Vesiculobullous & Papulosquamous Disorders for NEET PG 2026

Master pemphigus, pemphigoid, dermatitis herpetiformis, EM/SJS/TEN, psoriasis, lichen planus and pityriasis rosea for NEET PG 2026 with immunofluorescence.

Pemphigus foliaceus

• Antigen: desmoglein-1 only.
• Level: subcorneal cleavage; "cornflake" scales.
• Clinical: crusted erosions on seborrheic areas; no oral involvement.
• Variants: fogo selvagem (Brazilian endemic), pemphigus erythematosus (Senear-Usher).

Bullous pemphigoid (BP)

• Antigen: BP180 (BPAG2, hemidesmosome) and BP230.
• Level: subepidermal.
• Clinical: elderly patient, tense bullae on flexures and trunk, intensely pruritic, Nikolsky negative, oral involvement rare (~10–20%).
• DIF: linear IgG and C3 along the basement membrane zone.
• Salt-split skin: IgG on the roof (epidermal side).
• Treatment: topical clobetasol (mild–moderate); systemic steroids + steroid-sparing agents (severe); dupilumab emerging.

Dermatitis herpetiformis (DH)

• Antigen: epidermal transglutaminase (TG3) — cousin of tissue transglutaminase.
• Level: subepidermal (papillary dermis).
• Clinical: intensely pruritic grouped vesicles on extensor surfaces (elbows, knees, buttocks, scalp); strongly associated with coeliac disease (anti-tTG, anti-endomysial).
• DIF: granular IgA at the tips of dermal papillae — pathognomonic.
• HLA: DQ2 / DQ8.
• Treatment: dapsone (rapid relief, check G6PD first) + strict gluten-free diet (definitive, allows dapsone tapering).

Linear IgA bullous dermatosis (LAD)

• Antigen: LABD97 (a fragment of BP180).
• Level: subepidermal.
• Clinical: "string-of-pearls" or "cluster-of-jewels" annular vesicles in children (chronic bullous disease of childhood); drug-induced (vancomycin) in adults.
• DIF: linear IgA at the BMZ.
• Treatment: dapsone, sulfapyridine; stop offending drug.

Epidermolysis bullosa acquisita (EBA)

• Antigen: type VII collagen (anchoring fibrils).
• Clinical: trauma-induced blisters on extensor surfaces; scarring, milia. Mimics dystrophic EB.
• Salt-split skin: IgG on the dermal floor (vs roof in BP).

Erythema multiforme / SJS / TEN

A spectrum of severe mucocutaneous reactions:

• Histology: full-thickness epidermal necrosis with subepidermal split.
• Nikolsky: positive in SJS/TEN.
• SCORTEN score — 7 variables (age >40, malignancy, HR >120, BSA >10%, urea >10 mmol/L, glucose >14 mmol/L, HCO3 <20); predicts mortality.
• Treatment: stop drug, supportive care in burns/ICU unit; cyclosporine (4 mg/kg/day) and IVIG most-used disease-modifying agents in India.

Herpes infections — eczema herpeticum

• HSV-1/2 vesicles on erythematous base; positive Tzanck smear (multinucleated giant cells).
• Eczema herpeticum — disseminated HSV in atopic dermatitis; medical emergency. Treat with IV acyclovir.
• Varicella zoster — dermatomal vesicles. Post-herpetic neuralgia in elderly. Treat within 72 hours of rash onset (acyclovir, valacyclovir, famciclovir).

Papulosquamous disorders

Psoriasis

• Pathogenesis: TNF-alpha → IL-23 → Th17 → IL-17 axis driving keratinocyte hyperproliferation.
• Clinical: well-demarcated erythematous plaques with silvery scales on extensors (elbows, knees, scalp, lower back); Auspitz sign (pinpoint bleeding on scale removal); Koebner phenomenon (lesions at trauma sites).
• Histology: parakeratosis, neutrophilic Munro microabscesses, regular acanthosis with elongated rete ridges, thinning of suprapapillary plates.
• Variants: chronic plaque (most common), guttate (post-streptococcal), pustular (von Zumbusch — life-threatening), erythrodermic, inverse, palmoplantar, nail (pitting, oil drops, onycholysis).
• Comorbidities: psoriatic arthritis (10–30%), metabolic syndrome, IBD.
• Treatment ladder:
  • Mild (BSA <3%): topical corticosteroids + vitamin D analogues (calcipotriol), tar, salicylic acid.
  • Moderate: phototherapy (NB-UVB first line; PUVA second line).
  • Moderate-severe (BSA >10%, PASI >10, DLQI >10): methotrexate, cyclosporine, acitretin, apremilast.
  • Severe / refractory: biologics — TNF-alpha (etanercept, adalimumab, infliximab); IL-17 (secukinumab, ixekizumab, brodalumab); IL-23 (guselkumab, risankizumab, tildrakizumab).

Lichen planus

• Mnemonic — 6 P's: Purple, Pruritic, Polygonal, Planar (flat-topped), Papules, Plaques.
• Distribution: flexor wrists, ankles, lower back, oral mucosa (Wickham striae — lacy white network).
• Histology: "saw-tooth" rete ridges, hypergranulosis, band-like lymphocytic infiltrate, Civatte bodies.
• Associations: hepatitis C (especially oral LP), Wilson disease (penicillamine-induced), graft-versus-host disease.
• Treatment: topical corticosteroids; oral prednisolone for severe; phototherapy.

