Exam Prep: Skin Infections, Psoriasis & OmpathStudy

SECTION 1: SKIN PATHOLOGY (DERMATOPATHOLOGY) Intro: This section covers the major disease categories of the skin — infections, chronic inflammatory dermatoses, blistering disorders, disorders of epidermal appendages, and disorders of pigmentation/melanocytes (including melanoma). Focus areas for exams: pathogenesis mechanisms, key morphological buzzwords, and distinguishing features between similar-looking conditions (e.g., pemphigus vs. pemphigoid). --- 1. INFECTIOUS DERMATOSES A. Bacterial Infections (Impetigo) Range: superficial (impetigo) → deep dermal abscesses (e.g., Pseudomonas, puncture wounds) Organism: S. aureus (most common) or S. pyogenes Morphology: neutrophils beneath stratum corneum → subcorneal pustule ; Gram stain shows cocci Clinical: mainly children; starts as small macule (face/extremities) → honey-colored crust Bullous variant of childhood impetigo can mimic autoimmune blistering disease B. Fungal Infections Spectrum: superficial (Tinea, Candida) → deep/systemic (Aspergillus in immunosuppressed) Morphology: superficial → neutrophilic epidermal infiltrate; Candida → psoriasiform hyperplasia; deep → granulomatous response; Aspergillus = angioinvasive Stains: PAS and Gomori methenamine silver (GMS) Clinical: superficial = pruritic erythematous scaly macules (can mimic psoriasis — always exclude fungal cause before diagnosing new psoriasis) C. Viral – Verrucae (Warts) Caused by HPV ; self-limited (resolve in 6 mo–2 yrs) Low-risk HPV → warts (no transforming potential); high-risk HPV → anogenital cancers (via E6/E7 oncoproteins) Types: Verruca vulgaris (hands, most common), Verruca plana (flat, face), Verruca plantaris/palmaris (soles/palms), Condyloma acuminatum (genital) Morphology: verrucous epidermal hyperplasia + koilocytosis (perinuclear vacuolization/halo) --- 2. CHRONIC INFLAMMATORY DERMATOSES A. Psoriasis Affects 1–2%; linked to ↑ CV risk, arthritis (10%) Pathogenesis: multifactorial immune disease — CD4+ TH17/TH1 and CD8+ T cells → keratinocyte hyperproliferation; Koebner phenomenon (trauma-induced lesions); HLA association Morphology: well-demarcated salmon plaque with silvery scale; acanthosis with "test-tube in rack" rete ridges; loss of stratum granulosum; parakeratosis ; thin suprapapillary plates with dilated vessels → Auspitz sign (pinpoint bleeding); neutrophil microabscesses (Munro) Clinical: elbows, knees, scalp, lumbosacral, glans penis; nail pitting (30%) Treatment: NSAIDs, cyclosporine, TNF antagonists B. Lichen Planus Mnemonic: "Pruritic, Purple, Polygonal, Planar Papules and Plaques" Pathogenesis: CD8+ T cell cytotoxic response vs. basal layer antigens (post-viral/drug) Morphology: Wickham striae (white lines on papules); interface dermatitis; sawtooth rete ridges; Civatte/colloid bodies (necrotic basal cells); squamatization Clinical: middle-aged adults; wrists, elbows, glans penis; 70% oral mucosa (reticulate white pattern); skin lesions resolve in 1–2 yrs, oral lesions persist C. Lichen Simplex Chronicus Response to chronic rubbing/scratching; nodular form = prurigo nodularis Morphology: acanthosis, hyperkeratosis, hypergranulosis, dermal fibrosis (resembles thickened volar skin) Clinical: can mask underlying pruritic dermatosis — rule out cause --- 3. BLISTERING (BULLOUS) DISORDERS A. Inflammatory — Pemphigus Group Common mechanism: IgG autoantibodies vs. desmogleins → acantholysis (loss of cell-cell adhesion) Type Level of blister Key feature --- --- --- Pemphigus vulgaris ( 80%) Suprabasal "Row of tombstones"; oral ulcers first Pemphigus vegetans Suprabasal Verrucous plaques, no true blisters Pemphigus foliaceus Subcorneal (superficial) Fogo selvagem (Brazil); mucosa spared Pemphigus erythematosus Superficial Localized, malar/lupus-like Paraneoplastic pemphigus — Associated with NHL IF: net-like intercellular IgG deposits B. Bullous Pemphigoid Elderly patients; thighs, forearms, axillae, groin Pathogenesis: autoantibodies vs. BPAG2 (hemidesmosome component) → complement activation → eosinophil/neutrophil recruitment Morphology: tense bullae (don't rupture easily, unlike pemphigus); subepidermal, nonacantholytic blister; eosinophils beneath basal layer C. Dermatitis Herpetiformis Associated with celiac disease ; males, 3rd–4th decade; intensely pruritic Pathogenesis: IgA anti-gliadin cross-reacts with reticulin → subepidermal blister Morphology: microabscesses at dermal papillary tips (fibrin + neutrophils); IF = granular IgA at papillary tips Responds to gluten-free diet D. Noninflammatory Blistering Disorders Epidermolysis Bullosa (defects in structural proteins; blisters at trauma sites from birth): Simplex — keratin 5/14 mutation (AD, most common) Junctional — laminin or BPAG2 mutation (AR), lamina lucida split Dystrophic — COL7A1 mutation, beneath lamina densa Mixed — multiple levels Porphyria: disturbed porphyrin metabolism; 5 types (congenital erythropoietic, erythrohepatic protoporphyria, acute intermittent, porphyria cutanea tarda, mixed); photosensitiv