Explore acute inflammatory dermatoses. Learn about urticaria (hives), its causes like mast cell degranulation & angioedema, and the pathology of eczematous derm
SKIN PATHOLOGY --- ACUTE INFLAMMATORY DERMATOSES Acute lesions last days to weeks. Characterized by inflammation (predominantly mononuclear cells, not neutrophils), oedema, and sometimes epidermal, vascular, or subcutaneous injury. Some resolve; others transition to a chronic phase. --- 1. URTICARIA (Hives) Definition: Common disorder caused by localized mast cell degranulation → dermal microvascular hyperpermeability → erythematous, oedematous, pruritic plaques called wheals . Pathogenesis: - Most cases: Type I (immediate) hypersensitivity — antigens bind IgE on mast cells → degranulation - Triggers: pollens, foods, drugs, insect venom - IgE-independent: opiates and certain antibiotics directly cause mast cell degranulation - Hereditary angioedema: inherited deficiency of C1 esterase inhibitor → uncontrolled complement activation → affects lips, throat, eyelids, genitals, distal extremities. Laryngeal involvement can compromise the airway — potentially dangerous - In the vast majority of cases, no cause is found despite extensive investigation Morphology (Histology): - Subtle findings - Sparse superficial perivenular infiltrate of mononuclear cells, rare neutrophils, sometimes eosinophils - Superficial dermal oedema → wider-spaced collagen bundles - Mast cell degranulation difficult to see on H&E; highlighted by Giemsa stain Clinical Features: - Affects any age, but most common 20–40 years - Individual lesions develop and fade within hours; episodes can last days to months - Ranges from small pruritic papules to large oedematous erythematous plaques - Can be localized or generalized - Pressure urticaria: lesions only in pressure-bearing areas (feet, buttocks) - Persistent lesions may indicate urticarial vasculitis (complement deposition in dermal venules) - Treatment: antihistamines; systemic steroids for severe/refractory cases --- 2. ACUTE ECZEMATOUS DERMATITIS Definition: A clinical term covering multiple conditions with varied aetiologies. Presents as red papules with overlying vesicles that ooze and crust. With persistence → raised, scaling plaques. Subtypes: - Allergic contact dermatitis — topical allergen exposure (e.g., poison ivy) - Atopic dermatitis — genetic defects in keratinocyte barrier function; not purely allergen-driven - Drug-related eczematous dermatitis — hypersensitivity to a systemic drug - Photoeczematous dermatitis — abnormal reaction to UV or visible light - Primary irritant dermatitis — chemical, physical, or mechanical skin damage Pathogenesis (Contact Dermatitis as the model): - Allergen (e.g., poison ivy) chemically modifies self-proteins - Epidermal Langerhans cells process and present antigen to naive T cells in draining lymph nodes → immunologic memory - On re-exposure: memory CD4+ T cells migrate to skin → cytokine release → inflammatory cell recruitment + epidermal damage (delayed-type hypersensitivity) Morphology (Histology): - Hallmark: Spongiosis (intercellular epidermal oedema) → synonym: spongiotic dermatitis - Oedema fluid splays apart keratinocytes; intercellular bridges become stretched and more visible - Superficial perivascular lymphocytic infiltrate - Oedema of dermal papillae + mast cell degranulation - Eosinophils prominent in drug-induced cases - Histology is similar regardless of cause → clinical correlation is essential Clinical Features: - Pruritic, oedematous, oozing plaques with vesicles/bullae - Persistent antigen exposure → progressive scaling (hyperkeratosis) + epidermal thickening (acanthosis) - Scratching/rubbing can produce or worsen lesions → may evolve into Lichen Simplex Chronicus - Resolves when offending stimulus is removed - "Inside jobs" (internal antigen e.g., ingested food/drug) vs. "outside jobs" (external contact antigen) - Atopic dermatitis: strong genetic basis; 80% concordance in identical twins, 20% in fraternal twins. Usually begins in childhood, clears in adulthood. Often