Dermatology

Dermatology is one of the highest-yield-per-hour subjects in the NEET PG and INI-CET examinations. Although the absolute number of questions is modest compared with Medicine or Surgery, the subject is small, finite, image-heavy and pattern-driven, which means a focused student can convert almost every dermatology question into a guaranteed mark. The examiners reward recognition of classic morphology, knowledge of fixed associations, and command over a handful of "first-line drug / diagnostic test / pathognomonic sign" facts. This mother page maps the entire subject the way the exam actually tests it, group by group, with the traps, values, criteria, integrations and revision strategy you need.

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How Dermatology is Tested in NEET PG / INI-CET

Weightage

• NEET PG: Approximately 8–12 questions out of 200 (roughly 4–6%). Dermatology, Venereology and Leprosy (DVL) is examined as a combined unit, and in some papers leprosy + STDs alone account for nearly half the dermatology questions.
• INI-CET: Slightly higher conceptual depth, 6–10 questions, with a strong tilt toward image-based recognition, immunofluorescence patterns, and recent guideline updates (e.g., NLEP, NACO).
• FMGE: High yield (10–15 questions), heavily leprosy- and STD-weighted.

Recurrent question styles

Question style	What it looks like	Example theme
Clinical image / spot diagnosis	Photograph or description of a lesion → identify	Target lesions → erythema multiforme
"Pathognomonic sign" recall	A named sign → disease	Auspitz sign → psoriasis
First-line / drug of choice	Best treatment	Scabies → permethrin 5%
Histopathology / IF pattern	Microscopy or immunofluorescence → diagnosis	Fishnet/chicken-wire IgG → pemphigus vulgaris
Criteria / classification	WHO / clinical grouping	Ridley–Jopling spectrum of leprosy
Associations & syndromes	Cutaneous marker of systemic disease	Acanthosis nigricans → insulin resistance / GI adenocarcinoma
Single-best-answer integration	Pharmacology / pathology overlap	Mechanism of dapsone, MTX side effects

The single most important exam skill is morphological vocabulary: macule, papule, plaque, vesicle, bulla, pustule, wheal, nodule, scale, crust, erosion, ulcer, lichenification. Almost every stem is built on these primitives, and a student who confuses a vesicle (<0.5 cm) with a bulla (>0.5 cm) loses easy marks.

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Group 1: Infections

Cutaneous infections (bacterial, fungal, viral, parasitic infestations) are the single largest contributor of dermatology MCQs after leprosy and STDs. They are loved by examiners because each organism has a fixed lesion, a fixed investigation, and a fixed first-line drug.

Bacterial (pyodermas)

• Impetigo: Staphylococcus aureus (now commonest) and Streptococcus pyogenes. Honey-coloured crusts = non-bullous impetigo. Bullous impetigo = S. aureus exfoliative toxin (cleaves desmoglein-1). Post-streptococcal glomerulonephritis can follow, but rheumatic fever does not follow skin streptococcal infection — a classic trap.
• Erysipelas: Upper dermis + lymphatics, sharply demarcated, raised border, "tomato-red", commonly face/leg, Strep pyogenes.
• Cellulitis: Deeper, ill-defined border.
• Staphylococcal scalded skin syndrome (SSSS): Toxin-mediated, subcorneal/granular split, Nikolsky positive, children, spares mucosa (vs TEN which involves mucosa and splits at the dermo-epidermal junction).

Fungal (dermatophytes / superficial mycoses)

• Dermatophytoses (tinea): Trichophyton, Microsporum, Epidermophyton. KOH mount shows septate hyaline hyphae. Wood's lamp: Microsporum fluoresces green.
• Tinea versicolor: Malassezia furfur. "Spaghetti and meatballs" (hyphae + spores) on KOH. Coppery-orange/pale yellow Wood's lamp fluorescence. Hypo- or hyperpigmented macules.
• Recent epidemic trap: India is facing recalcitrant/steroid-modified tinea (Trichophyton indotineae) with terbinafine resistance; itraconazole is now the practical first-line oral agent for extensive disease — a high-yield recent-update point.
• Candidiasis: Satellite lesions, intertrigo; pseudohyphae + budding yeast.

