---

🩺 DERMATOLOGY — Complete NEET PG / INI-CET 2026 Notes

Sources: Fitzpatrick's Dermatology (Editors Vol 1 & 2) | Dermatology 2-Volume Set 5e (Bolognini) | Andrews' Diseases of the Skin

---

1. INTRODUCTION TO DERMATOLOGY

Basic Concepts

• Dermatology deals with skin, its appendages (hair, nails, glands), and mucous membranes
• Skin is the largest organ of the body (~1.5–2 m², weight ~4 kg)
• Three primary layers: Epidermis → Dermis → Subcutaneous fat (hypodermis)

Functions of Skin (High-Yield)

---

2. LAYERS OF SKIN

Epidermis (From Basal to Surface: "Californians Like Girls in Bikinis" / CBSGS)

NEET Key: Keratinization (cornification) begins at stratum granulosum. Transit from basal layer → shed = ~4 weeks total; nucleated compartment = 2 weeks; stratum corneum = 2 weeks.

Dermis

• Divided into papillary dermis (superficial; collagen type III, fine; interdigitates with epidermis via rete ridges) and reticular dermis (deep; collagen type I, coarse; contains adnexal structures)
• Composition: Glycosaminoglycan gel + fibrous matrix (collagen + elastin)
• Cellular residents: Fibroblasts, macrophages, dermal dendritic cells, mast cells, vascular endothelium
• Collagen type I = 85% of dermal collagen (thick bundles, reticular dermis)
• Collagen type III = 15% (thin fibers, papillary dermis, fetal skin)
• Elastin provides recoil; decreased in solar elastosis (sun damage)

Subcutaneous Fat (Hypodermis)

• Mainly adipocytes + fibrous septa
• Contains large vessels, nerves
• Panniculitis (inflammation here) → Erythema nodosum (septal), erythema induratum (lobular)

---

3. EPIDERMAL CELLS (4 Resident Populations)

1. Keratinocytes (80–85%)

• Ectodermal origin; stem cells in basal layer
• Produce keratin intermediate filaments (K5/K14 in basal; K1/K10 in suprabasal)
• Average epidermis = 50 microns thick; surface density ~50,000 nucleated cells/mm²
• In disease (psoriasis, eczema): proliferation ↑, maturation ↑

2. Melanocytes (~5–10%)

• Neural crest origin
• Located in stratum basale (1 per 10 keratinocytes in general skin)
• Produce melanin in melanosomes → transferred to keratinocytes
• Melanosome sits above the nucleus of keratinocytes → protects DNA from UV
• DOPA-positive staining identifies melanocytes
• Two types of melanin: Eumelanin (black-brown, photoprotective) and Phaeomelanin (red-yellow, less protective)
• 1 melanocyte: 36 keratinocytes = "epidermal melanin unit"

3. Langerhans Cells (~3–5%)

• Bone marrow origin (monocyte/macrophage lineage)
• Located in stratum spinosum
• Contain Birbeck granules (tennis-racket / rod-shaped on EM) — PATHOGNOMONIC
• Markers: CD1a, Langerin (CD207), S100
• Function: Phagocytose & process antigens → migrate to lymph nodes → activate T cells
• Depleted by UV radiation, glucocorticoids
• Proliferate in Langerhans Cell Histiocytosis (Letterer-Siwe, Hand-Schüller-Christian, Eosinophilic granuloma)

4. Merkel Cells

• Located in stratum basale (not always visible on H&E)
• Neuroendocrine origin
• Function: Slow-adapting mechanoreceptors (touch discrimination)
• Marker: CK20 (dot-like perinuclear staining) — key for Merkel cell carcinoma
• Merkel cell carcinoma: aggressive, associated with Merkel cell polyomavirus (MCPyV); CK20+ dot-like pattern

Memory Aid for Langerhans vs Merkel:

• Langerhans = CD1a + Birbeck granule → immunologic; spinosum
• Merkel = CK20 → mechanoreceptor; basale

---

4. INTRODUCTION TO COMMON SKIN CONDITIONS

Morphology of Lesions (Primary → Secondary)

• Scale (psoriasis), Crust (impetigo — honey-colored), Erosion (loss of epidermis only), Ulcer (loss of epidermis + dermis), Lichenification (thickened skin from chronic scratching), Excoriation, Atrophy, Scar, Fissure, Comedone

Psoriasis (High-Yield)

• Chronic, immune-mediated (Th17/IL-17 driven)
• Turnover time ↓ to 3–4 days (normal ~4 weeks); epidermal transit ~4 days
• ABCD of psoriasis: Acanthosis, Parakeratosis, Munro microabscesses (neutrophils in stratum corneum), Dilated tortuous capillaries in dermal papillae
• Auspitz sign (pinpoint bleeding on removing scale), Koebner phenomenon
• Woronoff ring (blanching around a psoriatic plaque)
• Nail changes: Pitting (most common), oil drop sign, onycholysis, subungual hyperkeratosis

Eczema / Atopic Dermatitis

• Spongiosis (intercellular edema in epidermis) is hallmark histologically
• Atopic triad: Asthma + allergic rhinitis + atopic dermatitis
• IgE elevated; Th2 response (IL-4, IL-5, IL-13)
• Dennie-Morgan lines (infra-orbital folds), Hertoghe sign (lateral eyebrow thinning)

---

5. ADNEXAL DISORDERS

Hair Follicle Anatomy

• Three segments: Infundibulum (upper), isthmus (middle), inferior segment (lower, cycling)
• Bulge region = hair follicle stem cells; permanent portion
• Bulb = hair matrix (rapidly dividing cells) + dermal papilla

Sebaceous Glands

• Holocrine secretion (entire cell disintegrates to release sebum)
• Present everywhere except palms and soles
• Fordyce spots = ectopic sebaceous glands on lips/buccal mucosa (normal variant)
• Sebaceous hyperplasia = benign enlargement on face (yellowish papules with central dell)

Eccrine Sweat Glands

• Distributed all over body; highest density: palms, soles, axillae, forehead
• Secretion: merocrine (exocytosis); clear, hypotonic sweat
• Anhidrosis → risk of hyperthermia
• Miliaria (prickly heat): eccrine duct occlusion → miliaria crystallina (superficial), miliaria rubra (deeper), miliaria profunda (deepest, rare)
• Hyperhidrosis: excessive sweating; Tx: Botulinum toxin injection (palms/axillae), anticholinergics, iontophoresis

Apocrine Glands

• Found: axillae, groin, periumbilical, perianal, areolae
• Become active at puberty; secrete odorless secretion → odor on bacterial decomposition
• Apocrine secretion = "decapitation secretion"
• Fox-Fordyce disease = apocrine duct occlusion → pruritic papules in axillae (young women)
• Hidradenitis suppurativa (HS): Chronic, recurrent, deep inflammatory disease of apocrine gland-bearing skin; Hurley staging (I–III); Rx: antibiotics (doxycycline), adalimumab (anti-TNF-α), isotretinoin

Nails (Adnexal)

• Nail plate: keratinized; originates from nail matrix (proximal → produces dorsal nail plate; distal → ventral)
• Lunula = visible part of nail matrix (whitish)
• Nail bed = epithelium under nail plate
• Nail growth: fingernails ~3 mm/month; toenails ~1 mm/month
• Beau's lines = transverse ridges → systemic illness, high fever, chemotherapy
• Mees' lines = transverse white bands → arsenic poisoning, renal failure
• Muehrcke's lines = paired white transverse bands → hypoalbuminemia
• Half-and-half nails (Lindsay's nails) = proximal white + distal red/brown → CKD
• Terry's nails = proximal 2/3 white → cirrhosis, CHF, diabetes
• Koilonychia (spoon-shaped) → iron deficiency anemia (IDA)
• Onycholysis = separation of nail plate from nail bed → psoriasis, trauma, fungal
• Subungual hyperkeratosis → psoriasis, fungal infection
• Paronychia = inflammation of nail fold; acute = Staph. aureus; chronic = Candida
• Onychomycosis: most common nail disease; caused by dermatophytes (T. rubrum most common)

---

6. MELANIN DISORDERS

Hyperpigmentation

Hypopigmentation / Depigmentation

---

7. SKIN CANCERS

Basal Cell Carcinoma (BCC)

• Most common skin cancer overall
• Originates from basal cells of epidermis and hair follicles; never from palms/soles
• Caused by: UV exposure (primary), arsenic exposure, Gorlin syndrome (PTCH1 gene mutation) → multiple BCCs
• Morphology: Pearly/translucent papule with rolled edges + central ulceration + telangiectasia
• Subtypes: Nodular (most common), superficial, morpheaform (most aggressive/invasive), pigmented
• Histology: Peripheral palisading of cells + clefting artifact; fibromyxoid stroma; mucin
• Rarely metastasizes (<0.1%); locally destructive
• Treatment: Excision (gold standard), Mohs surgery (for recurrent/periorbital), imiquimod (superficial BCC), vismodegib (Hedgehog pathway inhibitor — for advanced/metastatic)
• Immunostain: BerEP4+, CK5/6+

Squamous Cell Carcinoma (SCC)

• Second most common; can metastasize (~2–6%); arises in sun-exposed skin, scars, mucous membranes
• Risk factors: UV, chronic scars (Marjolin's ulcer), HPV (SCCs in mucous membranes), arsenic, radiation, immunosuppression, xeroderma pigmentosum
• Precursor lesion: Actinic keratosis (AK) — scaly, erythematous papule on sun-damaged skin; 0.1–10% progress to SCC/year
• Bowen's disease = SCC in situ; full-thickness epithelial atypia; "erythroplakia" on mucous membrane
• Erythroplasia of Queyrat = Bowen's disease on glans penis
• Histology: Atypical keratinocytes invading dermis; keratin pearls; intercellular bridges; EMA+
• Marjolin's ulcer: well-differentiated SCC in chronic ulcer/scar/burn → high metastatic risk
• Treatment: Excision, Mohs, radiotherapy; systemic: cetuximab, pembrolizumab

Melanoma

• Most deadly skin cancer; neural crest origin
• Major subtypes:
  • Superficial spreading melanoma (SSM) — most common (~70%); radial growth phase; ABCDE criteria
  • Nodular melanoma — aggressive, vertical growth; amelanotic variants exist
  • Lentigo maligna melanoma — elderly; sun-damaged face; begins as Hutchinson's melanotic freckle
  • Acral lentiginous melanoma (ALM) — palms, soles, subungual; most common in dark-skinned individuals (Asians, Africans); Hutchinson's sign (pigmentation extending to proximal nail fold)
• ABCDE criteria: Asymmetry, Border irregularity, Color variation, Diameter >6 mm, Evolution
• Risk factors: UV (intermittent intense exposure), fair skin, family history, dysplastic nevi syndrome
• Breslow thickness = most important prognostic factor (depth from granular layer to deepest tumor cell)
• Clark levels (I–V) = anatomic invasion level (less important than Breslow for prognosis)
• Sentinel lymph node biopsy for Breslow >1 mm (or <1 mm with ulceration/high mitosis)
• Markers: S100, HMB-45, Melan-A/MART-1, MiTF
• Treatment: Wide excision ± SLNB; Metastatic: BRAF inhibitors (vemurafenib, dabrafenib) if BRAF V600E mutation (50% of melanomas); anti-PD-1 (pembrolizumab, nivolumab); CTLA-4 (ipilimumab)
• Desmoplastic melanoma: S100+, HMB-45 negative or focally positive; highly neurotropic

Merkel Cell Carcinoma

• Rare, aggressive neuroendocrine carcinoma; elderly immunosuppressed patients
• Associated with Merkel cell polyomavirus (MCPyV)
• CK20 dot-like perinuclear staining + synaptophysin, chromogranin (neuroendocrine markers)
• CK7 negative (helps distinguish from metastatic small cell lung cancer which is CK7+, CK20−)

