Family Medicine EOR (Dermatologic): New for 2026 Topic List (Smarty PANCE)

What is Acne Vulgaris?

A chronic inflammatory disease of the pilosebaceous unit caused by androgen-driven sebum production, follicular hyperkeratinization, Cutibacterium acnes proliferation, and inflammation, presenting with comedones, papules, pustules, nodules, and cysts.

What are the four pathogenic factors of acne vulgaris (mnemonic: FISH)?

Follicular hyperkeratinization, Increased sebum production (androgen-driven), Cutibacterium acnes (formerly Propionibacterium) colonization, Inflammation/Hormones.

What distinguishes comedonal vs inflammatory vs nodulocystic acne?

Comedonal: open (blackheads) and closed (whiteheads) comedones; Inflammatory: papules and pustules; Nodulocystic: deep nodules and cysts with high scarring risk.

What is the first-line treatment for mild comedonal acne?

Topical retinoids (tretinoin, adapalene) ± benzoyl peroxide; adapalene now OTC.

What is the first-line treatment for moderate inflammatory acne?

Topical retinoid + benzoyl peroxide + topical antibiotic (clindamycin); never use topical antibiotic as monotherapy (resistance).

What is the treatment for severe nodulocystic or scarring acne?

Oral isotretinoin (Accutane); requires iPLEDGE enrollment, monthly pregnancy tests in females, baseline lipids/LFTs.

What are the major side effects and contraindications of isotretinoin?

Teratogenic (Category X), cheilitis, xerosis, elevated triglycerides/LFTs, depression/suicidal ideation; absolutely contraindicated in pregnancy.

What oral antibiotic is first-line for moderate-severe inflammatory acne?

Doxycycline or minocycline; avoid tetracyclines in pregnancy and children <8 years.

What hormonal therapy benefits female patients with acne?

Combined OCPs and spironolactone (anti-androgen); useful for adult women with hormonal flares along jawline.

What is Contact Dermatitis?

An inflammatory skin reaction from direct contact with an irritant (irritant contact dermatitis) or allergen (allergic contact dermatitis, a type IV delayed hypersensitivity reaction).

How do you distinguish irritant from allergic contact dermatitis?

Irritant: immediate burning/stinging, sharp borders matching exposure, most common type (soaps, detergents); Allergic: delayed 24-72 hr pruritic reaction, type IV hypersensitivity (poison ivy/oak, nickel, fragrances).

What is the classic distribution of poison ivy/oak contact dermatitis?

Linear streaks of vesicles and bullae from urushiol oil exposure; can spread via contaminated clothing/pets, NOT via blister fluid.

What is the gold standard test for allergic contact dermatitis?

Patch testing — applied to back, read at 48 and 96 hours.

What is the treatment for localized contact dermatitis?

Remove offending agent, cool compresses, topical mid-to-high potency corticosteroids (triamcinolone, clobetasol), oral antihistamines for pruritus.

When are systemic corticosteroids indicated for contact dermatitis?

Severe/widespread reactions (>20% BSA), facial/genital involvement, or severe poison ivy; prednisone taper over 2-3 weeks (shorter tapers cause rebound).

What is a Drug Eruption?

An adverse cutaneous reaction to a medication, ranging from benign morbilliform rashes to life-threatening reactions like SJS/TEN, DRESS, and AGEP.

What is the most common type of drug eruption?

Morbilliform (maculopapular) exanthem — symmetric erythematous macules and papules beginning on trunk, appearing 5-14 days after starting drug (sooner with re-exposure).

What are the most common causes of drug eruptions (mnemonic: PNAS)?

Penicillins/sulfonamides, NSAIDs, Allopurinol/Anticonvulsants, Statins; also TMP-SMX, aromatic anticonvulsants (phenytoin, carbamazepine, lamotrigine).

What is DRESS syndrome?

