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🩺 SKIN TUMORS - Surgery Final Year MBBS

Exam-Ready Points in Hinglish | Robbins + Sabiston se

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📋 CLASSIFICATION (Yaad karo - EXAM FAVOURITE!)

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1. SEBORRHEIC KERATOSIS

• Kya hota hai: Middle-age/elderly mein common, pigmented epidermal tumor
• Site: Trunk sabse zyada, phir face, neck, extremities
• Mutation: FGFR3 activating mutation (RAS/PI3K pathway)
• Appearance: Tan to dark brown, "stuck-on" / waxy, granular surface, coin-like plaques
• Micro: Basaloid cells + horn cysts + pseudo-horn cysts (PATHOGNOMONIC)

⚠️ EXAM TRAP - Sign of Leser-Trelat:

Sudden eruptive seborrheic keratoses (bahut saare ek saath) = Paraneoplastic syndrome - GI tract carcinoma socho!

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2. ACTINIC KERATOSIS (Premalignant!)

• Cause: UV-induced TP53 mutation (same mutations as SCC - isliye PREMALIGNANT)
• Site: Sun-exposed areas - face, arms, dorsum of hands, cheek/nose
• Appearance: <1 cm, tan-brown or red, rough "sandpaper" texture
• Progression to SCC: 0.1% to 2.6% per year (low, but treat karo)
• Micro: Basal cell atypia + hyperkeratosis + parakeratosis + solar elastosis (dermis mein blue-gray elastic fibers)

Treatment:

• Cryotherapy (superficial freezing) - simple and effective
• Topical agents (5-Fluorouracil, imiquimod)

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3. SQUAMOUS CELL CARCINOMA (SCC)

Pathogenesis (Mutation list - exam mein aata hai!):

• UV light → TP53 mutation (most common)
• RAS activating mutation
• NOTCH receptor loss of function
• Immunosuppression (organ transplant patients - HIGH risk!)

Risk Factors:

• Sun exposure (UV), xeroderma pigmentosum
• Oncogenic HPV (genital skin)
• Industrial carcinogens (tars, oils)
• Chronic non-healing ulcers, burn scars → Marjolin's ulcer (aggressive SCC!)
• Arsenical keratoses, ionizing radiation

Clinical Features:

• Nodular, scaly, often ulcerated lesion
• Men > Women, fair skin, older adults
• ~4% mein regional lymph node metastasis at diagnosis

Bowen's Disease = SCC in situ

• Plaque-like lesion with crusting
• Full-thickness epidermal atypia

Treatment:

• <2.5 cm: Wide excision with 6mm clear margin
• Large/invasive: Radical excision, consider Mohs surgery
• Metastatic: Highly responsive to immune checkpoint inhibitors (high mutational burden ke wajah se)

Marjolin's Ulcer (EXAM FAVOURITE!):

SCC arising in chronic scar/burn wound / cicatricial tissue. Poorer prognosis, more aggressive behavior.

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4. BASAL CELL CARCINOMA (BCC)

Pathogenesis:

• PTCH1 mutation (loss of function) → Hedgehog pathway constitutively active
• Gorlin Syndrome (Nevoid BCC syndrome): Autosomal dominant, germline PTCH1 mutation → Familial BCC + odontogenic keratocysts + medulloblastoma
• TP53 mutation also common (UV-induced)

Clinical Features:

• Raised nodule/papule with rolled edges ± ulceration
• Telangiectasia (dilated subepidermal vessels) - PATHOGNOMONIC
• Light skin: erythematous; Dark skin: pigmented (melanoma jaisi dikh sakti hai)
• Most common skin cancer (>1 million cases/year US mein)

Morphology (Micro):

• Basaloid cells, peripheral palisading of nuclei
• Cleft between tumor nests and stroma (artifact of sectioning) - CHARACTERISTIC
• Fibrotic or mucinous stromal matrix
• Never on mucosal surfaces (only epidermis/follicular epithelium se arise)

Treatment:

• Local excision curative
• 40% patients mein 5 years ke andar doosra BCC develop hota hai
• Advanced: PTCH1/Hedgehog inhibitor (vismodegib)

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5. MELANOCYTIC NEVI (Moles)

• Mutation: BRAF or RAS gain-of-function → proliferation then senescence (isliye benign rahta hai)
• Types:
  • Junctional nevus: Cells at dermoepidermal junction only
  • Compound nevus: Junction + dermis dono mein
  • Intradermal nevus: Only dermis (most elevated)
• Micro: Superficial cells - large, pigmented, nests; Deep cells - small, no pigment, cords → "Maturation" hoti hai depth ke saath (BENIGN ka sign)

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6. DYSPLASTIC NEVI

• Sporadic ya familial
• Familial → increased melanoma risk
• Size >5 mm, variable pigmentation, irregular borders, "pebbly" surface
• Bridging of nests, lentiginous hyperplasia at junction
• Cytologic atypia + linear fibrosis in dermis
• CDKN2A (p16) mutations common

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7. MELANOMA ⭐ (MOST IMPORTANT FOR EXAM!)

Pathogenesis - Step-by-Step Mutations:

Growth Phases (EXAM FAVOURITE!):

• Radial growth phase: Lateral spread in epidermis, NO metastasis capacity yet, flat lesion
• Vertical growth phase: Downward dermal invasion, nodule form karta hai, metastasis potential aata hai

ABCDE Rules (Warning Signs):

Histology:

• Pagetoid spread (cells at all levels of epidermis)
• Large nuclei, hyperchromatic, chromatin peripherally clumped
• "Cherry red" prominent nucleoli (PATHOGNOMONIC!)
• Atypical mitotic figures

Prognosis - Breslow Thickness:

Breslow thickness = depth of invasion in mm from granular layer to deepest tumor cell

• Thin lesion = curable surgically
• Thick + high mitotic rate + no lymphocytic response = poor prognosis
• Sentinel lymph node biopsy - routine at time of excision

Sites:

• Sun-exposed skin (most common)
• Acral melanoma: Sole, palm, nail bed (in darker skin individuals - KIT mutation)
• Subungual melanoma: Nail bed - diagnosis delay hoti hai! Biopsy karo
• Uveal melanoma: GNAQ/GNA11 mutations

Treatment:

• Surgery: Wide local excision + sentinel LN biopsy
• BRAF-mutated (V600E): Vemurafenib/dabrafenib (dramatic response, but resistance ho sakta hai)
• Immunotherapy: Immune checkpoint inhibitors (anti-PD1, anti-CTLA4) - metastatic disease mein "remarkable tumor regression"

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🔥 QUICK COMPARE TABLE (Copy karo apni notes mein!)

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💡 MNEMONICS FOR EXAM

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