Viral

• Herpes (HSV): Grouped vesicles on erythematous base; Tzanck smear shows multinucleated giant cells (also positive in varicella/zoster). DOC: acyclovir/valacyclovir.
• Molluscum contagiosum: Poxvirus, umbilicated papules, Henderson–Paterson (molluscum) bodies. In adults, profuse/facial molluscum is an HIV indicator.
• Warts: HPV. Plantar, periungual, genital (condyloma acuminata, HPV 6/11).

Infestations

• Scabies: Sarcoptes scabiei. Burrows, web spaces, genitalia; intense nocturnal itch; spares face in adults (not in infants). DOC: topical permethrin 5%; oral ivermectin for crusted (Norwegian) scabies / mass treatment. Crusted scabies → immunocompromised/HIV.
• Pediculosis: Lice; permethrin/malathion.

Traps in this group

• Honey-coloured crust = impetigo (not eczema).
• Nikolsky sign is positive in SSSS, pemphigus, TEN — but the level of split differs (subcorneal vs suprabasal vs subepidermal).
• Tzanck smear is not specific for one virus.

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Group 2: Papulosquamous Disorders

These are disorders with papules and scaling — the morphological hallmark. Psoriasis dominates this group and is among the most frequently asked single topics in all of dermatology.

Psoriasis

• Type: Chronic immune-mediated (Th17/IL-17, IL-23, TNF-α), hyperproliferative epidermis.
• Lesion: Well-defined erythematous plaques with silvery-white scales, extensor surfaces, scalp, lumbosacral.
• Signs (very high-yield):
  • Auspitz sign: Pinpoint bleeding on scale removal (dilated dermal papillae capillaries).
  • Candle grease sign (grattage).
  • Koebner phenomenon: Lesions at sites of trauma (also in lichen planus, vitiligo, warts).
• Histology: Munro microabscesses (neutrophils in stratum corneum), parakeratosis, regular acanthosis, thinned suprapapillary plates, Kogoj spongiform pustules.
• Nail changes: Pitting (commonest), oil-drop sign, onycholysis, subungual hyperkeratosis.
• Associations: Psoriatic arthritis, metabolic syndrome, uveitis, IBD. Aggravated by lithium, beta-blockers, antimalarials, abrupt systemic steroid withdrawal (→ pustular psoriasis).
• Treatment ladder: Topical (calcipotriol, steroids) → phototherapy (NB-UVB) → systemic (methotrexate, acitretin, cyclosporine) → biologics (anti-TNF, anti–IL-17 secukinumab, anti–IL-23 guselkumab). Recent-update theme: IL-17/IL-23 biologics are now standard for moderate-to-severe disease.

Lichen planus (the "6 Ps")

Pruritic, Purple, Polygonal, Planar, Papules and Plaques.

• Wickham's striae: White lacy lines over papules.
• Sites: flexor wrists, oral mucosa (Wickham's striae, lacy white), genitalia, nails (longitudinal ridging, pterygium).
• Histology: Sawtooth rete ridges, Civatte (apoptotic) bodies, band-like (lichenoid) lymphocytic infiltrate at DEJ, hypergranulosis (wedge-shaped), Max Joseph spaces.
• Association: Hepatitis C (especially oral LP). Drug-induced lichenoid eruption: thiazides, antimalarials, gold.

Pityriasis rosea

• Herald patch first → "Christmas tree" distribution on trunk along Langer's lines. Self-limiting; HHV-6/7 association. Collarette scale.

Pityriasis rubra pilaris

• Orange-red plaques with islands of sparing, follicular hyperkeratosis, palmoplantar keratoderma.

Traps

• Auspitz = psoriasis; Wickham's striae = lichen planus — do not swap.
• Koebner is shared (psoriasis, LP, vitiligo).
• Herald patch precedes pityriasis rosea by 1–2 weeks.

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Group 3: Vesiculobullous Disorders

This is the immunofluorescence group — INI-CET examiners particularly love the IF patterns and the target antigens. The key discriminator is the level of the split.

