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Dermatitis is the inflammation of the skin -that is characterized by certain clinical (erythema, scales & vesicles) and histopathological changes (spongiosis)-
CLASSIFICATION:
1. EXOGENOUS "contact" eczema: Allergic contact dermatitis Irritant contact dermatitis Photocontact dermatitis Infective dermatitis Dermtophytide
2.
ENDOGENOUS: Atopic dermatitis Seborrhoeic dermatitis Discoid eczema Pompholyx Gravitational 'stasis' dermatitis Pityriasis alba. Asteatotic eczema Neurodermatitis ' Lichen Simplex chronicus '. Juvenile plantar dermatosis.
STAGES OF ECZEMA
ACUTE ECZEMA
Non-allergic reaction that results from exposure to an irritating agent ( Physical or chemical ) producing cell damage and an inflammatory reaction Sufficient amount, concentration and time occurs in any person, no immunological factors and previous sensitization. common causes: - Chemicals: acids, alkalis, soap, detergent. - Physical: dusts, gases, heat, cold, humidity. - Mechanical: Friction, rubbing, scratching. E.G. Napkin dermatitis, Housewives dermatitis
Delayed type IV hypersensitivity reaction SENSITIZER: - chemical agent with low molecular weight which is able to sensitize certain individuals and induce cell mediated immune reaction that end with dermatitis only in previously sensitized persons. Pathogenesis: - Induction (sensitization) phase: 18-24 days - Elicitation phase: 2-4 days Antigen binds Langerhans cells in the epidermis or macrophages in the dermis Interaction with CD4+ T lymphyocytes at the regional lymph nodes causes release of inflammatory cytokines
Contact Dermatitis
Common causes: nickel, rubber, potassium dichromate, paraphenylenediamine Contact dermatitis with Nickel. Reddish marking and itching will occur.
Patch Test
Atopic Dermatitis
Atopy : -
genetically determined condition characterized by excessive response to an environmental antigen by production of large amounts of IgE anti bodies and these include asthma, hay fever and atopic Dermatitis
Aetiology:
1. Genetic tendency: family history of atopy is found in about 70 % of patients 2. Immunological abnormalities 1. Increased IgE level. 2. Increased immediate anaphylactic reactions to food and drugs. 3. Decreased delayed type hypersensitivity. 4. Increased tendency for vasoconstriction. 5. Increased susceptibility to bacterial,, viral and dermatophyte inf. 6. Decreased function of the monocyte and neutrophils. 7. Decreased itching threshold.
Clinical Features
MANAGEMENT:
1. Explanation and reassurance of the patient or his parents 2. Avoidance of irritant materials 3. Emollients 4. Mild to moderate topical steroid ointment 5. Sedative antihistamines 6. Systemic antibiotics 7. Tacrolimus & Pimecrolimus. 8. In very severe and resistant cases systemic steroids, azathioprime, PUVA and cyclosporine
SEBORRHOEIC DERMATITIS
Presentations
2. petaloid form 3. Trunk: pityriasiform 4. Intertriginous or flexural lesions 5. Severe wide spread form erythroderma.
Treatment
1.
Topical imidazoles are the first line of treatment. 2. 2% sulpher + 2 % salicylic acid in a solution form especially on hairy areas. 3. Mild to moderate topical steroids. 4. Antibiotics in case of secondary infection. 5. UVB may be useful in some cases. 6. Systemic antifungal, Systemic steroids and other immunosuppressive drugs
DISCOID ECZEMA
POMPHOLYX
1. Severe irritant or allergic contact dermatitis. 2. Ingested metals. Nickel, Chromate or Cobalt. 3. Ide reaction to the presence of active T. pedis, T. capitis, severe irritated dermatitis. 4. Emotional stress.
Clinical features
Treatment:
1. Avoidance and treatment of the precipitating factors. 2. Potassium permanganate soaks and very potent corticosteroid creams. 3. Systemic steroids may be needed in severe cases. 4. Antibiotics in the presence of infection.
Asteatotic Eczema