Complete Guide to NEET PG Dermatology High-Yield Topics

Version 1.0 — Published April 2026

Dermatology is the visual specialty — a field where the diagnosis often rests on recognizing a morphological pattern, knowing a pathognomonic sign, or distinguishing two conditions that look superficially similar. NEET PG tests dermatology through image-based questions, clinical vignettes with described lesion morphology, and classification-based questions (especially leprosy). The rewarding part: the question pool is predictable, and the same signs, diseases, and differentials repeat with high fidelity.

This guide covers the eight areas that generate the highest question density. Each section gives you the diagnostic criteria, pathognomonic features, and clinical associations that NBE tests. Pair it with the psoriasis vs eczema image walkthrough for visual pattern training and the medicine high-yield guide for systemic disease manifestations in skin.

Papulosquamous disorders: psoriasis, lichen planus, and pityriasis rosea

Papulosquamous disorders are characterized by scaly papules and plaques. Psoriasis is the most tested condition in this group, followed by lichen planus.

Psoriasis

Psoriasis is a chronic, relapsing, immune-mediated inflammatory disease characterized by well-defined, erythematous plaques with silvery-white micaceous scales, most commonly on extensor surfaces (elbows, knees), scalp, and lumbosacral area.

Pathognomonic signs:

• Auspitz sign — pinpoint bleeding on removing the scale (damaged dermal papillary capillaries exposed after removal of parakeratotic scale). This is the most tested clinical sign.
• Koebner phenomenon — new psoriatic lesions at sites of trauma (linear lesions along scratch marks, surgical scars)
• Candle grease sign — silvery scales come off in layers like scraping a candle
• Woronoff ring — blanching ring around a resolving psoriatic plaque

Histopathology: Acanthosis, parakeratosis (nuclei retained in stratum corneum), Munro microabscesses (neutrophils in the stratum corneum), spongiform pustules of Kogoj (neutrophils in the stratum spinosum), suprapapillary thinning with dilated tortuous capillaries.

Nail changes in psoriasis (tested as image or description):

• Pitting — most common (thimble pitting, irregular shallow depressions)
• Oil drop sign — translucent yellow-brown discoloration under the nail plate
• Onycholysis — distal separation of nail plate from nail bed
• Subungual hyperkeratosis — thickening under the nail

Psoriatic arthritis affects 10-30% of psoriasis patients. Five patterns: asymmetric oligoarthritis (most common), symmetric polyarthritis (mimics RA), DIP predominant (pathognomonic), spondylitis, and arthritis mutilans (opera glass hand). DIP involvement distinguishes psoriatic arthritis from RA (RA spares DIP).

Lichen planus

Lichen planus is a chronic inflammatory condition affecting skin, mucous membranes, hair, and nails. The classic description uses the 6 Ps: Purple, Polygonal, Planar (flat-topped), Pruritic Papules and Plaques.

Wickham striae — fine white reticular lines on the surface of lichen planus papules, best seen with a dermatoscope or after applying oil. This is the pathognomonic sign.

Histopathology: Interface dermatitis with a band-like (lichenoid) lymphocytic infiltrate hugging the basal layer, saw-tooth acanthosis, civatte bodies (colloid/apoptotic bodies at the dermoepidermal junction), and Max-Joseph spaces (clefts at the DEJ from basal cell destruction). This histological pattern is the most tested aspect of lichen planus in NEET PG.

Oral lichen planus — white reticular lesions on buccal mucosa. Considered a premalignant condition (1-2% risk of squamous cell carcinoma). Erosive oral lichen planus is the variant with highest malignant potential (IADVL Textbook of Dermatology, 4th Edition).

Pityriasis rosea

Pityriasis rosea is a self-limiting papulosquamous disorder, likely viral in etiology (HHV-6, HHV-7 association).

Herald patch — a single, oval, salmon-pink plaque with a "collarette" scale (fine scale at the periphery with central clearing) that appears 1-2 weeks before the generalized eruption. The herald patch is the diagnostic clue in NEET PG vignettes.

Christmas tree pattern — the generalized eruption follows skin cleavage lines (Langer lines) on the trunk, creating a "Christmas tree" distribution on the back. Lesions are smaller versions of the herald patch.

Key differential: Secondary syphilis can mimic pityriasis rosea. Always order VDRL/RPR in sexually active patients with a pityriasis rosea-like rash, especially if palms and soles are involved (pityriasis rosea typically spares palms and soles; syphilis involves them).