Disease	Antigen / target	Split level	DIF pattern	Nikolsky	Mucosa
Pemphigus vulgaris	Desmoglein 3 (±1)	Suprabasal (intraepidermal)	Fishnet / chicken-wire IgG + C3	Positive	Involved (often first)
Pemphigus foliaceus	Desmoglein 1	Subcorneal	Fishnet, superficial	Positive	Spared
Bullous pemphigoid	BP180, BP230 (hemidesmosome)	Subepidermal	Linear IgG + C3 along BMZ	Negative	Usually spared
Dermatitis herpetiformis	Tissue transglutaminase / epidermal TG	Subepidermal	Granular IgA in dermal papillae	Negative	Spared
Linear IgA disease	BP180 fragment	Subepidermal	Linear IgA along BMZ	Negative	Variable

High-yield specifics

• Pemphigus vulgaris: Flaccid bullae, Tzanck smear → acantholytic cells, oral lesions often the first sign. Most lethal of the group historically. DOC: systemic corticosteroids + rituximab (rituximab now first-line steroid-sparing — a major recent guideline shift).
• Bullous pemphigoid: Elderly, tense bullae, intense pruritus, eosinophils, salt-split skin → roof (epidermal) binding.
• Dermatitis herpetiformis: Intensely pruritic grouped vesicles on extensor surfaces (elbows, knees, buttocks), gluten-sensitive enteropathy (celiac), responds to dapsone and gluten-free diet. Neutrophilic microabscesses in dermal papillae.
• Epidermolysis bullosa acquisita: Anti–type VII collagen; salt-split skin → floor (dermal) binding.

Erythema multiforme / SJS / TEN spectrum

• Erythema multiforme: Target (iris) lesions; commonest trigger HSV.
• SJS (<10% BSA), SJS-TEN overlap (10–30%), TEN (>30% BSA): Drug-induced (sulfonamides, anticonvulsants, allopurinol, NSAIDs). SCORTEN prognostic score. Stop the drug; supportive ICU/burns-unit care. Nikolsky positive, mucosal involvement.

Traps

• DH → granular IgA; Linear IgA disease → linear IgA. Easy to confuse.
• Pemphigus = intraepidermal, Nikolsky +; pemphigoid = subepidermal, Nikolsky −.
• Target lesion ≠ erythema chronicum migrans (Lyme).

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Group 4: Leprosy (Hansen's Disease)

Leprosy is the single most exam-dense topic in DVL for Indian exams — expect 2–4 questions. Mycobacterium leprae (acid-fast, cannot be cultured in vitro, grows in mouse footpad / nine-banded armadillo). Generation time ~12–14 days (slowest of all bacteria).

Ridley–Jopling classification (immunological spectrum)

Type	Lesions	Bacillary load	Lepromin test	Immunity
TT (tuberculoid)	Few, large, anaesthetic, well-defined	Paucibacillary	Strongly +	Strong CMI (Th1)
BT	Few	Low	+
BB (mid-borderline)	"Punched-out" / Swiss-cheese	Intermediate	±	Unstable
BL	Many	High	−
LL (lepromatous)	Numerous, symmetric, leonine facies, madarosis	Multibacillary	Negative	Th2, poor CMI

• Indeterminate leprosy: Earliest, hypopigmented macule, may heal or progress.

WHO operational classification (for treatment)

• Paucibacillary (PB): 1–5 lesions / single nerve.
• Multibacillary (MB): ≥6 lesions / smear positive.

WHO MDT (recent update — high yield)

WHO now recommends a uniform 3-drug regimen (rifampicin + dapsone + clofazimine) for both PB and MB:

• PB: 6 months.
• MB: 12 months.
• Rifampicin is the key bactericidal drug (monthly supervised).
• Clofazimine → reddish-black skin pigmentation, ichthyosis.
• Dapsone → haemolysis (G6PD), methaemoglobinaemia, dapsone hypersensitivity syndrome.

Lepra reactions (very high-yield)

Feature	Type 1 (Reversal)	Type 2 (ENL)
Mechanism	Type IV (cell-mediated)	Type III (immune complex)
Spectrum	Borderline (BT–BL)	LL, BL
Features	Existing lesions inflamed, nerve damage / neuritis	Erythema nodosum leprosum — crops of tender nodules, fever, systemic
Treatment	Corticosteroids	Thalidomide (DOC; teratogenic), steroids, clofazimine

Nerve / deformity facts

• Ulnar nerve = most commonly involved nerve. Others: median, common peroneal (foot drop), posterior tibial, great auricular, facial.
• Lucio phenomenon: Diffuse non-nodular lepromatous leprosy (Latin America) with necrotic lesions.
• Lepromin test is prognostic, not diagnostic.
• Slit-skin smear: Bacteriological Index (BI) and Morphological Index (MI).

