3rd Year Dermatology PG Theory Examination — 10-Mark Model Answers

A) PROTEIN ENERGY MALNUTRITION (PEM)

Definition

Classification

Cutaneous Features

• Dry, loose, wrinkled, "old man" skin
• Loss of subcutaneous fat (emaciation)
• Hyperpigmentation, especially scalp
• Erosions and desquamation

• Peripheral edema, ascites, anasarca
• "Flaky paint" / "enamel paint" dermatosis - superficial desquamation and erosions over pressure areas, flexures, and perineum
• Alternating hyperpigmentation and hypopigmentation
• "Flag sign" of hair (bands of normal and depigmented hair)
• Easy hair pluckability; reddish discoloration of hair
• Sparse, silky, straight hair
• Angular stomatitis, glossitis, cheilitis
• Delayed wound healing

Pathophysiology

• Marasmus: prolonged total caloric deficit -> fat and muscle wasting; protein-sparing response operative
• Kwashiorkor: acute stress (infection, illness) superimposed on chronic malnutrition -> blocks protein-sparing response -> hypoalbuminemia -> reduced oncotic pressure -> edema
• Current evidence: gut microbiome dysbiosis (deficiency of anti-inflammatory taxa, increased inflammatory bacteria) plays a role in kwashiorkor
• Hypoalbuminemia also causes exudative protein loss into skin, impairing barrier function

Systemic Features

• Growth retardation, hepatomegaly (fatty liver in kwashiorkor)
• Recurrent infections (impaired cell-mediated immunity)
• Anemia, diarrhea
• Mental/developmental retardation if prolonged
• Delayed wound healing

Diagnosis

• Anthropometric measurements (weight-for-height, mid-upper arm circumference)
• Serum albumin (< 2.8 g/dL in kwashiorkor), pre-albumin, transferrin
• CBC, LFT, RFT, urinalysis

Management

1. Treat hypoglycemia (glucose 10% orally/NG)
2. Treat hypothermia
3. Treat dehydration (oral rehydration solution - ORS)
4. Correct electrolyte imbalances (potassium, magnesium)
5. Treat infections (empirical antibiotics: amoxicillin + gentamicin)
6. Correct micronutrient deficiencies (Vitamin A, zinc, folic acid, multivitamins)
7. Begin cautious feeding (F-75 formula: 75 kcal/100 mL)
8. Achieve catch-up growth (F-100 formula: 100 kcal/100 mL)
9. Provide sensory stimulation and emotional support
10. Prepare for follow-up after recovery

B) CONTACT DERMATITIS - PATHOPHYSIOLOGY

Definition

1. Irritant Contact Dermatitis (ICD) - non-immunologic
2. Allergic Contact Dermatitis (ACD) - immunologically mediated (Type IV hypersensitivity)

Irritant Contact Dermatitis - Pathophysiology

1. Irritant substance (alkalis, acids, detergents, solvents) directly damages the stratum corneum lipid bilayer and tight junctions
2. Disruption of skin barrier -> water loss and antigen penetration
3. Keratinocytes release pro-inflammatory cytokines: IL-1α, IL-1β, TNF-α, IL-6, IL-8
4. These cytokines activate resident macrophages and dendritic cells
5. Neutrophil and T-cell recruitment -> acute inflammatory response
6. No prior sensitization needed; dose-dependent response
7. With repeated exposure -> hardening effect (skin becomes more resistant)

Allergic Contact Dermatitis - Pathophysiology

Phase 1: Sensitization (Afferent Phase)

1. Allergen (hapten, e.g., nickel, urushiol from poison ivy, paraphenylenediamine) penetrates the epidermis
2. Hapten binds to carrier protein to form a complete antigen (hapten-protein complex)
3. Langerhans cells (epidermal antigen-presenting cells, CD1a+, Birbeck granules) internalize and process the antigen
4. Langerhans cells mature, upregulate MHC class II, CD80, CD86, and CCR7; migrate to regional lymph nodes
5. In lymph nodes, Langerhans cells present antigen to naive T cells (CD4+ Th1 and CD8+) via MHC II-TCR interaction + costimulatory signals (CD28-CD80/86)
6. T cells proliferate and differentiate into antigen-specific effector and memory T cells
7. Sensitization takes 10-15 days; patient is asymptomatic during this phase
8. Memory T cells circulate in peripheral blood and migrate back to skin (skin-homing via CLA - cutaneous lymphocyte-associated antigen + CCR4, CCR10)

