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DR13.1-2 | Vesiculobullous Lesions — Graded Quiz
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A 50-year-old woman presents with 6-week history of painful mouth ulcers that failed antibiotic therapy, followed by skin blisters that rupture within hours of formation. Examination reveals multiple erosions on the buccal mucosa and flaccid, easily ruptured bullae on the chest. Nikolsky sign is positive. The MOST likely diagnosis is:
Correct. Oral prodrome → flaccid cutaneous bullae → positive Nikolsky sign = the classical presentation of PV, caused by anti-Dsg3 IgG suprabasal acantholysis.
The triad of oral-first onset, flaccid blisters, and Nikolsky positivity is pathognomonic for pemphigus vulgaris. Bullous pemphigoid spares mucosae, has tense blisters, and Nikolsky is negative.
Incorrect. Oral erosions preceding skin blisters + flaccid bullae + positive Nikolsky sign is the defining triad of pemphigus vulgaris.
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A 70-year-old man with bullous pemphigoid confirmed on DIF is started on systemic prednisolone. Six weeks later he develops polyuria, polydipsia, and a fasting blood glucose of 220 mg/dL. This complication is MOST directly attributable to:
Correct. Steroid-induced hyperglycaemia is a well-recognised complication of systemic corticosteroids used to treat autoimmune blistering diseases. DR13.2 includes anticipating these complications before referral.
Systemic corticosteroids — the cornerstone of treatment for both PV and BP — cause steroid-induced diabetes mellitus (and also osteoporosis, cataracts, adrenal suppression). Primary management counselling must include these risks.
Incorrect. This is steroid-induced diabetes from the systemic prednisolone used to treat bullous pemphigoid. Recognising and monitoring for steroid side effects is part of DR13.2 primary management.
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You receive a patient at the emergency department with known bullous pemphigoid now covering 40% BSA with several ruptured blisters, oral temperature 39.2°C, and serum albumin 2.4 g/dL. Which pathophysiological mechanism accounts for the hypoalbuminaemia in this patient?
Correct. Denuded skin acts as a massive wound: plasma proteins (especially albumin) weep continuously from erosions, and poor oral intake (due to mouth erosions in PV, or general debility in BP) compounds the deficit.
Extensive blistering and erosion causes transepidermal protein and fluid loss — analogous to a major burn. This is the clinical rationale for fluid and nutritional support in the primary management of extensive vesiculobullous disease.
Incorrect. In extensive vesiculobullous disease, protein loss through denuded skin (analogous to burns) plus reduced intake accounts for hypoalbuminaemia.
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Direct immunofluorescence (DIF) is performed on a perilesional skin biopsy from a 44-year-old man with suspected autoimmune blistering disease. The result shows intercellular IgG deposits in a 'chicken-wire' pattern throughout the epidermis. This pattern is DIAGNOSTIC of:
Correct. Intercellular IgG binding to desmoglein on cell surfaces creates the 'chicken-wire' or 'fish-net' pattern on DIF — the DIF hallmark of pemphigus vulgaris.
DIF patterns: PV = intercellular (chicken-wire) IgG + C3 in epidermis. BP = linear IgG + C3 at BMZ. DH = granular IgA at dermal papillae. LAD = linear IgA at BMZ. These patterns map directly to the target antigen location.
Incorrect. Intercellular IgG in a chicken-wire pattern = pemphigus vulgaris (anti-Dsg IgG binding to keratinocyte surfaces). Linear BMZ IgG = bullous pemphigoid.
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A general practitioner calls you about a 62-year-old woman she has seen with suspected bullous pemphigoid. She asks what primary management she should provide before the dermatology appointment in 5 days. The patient has 10–15 intact tense blisters covering <5% BSA, is afebrile, eating well, and her oral mucosa is normal. Which management plan is MOST appropriate?
Correct. For limited, stable BP before specialist review: supportive wound care + itch control + safety-netting. Initiating systemic steroids without specialist guidance is outside the scope of primary management.
DR13.2 primary management for localised stable BP: gentle blister drainage (roof intact), non-adherent dressings, oral antihistamines for itch, avoid trauma to skin, and clear safety-netting for red flags. High-dose systemic steroids and IV treatment are specialist-initiated decisions.