Traps

• Lepromin positive = good immunity (TT), not active disease.
• M. leprae cannot be cultured — a recurring single-line MCQ.
• Thalidomide for ENL (Type 2), steroids for Type 1.

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Group 5: Sexually Transmitted Diseases (STDs / Venereology)

STDs are tested heavily and integrate with Microbiology and Community Medicine (NACO, syndromic management). The key discriminator is painful vs painless ulcer and incubation period.

Genital ulcer disease

Disease	Organism	Ulcer	Lymphadenopathy	Diagnosis
Syphilis (1°)	Treponema pallidum	Painless, indurated (hard chancre), clean	Painless, rubbery, bilateral	Dark-ground microscopy; VDRL/RPR; TPHA/FTA-ABS
Chancroid	Haemophilus ducreyi	Painful, soft, ragged, undermined	Painful, suppurative bubo	"School of fish" Gram stain
LGV	Chlamydia trachomatis L1–L3	Transient	Groove sign, matted	NAAT
Granuloma inguinale (Donovanosis)	Klebsiella granulomatis	Beefy-red, painless	"Pseudobubo"	Donovan bodies (Giemsa)
Herpes genitalis	HSV-2	Painful grouped vesicles → ulcers	Tender	Tzanck / PCR

Syphilis staging (high-yield)

• Primary: Hard chancre (3 weeks).
• Secondary: Condyloma lata, palms & soles maculopapular rash, mucous patches, generalized lymphadenopathy.
• Latent: Asymptomatic, serology positive.
• Tertiary: Gummas, cardiovascular (aortitis), neurosyphilis (tabes dorsalis, Argyll Robertson pupil, general paresis).
• Jarisch–Herxheimer reaction: Fever after penicillin (release of treponemal antigens).
• DOC: Benzathine penicillin G; doxycycline if allergic; neurosyphilis → aqueous crystalline penicillin IV.

Urethritis / discharge

• Gonococcal: Neisseria gonorrhoeae, purulent, short incubation. DOC: ceftriaxone + azithromycin/doxycycline (dual therapy for co-infection and resistance).
• Non-gonococcal: Chlamydia trachomatis (D–K), Ureaplasma, Mycoplasma genitalium.

Recent updates

• NACO syndromic management kits (colour-coded) and the emphasis on dual therapy for gonorrhoea due to rising cephalosporin resistance.
• HIV: Cutaneous markers — Kaposi sarcoma (HHV-8), eosinophilic folliculitis, oral hairy leukoplakia (EBV), severe seborrheic dermatitis, bacillary angiomatosis.

Traps

• Painless ulcer = syphilis/donovanosis/LGV; painful = chancroid/herpes.
• VDRL is non-treponemal (screening, can be falsely positive in SLE, pregnancy, leprosy); TPHA confirms.
• Condyloma lata (syphilis) vs condyloma acuminata (HPV).

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Group 6: Pigmentary Disorders

Tested for mechanism (melanocyte destruction vs dysfunction), associations and Wood's lamp findings.

Vitiligo

• Autoimmune destruction of melanocytes → depigmented (not hypopigmented) macules, chalk-white, accentuated under Wood's lamp.
• Koebner positive. Associations: thyroid disease (Hashimoto's), pernicious anaemia, T1DM, Addison's, alopecia areata (autoimmune polyendocrine cluster).
• Treatment: topical steroids/calcineurin inhibitors, NB-UVB, surgical grafting. Recent update: topical ruxolitinib (JAK inhibitor) approved for non-segmental vitiligo.

Melasma (chloasma)

• Hyperpigmentation, malar/centrofacial, women, pregnancy ("mask of pregnancy"), OCP, sun exposure. Triple combination (hydroquinone + tretinoin + steroid), sunscreen.

Albinism

• Tyrosinase deficiency (OCA1) — autosomal recessive; ↑ skin cancer, nystagmus, photophobia.