Phase 2: Elicitation (Efferent Phase) - on re-exposure

1. Re-exposure to the same allergen (even small amounts) -> hapten-protein complex re-formed
2. Keratinocytes present antigen; resident memory T cells in skin are activated rapidly
3. Memory T cells release IFN-γ, IL-17, IL-4, IL-5, TNF-α
4. IFN-γ activates keratinocytes and macrophages; upregulates ICAM-1 and MHC II on keratinocytes
5. Recruitment of CD4+ Th1 cells and CD8+ cytotoxic T cells
6. CD8+ T cells (Tc1) cause direct keratinocyte damage (spongiosis, vesicle formation) via perforin/granzyme and Fas-FasL
7. Mast cell activation and histamine release contribute to pruritus
8. Reaction peaks at 48-72 hours (hence "delayed-type")

Comparison Table

Common Allergens (ACD)

• Metals: Nickel (jewellery, belt buckles), chromium (cement), cobalt
• Topicals: Neomycin, bacitracin, benzocaine, lanolin
• Cosmetics: Paraphenylenediamine (PPD) in hair dye; fragrance mix; preservatives (formaldehyde, parabens)
• Plants: Urushiol (Rhus/Toxicodendron), primula, compositae
• Rubber: Thiuram, carbamates, mercaptobenzothiazole
• Occupational: Epoxy resin (construction), acrylates (dental), glutaraldehyde (healthcare)

Diagnosis

• Patch testing (gold standard for ACD): TRUE test, European standard series (30 allergens)
• Readings at D2 (48h) and D4 (96h); graded + to +++ (erythema, papules, vesicles)
• Photo-patch testing for photoallergic contact dermatitis

Management

• Wet compresses (Burrow's solution / normal saline) for weeping lesions
• Topical corticosteroids (moderate-potency for body; low-potency for face/flexures)
• Systemic steroids (prednisolone 1 mg/kg/day tapered over 2-3 weeks) for severe/widespread ACD (e.g., Rhus dermatitis)
• Oral antihistamines for itch (2nd generation: cetirizine, fexofenadine)

• Tacrolimus 0.1% / pimecrolimus 1% ointment (steroid-sparing, especially face)
• Emollients and barrier creams
• Phototherapy (NBUVB or PUVA) for chronic hand eczema

C) IMMUNOBULLOUS DISORDERS

Introduction

Classification

I. Intraepidermal Blistering (Pemphigus Group)

II. Subepidermal Blistering

Diagnosis of Immunobullous Disorders

• Pemphigus: intraepidermal acantholysis; "row of tombstones" (basal cells attached to BMZ)
• Pemphigoid: subepidermal blister with eosinophils; no acantholysis
• DH: microabscesses of neutrophils at dermal papillary tips; subepidermal split

• Pemphigus: monkey esophagus substrate
• BP: human skin or 1M NaCl salt-split skin (IgG on epidermal side)
• DH: endomysial antibodies, anti-tTG antibodies (ELISA)

Management (Focus on Pemphigus Vulgaris and Bullous Pemphigoid)

• First-line: Systemic corticosteroids (prednisolone 1-1.5 mg/kg/day) + Rituximab (anti-CD20, 1g IV x 2 doses 2 weeks apart OR 375 mg/m² x 4 weekly - now first-line per international guidelines)
• Adjuvants: Azathioprine (2-2.5 mg/kg/day), Mycophenolate mofetil (MMF, 2-3 g/day), Cyclophosphamide (IV pulse), Dapsone (for mild disease)
• IVIG (2 g/kg/cycle) for refractory cases
• Oral hygiene, antiseptic mouthwashes, topical steroids for oral lesions
• Monitor for steroid complications; PCP prophylaxis with co-trimoxazole