Vesiculobullous diseases: pemphigus, pemphigoid, and DH

Vesiculobullous diseases generate 2-3 questions per NEET PG paper. The key is distinguishing the level of blister formation and the immunofluorescence pattern.

Pemphigus vulgaris versus bullous pemphigoid

Tzanck smear shows acantholytic cells (rounded keratinocytes with large nuclei and perinuclear halo) in pemphigus. It is a bedside diagnostic test — scrape the base of a fresh blister, smear on a slide, stain with Giemsa. Positive Tzanck smear + positive Nikolsky sign = strong pemphigus support.

Pemphigus variants

• Pemphigus vulgaris — most common and most severe. Suprabasal acantholysis. Anti-desmoglein 3 (with or without anti-desmoglein 1).
• Pemphigus foliaceus — superficial (subcorneal acantholysis). Anti-desmoglein 1 only. No oral involvement (desmoglein 3 in oral mucosa provides compensation — desmoglein compensation theory). Presents with superficial crusted erosions, "corn flake" scales. Fogo selvagem is the endemic form in Brazil.
• Paraneoplastic pemphigus — associated with lymphoma and CLL. Severe mucositis + polymorphous skin lesions + anti-plakin antibodies.

Dermatitis herpetiformis (DH)

Dermatitis herpetiformis is a vesiculobullous disease with grouped (herpetiform) vesicles on extensor surfaces (elbows, knees, buttocks, upper back).

Association: Nearly 100% of DH patients have celiac disease (gluten-sensitive enteropathy) on jejunal biopsy, even if asymptomatic. This is the most tested association in NEET PG.

DIF: Granular IgA deposits at the dermal papillae tips — this is pathognomonic and distinguishes DH from linear IgA bullous dermatosis (which shows linear IgA at the BMZ).

Treatment: Dapsone provides rapid symptomatic relief (within 24-48 hours). Gluten-free diet is the definitive long-term treatment and allows eventual dapsone discontinuation (Rook's Textbook of Dermatology, 9th Edition).

Leprosy: Ridley-Jopling classification and management

Leprosy (Hansen disease), caused by Mycobacterium leprae, is the most tested dermatology topic in NEET PG. It covers classification, clinical features, treatment, and reactions — generating 2-3 questions per paper.

Ridley-Jopling classification

The spectrum from tuberculoid to lepromatous reflects the host immune response:

WHO operational classification simplifies this for treatment purposes: Paucibacillary (PB) = 1-5 skin lesions, 0-1 nerve involved (covers TT, BT). Multibacillary (MB) = >5 skin lesions or >1 nerve involved (covers BB, BL, LL) or skin smear positive.

WHO MDT regimens

Single-lesion PB: ROM regimen (single dose of Rifampicin 600 mg + Ofloxacin 400 mg + Minocycline 100 mg) — though WHO now recommends standard PB-MDT.

Leprosy reactions

Type 1 reaction is the most common cause of nerve damage in leprosy. The nerves at highest risk are the ulnar nerve (most commonly affected in leprosy overall), lateral popliteal (common peroneal), posterior tibial, and facial nerve.

Thalidomide is the drug of choice for severe ENL but is absolutely contraindicated in women of childbearing age due to teratogenicity (phocomelia). Prednisolone is used when thalidomide is contraindicated (WHO leprosy treatment guidelines).

Pigmentary disorders: vitiligo, melasma, and albinism

Pigmentary disorders test the ability to differentiate depigmented from hypopigmented lesions and to identify the pathogenic mechanism.

Vitiligo

Vitiligo is an autoimmune disorder causing progressive depigmentation through destruction of melanocytes. It affects 0.5-2% of the population globally, with onset most commonly in the second or third decade.

Clinical features: Well-defined, chalk-white (not cream or off-white) macules and patches, often symmetric. Common sites: periorbital, perioral, acral (fingers, toes), genital, axillary. Wood lamp examination shows bright white fluorescence with sharp borders (enhanced contrast) — this helps detect early or subtle lesions in fair-skinned individuals.

Types:

• Non-segmental (generalized) — most common type (85-90%). Bilateral, symmetric. Progressive. Associated with autoimmune diseases (thyroid disease in 20-30%, pernicious anemia, Addison disease, diabetes mellitus type 1).
• Segmental — unilateral, dermatomal distribution. Stable after initial progression. Earlier onset. Less responsive to medical therapy but responds better to surgical methods (melanocyte transplantation).

