Type I (IgE) hypersensitivity inflammatory reaction
Risk factors: Family history of atopy. Exacerbated by scratching, stress
Epidemiology: Usually begins prior to 6m of age.
(FACE): flexor surfaces get adults, children extensor)
Appear erythematous, edematous with papules/plaques.
Scaling, weeping, and crusting
Cell mediated reaction involving sensitized T lymphocytes.
Irritant form: Chemical insult to skin. No previous sensitizing event.
Allergic form is delayed-hypersensitivity reaction. Skin sensitized from initial exposure. During next exposure patient has reaction.
Develop 24-96h post exposure
Acute present as vesicles with clear fluid on erythematous edematous skin.
Sub-acute is edema and papules
Inflammatory skin disease that occurs on lower extremities
Extravasation of plasma proteins and RBC into subcutaneous tissues. Becomes brown in color due to hemosiderin deposits
Results in interstitial fluid accumulation . Leads to reduced capillary blood flow
Can progress to venous stasis ulcers and fibrosis
Found in 6-7% of elderly population
Cutaneous Candidiasis infection (C. Albicans )
Risks: areas where warmth and moisture lead to maceration of skin or mucous membranes
Skin rash that occurs in areas of high sebaceous gland concentration
Cutaneous inflammation to dermis
Etiology: Immune response to endogenous yeast Pityrosporum
Triggered by seasonal changes, scratching, emotional stress, medications...