---

8. FACIAL SKIN LESIONS

Acne Vulgaris

• Pathogenesis: Follicular hyperkeratosis → plugging → C. acnes colonization → inflammation
• Lesions: Comedones (open = blackhead; closed = whitehead) → papules → pustules → nodules → cysts → scars
• Grade I: Comedones; Grade II: Papules/pustules; Grade III: Nodules; Grade IV: Nodulocystic (Acne conglobata — most severe)
• Rx ladder: Topical retinoids → topical BPO/antibiotics → oral antibiotics (doxycycline/minocycline) → isotretinoin (for severe nodulocystic or refractory)
• Isotretinoin (13-cis retinoic acid): MOA = ↓ sebum production, normalizes follicular keratinization; teratogenic (Category X), monitor LFTs, lipids; iPLEDGE program
• Acne fulminans: Sudden onset, ulcerating, systemic symptoms (fever, arthralgia) — rx: oral steroids + isotretinoin

Rosacea

• Chronic facial erythema (central face: cheeks, nose, chin, forehead); telangiectasia
• Subtypes: Erythematotelangiectatic, Papulopustular, Phymatous (rhinophyma = enlarged bulbous nose), Ocular
• Trigger: Sun, heat, spice, alcohol, stress
• Demodex folliculorum involved in pathogenesis
• Rx: Topical metronidazole, azelaic acid, ivermectin; Oral doxycycline (anti-inflammatory dose); laser for telangiectasia

Sebaceous Gland Lesions

• Sebaceous hyperplasia: Yellowish umbilicated papules on nose/cheeks; elderly; benign
• Steatocystoma multiplex: Multiple cysts on trunk; keratinous + sebaceous content
• Xanthelasma: Yellow plaques on eyelids (medial canthus); ↑ lipids (but 50% have normal lipids); not resolved with statins typically

---

9. ALOPECIA

Non-Scarring Alopecia (Follicle Preserved — Reversible)

Androgenetic Alopecia (AGA)

• Most common type; males: Hamilton-Norwood pattern (frontotemporal recession → vertex); females: Ludwig pattern (diffuse crown thinning, frontal hairline preserved)
• DHT (dihydrotestosterone) from 5α-reductase converts testosterone → DHT → miniaturization of follicles
• Rx: Minoxidil (topical/oral; ↑ blood flow, prolongs anagen); Finasteride (5α-reductase inhibitor, oral, males only); Hair transplant

Alopecia Areata (AA)

• Autoimmune (T-cell mediated); lymphocytic infiltrate around anagen bulb ("swarm of bees" pattern)
• CD8+ T cells and IFN-γ are key effectors; loss of hair follicle immune privilege (↓ MHC class I expression)
• Non-scarring; well-demarcated, oval/circular patches of hair loss
• Exclamation mark hairs (dystrophic hairs tapered at base) — pathognomonic
• Variants: Alopecia totalis (total scalp loss), alopecia universalis (entire body)
• "Ophiasis pattern" = band-like loss along occipital/temporal periphery (worse prognosis)
• Associated: Thyroid disease, vitiligo, diabetes, Down syndrome
• Nail: Geometric pitting (most specific for AA); trachyonychia
• Rx: Intralesional triamcinolone (first-line for patchy), topical minoxidil, anthralin; systemic: JAK inhibitors (baricitinib, ritlecitinib — FDA approved)

Telogen Effluvium (TE)

• Diffuse, non-scarring; trigger shifts hairs from anagen → telogen prematurely
• Causes: Post-partum (most common), fever, surgery, crash dieting, hypothyroidism, iron deficiency
• Telogen shed 2–3 months after trigger (telogen duration = ~100 days)
• Hair pull test: >10% telogen hairs (normally <10%)
• Self-limiting in most; treat underlying cause

Tinea Capitis

• Fungal (Trichophyton, Microsporum); children predominantly
• Endothrix (T. tonsurans — "black dot ringworm") vs. ectothrix (M. canis — Wood's lamp: greenish fluorescence)
• Rx: Oral griseofulvin (drug of choice in children), terbinafine

Scarring Alopecia (Follicle Destroyed — Irreversible)

• Discoid lupus erythematosus (DLE): Follicular plugging; atrophy; dyspigmentation; "burnt-out" scarring on scalp
• Lichen planopilaris: Follicular lichen planus on scalp; "follicular spines"; Rx: cyclosporin, hydroxychloroquine
• Frontal fibrosing alopecia (FFA): Variant of LPP; recession of frontal hairline; postmenopausal women
• Folliculitis decalvans: S. aureus; pustular alopecia; tufted folliculitis (doll's hair appearance)
• Central centrifugal cicatricial alopecia (CCCA): Most common scarring alopecia in African-American women

---

10. MAST CELL DISORDERS (MASTOCYTOSIS)

Cutaneous Mastocytosis

• Mast cell proliferation in skin due to KIT (c-KIT / CD117) gain-of-function mutation (D816V most common)
• Mast cells release: Histamine, tryptase, prostaglandins, heparin, TNF-α

• Darier's sign: Rubbing of a lesion → urtication (mast cell degranulation) — classic for mastocytosis
• Tryptase level is elevated → systemic involvement screening
• Triggers of degranulation: Heat, friction, aspirin, NSAIDs, opiates, alcohol, contrast dye
• Histology: Giemsa stain / Toluidine blue stain shows metachromatic granules in mast cells
• CD117 (c-KIT)+, CD2+, CD25+ in systemic mastocytosis
• Rx: Antihistamines (H1 + H2), cromolyn sodium; imatinib (c-KIT mutation); midostaurin/avapritinib for advanced systemic mastocytosis

---

11. WOOD'S LAMP EXAMINATION

• Emits long-wave UV light (365 nm); examination in dark room
• Used for fluorescence of skin infections and pigmentary disorders

NEET Key: Coral-pink = Erythrasma; Bright green = Microsporum capitis; Chalky white = Vitiligo; Golden-yellow = Tinea versicolor

---

12. MISCELLANEOUS INFLAMMATORY DERMATOSES

Lichen Planus (LP)

• 6 P's: Pruritic, Purple, Polygonal, Planar (flat-topped), Papules, Plaques
• Sites: Flexor wrists, ankles, genitalia, oral mucosa
• Wickham's striae = white lacy pattern on surface (better seen with oil + dermoscopy)
• Oral LP = Wickham's striae on buccal mucosa (lace-like pattern); erosive type → risk of SCC
• Koebner phenomenon +
• Histology: Band-like lymphocytic infiltrate at DEJ, "saw-tooth" rete ridges, Civatte bodies (apoptotic keratinocytes), Max Joseph spaces (subepidermal clefts)
• Associated: Hepatitis C virus (HCV), drugs (gold, antimalarials, beta-blockers, thiazides — lichenoid drug reactions)
• Rx: Topical/systemic steroids, retinoids, cyclosporin; acitretin for hypertrophic LP