• Mild-moderate: Super-potent topical steroids (clobetasol propionate 0.05% cream, 40 g/day) - equal efficacy to systemic steroids with better safety profile
• Moderate-severe: Prednisolone 0.5-1 mg/kg/day
• Steroid-sparing: Doxycycline + nicotinamide (anti-inflammatory), MMF, azathioprine
• Rituximab for refractory cases
• Wound care, prevent secondary infection

D) VASCULITIS - CLASSIFICATION AND SMALL VESSEL VASCULITIS: CLINICAL FEATURES AND MANAGEMENT

Classification of Cutaneous Vasculitis

By Vessel Size (Chapel Hill Consensus Conference 2012 - Revised):

• Giant cell arteritis (Temporal arteritis)
• Takayasu arteritis

• Polyarteritis nodosa (PAN)
• Kawasaki disease

• Granulomatosis with polyangiitis (GPA, formerly Wegener's)
• Microscopic polyangiitis (MPA)
• Eosinophilic granulomatosis with polyangiitis (EGPA, formerly Churg-Strauss)

• IgA vasculitis (Henoch-Schonlein purpura, HSP)
• Cryoglobulinemic vasculitis
• Hypersensitivity vasculitis (cutaneous small vessel vasculitis, CSVV)
• Anti-GBM disease

• Behcet's disease

Dermatological Classification (Lever):

• Small vessel vasculitis: Leukocytoclastic vasculitis (LCV), HSP, urticarial vasculitis
• Medium vessel vasculitis: PAN, nodular vasculitis
• Large vessel vasculitis: Giant cell arteritis

Cutaneous Small Vessel Vasculitis (CSVV) / Leukocytoclastic Vasculitis (LCV)

Definition

Etiopathogenesis

• Immune complex deposition in vessel walls -> complement activation (C3a, C5a) -> neutrophil chemotaxis -> neutrophil degranulation -> release of proteolytic enzymes (elastase, collagenase) -> vessel wall destruction -> fibrinoid necrosis -> hemorrhage
• Causes: drugs (most common - penicillin, sulfonamides, allopurinol, NSAIDs), infections (streptococcus, hepatitis B/C, HIV), connective tissue diseases (SLE, RA), malignancy (paraneoplastic), inflammatory bowel disease, idiopathic (50%)

Clinical Features of Small Vessel Vasculitis

• Bilateral, symmetrical distribution
• Predominantly on dependent areas (lower limbs, especially below knees; buttocks in bedridden patients)
• Lesions 1-3 mm; crops appear over 1-4 weeks
• May progress to: urticarial papules, vesicles, bullae (hemorrhagic), pustules, necrosis, ulceration

• Tetrad: palpable purpura + arthritis/arthralgia + abdominal pain + glomerulonephritis
• Mainly children (peak 3-15 years), but can occur in adults (more severe renal disease)
• Upper respiratory tract infection (usually streptococcal) precedes by 1-3 weeks
• Purpura on buttocks and lower limbs (gravity-dependent areas)
• IgA deposits in skin and mesangium (IgA nephropathy)
• Self-limiting in most children

• Urticarial lesions lasting >24 hours (unlike ordinary urticaria which lasts <24 hours)
• Burning/pain more than itch
• Residual pigmentation after resolution
• Two subtypes: normocomplementemic (usually idiopathic, benign) and hypocomplementemic (HUVS - associated with SLE, COPD, angioedema; anti-C1q antibodies)

• GPA: saddle-nose deformity, necrotizing granulomas in upper/lower respiratory tract, glomerulonephritis; c-ANCA (anti-PR3)
• MPA: rapidly progressive glomerulonephritis; p-ANCA (anti-MPO)
• EGPA: asthma, eosinophilia, necrotizing granulomas; p-ANCA; cardiac involvement

• Fever, malaise, arthralgia/arthritis
• Hematuria, proteinuria (renal involvement)
• Abdominal pain, GI hemorrhage
• Peripheral neuropathy (mononeuritis multiplex)

