Dermatology Board cheat sheet

Psoriasis plaques are well demarcated, erythematous, and silvery-scaled; Auspitz sign is pinpoint bleeding after scale removal; more than 10% body surface area or special-site involvement supports systemic or phototherapy.

Atopic dermatitis is pruritic and chronic relapsing; infantile disease favors the face and extensor surfaces, while childhood disease favors flexures; emollients plus topical corticosteroids are first-line.

Acute allergic contact dermatitis shows weeping vesicles and linear streaking from allergen transfer; irritant contact dermatitis does not require prior sensitization; patch testing identifies delayed allergens.

Urticaria consists of wheals that usually resolve within 24 hours; chronic urticaria lasts more than 6 weeks; second-generation H1 antihistamines are first-line and systemic steroids are avoided long term.

Erythema multiforme shows target lesions, often acrally, and is commonly triggered by herpes simplex virus; Stevens-Johnson syndrome and toxic epidermal necrolysis feature mucosal involvement and epidermal detachment.

Cellulitis is unilateral warmth, tenderness, edema, and erythema; beta-hemolytic streptococci and Staphylococcus aureus are common causes; marked pain out of proportion suggests necrotizing infection.

Acne treatment is stratified: comedonal acne responds to topical retinoids; inflammatory acne adds benzoyl peroxide or antibiotics; severe nodulocystic or scarring acne may require isotretinoin.

Lichen planus presents as purple, polygonal, pruritic papules with Wickham striae and oral involvement; hepatitis C association warrants testing when risk factors are present.

Psoriasis histology shows regular acanthosis, thin suprapapillary plates, parakeratosis, Munro microabscesses, and dilated capillaries in dermal papillae.

Lichen planus histology shows hyperkeratosis, wedge-shaped hypergranulosis, saw-tooth rete ridges, a band-like lymphocytic infiltrate, and Civatte bodies at the dermoepidermal junction.

Pemphigus vulgaris shows suprabasal intraepidermal acantholysis; direct immunofluorescence shows intercellular IgG and C3 in a net-like epidermal pattern; desmoglein 3 is the main target.

Bullous pemphigoid shows a subepidermal blister with eosinophils; direct immunofluorescence shows linear IgG and C3 along the basement membrane zone; BP180 and BP230 are target antigens.

Dermatitis herpetiformis shows subepidermal vesicles with neutrophils at dermal papillae; direct immunofluorescence shows granular IgA at papillary tips; celiac disease is strongly associated.

Mycosis fungoides shows epidermotropic atypical CD4 T cells, Pautrier microabscesses, and a band-like dermal infiltrate; patch, plaque, and tumor stages have different histologic features.

Melanoma histology may show asymmetry, poor circumscription, pagetoid scatter, atypical melanocytes, and dermal mitoses; Breslow depth is measured from the granular layer to the deepest tumor cell.

Special stains include periodic acid-Schiff for fungi and basement membrane, Fontana-Masson for melanin, Prussian blue for iron, and Congo red for amyloid under polarized light.

Low-risk basal cell carcinoma is excised with about 4 mm clinical margins; low-risk squamous cell carcinoma with about 4 to 6 mm; melanoma in situ with about 5 mm; invasive melanoma margins range from 1 to 2 cm by Breslow depth.

Mohs micrographic surgery is indicated for high-risk basal or squamous cell carcinoma, recurrent tumors, ill-defined borders, and anatomically sensitive sites where tissue conservation is important.

A punch biopsy reaches deep dermis and is preferred for inflammatory dermatoses and suspected deep tumors; a shave biopsy samples superficial epidermis and upper dermis; excisional biopsy is preferred for suspected melanoma.

Lidocaine maximum dose is about 4.5 mg/kg without epinephrine and about 7 mg/kg with epinephrine; epinephrine prolongs anesthesia and reduces bleeding; buffering reduces injection pain.

Simple interrupted sutures provide tension control; running sutures provide speed; deep absorbable sutures close dead space; facial sutures are typically removed at 5 to 7 days and trunk sutures at 10 to 14 days.

Cryotherapy with liquid nitrogen freezes tissue to about minus 195 degrees Celsius, causing ice crystal formation, vascular stasis, and necrosis; freeze-thaw cycles increase tissue injury.

Pulsed dye laser at about 595 nm targets vascular lesions such as port-wine stains and infantile hemangiomas; Q-switched lasers target pigment; fractional carbon dioxide lasers create columns of controlled injury.

Procedural complications include infection, dehiscence, hypertrophic scar, keloid, dyspigmentation, and nerve injury; anticoagulants are not routinely stopped before cutaneous surgery when indication is strong.

Atopic dermatitis in infants favors the face and extensor surfaces; in older children it favors flexures; emollients plus low-potency topical corticosteroids are first-line; food elimination requires proven allergy.

Diaper dermatitis is most often irritant; beefy red erythema with satellite pustules suggests Candida, treated with topical nystatin or clotrimazole; barrier ointments help irritant disease.

Seborrheic dermatitis of infancy presents as cradle cap with greasy scale on the scalp; gentle oil and shampoo are used; it is self-limited and usually resolves by infancy.

Infantile hemangiomas appear after birth, proliferate during early infancy, and then involute; problematic lesions threatening airway, vision, or function are treated with oral propranolol.

Port-wine stains are present at birth and do not involute; pulsed dye laser is first-line; a V1 trigeminal distribution warrants evaluation for Sturge-Weber syndrome and glaucoma.

Kawasaki disease requires fever for at least 5 days plus 4 of 5 features: conjunctivitis, oral changes, rash, extremity changes, and cervical lymphadenopathy; IVIG prevents coronary artery complications.

Scarlet fever from group A streptococcus causes a sandpaper-like rash, strawberry tongue, and Pastia lines; penicillin is first-line and reduces rheumatic fever risk.

Hand-foot-mouth disease, usually from coxsackievirus, causes oral ulcers and acral vesicles; it is self-limited and managed with supportive hydration and analgesia.

Type I hypersensitivity is IgE-mediated mast cell degranulation; it causes urticaria, angioedema, bronchospasm, or anaphylaxis; intramuscular epinephrine is first-line for anaphylaxis.

Type II hypersensitivity involves IgG against cell-bound antigens; type III involves immune complexes and complement consumption; type IV is T-cell mediated and delayed, as in allergic contact dermatitis.

Anaphylaxis criteria include acute skin or mucosal involvement plus respiratory compromise or hypotension, or involvement of two organ systems after exposure to a likely allergen.

Morbilliform drug eruption is the most common drug reaction; Stevens-Johnson syndrome involves less than 10% body surface epidermal detachment; toxic epidermal necrolysis involves more than 30%.

Systemic lupus erythematosus has sensitive antinuclear antibody and specific anti-double-stranded DNA and anti-Smith antibodies; photosensitivity, malar rash, and discoid lesions are common.

Dermatomyositis shows heliotrope eruption, Gottron papules, and proximal muscle weakness; anti-Mi-2, anti-TIF1 gamma, and anti-MDA5 antibodies have different associations; adults need malignancy screening.

Allergic contact dermatitis is a delayed type IV reaction to haptens such as nickel or urushiol; patch testing confirms the allergen; avoidance leads to resolution.

Serum sickness is a type III reaction with fever, urticaria, arthralgia, and lymphadenopathy occurring 1 to 3 weeks after antigen exposure; complement may be low.