INFLAMMATORY RASHES

Atopic Dermatitis (Eczema) - itchy, red, oozing rash with vesicles and edema. Often involves face and flexors. Atopic means allergic, so it’s (most likely) a Type 1 hypersensitivity reaction. As such, IgE levels are high. It’s similar to urticaria, but Eczema is chronic, recurring and a tad more severe. The pathogenesis is poorly understood (may involve Filaggrin problems). It flares up in cycles. After years of rashes, the flexor surfaces become leathery (lichenified). Common in patients/families with asthma and allergic rhinitis (atopic march). Treatment is topical steroids and moisturizers. You can give a short dose of steroids as needed.. 

Contact Dermatitis - it looks like Eczema, but the cause is different. There is localized dermatitis caused by an irritant (eg, poison ivy, detergent, drugs or nickel jewelry). It is a Type 4 hypersensitivity reaction. The treatment is removing the offending agent & topical steroids.

Seborrheic Dermatitis - red scaly plaques on the face/scalp. It involves the nasolabial folds (Lupus avoids the folds). Poorly understood, but might involve the harmless fungus Malassezia furfur digesting the skin’s sebum (which releases some inflammatory digestive byproducts). Anywhere there’s oily skin (nasolabial folds, hair follicles) this rash can occur. In young kids, it likes to affect the scalp. Give ‘em topical antifungals and steroids. 

Acne Vulgaris - good ol’ acne. It refers to pilosebaceous inflammation. Sex hormones (eg, Androgens) thicken the keratin-rich hair follicle lumen wall (combat this growth with teratogenic Vitamin A derivatives like Isotretinoin). The hair follicle tube gets clogged, and sebaceous fluid (sebum) can’t escape. Stagnant sebum gets infected by Proprionibacterium acnes (Gram + anaerobe), which can be treated by topical keratolytics like Benzoyl Peroxide or topical antibiotics like Clindamycin, Doxy or Erythromycin. P. acnes are part of the normal skin flora, and it contributes to inflammation (but doesn’t cause it in and of itself). Acne has a range of lesions. Closed comedones (whiteheads), open comedones (blackheads), pustules (pimples) and nodules (scarring). Due to chronic inflammation of hair follicles and sebaceous glands in the dermis.  

Psoriasis - a very high yield derm condition, with a very distinctive rash -- well-circumscribed salmon-colored plaques (acanthosis) covered with a silvery scale (hyperkeratosis/parakeratosis). Usually on extensor surfaces and scalp. Auspitz Sign - if you remove the silvery scale, there will be pinpoint bleeding (thick AND thin stratum spinosum in acanthosis). Pitting of nails occurs too. The cause is unknown (likely AI), but what we see under the microscope is excessive keratinocyte proliferation. WBCs accumulate in the stratum corneum in clusters that are called Munro’s microabscesses. Since it’s likely AI, treatment with steroids and immune-modulators helps. Since this disease is due to hyperkeratosis, if we damage the keratin with UV light or slow it with Vitamin D, we can mitigate the rash. 1/3rd of patients get arthritis (seronegative). Treat with topical steroids. DON”T give oral steroids, it will induce pustular psoriasis

Rosacea - “adult acne.” MOA is unknown. If left untreated, it will make the patient's nose become enlarged and bulbous. Looks like acne but without comedones. Triggered by fun things (alcohol, spicy food, hot showers). 

Pityriasis Rosea - A single golf ball-sized red oval scaly patch (herald lesion) will appear. A few days later, a lot of pink plaques will erupt on the trunk (in a christmas tree pattern). Self-limiting. Unknown MOA. 

Lichen Planus - Pruritic, Planar, Polygonal, Purple Papules. Super itchy. Commonly involves wrists, elbows and mucosa. Often with reticular white lines (Wickham striae) caused by hypergranulosis. The cause is unknown. But it is associated with Hep C. Topical steroids