Drug Reaction with Eosinophilia and Systemic Symptoms — fever, morbilliform rash, lymphadenopathy, eosinophilia, hepatitis; onset 2-8 weeks after drug start; mortality 10%.

What are the red flag features that suggest a severe cutaneous adverse reaction?

Mucosal involvement, skin pain/tenderness, blistering/skin sloughing, facial edema, fever, lymphadenopathy, eosinophilia, atypical lymphocytes, hepatitis.

What is the management of any suspected drug eruption?

Immediately discontinue suspected drug, supportive care, antihistamines for pruritus; severe reactions require hospitalization and systemic steroids/IVIG.

What is Urticaria?

Pruritic, well-circumscribed, raised wheals (hives) caused by mast cell degranulation and histamine release, with individual lesions resolving within 24 hours (otherwise consider urticarial vasculitis).

How do you distinguish acute from chronic urticaria?

Acute: <6 weeks duration, usually identifiable trigger (infection, food, drug); Chronic: ≥6 weeks, often idiopathic (chronic spontaneous urticaria).

What is angioedema and how does it differ from urticaria?

Deeper dermal/subcutaneous swelling involving lips, eyelids, tongue, larynx; non-pitting, less pruritic, more painful; can be life-threatening if airway involved.

What is the most common cause of ACE inhibitor-induced angioedema and its treatment?

Bradykinin accumulation (not histamine-mediated); does NOT respond to antihistamines/steroids; discontinue ACEI, airway management, icatibant or C1 esterase inhibitor for severe cases.

What is the first-line treatment for urticaria?

Second-generation H1 antihistamines (cetirizine, loratadine, fexofenadine); can up-titrate to 4x standard dose before adding other agents.

When is epinephrine indicated in urticaria/angioedema?

Any signs of anaphylaxis — laryngeal edema, hypotension, bronchospasm, GI symptoms; epinephrine 0.3-0.5 mg IM in anterolateral thigh.

What is Acanthosis Nigricans?

Velvety, hyperpigmented, hyperkeratotic plaques on flexural surfaces (axillae, neck, groin) caused by insulin resistance, obesity, endocrinopathy, or malignancy.

What conditions are most commonly associated with acanthosis nigricans?

Insulin resistance (type 2 diabetes, obesity, PCOS, metabolic syndrome); rapid-onset in non-obese adult raises concern for occult malignancy (especially gastric adenocarcinoma).

What is the workup for new-onset acanthosis nigricans?

Fasting glucose/HbA1c, lipid panel, BMI assessment; if sudden onset in non-obese adult, evaluate for underlying malignancy (CT abdomen, age-appropriate cancer screening).

What is the treatment for acanthosis nigricans?

Treat underlying cause — weight loss, metformin for insulin resistance; topical retinoids, ammonium lactate, or keratolytics (urea) for cosmetic improvement.

What is Alopecia?

Hair loss that can be scarring (cicatricial, permanent) or non-scarring (reversible), with subtypes including androgenetic, alopecia areata, telogen effluvium, and tinea capitis.

What characterizes androgenetic alopecia?

Genetic, androgen-mediated hair loss; men: bitemporal/vertex thinning; women: diffuse thinning preserving frontal hairline; treatment: minoxidil (topical), finasteride (men only).

What is alopecia areata and its classic finding?

Autoimmune attack on hair follicles causing well-circumscribed round patches of non-scarring hair loss; "exclamation point hairs" at margins; associated with thyroid disease, vitiligo, atopy.

What is telogen effluvium?

Diffuse non-scarring hair shedding 2-4 months after major physiologic stressor (childbirth, surgery, severe illness, crash diet, medication); self-limited, regrows in 6-12 months.

What is traction alopecia?

Hair loss from chronic tension (tight braids, ponytails, weaves); reversible early, becomes scarring if chronic.

What is the treatment for alopecia areata?

Intralesional corticosteroids (triamcinolone) for limited disease; topical steroids, minoxidil; JAK inhibitors (baricitinib) for severe/extensive disease.