Psoriasis (Detailed Histology)

• Acanthosis + Parakeratosis + Munro microabscesses + Kogoj spongiform pustules (in stratum spinosum/granulosum) + Dilated capillaries in dermal papillae + Loss of stratum granulosum

Pityriasis Rosea

• Herald patch (single large lesion, 2–10 cm) → 7–14 days later: secondary eruption of smaller oval lesions along skin lines → "Christmas tree" pattern on back
• Follows Langer's lines
• Caused by HHV-6 and HHV-7 reactivation
• Self-limiting; resolves in 6–8 weeks; Rx: NB-UVB (shorten duration), oral acyclovir (severe cases)

Urticaria

• Wheal and flare; caused by mast cell degranulation → histamine release
• Acute (<6 weeks): Infection, food, drugs; Chronic (>6 weeks): idiopathic in most
• Dermographism (factitious urticaria): "writing on skin" — most common physical urticaria
• Rx: Nonsedating H1 antihistamines (cetirizine, fexofenadine); Omalizumab (anti-IgE) for chronic refractory urticaria

Bullous Disorders

---

13. DERMOEPIDERMAL JUNCTION (DEJ) & DIRECT IMMUNOFLUORESCENCE (DIF)

DEJ Structure (Basement Membrane Zone — BMZ)

• 4 layers from top to bottom:
  1. Lamina lucida — contains laminin 332 (laminin 5), integrins (α6β4), BPAG2 (BP180)
  2. Lamina densa — contains Type IV collagen, perlecan, nidogen
  3. Sub-lamina densa — contains Type VII collagen (anchoring fibrils), fibronectin
  4. Anchoring fibrils (Type VII collagen) loop around collagen VII into dermis
• Hemidesmosomes: connect keratinocytes to basement membrane; contain BPAG1 (BP230), BPAG2 (BP180), integrin α6β4
• Mutations in DEJ proteins → Epidermolysis Bullosa (EB):
  • Keratin 5/14 → EB Simplex
  • Laminin-332 → Junctional EB (Herlitz — lethal)
  • Type VII collagen → Dystrophic EB

Direct Immunofluorescence (DIF) — Key Patterns

NEET Key: DIF is done on perilesional skin for blistering diseases (except DH where it's done on normal perilesional skin)

---

14. SCALP HAIR CYCLE

Phases of Hair Growth

Hair Anatomy

• Hair shaft zones: Medulla (center) → Cortex (bulk) → Cuticle (outer)
• Root sheaths: Internal root sheath (Henle, Huxley, cuticle layers) + External root sheath
• Bulge region = Stem cell niche (CD34+ in mice; K15+ in humans) → permanent; not destroyed in non-scarring alopecia
• Dermal papilla = mesenchymal component; dictates hair follicle cycling

Types of Hair

• Lanugo: Fetal fine unpigmented hair; shed before birth (except premature infants)
• Vellus: Fine, short, unpigmented; body
• Terminal: Coarse, long, pigmented; scalp, beard, pubic, axillary

Clinical Correlations

• Anagen effluvium: Hair loss during anagen; cause = chemotherapy (MTX, cyclophosphamide); immediate hair loss within weeks
• Telogen effluvium: Premature shift to telogen; loss 2–3 months after trigger; post-partum most common
• Trichoscopy (dermoscopy of scalp): Used to evaluate hair disorders; yellow dots = follicular openings (AA); black dots = broken hairs (AA); peripilar sign (LP)

---

15. NAIL DISEASES

Structural Disorders

Nail Infections

• Onychomycosis: T. rubrum most common; Tinea unguium = dermatophyte onychomycosis; Rx: oral terbinafine (drug of choice, pulse/continuous), itraconazole
• Candida onychomycosis: Immunosuppressed, water-exposure; proximal subungual type common in HIV
• Acute paronychia: Bacterial (Staph. aureus); Rx: I&D + antibiotics
• Chronic paronychia: Candida; occupational (water exposure); Rx: antifungals + keep dry
• Herpetic whitlow: HSV-1/2; painful vesicles on periungual area; Rx: acyclovir
• Green nail syndrome: Pseudomonas aeruginosa — green-black discoloration

---

16. CUTANEOUS TUBERCULOSIS & ERYTHEMA NODOSUM

Cutaneous TB

• Papulonecrotic tuberculid: Recurrent necrotic papules on extensor limbs
• Lichen scrofulosorum: Groups of lichenoid papules; children; perifollicular
• Erythema induratum (Bazin's disease): Nodular vasculitis of legs (calves); women; lobular panniculitis (fat necrosis + granulomas)

Erythema Nodosum (EN)

• Most common panniculitis; septal panniculitis (inflammation of fat septa)
• Bilateral, tender, red nodules on anterior shins (pretibial); no ulceration
• Histology: Septal thickening + lymphocytic infiltrate + Miescher's radial granuloma (in fat septae)

• Streptococcal infection (most common in children)
• Sarcoidosis (Löfgren's syndrome: EN + bilateral hilar lymphadenopathy + fever + arthritis)
• Tuberculosis
• Reactive: IBD (Crohn's > UC), behcet's
• Infections: Yersinia, fungi (histoplasma, coccidioides), leprosy
• Pregnancy/OCP (estrogen)
• Etc: drugs (sulfonamides, penicillins), lymphoma
• Löfgren's syndrome = acute sarcoidosis: EN + bilateral hilar adenopathy + uveitis + arthritis → good prognosis
• Rx of EN: Treat underlying cause; NSAIDs (first-line for pain); KI (potassium iodide) for refractory; systemic steroids

---

17. DRUG REACTIONS IN DERMATOLOGY

Classification by Mechanism

Common Cutaneous Drug Reactions

Morbilliform (Exanthematous) Drug Eruption

• Most common drug reaction
• Symmetrical maculopapular rash; starts trunk → extremities
• Causes: Penicillin (most common), amoxicillin (90% in infectious mononucleosis!), sulfonamides
• Onset: 7–14 days after starting drug
• Self-limiting; Rx: Stop drug, antihistamines, topical steroids