Other discriminators

• Pityriasis alba: Hypopigmented (not depigmented) patches, atopic children.
• Post-inflammatory hypo/hyperpigmentation.
• Café-au-lait macules: ≥6 (>5 mm pre-pubertal / >15 mm post-pubertal) → NF-1; also McCune–Albright (coast-of-Maine borders).
• Ash-leaf macules: Tuberous sclerosis (Wood's lamp enhanced).

Traps

• Vitiligo = depigmented; pityriasis alba/versicolor/leprosy = hypopigmented.
• Wood's lamp accentuates vitiligo (epidermal pigment loss).
• NF-1 vs McCune–Albright café-au-lait border morphology (coast of California vs coast of Maine).

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Group 7: Tumours

Tested for risk factors, histology and the "premalignant → malignant" progression.

Premalignant

• Actinic (solar) keratosis → SCC.
• Bowen's disease: SCC in situ.
• Leukoplakia / erythroplakia of mucosa.

Malignant

Tumour	Cell of origin	Key features	Spread
Basal cell carcinoma (BCC)	Basal keratinocytes	Rodent ulcer, pearly border, telangiectasia, sun-exposed face (above a line from angle of mouth to ear lobe)	Locally invasive, rarely metastasises
Squamous cell carcinoma (SCC)	Keratinocytes	Keratin pearls, arises in scars (Marjolin ulcer), lower lip, can metastasise	Lymphatic
Malignant melanoma	Melanocytes	ABCDE, Breslow thickness = key prognostic factor	Highly metastatic

Melanoma high-yield

• ABCDE: Asymmetry, Border irregularity, Colour variegation, Diameter >6 mm, Evolution.
• Breslow thickness (depth in mm) is the most important prognostic indicator; Clark's level is older.
• Types: superficial spreading (commonest), nodular (worst prognosis, vertical growth early), lentigo maligna, acral lentiginous (palms/soles/nails — commonest in Indians/dark skin).
• Recent update: BRAF inhibitors (vemurafenib/dabrafenib) and immune checkpoint inhibitors (anti–PD-1 nivolumab/pembrolizumab, anti–CTLA-4 ipilimumab) for metastatic melanoma.

Mycosis fungoides

• Cutaneous T-cell lymphoma; Pautrier microabscesses; Sézary syndrome (leukaemic, erythroderma + atypical cerebriform Sézary cells).

Traps

• BCC rarely metastasises; SCC and melanoma do.
• Marjolin ulcer (SCC in chronic wound/scar/burn).
• Acral lentiginous melanoma is most relevant to Indian skin.

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Cross-Subject Integration Points

Dermatology is a connective subject; many MCQs are deliberately placed in other papers.

Overlap	Where it appears	Key fact
Pharmacology	Methotrexate (folate antagonist, hepatotoxic, pancytopenia), dapsone (haemolysis/G6PD), retinoids (teratogenic, ↑ triglycerides), thalidomide (teratogenic, ENL)	Drug + side effect pairing
Pathology / IF	Pemphigus, pemphigoid, DH, lupus band test	Split level + IF pattern
Microbiology	Leprosy, syphilis, dermatophytes, HSV/VZV	Organism + stain
Medicine	Cutaneous markers of systemic disease	Acanthosis nigricans, erythema nodosum, pyoderma gangrenosum (IBD), necrolytic migratory erythema (glucagonoma), dermatomyositis (heliotrope, Gottron)
Community Medicine	NLEP, NACO, syndromic STD management	Programme indicators
Endocrinology	Acanthosis nigricans (insulin resistance), pretibial myxoedema (Graves'), necrobiosis lipoidica (diabetes)	Skin–endocrine link

Cutaneous markers worth memorising

• Acanthosis nigricans: Insulin resistance, obesity; sudden onset → GI adenocarcinoma (paraneoplastic).
• Erythema nodosum: Sarcoidosis, streptococcal infection, TB, IBD, OCP, drugs.
• Pyoderma gangrenosum: IBD, RA; pathergy positive.
• Dermatitis herpetiformis: Celiac disease.
• Necrolytic migratory erythema: Glucagonoma.
• Sign of Leser–Trélat: Sudden eruptive seborrheic keratoses → internal malignancy.

