Eczema is a clinical term describing many pathogenically different conditions. The Greek word eczema means "to boil over". All are characterized by red, papilovesicular, oozing, and crusted lesions which develop over time into raised, scaling plaques. Small and larger blisters (vesicles and bullae) may be present.
Over time, vesicles can become progressively scaly (hyperkeratotic) as the epidermis thickens (acanthosis).
The itch that rashes
acute:
chronic, or secondary:
cultures and fungal scrapings may be done
skin biopsy apparently reveals something
allergy testing: patch tests, rast tests, prick tests
Edema occurs within the intercellular spaces of the epidermis, primarily the stratum spinosum. Mechanical shearing of desmosomes and cell membranes by fluid accumulation results in intraepidermal vesicles.
Epidermal antigens are taken up by Langerhans cells, which then migrate to draining lymph nodes. Antigens are processed and presented to naitve CD4+ T cells, which are activated and develop into effector and memory T cells.
On re-exposure, these T cells migrate to affected skin sites, releasing cytokines and other factors recruiting inflammatory cells.
Early cytokine release causes venule endothelial activation, promoting memory T cell adhesion and extravasation. Expression of an array of lymphokines recruits large numbers of inflammatory cells within 24 hours. This accounts for initial erythema and pruritus acompanying cutaneous delayed hypersensitivity.
Chronic exposure to UV damages epidermal Langerhans cells, required for the development of contact hypersensitivity. Neuropeptides also appear to affect Langerhans cell function, suggesting implications for neural roles in the development and severity of certain dermatidites.
Local irritants more often contribute than foods - wool clothing, sand/dirt, saliva, heat/cold, dry air
take a really good history; ask all about what products they use
Acute:
no thinning of the skin with tacrolimus/pimocrolimus
chronic: