Image MCQ Walkthrough: Dermatology Vesiculobullous Diseases — Pemphigus, Pemphigoid, DH and More (NEET PG)

Version 1.0 — Published March 2026

Clinical image presentation

A 52-year-old man presents to the dermatology outpatient clinic with a 6-week history of painful oral erosions that have progressed to involve the lips, buccal mucosa, and hard palate. He has difficulty eating and has lost 4 kg. Over the past 2 weeks, flaccid blisters have appeared on the scalp, upper chest, and back — they rupture within hours of forming, leaving raw, weeping erosions that slowly re-epithelialize. No significant past medical history. No recent medication changes. No family history of skin disease.

On examination: vitals normal, temperature 37.4 C. Extensive oral mucosal erosions involving buccal mucosa, tongue, lips, and soft palate — the hard palate shows denuded epithelium. On the scalp, upper chest, and interscapular region: multiple flaccid, easily ruptured bullae on apparently normal skin, with widespread shallow erosions and crusting. Peri-lesional skin demonstrates a positive Nikolsky sign — lateral pressure causes epidermal slide. Asboe-Hansen sign is positive — lateral pressure on an existing intact bulla extends it into adjacent normal skin.

A student interpreting the dermatology photograph and clinical history should systematically identify:

Lesion morphology:

• Flaccid bullae (roof thin, easily ruptured, often only erosions visible)
• No tense, dome-shaped intact blisters
• No grouped vesicles
• Widespread erosions without new vesicle formation at the edges

Lesion distribution:

• Mucosal-dominant (oral, sometimes conjunctival, genital) — often the presenting and most severe site
• Cutaneous lesions on scalp, upper chest, back — seborrheic distribution
• Not flexural (rules out BP)
• Not extensor/grouped (rules out DH)
• Not annular with peripheral vesicle rim (rules out linear IgA)

Bedside signs:

• Nikolsky sign POSITIVE — indicates loss of intercellular cohesion (epidermal split)
• Asboe-Hansen sign POSITIVE — lateral bulla extension from pressure

Age and course:

• 52-year-old adult (middle age — typical PV; BP is elderly above 70; DH is young adult 20-40)
• 6-week chronic progressive course (rules out acute drug reaction)

Investigations ordered:

• Skin biopsy (H&E) from a fresh blister: suprabasal acantholysis with basal keratinocytes lined up in a tombstone row along the floor of the intraepidermal blister cavity; rounded acantholytic cells within the blister cavity
• Perilesional skin biopsy for DIF: intercellular IgG and C3 deposition in a net-like (fishnet) pattern throughout the epidermis
• Serum indirect immunofluorescence (IIF) on monkey esophagus: circulating anti-desmoglein 3 antibodies, titer 1:640
• ELISA: anti-desmoglein 3 (Dsg3) antibody positive at high titer; anti-desmoglein 1 (Dsg1) negative (mucosal-dominant PV)

MCQ question as it appears in NEET PG

A 52-year-old man presents with a 6-week history of painful oral erosions that are worsening, and 2 weeks of flaccid blisters on the scalp, chest, and back. The blisters rupture within hours. Nikolsky sign is positive on peri-lesional skin. Histology shows suprabasal acantholysis with a tombstone row of basal keratinocytes. DIF of peri-lesional skin shows intercellular IgG and C3 in a fishnet pattern. Which of the following is the most likely diagnosis and its target antigen?

• (a) Bullous pemphigoid — IgG against BP180 (hemidesmosome)
• (b) Pemphigus vulgaris — IgG against desmoglein 3
• (c) Dermatitis herpetiformis — IgA against epidermal transglutaminase (TG3)
• (d) Linear IgA bullous dermatosis — IgA against BP180

Take a moment to work through this before reading the analysis below.

Step-by-step visual analysis

A systematic reading protocol is critical — missing a single criterion (bulla tension, Nikolsky, DIF) can push you toward the wrong diagnosis. Use this protocol every time a vesiculobullous image or case appears in an NEET PG MCQ.

Step 1: Assess bulla morphology — flaccid vs tense

Bulla tension directly predicts the level of epidermal split.

In this patient: flaccid bullae → intraepidermal disease (pemphigus family).

Step 2: Test Nikolsky sign

• Positive Nikolsky = loss of intercellular cohesion in epidermis; characteristic of:
  • Intraepidermal blistering (pemphigus vulgaris, pemphigus foliaceus)
  • Epidermal necrolysis (SJS/TEN, staphylococcal scalded skin syndrome, severe burns)
• Negative Nikolsky = intact epidermis; characteristic of:
  • Subepidermal blistering (bullous pemphigoid, dermatitis herpetiformis, linear IgA)

Asboe-Hansen sign (lateral extension of existing bulla by pressure) is the positive-Nikolsky equivalent applied to an intact bulla — positive in pemphigus.

In this patient: Nikolsky positive + flaccid bullae + chronic course with mucosal involvement → pemphigus vulgaris (not SJS/TEN which would be acute with widespread necrolysis).

Step 3: Correlate clinical distribution

Distribution narrows the differential dramatically.

In this patient: mucosal-dominant + flaccid + seborrheic cutaneous distribution + middle-age → pemphigus vulgaris.

Step 4: Review histology level

In this patient: suprabasal split with tombstone row → pemphigus vulgaris.

Step 5: Interpret DIF pattern

DIF on peri-lesional skin is the single most discriminatory test in vesiculobullous disease.

In this patient: intercellular IgG + C3 fishnet → pemphigus vulgaris, confirmed.

Step 6: Match to serology

• Anti-desmoglein 3 ELISA: positive in PV (mucosal + cutaneous or mucosal-only PV)
• Anti-desmoglein 1 ELISA: positive in pemphigus foliaceus and mucocutaneous PV
• Anti-BP180 and anti-BP230 ELISA: positive in bullous pemphigoid
• Anti-tissue transglutaminase (TG2) and anti-epidermal transglutaminase (TG3) IgA: positive in DH (and 90 percent have celiac disease with anti-TG2 positivity)

In this patient: anti-Dsg3 positive at 1:640 → confirms mucocutaneous pemphigus vulgaris.

Answer and detailed explanation

Correct answer: (b) Pemphigus vulgaris — IgG against desmoglein 3

This patient has classic mucocutaneous pemphigus vulgaris. Mucosal-dominant presentation, flaccid bullae, positive Nikolsky, suprabasal acantholysis with tombstone row on histology, and intercellular IgG/C3 fishnet DIF with high-titer anti-Dsg3 ELISA are pathognomonic. Pemphigus vulgaris is driven by IgG autoantibodies against desmoglein 3 (mucosal form) or desmoglein 1 and 3 (mucocutaneous form). Desmoglein 3 is the dominant desmosomal cadherin in mucosa and the deep epidermis — its loss disrupts keratinocyte-keratinocyte adhesion suprabasally.

Why each distractor is wrong:

NEET PG trap alert: The commonest wrong answer in a mucocutaneous bullous disease vignette is "bullous pemphigoid" because both diseases involve IgG. Remember: bullous pemphigoid is a subepidermal, Nikolsky-negative, tense-bulla, elderly, flexural, pruritic disease with linear DIF. Pemphigus vulgaris is intraepidermal, Nikolsky-positive, flaccid-bulla, middle-aged, mucocutaneous, with intercellular fishnet DIF. The three C's for pemphigus: Cohesion loss (Nikolsky+), Caudal-first (mucosa first), Crusting shallow erosions.

Practice dermatology MCQs with AI-powered explanations to build visual and DIF pattern recognition. For a full review, see the dermatology high-yield topics guide and the related psoriasis vs eczema image MCQ walkthrough.