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Recent Update Themes (Current Exam Cycle)

1. Steroid-modified, terbinafine-resistant tinea (T. indotineae) — itraconazole-based therapy, rational steroid-combination cream policy.
2. Rituximab as first-line (with steroids) for moderate-to-severe pemphigus vulgaris.
3. Biologics in psoriasis — IL-17 (secukinumab, ixekizumab) and IL-23 (guselkumab, risankizumab) inhibitors.
4. JAK inhibitors — topical ruxolitinib for vitiligo and atopic dermatitis; oral JAKi for alopecia areata.
5. WHO uniform MDT for leprosy (3 drugs for PB and MB) and post-exposure prophylaxis with single-dose rifampicin (SDR-PEP).
6. Dual therapy for gonorrhoea (ceftriaxone + azithromycin) due to resistance.
7. Immunotherapy/targeted therapy in melanoma (checkpoint inhibitors, BRAF/MEK inhibitors).
8. Dupilumab (anti–IL-4Rα) for moderate-to-severe atopic dermatitis.

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Practical Study Roadmap

Phase 1 — Build the vocabulary (Week 1)

Master the primary and secondary lesion definitions, Nikolsky/Auspitz/Wickham signs, and the KOH/Tzanck/Wood's lamp investigations. Without morphology, image questions are unsolvable.

Phase 2 — High-yield blocks (Weeks 2–4)

Prioritise in this order, matching exam density:

1. Leprosy (Ridley–Jopling, MDT, reactions).
2. STDs (ulcer table, syphilis staging).
3. Vesiculobullous + IF patterns.
4. Psoriasis & lichen planus.
5. Infections (tinea, scabies, impetigo).
6. Tumours & pigmentary.

Phase 3 — Integration & images (Weeks 5–6)

Solve image-based question banks and link skin findings to systemic disease (Medicine/Endocrine overlaps). Drill the drug side-effect table with Pharmacology.

Last-Week Revision Strategy

• Revise only tables and one-liners — IF patterns, ulcer table, MDT regimen, lepra reactions, signs.
• Flip through a clinical image atlas once daily for spot diagnosis.
• Memorise DOCs: scabies (permethrin), pemphigus (steroid + rituximab), DH (dapsone), ENL (thalidomide), syphilis (benzathine penicillin), tinea (itraconazole for resistant).
• Do one full DVL test and review every wrong association.
• Do not start new topics; consolidate the fixed-fact pairs that the exam repeats year after year.

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High-Yield Mnemonics

• Lichen planus — 6 Ps: Pruritic, Purple, Polygonal, Planar, Papules, Plaques.
• Melanoma — ABCDE: Asymmetry, Border, Colour, Diameter, Evolution.
• Causes of erythema multiforme/SJS-TEN drugs — "SANS": Sulfonamides, Anticonvulsants, NSAIDs, allopurinol (Sulfa/Anticonvulsant/NSAID/Allopurinol).
• DH = Dapsone + Diet (gluten-free) + Dermal papillae granular IgA + Duhring's disease.
• Pemphigus = Suprabasal, Superficial dgg-3, Nikolsky +, "fishneT" — Top of epidermis.
• Koebner shows up in "PVL-W": Psoriasis, Vitiligo, Lichen planus, Warts.

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Rapid-Fire One-Liners

1. Pinpoint bleeding on scale removal → Auspitz sign → psoriasis.
2. Fishnet/chicken-wire intercellular IgG → pemphigus vulgaris (anti–desmoglein 3).
3. Linear IgG along basement membrane → bullous pemphigoid (anti-BP180/230).
4. Granular IgA in dermal papillae + gluten enteropathy → dermatitis herpetiformis → dapsone.
5. Painless indurated genital ulcer → primary syphilis (hard chancre).
6. Painful, soft, undermined genital ulcer + suppurative bubo → chancroid (H. ducreyi).
7. Most common nerve involved in leprosy → ulnar nerve.
8. Thalidomide is the drug of choice for → Type 2 lepra reaction (ENL).
9. Spaghetti-and-meatballs KOH → pityriasis (tinea) versicolor (Malassezia).
10. Rodent ulcer with pearly telangiectatic border → basal cell carcinoma.
11. Breslow thickness → most important prognostic factor in melanoma.
12. Chalk-white depigmented macule, Koebner positive, thyroid association → vitiligo.
13. Herald patch followed by Christmas-tree truncal rash → pityriasis rosea.
14. Sudden eruptive seborrheic keratoses (Leser–Trélat) → internal (GI) malignancy.