Treatment: Topical corticosteroids or tacrolimus (face, intertriginous areas), narrowband UVB phototherapy (mainstay for generalized vitiligo), and surgical methods (suction blister melanocyte transplantation) for stable, localized disease unresponsive to medical therapy.

Melasma

Melasma is an acquired symmetric hypermelanosis affecting sun-exposed areas of the face, most common in women of reproductive age. Hormonal influences (pregnancy, oral contraceptives) and UV exposure are the primary triggers.

Types by Wood lamp:

• Epidermal — enhanced under Wood lamp (better prognosis, responds to topical treatment)
• Dermal — NOT enhanced under Wood lamp (poorer prognosis)
• Mixed — partial enhancement

Treatment: Strict sun protection (SPF 30+, physical sunscreens), triple combination cream (hydroquinone 4% + tretinoin 0.05% + fluocinolone 0.01% — "Kligman formula"), chemical peels (glycolic acid), and laser for refractory cases.

Oculocutaneous albinism (OCA)

Albinism results from defective melanin synthesis. The most commonly tested form is OCA type 1 (tyrosinase-negative) — complete absence of melanin in skin, hair, and eyes. Autosomal recessive inheritance. Clinical features: white hair, pink skin, translucent irides, nystagmus, photophobia. Increased risk of skin cancers (SCC, BCC) due to absent UV protection.

Connective tissue diseases: skin manifestations

Connective tissue diseases with dermatological manifestations are tested in both dermatology and medicine sections of NEET PG.

Systemic lupus erythematosus (SLE) — skin findings

SLE affects women of childbearing age (F:M ratio 9:1). The skin findings most tested:

• Malar (butterfly) rash — erythema over both cheeks and bridge of nose, sparing the nasolabial folds. The nasolabial fold sparing distinguishes SLE from rosacea and seborrheic dermatitis.
• Discoid lupus — coin-shaped plaques with follicular plugging, atrophy, and scarring. Can occur with or without systemic disease.
• Photosensitivity — rash triggered or worsened by UV exposure. Present in over 70% of SLE patients.
• Oral ulcers — usually painless, on the hard palate (differentiating feature from aphthous ulcers which are painful).

Key autoantibodies: ANA (sensitive but not specific, 95%+), anti-dsDNA (specific for SLE, correlates with renal disease activity), anti-Smith (most specific for SLE, low sensitivity).

Dermatomyositis

Dermatomyositis is an inflammatory myopathy with characteristic skin findings. The skin changes may precede muscle weakness (amyopathic dermatomyositis).

• Heliotrope rash — violaceous (purple-lilac) discoloration and edema of the upper eyelids. Pathognomonic.
• Gottron papules — violaceous papules over the knuckles (MCP and PIP joints). Pathognomonic.
• Shawl sign — erythema over the upper back, shoulders, and posterior neck (V-distribution).
• Mechanic's hands — roughened, cracked skin on the lateral and palmar surfaces of fingers (associated with anti-Jo-1 antibodies and ILD).

Malignancy association: Adult dermatomyositis has a 15-30% association with internal malignancy (ovarian, lung, GI, breast). Cancer screening is mandatory at diagnosis and for 3 years after (Fitzpatrick's Dermatology, 9th Edition).

Scleroderma

Scleroderma (systemic sclerosis) is characterized by skin fibrosis and internal organ involvement.

Limited (CREST): Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia. Anti-centromere antibody positive. Better prognosis. Pulmonary hypertension is the main cause of death.

Diffuse: Rapid skin thickening beyond elbows/knees, early internal organ involvement. Anti-Scl-70 (anti-topoisomerase I) antibody positive. Renal crisis (malignant hypertension) is the most feared complication — treated with ACE inhibitors.

Sexually transmitted infections: syphilis, chancroid, and LGV

STIs are tested through clinical vignette descriptions of genital ulcers, with emphasis on differentiating features.

Syphilis (Treponema pallidum)

Primary syphilis (3 weeks post-exposure): Painless chancre — a clean-based ulcer with indurated, rolled edges at the site of inoculation. Non-tender inguinal lymphadenopathy. The chancre heals spontaneously in 3-6 weeks. Darkfield microscopy shows spirochetes.

