Contact Dermatitis Flashcards
Irritant Dermatitis
caused by an agent acting an an irritant
Contact Dermatitis
caused by an allergen
Photophytodermatitis
inflammatory rxn due to exposure of a topical or oral photsensitizer followed by UV wavelength
Rhus dermatitis
inflamm rxn due to contact with a planet
Epidemiology of contact derm and irritant derm
occupation, leisure activities, hobbies play a factor in both
ACD
delayed hypersensitivity response which requires a prior sensitization. Once sensitied, only a small amount of offending substance is needed to cause an allergy
ID
irritant disrupts the skin permeability, mild damage occurs to keratinocytes causing inflammatory mediators , can be acute or chronic like frequent hand washing
Clinical features ACD
Shape, location and pattern are important: well demarcated eczematous eruption, extremely pruritic. Acute phase: erythematous weepy skin with vesicles and bullae. Chronic: lichenification, erythematous plaques
Clinical Features: ID
NOT well demarcated, erythematous scaling, prominent lichenification, stinging is more common than pruritus
Dermatopathology ACD
Spongiotic dermatitis with mixed inflammatory infiltrate with lymphocytes, histiocytes and eosinophils
ID Dermatopathology
mild spogiosis with inflammatory infiltrate. Necrosis of epidermal keratinocytes.
Top Allergens
nickel, balsam of peru, fragrance, neomycin sulfate, bacitracin, formaldehyde, cobalt chlorida, black dye
Allergens can be found in
preservatives, rubber, textiles, adhesives, cosmetics, hygeine products
Allergens for ID
Acids, metal salts, solvents, disinfectants, chronic water exposure, alcohol, plastics, body fluids like in lip lickers and diaper derm
ACD Patch Testing
True test: 36 pre-impregnated allergens on 3 panels on the patients back. Keep dry. Remove in 48 hours can interpret then and again in 72 hours. Again at one week. + = erythema and bullous rxn
Tx for ACD and ID
Avoiding offensive substance, pt ed on reading ingredient labels. Skin protection with emollients and cotton gloves. Corticosteroids for inflammation, Oral antihistamine to decrease urge to scratch
onset of ID is
gradual
onset of ACD is
rapid
borders with ID
indistinct
borders with ACD
clear areas of demarcation
Rhus dermatitis
contact w poison ivy, poison oak, poison sumac. 3 leaflets.
Rhus derm patho
urushiol oil = alergic reaction on the skin
Clinical s/s rhus derm
linear pattern of erythema causing vesicles and bullae, extreme pruritis. exposure to smoke from burning ivy will cause wide spread erythematous plaques and edema
tx Rhus dermatitis
burrows solution to dry vesicles. antihistamines, calamine to help with itch and weepy lesions to dry, topical steroids in a gel to help dry lesions, oral steroid if severe
Photophytodermatitis
fennel, celery, parsnip, parslep, lime, orange, lemon, grapefruit.
At risk for Photophytodermatitis
employment with fruit and vegetable processing, bartenders working outdoors, people making lemonade/limeade, gardeners.
pathogenesis Photophytodermatitis
plants with Furoocumarins that protect the plant from fungal attacks followed by UV causes skin injury
Clinical signs Photophytodermatitis
erythema, edema, bullae in bizarre pattern 24-48 hrs after exposure. not painful, not pruritic. Hyperpigmentation after can remain for months to years
tx Photophytodermatitis
prevention is key, rapid washing of skin immediately after exposure may prevent a reaction, high potent topical steroids can decrease intensity of rxn and reduce PIH
