Dermatology for NEET PG 2026: Bullous Disorders, Lichen Planus, Leprosy, and High-Yield Signs

Dermatology contributes 3 to 5 percent of the NEET PG paper — approximately 5 to 9 questions out of 180. Unlike some subjects where questions test broad recall, Dermatology questions are frequently morphology-based, pattern-recognition, or classic clinical presentation MCQs. Once you learn the patterns, Dermatology becomes one of the most reliably scorable subjects in the paper.

This guide covers every high-yield Dermatology topic with the depth NEET PG actually demands. Not a textbook overview — a focused breakdown of what appears in PYQs, what the examiners test, and how to answer correctly under exam conditions. For how this subject sits against the rest of the paper, see the complete Dermatology subject wise weightage; for how to fit it into your timetable, see the NEET PG preparation strategy.

Before starting any subject revision, check the NEET PG 2026 score calculator to understand how your current mock test accuracy translates to rank. Getting all Dermatology questions correct versus none is a score swing of 20 to 36 marks — meaningful rank movement at every level.

Dermatology pairs well with the other small, high-repetition subjects. If you are working through them together, Anaesthesia for NEET PG 2026 follows the same approach: a short list of topics that repeat almost verbatim, cycle after cycle.

The 18 Most-Tested Dermatology Topics in NEET PG PYQs

Rank	Topic	Frequency	Question Format
1	Pemphigus vulgaris vs bullous pemphigoid — comparison	Very High	Comparison + IF pattern
2	Koebner phenomenon and reverse Koebner — disease lists	Very High	Direct factual
3	Auspitz sign and other psoriasis signs	Very High	Direct factual
4	Leprosy — Ridley-Jopling classification	Very High	Classification MCQ
5	Leprosy reactions — Type 1 vs Type 2	Very High	Clinical scenario
6	Lichen planus — clinical features, 4Ps, Wickham striae	High	Clinical + histology
7	Lichen planus pigmentosus	High	Direct factual
8	Psoriasis — treatment ladder and biologics	High	Pharmacology MCQ
9	Vitiligo — types and treatment	High	Direct factual
10	Scabies — causative organism and treatment	High	Pharmacology MCQ
11	Dermatophytosis — Wood's lamp findings	Moderate	Direct factual
12	SLE and skin manifestations	Moderate	Clinical scenario
13	Acne vulgaris — pathogenesis and treatment	Moderate	Pharmacology MCQ
14	Erythema multiforme, SJS, TEN — comparison	Moderate	Severity spectrum MCQ
15	Drug-induced skin reactions	Moderate	Pharmacology MCQ
16	Herpes zoster vs simplex	Moderate	Clinical MCQ
17	Pemphigus foliaceus — difference from PV	Low-Moderate	Comparison MCQ
18	DRESS syndrome	Low-Moderate	Drug reaction MCQ

Dermatological Signs — The Most Tested in NEET PG

Dermatology signs are consistently tested as direct recall questions. Know every sign, what condition it belongs to, and why it occurs.

Koebner Phenomenon (Isomorphic Response)

The appearance of the same skin lesion at sites of trauma or injury, in a patient who already has that skin disease.

Classic diseases showing Koebner — remember "WPAS": Warts (viral), Psoriasis, Alopecia areata, Syringoma. Also lichen planus, vitiligo, molluscum contagiosum, lichen nitidus, xanthoma and Darier's disease.

PYQ pattern: questions ask which diseases show Koebner. Psoriasis and lichen planus are always correct answers. Pemphigus does not show Koebner.

Pseudo-Koebner Phenomenon

Inoculation of infectious organisms at sites of trauma — the lesion is infectious, not a true isomorphic inflammatory response. Seen with molluscum contagiosum and viral warts, where organisms are physically implanted into traumatised skin.

The distinction: true Koebner means a non-infectious lesion appears at a trauma site; pseudo-Koebner means an infectious lesion is inoculated there.

Reverse Koebner Phenomenon

Clearance of existing skin lesions at sites of trauma or friction. The classic disease is vitiligo — paradoxically, trauma can cause localised repigmentation of vitiligo patches. Also reported in some psoriasis patients.