What is Atopic Dermatitis?

A chronic, relapsing, pruritic inflammatory skin disease characterized by impaired skin barrier function (filaggrin mutation), Th2 immune dysregulation, and associated atopy (asthma, allergic rhinitis).

What is the classic distribution of atopic dermatitis by age?

Infants: cheeks, scalp, extensor surfaces; Children: flexural areas (antecubital, popliteal fossae); Adults: hands, eyelids, flexural areas, neck.

What is the "atopic triad"?

Atopic dermatitis, asthma, allergic rhinitis — often presents sequentially as the "atopic march."

What is the cornerstone of atopic dermatitis treatment?

Daily emollients/moisturizers (thick creams/ointments), lukewarm short baths, gentle non-soap cleansers, identify/avoid triggers; topical corticosteroids for flares.

What are non-steroidal topical options for atopic dermatitis?

Topical calcineurin inhibitors (tacrolimus, pimecrolimus) — useful for face/folds to avoid steroid atrophy; crisaborole (PDE4 inhibitor); ruxolitinib cream (JAK inhibitor).

What systemic treatment is FDA-approved for moderate-severe atopic dermatitis?

Dupilumab (anti-IL-4/IL-13 monoclonal antibody); also JAK inhibitors (upadacitinib, abrocitinib); methotrexate, cyclosporine as alternatives.

What is the most common complication of atopic dermatitis?

Secondary bacterial infection (Staph aureus); also eczema herpeticum (HSV superinfection — dermatologic emergency, treat with IV acyclovir).

What is Bullous Pemphigoid?

An autoimmune subepidermal blistering disease of elderly patients, caused by IgG autoantibodies against hemidesmosomal proteins BP180 and BP230, producing tense bullae on erythematous or normal skin.

What is the classic presentation of bullous pemphigoid?

Elderly patient (>60) with intensely pruritic tense bullae on erythematous base, favoring flexural areas, axillae, groin, lower abdomen; mucosal involvement uncommon (<30%).

How does bullous pemphigoid differ from pemphigus vulgaris?

BP: tense bullae, subepidermal, elderly, mucosa rarely involved, negative Nikolsky, anti-BP180/230; Pemphigus vulgaris: flaccid bullae, intraepidermal, middle-aged, mucosal involvement common, POSITIVE Nikolsky, anti-desmoglein.

What is the gold standard for diagnosing bullous pemphigoid?

Skin biopsy with direct immunofluorescence (DIF) showing linear IgG and C3 deposition along the basement membrane zone.

What is the first-line treatment for bullous pemphigoid?

High-potency topical corticosteroids (clobetasol) for localized disease; oral prednisone for widespread; steroid-sparing agents: doxycycline + nicotinamide, methotrexate, rituximab.

What is Erythema Multiforme?

An acute, self-limited, immune-mediated cutaneous reaction characterized by target lesions (3 zones), most commonly triggered by HSV infection or medications.

What is the classic "target lesion" of erythema multiforme?

Three concentric zones: central dusky/dark area (or vesicle), middle pale ring of edema, outer erythematous ring; typically on extensor surfaces of extremities.

What is the most common trigger for erythema multiforme?

Herpes simplex virus (HSV) — accounts for >50% of cases; second most common: Mycoplasma pneumoniae (especially in children); drugs less common.

How is erythema multiforme classified?

EM minor: target lesions, no/minimal mucosal involvement, no systemic symptoms; EM major: target lesions PLUS mucosal involvement of ≥1 site, systemic symptoms.

What distinguishes EM major from SJS?

EM major: classic target lesions on extremities, <10% BSA, HSV-triggered; SJS: atypical targets on trunk, painful skin, drug-induced, mucosal involvement severe, can progress to TEN.

What is the treatment for erythema multiforme?

Self-limited (resolves 2-4 weeks); symptomatic treatment (antihistamines, topical steroids); chronic suppressive antiviral therapy (acyclovir) for recurrent HSV-associated EM.