Investigations

• CBC with differential (leukocytosis, eosinophilia in EGPA)
• ESR, CRP, ANA, ANCA (c-ANCA/p-ANCA), anti-dsDNA, complement (C3, C4, CH50)
• Serum IgA (elevated in HSP)
• Hepatitis B surface antigen, HCV antibodies, cryoglobulins, RF
• Urinalysis (hematuria, RBC casts, proteinuria)
• Chest X-ray (GPA, EGPA)
• Skin biopsy: H&E staining showing fibrinoid necrosis of vessel walls + neutrophilic infiltrate + nuclear dust (leukocytoclasis)
• DIF of lesional skin (early lesion, <24 hours): IgA deposition in vessel walls diagnostic of HSP

Management

• Identify and remove the precipitating cause (stop offending drug, treat infection)
• Leg elevation, rest, compression stockings
• Most cases of CSVV are self-limiting (resolve within weeks)

• Observation + leg elevation
• NSAIDs for arthralgia
• Antihistamines for urticaria

• Prednisolone 0.5-1 mg/kg/day, tapering over 4-6 weeks
• Colchicine 0.5-1.5 mg/day (especially for urticarial vasculitis and mild HSP)
• Dapsone 50-100 mg/day (neutrophil inhibitor - effective in LCV)
• Hydroxychloroquine 200-400 mg/day (for urticarial vasculitis/SLE-associated)

• Azathioprine 1-2 mg/kg/day or MMF 2-3 g/day
• Cyclophosphamide (pulse IV or oral) for ANCA-associated vasculitis with systemic involvement
• Rituximab (anti-CD20) - now preferred over cyclophosphamide for GPA/MPA (RAVE trial)
• IVIG for resistant cases

• Usually self-limiting; supportive care
• Prednisolone for severe abdominal pain or nephritis
• Monitor renal function for 6 months

E) CUTANEOUS TUBERCULOSIS - CLASSIFICATION AND TB VERRUCOSA CUTIS: CLINICAL FEATURES AND MANAGEMENT

Classification of Cutaneous Tuberculosis

I. TRUE CUTANEOUS TUBERCULOSIS (Mycobacteria present in skin)

1. Tuberculous chancre (Primary inoculation TB): First infection in non-immune individuals; inoculation through broken skin -> painless ulcer + regional lymphadenopathy (TB complex)
2. Tuberculosis verrucosa cutis (TVC): Re-infection/exogenous inoculation in previously sensitized immune individuals (high immunity)

II. TUBERCULIDS (Immunologic/hypersensitivity reactions, organisms not demonstrable in skin)

1. Papulonecrotic tuberculid (PNT): Symmetrical papules with central necrosis and crust; extensor surfaces of limbs
2. Lichen scrofulosorum: Minute follicular/perifollicular papules on trunk; children; associated with lymph node or bone TB
3. Erythema induratum of Bazin (EIB): Nodular vasculitis of the calves in women; cold panniculitis; Mycobacterium DNA detectable by PCR
4. Nodular granulomatous phlebitis

Classification by Immune Status (Beyt's Classification, simplified):

TB VERRUCOSA CUTIS (TVC) - Clinical Features and Management

Definition

Epidemiology

• Also called "warty TB", "anatomist's wart", "prosector's wart" (when in pathologists/anatomists from cadavers), "verruca necrogenica"
• Common in India; affects adults (males > females due to outdoor occupational exposure)
• Sites: buttocks and lower limbs in children (from contaminated soil); hands, fingers in adults with occupational exposure

Pathogenesis

• Mycobacterium tuberculosis inoculated through traumatized skin
• Pre-existing strong cell-mediated immunity (positive Mantoux test) -> granulomatous reaction predominates -> warty/verrucous surface
• Tuberculin test strongly positive (>15 mm induration)

