—chronic inflammatory skin disorder characterized by dry skin and pruritus. Rubbing and scratching the skin promotes inflammation and leads to an itch–scratch cycle. It follows a relapsing course characterized by alternating periods of flares and remissions. Patients often have a personal or family history of eczema, asthma, or allergic rhinitis. Exacerbating factors may include cold weather, dust mites, pollens, infection, wool, pet fur, emotional stress, chemical irritants, and other allergens

—ill-defined pruritic erythematous plaques with excoriations. Neck and flexural prominence in adults and children. Pustules, honey-colored crusts, and weeping may be a sign of secondary infection

—dry skin care (unscented, hypoallergenic soaps, daily moisturizers). Topical corticosteroids BID × 3 weeks, off 1 week, repeat PRN (typically hydrocortisone 1–2.5% or desonide 0.05% for the face, triamcinolone 0.1% for the body), and topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%). Antihistamines (diphenhydramine, loratadine, fexofenadine, hydroxyzine, and doxepin). Oral antibiotics × 7 days for superimposed Staphylococcus aureus infections (typically flucloxacillin or other penicillinase-resistant penicillin for MSSA and clindamycin, doxycycline or trimethoprim-sulfamethoxazole for MRSA)

—a chronic inflammatory skin disorder with a polygenic predisposition and sometimes an environmental triggering factor (trauma/Koebner phenomenon, infections, drugs, alcohol ingestion, emotional stress)

—well-circumscribed, bright salmon red color, silvery micaceous scaly plaques. Predilection for the scalp and extensor regions. Nails may show pitting changes, “oil spots”, onycholysis, and subungual debris which may be helpful in making the diagnosis. All patients regardless of skin severity should be screened for inflammatory arthritis that is worse in the mornings, associated with joint stiffness and swelling ± dactylitis. Consider screening for hyperlipidemia, coronary artery disease, and diabetes in patients with risk factors as there is an increased predilection in patients with psoriasis

—topical therapy with corticosteroids (triamcinolone/fluocinolone, fluocinonide, betamethasone dipropionate and clobetasol) and vitamin D analogs. Topical calcineurin inhibitors may be used on the face and intertriginous areas. If unable to control, light therapy with either UVB or PUVA may be considered, but requires 2–3 visits/week for months. Traditional systemic therapies including acitretin, cyclosporine, and methotrexate should be considered in patients with moderate to severe psoriasis with >10% body surface involvement or severe functional impairment (hands, feet, arthritis, and genitals). If unresponsive or unable to tolerate these, biologic therapy such as the TNFα inhibitors (infliximab, adalimumab, golimumab, etanercept) or ustekinumab (anti-IL 12/23) should be considered for psoriatic arthritis. Avoid systemic steroids as discontinuation may cause generalized pustular psoriasis

—EGFR inhibitors (erlotinib, gefitinib, cetuximab, panitumumab) and oral corticosteroids (prednisone, dexamethasone) can cause pustular folliculitis

—drugs (steroids, phenytoin, lithium), androgen excess (PCOS, Cushing’s, congenital adrenal hyperplasia)

—teenager with open comedones (blackheads), closed comedones (white heads), erythematous papules, pustules, cysts and scarring over face, shoulders, upper chest, and back

—widespread erythematous maculopapular lesions that may be accompanied by fever and malaise

—discontinue any offending drugs. Usually resolve spontaneously

—slapped cheek rash on face and erythematous eruption on trunk, neck, and extremities. Also called fifth disease or erythema infectiosum. Fever may be present. Parvovirus B19 is also associated with aplastic anemia, polyarthritis, and fetal hydrops

—patients usually develop symptoms within 2–3 weeks after drug exposure, more rapidly in previously exposed patients. The prodrome involves a flu-like syndrome with fever, malaise, arthralgias, myalgias, and mucous membrane lesions. This is followed by the development of irregular targetlike lesions often with necrotic centers that coalesce over time. Flaccid blisters form that spread with pressure (Nikolsky sign) resulting in sheet-like loss of epidermis and exposure of the underlying dermis. Ninety percent of patients have mucous membrane involvement and 60% have ocular involvement

—pressing on the edges of an intact blister helps to discriminate between an intraepidermal blistering process (pemphigoid vulgaris, blister extends and breaks easily) and a subepidermal process (TEN, bullous pemphigoid, blister would not advance)