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Dermatitis is red and scaly. The differential is primarily clinical – breakdown the differential by distribution and appearance.

Atopic dermatitis (eczema)

  • Pathophysiology: Epidermal barrier dysfunction (e.g., filaggrin mutations), immune dysregulation (skewed Th2 response), and altered skin microbiota; often associated with allergic rhinitis and asthma (“atopic triad”)

  • Clinical features: Most commonly presents on the face and flexural areas (e.g., popliteal and antecubital fossa)

    • - ACUTE: Intensely pruritic erythematous papules and vesicles; may be super-infected with oozing and crusting

    • - CHRONIC: Dry, scaly, excoriated papules and plaques; may see lichenification and fissuring

    • - Subtypes (descriptive terms of subtypes of atopic dermatitis)

      • Xerotic (asteatotic) eczema: Erythematous lesions with “plate-like” cracked scales, typically on the lower extremities; seen in older adults; associated with dry weather and/or excessive bathing

      • Nummular (discoid) dermatitis: Coin-shaped, pruritic scaly plaques, commonly on the extremities

      • Dyshidrotic eczema: Pinpoint clear vesicles on the lateral sides of the fingers

  • Treatment: Emollients (e.g., petroleum jelly, Aquaphor ointment) + topical glucocorticoids. Consider topical calcineurin inhibitors (e.g., tacrolimus) or a less potent steroid for the face, genitals, and skin folds.

  • Pearl: History of atopic dermatitis as a child greatly increases the risk of dermatitis in adulthood. Atopic dermatitis increases the risk of contact dermatitis. If a patient’s atopic dermatitis worsens, consider co-existing pathologies.

Contact dermatitis

  • Pathophysiology: Two types – irritant is more common than allergic

    • - Irritant: Direct damage to the skin from harsh chemicals, soaps, or detergents

    • - Allergic: Type IV hypersensitivity reaction to a particular antigen (e.g., poison oak/ivy, nickel, iodine, bacitracin); sensitized T-cells trigger an eczematous eruption at the site of contact

  • Clinical features: Intensely pruritic erythematous papules and vesicles in the exposed areas

  • Treatment: Avoid causative agents; severe eruptions may require topical glucocorticoids or systemic steroids; if dermatitis is severe or life-altering (e.g., job threatening) consider patch testing to determine cause

Stasis dermatitis (“venous eczema”)

  • Pathophysiology: Innate immune response to fluid collection in tissues

  • Clinical features: Pruritic, erythematous lesions on the lower extremities in patients with chronic dependent edema; typically bilateral but may be unilaterally symptomatic; often confused with cellulitis

  • Treatment: Reduce the edema (leg elevation, compression stockings) and treat the eczema with emollients and topical steroids



  • Pathophysiology: Immune dysregulation (Th1, Th17, excess IFN-gamma) and keratinocyte hyperproliferation

  • Clinical features: Thick, well-demarcated salmon-colored plaques with overlying silvery scale; classically on the extensor surfaces (e.g., knees, elbows) but can also be seen on the scalp, palms/feet (palmoplantar psoriasis), nails (pitting, “oil spots”) and flexural areas (inverse psoriasis); lesions will bleed if picked (Auspitz sign); 30% of patients have concurrent psoriatic arthritis; associated with metabolic syndrome and greater risk of cardiovascular disease

  • Treatment: Depends on disease severity

    • - Limited: Topical glucocorticoids, topical vitamin D analogues (calcipotriene, calcitriol), and/or ...

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