Clinical Features

1. Initial lesion: Small, asymptomatic, brownish-red or violaceous papule or papulopustule at the site of inoculation
2. Progressive stage: Papule enlarges into a verrucous (warty) plaque with irregular, hyperkeratotic, papillomatous surface
3. Established lesion:
   • Well-defined, warty/verrucous plaque, 1-5 cm or larger (can be >10 cm with long duration)
   • Surface: hyperkeratotic, rough, fissured, papillomatous
   • Margin: irregular, serpiginous or gyrate border
   • "Papillomatous center, inflammatory halo" pattern
   • Color: brownish-red, violaceous
   • Pus may ooze from fissures on pressure ("squeezing test" / "mustard paste sign")
   • Horny projections from surface
   • No lymphadenopathy (high immunity)
   • No systemic symptoms usually
4. Healing: Central clearing with atrophic scarring, advancing peripheral border (centrifugal spread)

• Common warts (HPV verruca vulgaris): no inflammatory halo, positive paring
• Chromoblastomycosis: "black dots" on surface, KOH shows Medlar bodies
• Hypertrophic lichen planus: violaceous, Wickham's striae
• Verrucous/blastomycosis-like pyoderma
• Squamous cell carcinoma: advancing edge, ulceration
• Leishmaniasis (chronic): from endemic areas
• Psoriasis: silvery scales, Auspitz sign

Investigations

1. Tuberculin/Mantoux test: Strongly positive (>15 mm) - reflects high immunity
2. Histopathology: (most important)
   • Epidermis: hyperkeratosis, papillomatosis, acanthosis, pseudoepitheliomatous hyperplasia
   • Dermis: epithelioid cell granulomas with Langhans giant cells; central caseation necrosis (present in varying degrees)
   • Neutrophilic microabscesses in epidermis or superficial dermis
   • Dense lymphoplasmacytic infiltrate
   • AFB (acid-fast bacilli) on Ziehl-Neelsen stain: scanty or absent (paucibacillary - hence high tuberculin reactivity)
3. Culture: M. tuberculosis culture of tissue (Lowenstein-Jensen medium) - gold standard but slow (6-8 weeks)
4. PCR (GeneXpert/IS6110): Rapid, sensitive; detects mycobacterial DNA even when AFB not visible
5. Chest X-ray: To rule out underlying pulmonary TB
6. IGRA (Interferon-Gamma Release Assay): QuantiFERON-TB Gold - not affected by BCG vaccination

Management

• Isoniazid: 5 mg/kg/day (max 300 mg/day) + Pyridoxine 25-50 mg/day (to prevent peripheral neuropathy)
• Rifampicin: 10 mg/kg/day (max 600 mg/day) - given on empty stomach
• Pyrazinamide: 25 mg/kg/day (max 2 g/day) - intensive phase only
• Ethambutol: 15 mg/kg/day - monitor visual acuity (optic neuritis)

• LFTs at baseline and monthly (hepatotoxicity - H, R, Z)
• Visual acuity and color vision (ethambutol)
• Serum uric acid (pyrazinamide -> hyperuricemia)
• Response: clinical improvement (flattening of verrucous surface, reduced erythema) usually within 6-8 weeks

• Excellent with complete ATT
• Lesions heal with atrophic, hypopigmented scarring
• Relapse uncommon with full compliance

References: Fitzpatrick's Dermatology (10th Edition); Andrews' Diseases of the Skin (13th Edition); Dermatology 2-Volume Set, 5th Edition (Griffiths et al.); Rook's Textbook of DermatologyAll five model answers are now complete. Here is a summary of what was covered for each topic:

Summary of All 5 Answers

A) Protein Energy Malnutrition

B) Contact Dermatitis - Pathophysiology

• ICD: Direct keratinocyte damage -> IL-1α/TNF-α cytokines -> dose-dependent, no sensitization
• ACD: Two-phase Type IV hypersensitivity: Sensitization phase (Langerhans cells, hapten-carrier, lymph node priming of memory T cells, 10-15 days) and Elicitation phase (memory T cell re-activation, IFN-γ/IL-17, CD8+ cytotoxic damage, 48-72h peak)
• Comparison table, common allergens, patch testing, and management

C) Immunobullous Disorders

D) Vasculitis Classification + Small Vessel Vasculitis

E) Cutaneous TB Classification + TB Verrucosa Cutis