PYQ pattern: "Reverse Koebner phenomenon is seen in ______" — the answer is vitiligo.

Auspitz Sign

Pinpoint bleeding spots appearing when a psoriatic scale is removed, caused by thinning of the suprapapillary epidermis over dilated dermal capillaries. It is pathognomonic of psoriasis.

Mechanism: suprapapillary plate thinning exposes dermal capillaries, so forcibly removing the scale produces punctate bleeding.

PYQ pattern: "Auspitz sign is seen in ______" — always psoriasis. "Auspitz sign occurs due to ______" — thinning of the suprapapillary plate.

Complete Sign Reference Table

Sign	Disease	Description
Auspitz sign	Psoriasis	Pinpoint bleeding on scale removal
Nikolsky sign (positive)	Pemphigus vulgaris	Skin slides off with lateral pressure
Nikolsky sign (negative)	Bullous pemphigoid	Skin does not slide off
Bulla spread sign	Pemphigus vulgaris	Pressure on a bulla causes lateral extension
Koebner phenomenon	Psoriasis, LP, vitiligo, warts	Lesion appears at trauma site
Reverse Koebner	Vitiligo	Repigmentation at trauma sites
Pseudo-Koebner	Viral warts, molluscum	Infectious inoculation at trauma site
Wickham striae	Lichen planus	Whitish lacy network on papules
Candle grease sign	Psoriasis	Scales detach like scraping a candle
Carpet tack sign	Discoid lupus	Follicular plugging seen on scale removal
Leser-Trélat sign	Internal malignancy	Sudden eruption of multiple seborrhoeic keratoses
Darier sign	Mastocytosis (urticaria pigmentosa)	Urtication on stroking the lesion
Buttonhole sign	Neurofibromatosis	Nodules can be pushed through dermis
String of beads sign	Dermatitis herpetiformis	Grouped vesicles on elbows
Pathergy test positive	Behçet's disease	Pustule forms at needle prick site
Oil drop sign	Psoriasis (nail)	Translucent yellowish patch under nail
Pencil-in-cup deformity	Psoriatic arthritis	X-ray finding of DIP erosion

Bullous Disorders — The Most Tested Comparison

Pemphigus Vulgaris vs Bullous Pemphigoid

This comparison appears in virtually every NEET PG exam. Every row is exam-relevant.

Feature	Pemphigus Vulgaris	Bullous Pemphigoid
Age of onset	Middle-aged (40–60 years)	Elderly (over 60)
Blister level	Intraepidermal (suprabasal)	Subepidermal
Nikolsky sign	Positive	Negative
Bulla	Flaccid, ruptures easily	Tense, thick-roofed, does not rupture easily
Mucosal involvement	Always involved — oral lesions often first	Rare
Acantholysis	Yes — loss of intercellular adhesion	No
Target antigen	Desmoglein 3 (oral) and desmoglein 1 (skin)	BP180 and BP230 (hemidesmosomes)
Antibody	IgG against desmoglein 3/1	IgG against BP180 (collagen XVII) and BP230
Direct IF pattern	Net-like, fishnet or chicken-wire	Linear IgG and C3 at the BMZ
Indirect IF	IgG on epithelial cell surfaces	IgG along the basement membrane zone
Histology	Intraepidermal blister, acantholytic (Tzanck) cells, tombstone row of basal cells	Subepidermal blister with eosinophilic infiltrate
Prognosis	More severe, higher mortality	Better
Treatment	High-dose systemic steroids plus steroid-sparing agents (azathioprine, rituximab)	Topical or systemic steroids; doxycycline with niacinamide

Memory pearls: PV — Positive Nikolsky, Pemphigus, intra-epidermal. BP — Basement membrane, Bullous Pemphigoid, subepidermal, Tense blister. IF pattern: PV is net or chicken-wire (intercellular); BP is linear (at the basement membrane).

Pemphigus Histology

On light microscopy: a suprabasal split forming just above the basal layer; acantholytic cells — rounded keratinocytes that have lost cell-to-cell adhesion; a "tombstone" appearance where basal cells remain attached to the basement membrane in a row; and acantholytic cells on Tzanck smear, which is also positive in herpes infections.

On immunofluorescence: direct IF shows IgG deposits in a net-like, chicken-wire pattern on keratinocyte cell surfaces throughout the epidermis, with C3 deposited alongside. Indirect IF detects patient IgG against epidermal cell surfaces.

Bullous Pemphigoid Histology

On light microscopy: a subepidermal blister forming below the entire epidermis; an eosinophil-rich infiltrate in the blister cavity and dermis; no acantholysis, with the epidermis intact and basal cells in the blister roof.

On immunofluorescence: direct IF shows linear IgG and C3 along the basement membrane zone — the linearity is what distinguishes it from PV's net-like pattern. On salt-split skin, the IgG sits on the epidermal side of the split.

Drug-Induced Bullous Pemphigoid

Drug Class	Examples
Diuretics	Furosemide, spironolactone
Antihypertensives	Nifedipine, captopril, enalapril
Antibiotics	Amoxicillin, ciprofloxacin
Antidiabetics	Gliptins (DPP-4 inhibitors) — strong association
Antipsychotics	Chlorpromazine
Biologics	TNF-alpha inhibitors

PYQ pattern: the drug class most prominently associated with bullous pemphigoid in recent questions is the DPP-4 inhibitors (gliptins).

Other Bullous Disorders

Condition	Key Feature	Target Antigen
Pemphigus foliaceus	Superficial blistering, no mucosal involvement; endemic form in Brazil (fogo selvagem)	Desmoglein 1 only
Dermatitis herpetiformis	Intensely pruritic vesicles on elbows, knees, buttocks; associated with coeliac disease	Epidermal transglutaminase
Linear IgA disease	Linear IgA at BMZ; "string of pearls" in children	IgA against BP180
Epidermolysis bullosa acquisita	Mechanobullous, at trauma sites; below lamina densa	Collagen VII
Porphyria cutanea tarda	Sun-exposed areas, fragile skin, milia; urine fluorescence	Uroporphyrinogen decarboxylase deficiency

Lichen Planus

Clinical Features — the 4 Ps

Lichen planus is described by the classic four Ps: Pruritic, Purple, Planar (flat-topped) and Polygonal — plus Wickham striae, the whitish lacy lines on the lesion surface.

Sites are the flexor aspects of wrists and forearms, ankles, lower legs and mucosae. Mucosal involvement occurs in 50 to 70 percent of patients, most often as a reticular whitish pattern on the buccal mucosa; the erosive oral form is pre-malignant.

Nail changes include pterygium unguis — adhesion of the proximal nail fold to the nail plate, which is pathognomonic — along with longitudinal ridging and trachyonychia. Koebner phenomenon is positive.

Histology

Layer	Finding
Epidermis	Hyperkeratosis, focal hypergranulosis, irregular acanthosis with saw-tooth rete ridges
Dermoepidermal junction	Vacuolar degeneration of basal cells; colloid (Civatte) bodies
Dermis	Band-like lichenoid lymphocytic infiltrate hugging the DEJ

Saw-tooth rete ridges plus a band-like infiltrate is the classic LP pattern. Colloid bodies — also called Civatte or cytoid bodies — are apoptotic keratinocytes appearing as eosinophilic globular structures at the DEJ.

Variants

Variant	Site or Feature
Classic (papular)	Flexor wrists and forearms — most common
Oral LP	Buccal mucosa, reticular pattern; erosive form pre-malignant
Lichen planus pigmentosus	See below
Hypertrophic LP	Thick plaques on legs — the most pruritic variant
Bullous LP	Blisters within LP lesions
Actinic LP	Sun-exposed areas; commoner in the Middle East and India
Lichen planopilaris	Follicular LP causing scarring alopecia
Inverse LP	Flexural areas, groin, axillae
Ulcerative LP	Chronic painful ulcers on the soles

Lichen Planus Pigmentosus

Lichen planus pigmentosus is a variant characterised by hyperpigmented macular lesions on sun-exposed and flexural sites, without the classic papular morphology. It is far more common in South Asian and Middle Eastern populations than in Western ones, which makes it disproportionately high-yield for Indian exams.

Feature	Detail
Lesion type	Dark brown to black macules and patches
Distribution	Face (especially forehead and temples), neck, flexural folds
Sun exposure	Worse on sun-exposed areas — photodistributed
Pruritus	Mild to moderate; less intense than classic LP
Classic LP features	Usually absent — no Wickham striae, no flat-topped papules
Mucosal involvement	Uncommon
Course	Chronic; pigmentation may persist long after active disease resolves

Histology shows vacuolar degeneration of the basal layer and melanin incontinence — melanin within dermal macrophages (melanophages) — with a sparse lymphocytic infiltrate at the DEJ, less band-like than classic LP.

Treatment starts with mandatory sun protection, since UV exposure worsens the pigmentation. Topical corticosteroids of moderate potency are used for limited disease, and topical tacrolimus is the steroid-sparing option preferred on the face. Hydroxychloroquine or low-dose systemic steroids are reserved for resistant cases, and Q-switched Nd:YAG laser can address persistent pigmentation once the disease is inactive.

PYQ pattern: questions ask about the distribution (flexural and sun-exposed), the histological finding (melanin incontinence with melanophages), and the treatment.

Leprosy

Ridley-Jopling Classification

Based on the immunological status of the host — the standard classification tested in NEET PG.

Type	Bacteria	Lepromin Test	Histology	Clinical Features
Tuberculoid (TT)	None	Strongly positive	Well-formed granulomas surrounded by lymphocytes	1–3 hypopigmented, anaesthetic, dry patches with well-defined borders; prominent nerve enlargement
Borderline tuberculoid (BT)	Few	Positive	Less organised granulomas	More lesions than TT, less clear borders
Mid-borderline (BB)	Moderate	Equivocal	Mixed picture	Multiple asymmetric lesions, punched-out appearance
Borderline lepromatous (BL)	Many	Negative	Poor granulomas, foamy macrophages	Multiple lesions, nerve damage
Lepromatous (LL)	Very high	Strongly negative	Foamy macrophages (Virchow cells), no granulomas, globi of organisms	Diffuse thickening, madarosis, ear lobe thickening, leonine facies; nerve damage late
Indeterminate (I)	None to few	Variable	Non-specific	Early stage; may progress or regress

The lepromin test measures delayed hypersensitivity to Mycobacterium leprae antigens. It is positive in tuberculoid disease (good cell-mediated immunity) and negative in lepromatous disease (anergic). It is not diagnostic — it indicates immune status.

WHO Classification for Treatment

Classification	Lesions	Skin Smear	Treatment
Paucibacillary (PB)	1–5 patches	Negative	Rifampicin + dapsone for 6 months
Multibacillary (MB)	More than 5 patches	Positive	Rifampicin + dapsone + clofazimine for 12 months

Anti-Leprosy Drugs

Drug	Mechanism	Key Property
Rifampicin	RNA polymerase inhibitor	Bactericidal; most potent single agent; monthly supervised dose
Dapsone	Dihydropteroate synthase inhibition	Bacteriostatic; daily self-administered; causes haemolytic anaemia and methaemoglobinaemia
Clofazimine	DNA binding plus anti-inflammatory	Bacteriostatic and anti-inflammatory (used in Type 2 reactions); causes orange-red skin discolouration

Leprosy Reactions

Feature	Type 1 (Reversal)	Type 2 (ENL)
Mechanism	Delayed hypersensitivity (Type IV) — upregulated CMI	Immune complex deposition (Type III)
Spectrum	Borderline types (BT, BB, BL)	Lepromatous (LL, BL)
Skin lesions	Existing patches become red, oedematous, tender	New painful red nodules
Nerve involvement	Acute nerve function impairment — common	Less prominent
Systemic features	Minimal	Fever, malaise, iridocyclitis, orchitis, lymphadenopathy
Treatment	Systemic corticosteroids	Thalidomide first-line; systemic steroids

High-yield: thalidomide is the drug of choice for ENL. Steroids treat Type 1.

Psoriasis

Psoriasis presents as an erythematous plaque with silvery-white scale on extensor surfaces — elbows, knees, scalp, lumbar area and nails. The candle grease sign describes scales detaching in layers like scraping a candle; the Auspitz sign is pinpoint bleeding after scale removal; Koebner is positive.

Nail Changes

Change	Description
Pitting	Most common nail change — small punctate depressions
Oil drop sign	Translucent yellow-brown spot under the nail
Onycholysis	Separation of nail from nail bed
Subungual hyperkeratosis	Thickening under the nail
Leukonychia	White discolouration

Histology

Finding	Significance
Munro's microabscesses	Neutrophil collections in the stratum corneum — pathognomonic
Kogoj's spongiform pustule	Neutrophils between keratinocytes in the upper spinous layer
Parakeratosis	Retained nuclei in the stratum corneum
Regular acanthosis	Elongated rete ridges, test-tube and club shaped
Thin suprapapillary plate	Explains the Auspitz sign
Dilated tortuous capillaries	In the dermal papillae

Treatment Ladder

Topical therapy uses corticosteroids first-line for mild disease, with calcipotriol (a vitamin D analogue) — the steroid-calcipotriol combination is standard — plus coal tar, dithranol and tazarotene.

Phototherapy uses narrowband UVB first-line, with PUVA more effective but carrying a higher cancer risk.

Systemic options are methotrexate (most widely used for moderate to severe disease), cyclosporine for rapid control of severe flares, and acitretin for pustular and erythrodermic psoriasis.

Biologic	Target	Class
Adalimumab, etanercept, infliximab	TNF-alpha	Anti-TNF
Ustekinumab	IL-12 and IL-23	Anti-IL-12/23
Secukinumab, ixekizumab	IL-17A	Anti-IL-17
Guselkumab, risankizumab	IL-23 (p19 subunit)	Anti-IL-23

PYQ pattern: the drug targeting IL-17 is secukinumab; the drug for pustular psoriasis is acitretin.

Vitiligo

Feature	Detail
Pathogenesis	Autoimmune destruction of melanocytes
Lesion	Complete depigmentation — milk-white macules with normal skin texture
Wood's lamp	Enhanced chalk-white fluorescence
Koebner phenomenon	Positive
Reverse Koebner	Positive — trauma can cause repigmentation
Dermoscopy	Perifollicular pigmentation — a good prognostic sign, indicating a melanocyte reservoir in the follicles

Type	Features
Generalised (non-segmental)	Most common; bilateral and symmetric; associated with thyroid disease, type 1 diabetes and Addison's
Segmental	Unilateral, follows Blaschko's lines, early onset; responds better to grafting
Focal	Single or few macules in one body segment
Acrofacial	Distal digits and periorificial face
Universal	Over 80 percent body involvement — worst prognosis

Treatment uses topical corticosteroids first-line for limited disease, with topical tacrolimus or pimecrolimus preferred on the face and in children. Narrowband UVB is the most effective phototherapy, with PUVA for generalised disease and excimer laser for localised stable patches. Surgical options — split-thickness grafting and melanocyte transplantation — apply only to stable vitiligo. Oral mini-pulse steroids can arrest progression in active disease.

Scabies

Feature	Detail
Organism	Sarcoptes scabiei var. hominis
Pathognomonic lesion	Burrow — a 5–15 mm curved thread-like channel
Sites in adults	Finger web spaces, wrists, penis
Sites in infants	Palms, soles, face
Symptom	Intense pruritus, worse at night
Diagnosis	Dermoscopy shows the "jet with contrail" sign — mite plus burrow; microscopy of skin scraping

Drug	Notes
Permethrin 5% cream	First-line; head to toe, left 8–12 hours, repeated after a week
Oral ivermectin	200 mcg/kg, two doses two weeks apart; first-line for crusted scabies
Benzyl benzoate 25%	Traditional, effective, irritating
Lindane	Avoid in infants and pregnancy — neurotoxicity
Sulfur ointment	Safest in infants and pregnancy

Norwegian or crusted scabies is a hyperinfestation seen in immunocompromised patients — HIV, the elderly, long-term corticosteroid users — with millions of mites, high contagiousness and crusted hyperkeratotic plaques. Treatment combines ivermectin with a topical scabicide.