Secondary syphilis (6-8 weeks post-primary): Widespread symmetric maculopapular rash involving palms and soles (key feature — very few conditions cause palmar/plantar rash: syphilis, Rocky Mountain spotted fever, hand-foot-mouth disease, Kawasaki). Condylomata lata (moist, flat, highly infectious warts in intertriginous areas — distinguish from condylomata acuminata of HPV which are dry and pointed). Mucous patches. Moth-eaten alopecia. Generalized lymphadenopathy.

Tertiary syphilis (years later): Gumma (granulomatous lesions in skin, bone, liver), cardiovascular syphilis (aortitis of ascending aorta — tree bark appearance, aortic regurgitation, aortic aneurysm), neurosyphilis (tabes dorsalis — lightning pains, Argyll Robertson pupil — accommodates but does not react to light, Charcot joints).

Congenital syphilis — Hutchinson triad: Interstitial keratitis, Hutchinson teeth (peg-shaped, notched upper central incisors), and sensorineural deafness (VIII nerve).

Chancroid (Haemophilus ducreyi)

Chancroid produces a painful genital ulcer (unlike the painless chancre of syphilis). The ulcer has ragged, undermined edges and a necrotic base. Tender inguinal lymphadenopathy that may suppurate and form buboes (draining sinuses). Diagnosis: Gram stain shows "school of fish" pattern (parallel chains of gram-negative coccobacilli).

Lymphogranuloma venereum (LGV)

LGV is caused by Chlamydia trachomatis serovars L1, L2, L3. Three stages: painless papule/ulcer (often missed), then inguinal lymphadenopathy (the bubo stage — unilateral, fluctuant, may suppurate). The groove sign (sign of Greenblatt) — a groove between the inguinal and femoral lymph node groups created by the inguinal ligament — is pathognomonic. Late stage: proctitis, strictures, elephantiasis of genitalia.

Treatment: Doxycycline 100 mg BD for 21 days.

Drug reactions: SJS/TEN, FDE, and DRESS

Drug reactions are tested through clinical scenarios with the causative drug as the answer or through clinical description identification.

SJS and TEN — spectrum of severity

SJS and TEN are on the same spectrum, differentiated by the body surface area (BSA) of epidermal detachment:

Common causative drugs (high-yield for MCQs): Carbamazepine, allopurinol, sulfonamides (cotrimoxazole), phenytoin, nevirapine, NSAIDs (piroxicam, especially), and lamotrigine.

Clinical features: Prodromal fever and malaise, then painful skin involvement with target lesions, hemorrhagic erosions of mucous membranes (oral, ocular, genital), and progressive epidermal detachment. Nikolsky sign is positive (epidermis slides off with lateral pressure). Mucosal involvement is mandatory for diagnosis.

Management: Immediate withdrawal of the offending drug (the single most important step). Supportive care in a burns unit/ICU. IVIG and cyclosporine are used in severe cases. Corticosteroids are controversial. SCORTEN prognostic scoring system predicts mortality based on 7 parameters (age, malignancy, BSA, heart rate, BUN, glucose, bicarbonate).

Fixed drug eruption (FDE)

FDE is characterized by a round, well-defined, violaceous (dusky red-brown) plaque that recurs at the same site with each drug exposure. Post-inflammatory hyperpigmentation persists between episodes. Common culprits: cotrimoxazole (most common), tetracyclines, NSAIDs, metronidazole. The "same site recurrence" is the diagnostic clue in NEET PG.

DRESS syndrome

DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms) presents 2-8 weeks after starting the causative drug with fever, morbilliform rash, facial edema, lymphadenopathy, and internal organ involvement (hepatitis most common, also nephritis, pneumonitis). Peripheral eosinophilia (>1500/microL) or atypical lymphocytes are characteristic. Common drugs: anticonvulsants (carbamazepine, phenytoin, lamotrigine), allopurinol, dapsone, minocycline. HHV-6 reactivation plays a role in pathogenesis.

Hair and nail disorders: alopecia areata and onychomycosis

Hair and nail disorders appear as 1-2 questions per NEET PG, often as image-based or one-liner questions.

Alopecia areata

Alopecia areata is an autoimmune condition causing well-defined, oval or round patches of non-scarring hair loss. The scalp skin appears normal (no scarring, no scaling — distinguishing it from tinea capitis and discoid lupus).

Pathognomonic sign: "Exclamation mark hairs" — short, broken hairs (2-3 mm) that are narrower at the base than at the tip, found at the margins of the patch. These represent dystrophic anagen hairs and are diagnostic.