Pityriasis rosea

• Cause: HHV-6/HHV-7 reactivation.
• Clinical: herald patch (single oval salmon plaque on trunk) precedes a "Christmas tree" distribution along Langer lines, 1–2 weeks later.
• Self-limiting: resolves in 6–8 weeks.
• DDx: secondary syphilis — always check VDRL/RPR if palms/soles involved.

Seborrheic dermatitis

• Greasy, yellow scales on scalp, eyebrows, nasolabial folds, central chest.
• Cause: Malassezia yeast overgrowth.
• Treatment: ketoconazole shampoo, topical steroids (short course), topical calcineurin inhibitors.
• NEET PG association: severe in HIV (AIDS-defining when extensive) and Parkinson disease.

Secondary syphilis

• 6 weeks–6 months after primary chancre.
• Maculopapular rash including palms and soles (mimicker of pityriasis rosea); condylomata lata in moist areas; mucous patches; patchy alopecia ("moth-eaten").
• Diagnosis: VDRL/RPR (non-treponemal, used for screening and treatment monitoring); FTA-ABS / TPHA (treponemal, confirmatory).
• Treatment: benzathine penicillin G 2.4 MU IM weekly × 2–3 doses.

Immunofluorescence patterns — high-yield summary

Nikolsky sign — when is it positive?

Pseudo-Nikolsky (Asboe-Hansen) — extension of an already-formed blister on pressure — is positive in pemphigoid.

NEET PG MCQ traps (high-yield list)

1. PV affects oral mucosa first (>50% of cases); BP rarely involves oral mucosa.
2. Tombstone basal cells = pemphigus vulgaris (suprabasal acantholysis).
3. DH = granular IgA at papillae; LAD = linear IgA at BMZ. Different diseases, similar names.
4. Salt-split DIF — BP on roof; EBA on floor.
5. Auspitz sign — psoriasis (pinpoint bleeding on scale removal).
6. Koebner phenomenon — psoriasis, lichen planus, vitiligo, vitiligo, viral warts.
7. Wickham striae — oral lichen planus.
8. Herald patch + Christmas tree = pityriasis rosea; palms + soles rash = secondary syphilis.
9. TEN >30% BSA; SJS <10% BSA.
10. Eczema herpeticum — IV acyclovir, not topical steroid escalation.
11. Rituximab is first-line for moderate-severe pemphigus vulgaris (post-2018 evidence).
12. Dapsone before G6PD test is contraindicated — always check G6PD first.

Recent updates (2025–2026)

• Pemphigus 2024 guidelines: rituximab + tapered prednisolone preferred over high-dose monotherapy steroids — fewer relapses, lower cumulative steroid burden.
• IL-23 inhibitors (risankizumab, guselkumab) achieving PASI 90/100 in >70% at 16 weeks; preferred over older TNF-alpha agents in many Indian dermatology centres.
• Dupilumab has emerging evidence in bullous pemphigoid; trials ongoing in pemphigus.
• NMC 2024 dermatology continues to emphasise immunofluorescence patterns and SJS-TEN management as Phase 3 must-knows.

Frequently Asked Questions

How do you differentiate pemphigus vulgaris from bullous pemphigoid?

Pemphigus vulgaris is intraepidermal (suprabasal) with flaccid bullae, positive Nikolsky sign, prominent oral involvement, IgG against desmoglein-3 (and desmoglein-1 in mucocutaneous form), and a 'fishnet' or 'chicken-wire' direct immunofluorescence pattern. Bullous pemphigoid is subepidermal with tense bullae, negative Nikolsky, rare oral lesions, IgG against BP180/BP230, and a linear DIF pattern at the basement membrane zone.

What is Nikolsky sign and what is pseudo-Nikolsky?

Nikolsky sign is the lateral extension of a blister or shearing of normal-looking skin with sliding pressure — positive in pemphigus vulgaris, SSSS and toxic epidermal necrolysis (TEN). Pseudo-Nikolsky (Asboe-Hansen sign) is extension of an existing blister edge on direct pressure — seen in pemphigoid. Nikolsky reflects acantholysis or full epidermal detachment; pseudo-Nikolsky reflects fluid spread.

What is the immunofluorescence pattern in dermatitis herpetiformis?

Dermatitis herpetiformis shows granular IgA deposits in the dermal papillae on direct immunofluorescence — often described as 'granular IgA at tips of dermal papillae.' It is associated with coeliac disease (anti-tissue transglutaminase, anti-endomysial antibodies), HLA-DQ2/DQ8, and presents as intensely pruritic grouped vesicles on extensor surfaces. First-line treatment is dapsone plus a strict gluten-free diet.

What is the treatment ladder for chronic plaque psoriasis?

Mild (under 3% BSA): topical corticosteroids + vitamin D analogues (calcipotriol), tar, or salicylic acid. Moderate: phototherapy (NB-UVB, PUVA). Moderate-severe (over 10% BSA, PASI over 10, DLQI over 10): systemic methotrexate, cyclosporine, acitretin, or apremilast. Refractory or severe: biologics — TNF-alpha inhibitors (etanercept, adalimumab, infliximab), IL-17 inhibitors (secukinumab, ixekizumab), or IL-23 inhibitors (guselkumab, risankizumab).

How do you distinguish SJS from TEN clinically?

Stevens-Johnson syndrome involves under 10% body surface area (BSA) of epidermal detachment; SJS-TEN overlap is 10–30% BSA; toxic epidermal necrolysis is over 30% BSA. Both share mucosal involvement (more than 2 sites), positive Nikolsky sign, and full-thickness epidermal necrosis on histology. Mortality rises with BSA — TEN mortality reaches 25–35%. SCORTEN score predicts mortality based on 7 clinical variables.

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