Fixed Drug Eruption (FDE)

• Same site each time the drug is taken → hyperpigmented patch/plaque
• Residual hyperpigmentation after resolution
• Common causes: NSAIDs (especially phenylbutazone), tetracyclines, cotrimoxazole, paracetamol, barbiturates
• Histology: Basal layer vacuolation + melanophages in dermis + eosinophils

Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)

• Spectrum of severity based on BSA skin detachment:
  • SJS: <10% BSA
  • SJS-TEN overlap: 10–30% BSA
  • TEN: >30% BSA
• Mechanism: Drug-induced Fas-L/FasR mediated keratinocyte apoptosis → full-thickness epidermal necrosis
• Nikolsky sign + (Asboe-Hansen sign = lateral pressure extends bulla)
• Common causes: Allopurinol (most common overall/HLA-B5801), carbamazepine (HLA-B1502 in Asians), lamotrigine, phenytoin, NSAIDs (oxicam group), sulfonamides, nevirapine (HIV)
• HLA associations (NEET Key):
  • HLA-B*5801 → Allopurinol-induced SJS/TEN (Han Chinese, Thai)
  • HLA-B*1502 → Carbamazepine-induced SJS/TEN (South/Southeast Asian)
  • HLA-B*5701 → Abacavir hypersensitivity (non-skin but important)
• Mucosal involvement in 100% (oral, ocular, genital)
• Rx: Stop offending drug immediately; ICU/burn unit; IV fluids; eye care (prevent symblepharon); cyclosporin, IVIG (controversial); systemic steroids contraindicated in TEN (↑ sepsis risk)
• Mortality: SJS ~1–5%, TEN ~25–35%; SCORTEN score (prognostic scoring)

DRESS Syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms)

• Also called Drug-induced Hypersensitivity Syndrome (DIHS)
• Onset: 2–8 weeks after drug initiation (longer latency than other reactions)
• Triad: Extensive morbilliform rash + fever + internal organ involvement + lymphadenopathy + eosinophilia
• Atypical lymphocytosis on blood smear
• Organs: Liver (hepatitis most common), kidney, lung, heart (myocarditis), thyroid (late — weeks to months after)
• Causes: Anticonvulsants (phenytoin, carbamazepine, phenobarbital), dapsone, sulfonamides, allopurinol, minocycline
• HHV-6 reactivation during DRESS → marker of DRESS (↑ HHV-6 viral load)
• RegiSCAR criteria used for diagnosis
• Rx: Systemic steroids (prednisone 1–2 mg/kg/day); slow taper (months); IVIG for refractory

Urticaria and Angioedema

• Most common allergic drug reaction
• Type I (IgE-mediated) or direct mast cell activation
• Penicillin = classic cause
• ACE inhibitors → Angioedema (bradykinin-mediated, NOT IgE; C1 esterase inhibitor not involved; replace with ARB)

Drug-Induced Lupus

• Drugs: Hydralazine, Procainamide, Isoniazid, Minocycline, TNF-α inhibitors
• ANA +; Anti-histone antibodies + (most specific); complement normal; dsDNA usually negative
• Resolves on stopping drug

Photosensitivity Reactions

• Phototoxic (more common): Anyone exposed; no prior sensitization; like sunburn; dose-dependent
  • Drugs: Tetracyclines (doxycycline), fluoroquinolones, amiodarone, NSAIDs (ketoprofen), voriconazole, psoralens
  • "Photo-onycholysis" — doxycycline
• Photoallergic (less common): Prior sensitization required; type IV; eczematous; can spread beyond sun-exposed area
  • Drugs: Sulfonamides, thiazides, sunscreens (PABA), promethazine
• Berloque dermatitis: Phototoxic reaction to psoralen in perfumes (lime/bergamot oil) → drip-pattern hyperpigmentation on neck

Other Important Drug Reactions

---

QUICK-REFERENCE MNEMONICS FOR NEET PG / INI-CET

---

---

What's Covered (All 17 Topics):

1. Introduction to Dermatology — skin functions, structure, three layers
2. Layers of Skin — CBSGS mnemonic for epidermal layers, dermis (papillary vs reticular), hypodermis, collagen types
3. Epidermal Cells — Keratinocytes, Melanocytes (1:36 ratio, epidermal melanin unit), Langerhans cells (Birbeck granules, CD1a, CD207), Merkel cells (CK20)
4. Common Skin Conditions — Primary vs secondary morphology, psoriasis (Munro microabscess, Kogoj pustule, Auspitz sign), eczema (spongiosis, IgE, Th2)
5. Adnexal Disorders — Holocrine sebaceous glands, eccrine (miliaria, hyperhidrosis), apocrine (Fox-Fordyce, hidradenitis suppurativa)
6. Melanin Disorders — Melasma, vitiligo (JAK inhibitors), albinism, pityriasis versicolor (spaghetti & meatballs), leprosy, café-au-lait macules
7. Skin Cancers — BCC (peripheral palisading, PTCH1/Gorlin), SCC (Marjolin, Bowen's), Melanoma (ABCDE, Breslow, subtypes, BRAF V600E, immunotherapy), Merkel cell carcinoma
8. Facial Skin Lesions — Acne vulgaris (isotretinoin, iPLEDGE), Rosacea (rhinophyma, Demodex), xanthelasma
9. Alopecia — AGA (DHT, finasteride), Alopecia areata (swarm of bees, JAK inhibitors, exclamation mark hairs), Telogen effluvium, Tinea capitis, Scarring alopecias
10. Mast Cell Disorders — Mastocytosis, Darier's sign, D816V KIT mutation, CD117+/CD2+/CD25+, tryptase
11. Wood's Lamp — Coral-pink (erythrasma), Green (Microsporum), White (vitiligo), Golden-yellow (tinea versicolor), Blue-white (ash-leaf macule)
12. Inflammatory Dermatoses — Lichen planus (6 P's, Wickham's striae, HCV, lichenoid reactions), Pityriasis rosea (Herald patch, HHV-6/7), Urticaria, Bullous diseases (DIF patterns table)
13. DEJ & Direct Immunofluorescence — 4 BMZ layers, hemidesmosomes, Epidermolysis bullosa types, all DIF patterns with diseases
14. Scalp Hair Cycle — Anagen/Catagen/Telogen durations and percentages, bulge stem cells, lanugo/vellus/terminal, anagen vs telogen effluvium
15. Nail Diseases — Complete nail signs with associations, onychomycosis (terbinafine), paronychia, green nail syndrome
16. Cutaneous TB & Erythema Nodosum — All TB types (lupus vulgaris = apple-jelly, scrofuloderma, TBVC), tuberculids, EN (Löfgren's syndrome, septal panniculitis, SSTRIPE causes)
17. Drug Reactions — SJS/TEN (SCORTEN, HLA associations), DRESS (HHV-6, 2–8 week latency), FDE, morbilliform, photosensitivity, and drug-specific skin reactions table