Variants: Alopecia totalis (complete scalp hair loss), alopecia universalis (complete body hair loss). Nail changes in alopecia areata: fine pitting (regular, geometric "grid-like" pattern — in contrast to the irregular pitting of psoriasis).

Treatment: Intralesional triamcinolone (first-line for localized patches), topical minoxidil, contact immunotherapy (DPCP/SADBE) for extensive disease, and JAK inhibitors (baricitinib — FDA approved for severe alopecia areata).

Onychomycosis

Onychomycosis is fungal infection of the nail, most commonly caused by dermatophytes (Trichophyton rubrum is the most common organism). It accounts for 50% of all nail disorders.

Types: Distal and lateral subungual (most common), proximal subungual (associated with immunosuppression — HIV marker), superficial white, and total dystrophic.

Diagnosis: KOH mount of nail clippings shows septate hyphae. Fungal culture on Sabouraud dextrose agar confirms the species.

Treatment: Terbinafine oral (drug of choice for dermatophyte onychomycosis — 12 weeks for toenails, 6 weeks for fingernails). Itraconazole pulse therapy (200 mg BD for 1 week/month, 2-3 pulses for fingernails, 3-4 for toenails) is an alternative. Topical ciclopirox or amorolfine nail lacquer for mild, distal disease.

Sources and references

1. IADVL Textbook of Dermatology, 4th Edition (Valia & Valia, 2015) — standard Indian dermatology reference for NEET PG preparation.
2. Rook's Textbook of Dermatology, 9th Edition (Griffiths et al., 2016) — comprehensive international dermatology reference.
3. Fitzpatrick's Dermatology, 9th Edition (Kang et al., 2019) — gold-standard reference for dermatopathology and clinical dermatology.
4. WHO Guidelines for the Diagnosis, Treatment and Prevention of Leprosy (2018) — definitive source for leprosy classification and MDT regimens.

Frequently asked questions

How many dermatology questions appear in NEET PG?

Dermatology contributes 10-14 questions in NEET PG (2021-2024 analysis). Leprosy accounts for 2-3 questions almost every year. Psoriasis, pemphigus, drug reactions, and STIs are the next most tested. Image-based dermatology questions appear 3-4 times per paper.

What is the most tested dermatology topic in NEET PG?

Leprosy is the single most tested topic because it covers classification, microbiology, immunology, clinical features, treatment, and reactions. It appears in 2-3 questions per paper. Psoriasis is second, followed by vesiculobullous diseases.

How do I differentiate pemphigus from pemphigoid?

Pemphigus: flaccid blisters, intraepidermal, Nikolsky positive, acantholysis, fishnet DIF. Pemphigoid: tense blisters, subepidermal, Nikolsky negative, no acantholysis, linear DIF. Remember: pemphiGUS = GUShy (flaccid), pemphiGOID = GOod (tense).

What is the Ridley-Jopling classification of leprosy?

The spectrum from TT (tuberculoid) to LL (lepromatous) reflects host immunity. TT: few well-defined lesions, high CMI, low bacilli. LL: innumerable diffuse lesions, absent CMI, high bacilli. BB is the most unstable form.

What drug reactions are commonly tested?

SJS/TEN (differentiated by BSA: SJS less than 10%, TEN greater than 30%), DRESS (eosinophilia, systemic involvement), and FDE (same site recurrence). Key drugs: carbamazepine, allopurinol, sulfonamides, phenytoin.

How is vitiligo differentiated from other depigmented lesions?

Vitiligo: chalk-white, well-defined, normal texture, bright white on Wood lamp. Pityriasis versicolor: hypopigmented with scaling, KOH positive. Leprosy: hypopigmented with hypoesthesia. Nevus depigmentosus: stable from birth, not chalk-white.

What are the stages of syphilis tested in NEET PG?

Primary: painless chancre. Secondary: maculopapular rash on palms and soles, condylomata lata. Tertiary: gumma, aortitis, neurosyphilis (tabes dorsalis, Argyll Robertson pupil). Congenital: Hutchinson triad.

What is the Koebner phenomenon?

Koebner phenomenon is the development of disease-specific lesions at sites of trauma. Classic diseases: psoriasis, lichen planus, vitiligo, and warts. The linear/geometric distribution pattern following injury lines is the clinical clue.

Start your dermatology preparation today. Open the Dermatology subject page and solve your first 15 MCQs — the morphological patterns you learn now will unlock marks across dermatology and medicine on exam day. For AI-powered image-based MCQs with visual explanations, explore NEETPGAI Pro.

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

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