SDL Contact dermatitis atopic dermatitis and urticarial rash

Contact dermatitis hypersensitivity type

Type IV (delayed) T-cell-mediated hypersensitivity after allergen exposure

Atopic dermatitis hypersensitivity type

Type I (immediate) IgE-mediated hypersensitivity due to genetic predisposition (atopy)

Contact dermatitis pathogenesis

Allergen exposure → sensitization → memory T-cell activation on re-exposure → cytokine release → localized skin inflammation

Atopic dermatitis pathogenesis

Genetic predisposition → ↑IgE production → allergen sensitization → mast cell activation → chronic pruritic eczema

Contact dermatitis vs atopic dermatitis

Type IV vs Type I; T cells vs IgE; allergen exposure vs genetic predisposition; localized vs generalized; red itchy blisters vs dry itchy thickened skin; any age vs mainly infants/children

Urticarial rash mechanism

Mast cell activation → histamine release → vasodilation + increased vascular permeability → dermal edema → wheal and flare

Urticaria hallmark lesion

Pruritic, well-circumscribed, raised erythematous wheals (pale centre with surrounding flare) caused by dermal edema

Classic clinical clue for contact dermatitis

Localized rash confined to the site of allergen contact

Classic clinical clue for atopic dermatitis

Generalized intensely pruritic dry skin affecting mainly infants/children with an atopic (high IgE) background

Highest-yield associations

Contact dermatitis→Type IV→T cells; Atopic dermatitis→Type I→IgE; Urticaria→Mast cells→Histamine→Wheal & flare