---

🦠 HANSEN'S DISEASE (LEPROSY) — Complete NEET PG / INI-CET 2026 Notes

Sources: Andrews' Diseases of the Skin — Clinical Dermatology | Robbins, Cotran & Kumar — Pathologic Basis of Disease | Roitt's Essential Immunology | Sherris Medical Microbiology

---

1. INTRODUCTION & EPIDEMIOLOGY

• Hansen's disease = chronic granulomatous infection caused by Mycobacterium leprae (and rarely M. lepromatosis, proposed 2008)
• Obligate intracellular pathogen — infects dermal macrophages and Schwann cells
• Cannot be cultured in vitro (only in armadillo foot pads and mouse foot pads)
• Grows optimally at 32–34°C → prefers cooler tissues: skin, peripheral nerves, anterior eye, testes, upper airway
• Does NOT affect CNS, liver parenchyma, or bones directly (core temperature too high)
• Incubation period: 2–5 years (tuberculoid); 8–12 years (lepromatous) — longest incubation of any bacterial infection
• Global burden: ~200,000 new cases/year; endemic in India, Brazil, Indonesia, SE Asia, Africa
• India: elimination target <1/10,000; current prevalence ~0.45/10,000

Transmission

• Respiratory droplets (nasal secretions of LL patients) — primary route
• Skin-to-skin contact (prolonged close contact)
• Zoonotic reservoir: Nine-banded armadillo (Dasypus novemcinctus) — in southern USA
• NOT highly contagious — 95% of humans are naturally immune

---

2. MICROBIOLOGY OF M. LEPRAE

NEET Key: M. leprae has the longest doubling time of any bacterium (~13 days). Cannot be cultured on artificial media.

---

3. IMMUNOLOGY — THE SPECTRUM CONCEPT (RIDLEY-JOPLING)

HIGH CMI ←————————————————————————————→ LOW CMI
   TT        BT        BB        BL        LL
(Tuberculoid)              (Lepromatous)

---

4. CLASSIFICATION

A. Ridley-Jopling Classification (Standard/International)

B. WHO Classification (used for MDT regimen selection — NEET Favourite)

NEET Key: WHO PB = ≤5 lesions; MB = >5 lesions. Smear positivity alone = MB regardless of lesion count.

C. Indian Classification (IAL — used in Indian textbooks)

• Indeterminate (I) → Tuberculoid (T) → Borderline (B) → Lepromatous (L)

---

5. CLINICAL FEATURES

Indeterminate Leprosy

• Earliest form; often the first clinical sign
• Solitary, poorly defined hypopigmented macule on cheek, upper arm, thigh, buttock
• Sensory changes minimal or absent; no nerve enlargement; no nodules
• Histology: lymphocytic infiltrate without granulomas; few or no bacilli
• May spontaneously resolve (if CMI strong) or evolve into TT, BB, or LL
• Diagnosis is not indeterminate — the classification is indeterminate

Tuberculoid Leprosy (TT)

• 1–5 lesions, asymmetrically distributed
• Typical lesion: Large erythematous plaque; sharply elevated, indurated border sloping to a flattened atrophic center → "saucer right side up"
• Dry, scaly, hairless (anhidrotic), anesthetic
• Cardinal signs: Anesthesia + Anhidrosis + Alopecia within the lesion
• Enlarged peripheral nerves near the lesion → tender, cord-like
• "Feeding nerve" = enlarged nerve leading to the lesion (in BT especially)
• Common sites: face, limbs, trunk; NOT scalp, axillae, groin, perineum (these areas are warm/moist → not affected)
• Nerves commonly affected: Greater auricular, superficial peroneal, ulnar (most commonly affected nerve overall), posterior tibial, radial cutaneous, facial

Lepromatous Leprosy (LL)

• Numerous lesions, bilaterally symmetric
• Macular → papular → nodular; coalesce → "leonine facies" (diffuse infiltration of face)
• Skin thickening, loss of eyebrows (madarosis — loss of lateral eyebrows first) and eyelashes
• Sensation relatively preserved early (but eventually lost due to diffuse nerve damage)
• Symmetric peripheral neuropathy (unlike TT where asymmetric)
• Nasal involvement: Chronic nasal congestion → saddle-nose deformity (septal perforation)
• Testes: Orchitis → hyalinization → infertility, gynecomastia
• Lymph nodes: Foamy macrophages in paracortex
• Ocular: Corneal opacities ("iris pearls" = miliary lepromas of iris in BL/LL), lagophthalmos
• Glove and stocking anesthesia — due to symmetric polyneuropathy
• Lucio phenomenon: Specific to LL; hemorrhagic necrotic lesions (form of ENL in Lucio leprosy — diffuse non-nodular lepromatous leprosy in Mexico/Central America)

Borderline Leprosy (BB)

• Most unstable type on the spectrum
• "Punched out" lesions with irregular, vague edges
• Mixed features; may have satellite lesions
• BB leprosy is the most difficult to classify
• Liable to type 1 (reversal) reactions

Histoid Leprosy (Wade's histoid)

• Variant of LL (downgraded/relapsed); classically seen in dapsone resistance or after irregular treatment
• Well-defined, dome-shaped, shiny nodules (resembling dermatofibroma)
• Bacilli in spindle-shaped histiocytes arranged in a storiform pattern
• Highest bacterial index (BI) of all forms
• Can occur over bony prominences (elbows, knees)

---

6. NERVE INVOLVEMENT — HIGH-YIELD TABLE

Memory Aid: Ulnar = most commonly affected nerve in leprosy. Lateral popliteal = most commonly affected lower limb nerve.

• Ulnar claw = 4th & 5th fingers clawed (main-en-griffe)
• Median claw = Index + middle fingers
• Combined = all 4 fingers
• "Benediction sign" (Pope's blessing) = ulnar nerve → cannot flex 4th & 5th = they remain extended when asked to make fist
• "Ape hand" = median nerve → thenar wasting, thumb cannot oppose

---

7. HISTOPATHOLOGY

NEET Key — Grenz Zone: Pathognomonic of LL — normal collagen-free subepidermal zone between epidermis and the macrophage infiltrate.

Bacterial Index (BI) — Ridley's Logarithmic Scale

Morphological Index (MI)

• % of solid-staining (viable) bacilli in a smear
• Normal = ~25–60% solid bacilli
• After treatment: MI falls to 0 within 3–6 months (earlier than BI)
• MI falls before BI — used to monitor early treatment response

---

8. LEPROMIN TEST (MITSUDA REACTION)

• Not a diagnostic test — measures cell-mediated immunity (CMI)
• Intradermal injection of autoclaved M. leprae suspension (Mitsuda antigen)

Key: Lepromin positive = good prognosis; Lepromin negative = lepromatous/poor immunity. Diagnostic value = NIL.

---

9. LEPROSY REACTIONS (HIGH-YIELD)

Type 1 Reaction (Reversal Reaction — RR)

Type 2 Reaction — Erythema Nodosum Leprosum (ENL)

Type 3 Reaction — Lucio Phenomenon

• Specific to diffuse lepromatous (Lucio) leprosy in Mexico/Central America
• Hemorrhagic, necrotic plaques → ulceration
• Mechanism: immune complex vasculitis (similar to ENL but distinct)
• NOT a classic type 1 or type 2 — considered a separate category

Comparison — Type 1 vs Type 2 Reaction (Most Tested)

---

10. MDT — MULTIDRUG THERAPY (WHO REGIMEN)

Adult PB Leprosy (≤5 lesions) — 6 months

Adult MB Leprosy (>5 lesions) — 12 months

Pediatric MDT (10–14 years, weight-adjusted)

• PB: Rifampicin 450 mg monthly + Dapsone 50 mg daily × 6 months
• MB: Rifampicin 450 mg + Clofazimine 150 mg monthly; Dapsone 50 mg + Clofazimine 50 mg alternate days × 12 months
• Clofazimine 6 mg/kg/month (supervised) for children

Single-Lesion PB Leprosy — ROM Regimen

• Rifampicin 600 mg + Ofloxacin 400 mg + Minocycline 100 mg — single dose
• Only for single skin lesion with no nerve involvement (not indeterminate)

Drug Mechanisms & Side Effects

NEET Key: Rifampicin = most bactericidal drug in leprosy MDT. Clofazimine = reduces frequency/severity of ENL. Thalidomide = DOC for ENL but teratogenic.

---

11. DISABILITY GRADING (WHO)

NEET Key: Grade 2 disability = visible deformity. Grade 1 = only anesthesia/impairment without visible deformity.

---

12. DIAGNOSIS OF LEPROSY

Clinical Diagnosis (WHO Criteria — 3 Cardinal Signs)

1. Hypopigmented/erythematous skin lesion with loss of sensation
2. Thickened peripheral nerve with sensory/motor loss
3. Positive skin smear for AFB

• 1 or more cardinal signs → diagnosis of leprosy

Investigations

Sensory Testing Sequence (First to Last affected)

1. Temperature (cold sensation — FIRST to be lost)
2. Light touch
3. Pain (pin prick)
4. Deep pressure (last to be lost)

NEET Key: Temperature sensation is the FIRST to be lost in leprosy.

---

13. SPECIAL FORMS & ASSOCIATIONS

Pure Neural Leprosy

• Only nerve involvement, no skin lesions
• Can be TT, BT, or LL type
• Constitutes up to 5% of cases in Nepal/India
• Diagnosis: Nerve biopsy (sural nerve most commonly biopsied)

Leprosy in Children

• Indeterminate form most common
• Tuberculoid most common type overall in children
• BCG vaccination offers partial protection

Leprosy and Pregnancy

• Type 1 and type 2 reactions ↑ during pregnancy and postpartum
• Clofazimine: relatively contraindicated (crosses placenta → neonatal skin discoloration)
• Thalidomide: absolutely contraindicated in pregnancy
• MDT (rifampicin + dapsone) — safe in pregnancy

Leprosy and HIV

• HIV does not dramatically increase risk of leprosy
• Can cause immune reconstitution inflammatory syndrome (IRIS) → type 1 reactions after ART
• HIV + leprosy = more unusual presentations

---

14. VACCINES IN LEPROSY

NEET Key: MIP vaccine = developed in India (JALMA, Agra/Delhi — answer varies by source; JALMA is in Agra); used as adjunct in MB leprosy. BCG gives partial protection.

---

15. OCULAR, NASAL & SYSTEMIC INVOLVEMENT

Ocular (Lepromatous)

• Lagophthalmos (VII nerve) → exposure keratitis
• Corneal anesthesia (V nerve) → corneal ulcers
• Iris pearls (miliary lepromas of iris) — in BL/LL
• Corneal opacities, avascular keratitis, pannus formation
• Iridocyclitis (in ENL reactions)

Nasal

• Chronic nasal congestion → epistaxis
• Septal perforation → saddle-nose deformity
• Loss of upper incisor teeth (from alveolar infiltration in LL)

Testes

• Orchitis → destruction of seminiferous tubules → azoospermia, infertility, gynecomastia (LL)

Kidney

• ENL → immune complex glomerulonephritis (mesangial)

---

16. LEPROSY — KEY MNEMONICS

---

17. PREVIOUS YEAR QUESTIONS (PYQ) — NEET PG / INI-CET / AIPGMEE

---

🔴 PYQ BLOCK 1 — Bacteriology & Immunology

• A. 24 hours
• B. 6 days
• C. 13 days ✅
• D. 30 days

---

• A. Tuberculoid leprosy
• B. Normal adults
• C. Sarcoidosis
• D. Lepromatous leprosy ✅

---

• A. It is diagnostic of leprosy
• B. It requires a live bacillus suspension
• C. It measures cell-mediated immunity ✅
• D. Mitsuda reaction is read at 48–72 hours

---

• A. Producing anti-PGL-1 antibodies
• B. Activating Th2 cells
• C. Cross-reactive CMI against M. leprae ✅
• D. Directly neutralizing M. leprae

---

🔴 PYQ BLOCK 2 — Classification & Histology

• A. ≤3 lesions only
• B. Single lesion only
• C. ≤5 lesions with negative smear ✅
• D. >5 lesions with negative smear

---

• A. Epithelioid granuloma
• B. Caseous necrosis
• C. Foamy macrophages (lepra/Virchow cells) with globi ✅
• D. Neutrophilic microabscesses

---

• A. Tuberculoid leprosy
• B. Borderline leprosy
• C. Lepromatous leprosy ✅
• D. Indeterminate leprosy

---

• A. Well-defined shiny nodules
• B. Seen in previously untreated patients ✅ (Incorrect — seen in dapsone-resistant/relapsed patients)
• C. High bacterial index
• D. Spindle-shaped histiocytes in storiform pattern

---

• A. TT
• B. BB (mid-borderline) ✅
• C. BT
• D. LL

---

🔴 PYQ BLOCK 3 — Clinical Features & Nerve Involvement

• A. Posterior tibial nerve
• B. Ulnar nerve ✅
• C. Greater auricular nerve
• D. Facial nerve

---

• A. Radial nerve
• B. Ulnar nerve ✅
• C. Median nerve
• D. Peroneal nerve

---

• A. Posterior tibial nerve
• B. Femoral nerve
• C. Common peroneal (lateral popliteal) nerve ✅
• D. Sural nerve

---

• A. Fine touch
• B. Pain
• C. Temperature (cold) ✅
• D. Deep pressure

---

• A. LL leprosy
• B. Indeterminate leprosy
• C. BT (borderline tuberculoid) leprosy ✅
• D. BB leprosy

---

• A. Traumatic septal fracture
• B. Granulomatous infiltration of nasal septum (LL) ✅
• C. Type 1 reaction
• D. ENL

---

🔴 PYQ BLOCK 4 — Reactions

• A. TT leprosy only
• B. LL leprosy only
• C. Borderline spectrum (BT, BB, BL) ✅
• D. All forms of leprosy

---

• A. Type I hypersensitivity
• B. Type III (immune complex) hypersensitivity ✅
• C. Type IV hypersensitivity
• D. Type II hypersensitivity

---

• A. Prednisolone
• B. Clofazimine
• C. Thalidomide ✅
• D. Dapsone

---

• A. New lesions appear
• B. Systemic features like fever are common
• C. Existing lesions become erythematous and edematous ✅
• D. Immune complexes are deposited in vessel walls

---

• A. Borderline leprosy
• B. Tuberculoid leprosy
• C. ENL patients in India
• D. Diffuse lepromatous leprosy (Lucio leprosy) — mainly Mexico/Central America ✅

---

🔴 PYQ BLOCK 5 — Treatment

• A. Rifampicin + Dapsone × 12 months
• B. Rifampicin + Dapsone + Clofazimine × 12 months ✅
• C. Rifampicin + Clofazimine × 6 months
• D. Rifampicin + Dapsone × 6 months

---

• A. Dapsone
• B. Rifampicin
• C. Clofazimine ✅
• D. Minocycline

---

• A. Methemoglobinemia
• B. Hemolytic anemia in G6PD deficiency
• C. Hepatocellular carcinoma ✅ (Not a known effect)
• D. Agranulocytosis

---

• A. Rifampicin, Ofloxacin, Metronidazole
• B. Rifampicin, Ofloxacin, Minocycline — single dose ✅
• C. Rifampicin, Ofloxacin, Moxifloxacin
• D. Rifampicin, Ofloxacin, Minocycline × 6 months

---

• A. Vitiligo
• B. Nevus depigmentosus ✅ (Note: Some sources say indeterminate leprosy — the KEY differentiator is white accentuation on Wood's lamp WITHOUT complete depigmentation)
• C. Nevus anemicus
• D. Indeterminate leprosy

---

🔴 PYQ BLOCK 6 — Miscellaneous

• A. Number of bacilli per field
• B. Percentage of solid (viable) bacilli ✅
• C. Granuloma density
• D. Nerve damage extent

---

• A. Visible deformity or damage
• B. Claw hand
• C. Anesthesia of the palm (no visible deformity) ✅
• D. Loss of digits

---

• A. NIMHANS, Bangalore
• B. JALMA, Agra (ICMR) ✅
• C. AIIMS, New Delhi
• D. CMC, Vellore

---

• A. Inhibiting RNA polymerase
• B. Inhibiting PABA synthesis
• C. Binding to mycobacterial DNA + anti-inflammatory effect ✅
• D. Inhibiting cell wall synthesis

---

• A. Symmetric skin lesions
• B. Leonine facies
• C. Lepromin test positive ✅
• D. Highest bacterial index

---

RAPID REVISION TABLE — NEET PG FAVOURITE COMPARISONS

---

---

1. Ridley-Jopling vs WHO classification — lesion counts, smear status
2. Type 1 vs Type 2 reactions — mechanism, spectrum, treatment
3. Nerve involvement table — ulnar (most common), peroneal (foot drop), facial (lagophthalmos)
4. MDT regimens — 6 months PB vs 12 months MB; ROM single dose
5. Lepromin test — not diagnostic; Mitsuda reaction at 3–4 weeks
6. Histology — epithelioid granuloma (TT) vs foamy lepra cells + Grenz zone (LL)
7. Thalidomide for ENL; Prednisolone for Type 1/RR
8. First sensation lost = Temperature (cold)

1. Extract all the content exactly as written — no additions from outside sources
2. Reformat it into beautiful, aesthetic one-page revision notes styled for quick NEET PG / INI-CET revision