(Hives): localized mast cell degranulation resulting in erythematous, edematous, and pruritic plaques. Usually result of antigen-induction from sensitization with specific IgE antibodies (Type I hypersensitivity). Typical time course: <24hrs
Acute Eczematous Dermatitis
Clinical term for several conditions characterized by red, papulovesicular, oozing, crusted lesions, followed by raised, scaling plaques. Pathology similar to type IV hypersensitivity. Histologically: spongiosis (edema), eosinophils (occasionally).
"Multiform" lesions (including targetoid) throughout body, probably caused by certain infections. Lichenoid lymphocytic assault (epidermal interface), but without chronic features. Infection-caused are usually less severe than drug-caused.
Chronic condition. Typical lesions: pink plaque covered by white scale. Epidermal thickening w/ regular elongation of rete ridges (psoriasoform acanthosis), loss of stratum granulosum resulting in parakeratosis and hyperkeratosis. Neutrophils present.
Pruritic, purple, polygonal, planar papules, and plaques on skin and mucosa. Chronic, usually resolves after 1/2yrs. Lymphocytic infiltrate at epidermal interface: zigzag contour. Anucleate/necrotic basal cells in papillary dermis. Commonly: wrist
Bacterial Skin Infection
Often Staphylococcus Aureus (catalase +) or Streptococcus Pyogenes (catalase -)
Impetigo: superficial epidermis infection
Erysipelas: acute S. pyogenes in deep epidermis w/ lymphatic spread
Cellulitis: deep (usually hypodermis--subcutaneous)
Often caused by Candida species. Superficial infections (even as superficial as stratum corneum) are accompanied by neutrophilic infiltrate and lesions look similar to those of psoriasis.
(Warts): caused by HPV, subverts cell cycle controls to proliferate. Histologic features: papillary epidermal hyperplasia (looks like points of a crown), vacuolization of cytoplasm primarily in superficial epidermal layers (halos of pallor).
Usually elderly population. Autoimmune: IgG antibodies attack at basement membrane/hemidesmosomes at bullus pemphigoid antigen (BPAG)-complement fixing-neutrophils/eosinophils. Nonacantholytic, subepidermal blister, resistant to rupture.
Pruritic uticaria and grouped vesicles. Caused from IgA antibodies against gluten cross reacting with reticulin in epidermal basement. Fibrin/neutrophils accumulate at dermal papillae to form microabsecesses. Subepidermal blistering.
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