Drug-Induced Skin Reactions

Reaction	Drug	Key Feature
Fixed drug eruption	Tetracyclines, NSAIDs, cotrimoxazole	Recurs at the same site on re-exposure
Stevens-Johnson syndrome	Sulfonamides, carbamazepine, allopurinol, lamotrigine	Under 10 percent BSA, mucosal involvement
Toxic epidermal necrolysis	Same drugs, more severe	Over 30 percent BSA; Nikolsky positive
DRESS syndrome	Anticonvulsants, allopurinol, sulfonamides	Eosinophilia with organ involvement; onset 2–8 weeks
Photosensitivity	Tetracyclines, amiodarone, chlorpromazine, fluoroquinolones	Sun-exposed distribution
Lichenoid drug reaction	Antimalarials, gold, captopril, thiazides	Mimics lichen planus
Acneiform eruption	Steroids, isoniazid, lithium, OCP	Monomorphic comedones
Alopecia	Cytotoxics, heparin, anticoagulants, retinoids	Diffuse hair loss

Wood's Lamp Findings

Organism or Condition	Colour
Microsporum canis (tinea capitis)	Green to yellow-green
Microsporum audouinii	Brilliant green
Trichophyton schoenleinii (favus)	Pale greenish-white
Pityriasis versicolor (Malassezia)	Yellow-green, coppery-orange
Pseudomonas aeruginosa	Green
Erythrasma (Corynebacterium minutissimum)	Coral red
Porphyria cutanea tarda	Pink-red urine fluorescence
Vitiligo	Chalk-white enhancement

PYQ pattern: erythrasma fluoresces coral red because Corynebacterium produces porphyrins; Microsporum tinea capitis fluoresces green to yellow-green.

High-Yield Dermatology PYQ Checklist

Work through this alongside a timed NEET PG HAMMER test to see which items actually hold up under exam conditions.

• Nikolsky sign — positive in PV, negative in BP
• Koebner phenomenon — psoriasis, LP, vitiligo, not pemphigus
• Reverse Koebner — vitiligo
• Pseudo-Koebner — viral warts, molluscum
• Auspitz sign — psoriasis; mechanism is suprapapillary thinning
• PV target antigen — desmoglein 3 (oral), desmoglein 1 (skin)
• BP target antigen — BP180 (collagen XVII), BP230
• PV immunofluorescence — net or chicken-wire, intercellular
• BP immunofluorescence — linear at the BMZ
• Colloid (Civatte) bodies — lichen planus
• Saw-tooth rete ridges with band-like infiltrate — lichen planus
• Munro's microabscesses — psoriasis, pathognomonic
• Kogoj's spongiform pustule — psoriasis
• Lichen planus pigmentosus — melanin incontinence; flexural and sun-exposed
• Ridley-Jopling TT — lepromin strongly positive, no AFB, well-formed granulomas
• Ridley-Jopling LL — lepromin negative, very high AFB, Virchow cells
• WHO paucibacillary — 5 or fewer lesions; rifampicin and dapsone for 6 months
• WHO multibacillary — more than 5 lesions; add clofazimine, 12 months
• Type 1 leprosy reaction — borderline types; steroids
• Type 2 leprosy reaction (ENL) — LL and BL; thalidomide first-line
• Anti-IL-17 for psoriasis — secukinumab, ixekizumab
• Anti-IL-23 for psoriasis — guselkumab, risankizumab
• Permethrin 5% — first-line for scabies
• Norwegian scabies — immunocompromised; ivermectin
• Erythrasma on Wood's lamp — coral red
• Microsporum tinea capitis on Wood's lamp — green to yellow-green
• Dermoscopy in vitiligo — perifollicular pigmentation indicates good prognosis
• Pterygium unguis — nail lichen planus, pathognomonic