Incorrect. The primary physician should provide supportive care (drainage, dressings, antihistamines, safety-netting) while arranging specialist review — not either nothing or high-dose immunosuppression without specialist input.
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A clinical photograph shows a fresh blister from a patient with pemphigus vulgaris. When gentle downward pressure is applied to the roof of the blister, the blister margin visibly extends laterally. This phenomenon is termed:
Correct. The Asboe-Hansen sign (bulla-spread sign) is elicited by pressing down on a blister; the fluid spreads laterally, extending the blister margin — evidence of a propagating intra-epidermal cleavage plane.
Asboe-Hansen sign = lateral spread of an EXISTING blister under downward pressure. Nikolsky sign = new blister formation on NORMAL perilesional skin under tangential pressure. Both indicate fragile intra-epidermal adhesion.
Incorrect. Lateral extension of an existing blister under downward pressure = Asboe-Hansen sign. Nikolsky sign = shearing of normal perilesional skin with tangential pressure.
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Which of the following comparisons between pemphigus vulgaris and bullous pemphigoid is ACCURATE?
Correct. Oral involvement is prominent in PV (often the initial manifestation in >50% of patients) and is characteristically absent in BP.
Mnemonic: 'Pemphigus is high, flaccid, positive (Nikolsky+), oral, middle-aged. Pemphigoid is deep, tense, negative (Nikolsky−), mucosal-sparing, elderly.' Reversing any of these is a common examination trap.
Incorrect. Remember: PV = flaccid blisters, Nikolsky positive, oral mucosa involved, middle-aged. BP = tense blisters, Nikolsky negative, oral spared, elderly.
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A 58-year-old man with pemphigus vulgaris develops a rapidly spreading, warm, tender, erythematous area around multiple skin erosions on the back, with fever and leukocytosis (WBC 18,000/μL). The MOST likely complication and the MOST appropriate next step are:
Correct. Spreading erythema + warmth + fever + leukocytosis around erosions in PV = secondary bacterial infection. The correct response is microbiological sampling + empirical antibiotics + NOT increased immunosuppression.
Denuded skin in PV/BP is highly vulnerable to secondary bacterial infection (Staphylococcus aureus, Streptococcus). Recognising superinfection vs disease flare is a key DR13.2 clinical decision point — infection requires antibiotics, NOT increased immunosuppression.
Incorrect. Spreading warmth, fever, and leukocytosis around skin erosions indicates secondary bacterial infection — not a PV flare. Increasing steroids in the presence of infection would be harmful.
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Serology for a suspected autoimmune blistering disease shows ELISA-positive anti-desmoglein 1 (Dsg1) antibodies but NEGATIVE anti-desmoglein 3 (Dsg3) antibodies. The clinical finding you would MOST expect is:
Correct. Isolated anti-Dsg1 produces pemphigus foliaceus: superficial (subcorneal) splits on the skin only. Because Dsg3 is the dominant adhesion molecule in oral mucosa and is intact, there is no mucosal disease.
Desmoglein compensation: anti-Dsg1 alone → superficial (subcorneal) skin-only disease (pemphigus foliaceus); no oral disease because Dsg3 compensates in mucosae. Anti-Dsg3 alone → oral-only PV. Anti-Dsg1 + Dsg3 → mucocutaneous PV.
Incorrect. Anti-Dsg1 alone targets the most superficial epidermal layer and cannot overcome Dsg3 compensation in the oral mucosa — producing pemphigus foliaceus (skin only, no oral involvement).
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A 52-year-old woman with active, widespread pemphigus vulgaris is being prepared for transfer to a tertiary centre. Pending transfer, which of the following nursing and supportive care instructions is LEAST appropriate?
Correct — standard adhesive tape IS the least appropriate option. Removing adhesive tape from fragile perilesional skin strips the epidermis, creating new erosions. Non-adherent fixation (tubular bandage) must be used.
DR13.2 primary care principle: protect fragile skin from trauma. Adhesive tape on perilesional skin will strip the epidermis on removal — a harmful act of iatrogenic Nikolsky sign induction. All dressings must be non-adherent; fixation uses tubular bandage or foam without adhesive.
Incorrect. All the other options are correct supportive care measures. Adhesive tape on perilesional skin is contraindicated — removal generates new erosions by the same mechanism as Nikolsky's sign.
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