coexists with asthma and allergic rhinitis — the atopic triad --- 3. ERYTHEMA MULTIFORME Definition: Uncommon, usually self-limited hypersensitivity disorder triggered by infections or drugs. Triggers: - Infections: herpes simplex (most common), Mycoplasma, some fungi - Drugs: sulfonamides, penicillin, salicylates, hydantoins, antimalarials Pathogenesis: - Skin-homing cytotoxic T cells attack basal cells of skin and mucosae - These cells display antigens that cross-react with the inciting drug or microbe Morphology (Histology): - Gross: characteristic targetoid lesions — red macule/papule with pale vesicular or eroded center - Early: superficial perivascular lymphocytic infiltrate + dermal oedema + lymphocytes along dermoepidermal junction associated with degenerating keratinocytes - Later: discrete/confluent zones of basal epidermal necrosis + blister formation - Severe form ( Toxic Epidermal Necrolysis ): necrosis extends through full thickness of epidermis Clinical Features: - Wide diversity of lesions: macules, papules, vesicles, bullae, and targetoid lesions — hence "multiforme" - Infection-associated forms (especially HSV) are less severe - Drug-associated forms can progress to: - Stevens-Johnson Syndrome - Toxic Epidermal Necrolysis (TEN) — large areas of epidermis slough → fluid loss + secondary infection, similar to burn injuries. Life-threatening. Most often idiopathic drug reactions. --- INFECTIOUS DERMATOSES --- 1. BACTERIAL INFECTIONS Overview: Range from superficial (impetigo) to deep dermal abscesses (e.g., Pseudomonas aeruginosa from puncture wounds). Pathogenesis similar to microbial infections elsewhere in the body. Impetigo — Morphology: - Accumulation of neutrophils beneath the stratum corneum → subcorneal pustule - Nonspecific reactive epidermal changes + superficial dermal inflammation - Bacterial cocci visible in superficial epidermis on Gram stain Impetigo — Clinical Features: - Primarily affects children - Causative organisms: Staphylococcus aureus (most common) or Streptococcus pyogenes - Transmission: direct contact - Begins as a small macule on extremities or face (near nose/mouth) → rapidly evolves into a larger lesion with a honey-colored crust of dried serum - Nasal or anal colonization by S. aureus or S. pyogenes increases susceptibility - Microbiologic culture + antibiotic sensitivity testing is useful - A less common bullous form of childhood impetigo can mimic autoimmune blistering disorders --- 2. FUNGAL INFECTIONS Overview: Range from superficial infections (Tinea, Candida) to life-threatening infections in immunosuppressed patients (Aspergillus). Classification: - Superficial: stratum corneum, hair, nails - Deep: dermis or subcutis - Systemic: haematogenous spread, usually in immunocompromised patients Morphology: - Varies by organism, host response, and degree of superinfection - Superficial infections: neutrophilic infiltrate in epidermis; some show eczematous dermatitis with intraepidermal neutrophils - Candida: can induce psoriasiform hyperplasia - Deep infections: greater tissue damage + granulomatous response (vigorous immune response) - Aspergillus: angioinvasive - Special stains: PAS and Gomori methenamine silver (GMS) stains identify fungal organisms Clinical Features: - Superficial: erythematous macules with superficial scale, may be pruritic - Deep (e.g., Aspergillus in immunocompromised): erythematous, nodular lesions, sometimes with local haemorrhage - Superficial Candida infections can mimic psoriasis — always exclude fungal infection before diagnosing new-onset psoriasis --- 3. VERRUCAE (WARTS) Definition: Common HPV-induced lesions, mostly in children and adolescents but can occur at any age. Usually self-limited — most regress spontaneously within 6 months to 2 years. Transmission: Direct contact with infected individual or autoinoculation. Pathogenesis: - Caused by Human Papillomavirus (HPV) - Low-risk HPV subtypes cause warts (no malignant transformation); high-risk types associated with anogenital carcinoma - Low-risk HPV expresses E6 and E7 oncopr