Similar patterns comparison table

The five vesiculobullous diseases most commonly tested in NEET PG — memorize this comparison table, it covers approximately 90 percent of vesiculobullous image MCQs:

Clinical application: how to approach a vesiculobullous image in the exam

The systematic approach below solves 90 percent of NEET PG vesiculobullous image questions in under 90 seconds.

Frequently asked questions

What is the difference between tense and flaccid bullae and why does it matter?

Bulla tension is a direct clinical clue to the histologic level of blister formation. Flaccid bullae (easily ruptured, roof thin, often only erosions visible) indicate an intraepidermal split where the blister roof is just a few cell layers — classic of pemphigus vulgaris (suprabasal split) and pemphigus foliaceus (subcorneal split). Tense bullae (firm, intact, dome-shaped, persist for days) indicate a subepidermal split where the entire epidermis forms the roof — classic of bullous pemphigoid, dermatitis herpetiformis, linear IgA disease, epidermolysis bullosa acquisita, and bullous lupus. The single clinical sign of bulla tension reliably predicts the split level and narrows the differential by 50 percent before DIF.

How is Nikolsky sign elicited and what does it mean?

Nikolsky sign is the induction of epidermal detachment by lateral pressure on apparently normal or peri-lesional skin. Positive Nikolsky indicates loss of intercellular cohesion in the epidermis — a feature of intraepidermal blistering diseases (pemphigus vulgaris, pemphigus foliaceus) and acute epidermal necrolysis (SJS/TEN, staphylococcal scalded skin syndrome). Asboe-Hansen sign is related — lateral extension of an existing bulla with pressure, also positive in pemphigus. Negative Nikolsky is typical of subepidermal diseases (bullous pemphigoid, dermatitis herpetiformis, linear IgA). Key NEET PG trap: Nikolsky positive does NOT mean pemphigus by default — TEN, SSSS, and severe burns also show positive Nikolsky, and context distinguishes them.

What are the three direct immunofluorescence (DIF) patterns in vesiculobullous diseases?

DIF on peri-lesional skin shows three diagnostic patterns. First, intercellular IgG and C3 deposition in a net-like pattern throughout the epidermis — diagnostic of pemphigus vulgaris (IgG against desmoglein 3) and pemphigus foliaceus (IgG against desmoglein 1). Second, linear IgG and C3 at the basement membrane zone (BMZ) — diagnostic of bullous pemphigoid (IgG against BP180 and BP230 hemidesmosomes). A similar linear pattern with IgA alone is diagnostic of linear IgA disease. Third, granular IgA deposition in dermal papillae — pathognomonic of dermatitis herpetiformis (IgA against epidermal transglutaminase TG3). EBA (epidermolysis bullosa acquisita) shows linear IgG at BMZ like BP but on salt-split skin the deposits localize to the dermal side (vs epidermal side in BP).

What is the pathological level of blister formation in each major vesiculobullous disease?

Intraepidermal split diseases (flaccid bullae, Nikolsky positive): pemphigus vulgaris splits suprabasally (above basal cells, leaving tombstone row), pemphigus foliaceus splits subcorneally (just below stratum corneum), staphylococcal scalded skin syndrome splits in stratum granulosum (exfoliative toxin cleaves desmoglein 1), Hailey-Hailey shows full-thickness acantholysis (dilapidated brick wall). Subepidermal split diseases (tense bullae, Nikolsky negative): bullous pemphigoid splits at the lamina lucida (above PAS-positive basement membrane), dermatitis herpetiformis and linear IgA split at the lamina lucida, epidermolysis bullosa acquisita splits below the lamina densa (sublamina densa). SJS/TEN shows full-thickness epidermal necrosis — the split is at the dermo-epidermal junction because the entire epidermis is dead.

How is pemphigus vulgaris clinically distinguished from bullous pemphigoid?

