shows granular IgA in the dermal papillae. Coeliac serology (IgA anti-tissue transglutaminase) is usually positive.
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Name three important adverse effects of dapsone.
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Any three: haemolysis (severe in G6PD deficiency), methaemoglobinaemia, agranulocytosis, dapsone hypersensitivity syndrome (rash, fever, hepatitis).
Why? Check G6PD before starting, then monitor full blood count and liver function closely during the early months of treatment.
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Which class of oral diabetes drugs is associated with drug-induced bullous pemphigoid?
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DPP-4 inhibitors (gliptins), e.g. sitagliptin, vildagliptin, linagliptin.
Why? Bullous pemphigoid is listed as an adverse effect in gliptin product information; stop the gliptin if it develops.
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What is the molecular target of rituximab, used in pemphigus vulgaris?
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CD20 on B cells.
Why? B-cell depletion reduces production of anti-desmoglein autoantibodies; rituximab is given with corticosteroids in moderate-to-severe pemphigus.