Six clinical features separate PV from BP. Age: PV affects 40-60 years; BP affects elderly (above 70 years). Mucosal involvement: PV has almost 100 percent mucosal (oral, conjunctival, genital) — often the presenting feature; BP has only 10-20 percent mucosal. Bulla type: PV has flaccid bullae with widespread erosions because bullae rupture fast; BP has tense intact bullae that last days. Nikolsky sign: positive in PV, negative in BP. Itching: mild in PV, severe in BP (often precedes bullae by weeks — 'pre-bullous pemphigoid' phase). Mortality: untreated PV mortality is 60-90 percent (lethal disease before steroids); untreated BP is self-limiting over 1-5 years with 10-20 percent mortality mostly from comorbidities in the elderly.

What is the classic histology of pemphigus vulgaris?

Pemphigus vulgaris histology shows three pathognomonic features. First, suprabasal acantholysis — loss of desmosomes between keratinocytes creates an intraepidermal split just above the basal cell layer. Second, tombstone appearance — the basal keratinocytes remain attached to the basement membrane but lose lateral attachments to their neighbors, lining up like tombstones along the floor of the blister cavity. Third, acantholytic cells (Tzanck cells) within the blister cavity — rounded keratinocytes that have lost their intercellular connections. Tzanck smear from a fresh blister shows these rounded acantholytic cells (also seen in viral blisters — HSV, VZV — but without tombstone histology). DIF is diagnostic: intercellular IgG and C3 net-like pattern.

How is dermatitis herpetiformis linked to celiac disease and how is it treated?

Dermatitis herpetiformis (DH) is the cutaneous manifestation of gluten sensitivity — 90 percent of DH patients have small bowel villous atrophy (often subclinical). Both conditions are driven by IgA antibodies against tissue transglutaminase (TG2 in gut, TG3 in skin). DH presents as intensely itchy, grouped vesicles on extensor surfaces (elbows, knees, buttocks, scalp) — the grouped herpetiform distribution is the name origin. DIF shows pathognomonic granular IgA in dermal papillae. Treatment: strict lifelong gluten-free diet (addresses both skin and gut disease); dapsone 50-100 mg/day provides rapid symptomatic relief within 24-48 hours but does NOT address the underlying gluten enteropathy. G6PD screen is mandatory before dapsone (risk of hemolytic anemia in deficient patients).

How is vesiculobullous dermatology tested in NEET PG?

NBE tests vesiculobullous diseases through five patterns: clinical photograph recognition with bulla type (flaccid vs tense) and distribution (flexural in BP, extensor in DH, mucosal in PV), Nikolsky sign interpretation (positive in PV, SJS/TEN, SSSS; negative in BP, DH, linear IgA), histology level recognition (suprabasal in PV, subcorneal in PF, subepidermal in BP/DH/linear IgA), DIF pattern matching (intercellular net in pemphigus, linear BMZ in BP/linear IgA, granular BMZ in DH), and treatment choice (steroids for PV and BP, gluten-free diet plus dapsone for DH, withdraw offending drug plus supportive care in SCORTEN ICU for SJS/TEN). Expect 2-3 vesiculobullous questions per NEET PG paper in the dermatology section.

Sources and references

1. Bolognia JL, Schaffer JV, Cerroni L, Dermatology, 4th Edition (Elsevier, 2018) — comprehensive reference for autoimmune bullous diseases including histology, DIF patterns, and treatment algorithms.
2. Schmidt E, Kasperkiewicz M, Joly P, "Pemphigus," Lancet, 2019 — definitive review on pemphigus vulgaris pathogenesis, diagnosis, and first-line rituximab therapy.
3. IADVL Textbook of Dermatology, 5th Edition (Bhalani Publishing, 2022) — Indian standard dermatology reference with clinical photographs and DIF pattern recognition chapters for NEET PG preparation.

Strengthen your dermatology image pattern recognition by working through vesiculobullous and papulosquamous cases. Review the dermatology subject page, deepen psoriasis-vs-eczema reasoning with the dermatology psoriasis vs eczema image MCQ walkthrough, and drill targeted dermatology MCQs on NEETPGAI. Ready for unlimited AI-powered MCQs with detailed explanations? Explore NEETPGAI Pro.

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Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: March 2026

This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.