What is Hidradenitis Suppurativa?

A chronic inflammatory disease of the apocrine gland-bearing skin (axillae, groin, buttocks, inframammary), characterized by recurrent painful nodules, abscesses, sinus tracts, and scarring.

What is the typical patient profile for hidradenitis suppurativa?

Post-pubertal, female > male, obesity, smoking, family history; associated with metabolic syndrome, IBD, PCOS.

What is the Hurley staging for HS?

Stage I: isolated abscesses, no scarring/sinus tracts; Stage II: recurrent abscesses with sinus tracts and scarring, widely separated; Stage III: diffuse involvement with interconnected sinus tracts and abscesses.

What is the first-line treatment for mild hidradenitis suppurativa?

Lifestyle modifications (weight loss, smoking cessation), topical clindamycin, antibacterial washes (chlorhexidine, benzoyl peroxide); intralesional triamcinolone for acute flares.

What is the treatment for moderate-severe hidradenitis suppurativa?

Oral antibiotics (doxycycline, clindamycin + rifampin); hormonal therapy (spironolactone, OCPs); biologics (adalimumab — FDA approved, secukinumab); wide surgical excision for Stage III.

What is Lichen Planus?

A chronic inflammatory T-cell-mediated mucocutaneous disorder characterized by the "6 P's": Pruritic, Purple, Polygonal, Planar, Papules and Plaques, often with Wickham striae.

What are the 6 P's of lichen planus?

Pruritic, Purple (violaceous), Polygonal, Planar (flat-topped), Papules and Plaques; classic location: flexor wrists, ankles, lower back.

What are Wickham striae?

Fine white reticulated lines on the surface of lichen planus lesions or oral mucosa — pathognomonic finding.

What conditions are associated with lichen planus?

Hepatitis C (always check HCV serology!), medications (thiazides, ACE inhibitors, antimalarials, beta-blockers — "lichenoid drug eruption"), GVHD.

What is the treatment for lichen planus?

High-potency topical corticosteroids first-line; intralesional steroids for thick plaques; oral steroids, phototherapy, or acitretin for severe/widespread disease; usually self-limited (1-2 years).

What is Lichen Simplex Chronicus?

Localized, thickened, lichenified plaque from chronic rubbing and scratching of pruritic skin — the "itch-scratch cycle" — most common on posterior neck, ankles, scrotum, vulva.

What is the classic appearance of lichen simplex chronicus?

Well-demarcated thickened plaque with exaggerated skin lines (lichenification), hyperpigmentation, and excoriations from chronic scratching.

What is the treatment for lichen simplex chronicus?

Break the itch-scratch cycle: high-potency topical corticosteroids (clobetasol), occlusion (Unna boot), antihistamines (sedating at night — hydroxyzine), intralesional steroids for thick plaques.

What is Melasma?

Acquired symmetric hyperpigmentation of sun-exposed areas (face), driven by estrogen, pregnancy ("mask of pregnancy"/chloasma), OCPs, and UV exposure; more common in women with darker skin (Fitzpatrick III-V).

What is the classic distribution of melasma?

Symmetric hyperpigmented patches on the face — centrofacial (forehead, cheeks, upper lip, chin), malar, or mandibular patterns.

What is the first-line treatment for melasma?

Strict sun protection (broad-spectrum sunscreen SPF ≥50, physical blockers like zinc oxide), triple combination cream (hydroquinone 4% + tretinoin + corticosteroid) — Kligman's formula.

What is Nummular Eczema?

Pruritic, coin-shaped (nummular), well-circumscribed eczematous plaques, typically on extremities, often associated with dry skin (xerosis), more common in winter/elderly.

What distinguishes nummular eczema from tinea corporis?

Nummular eczema: round coin-shaped plaques without central clearing, KOH-negative; Tinea corporis: annular with central clearing and raised scaly border, KOH-positive for hyphae.

What is the treatment for nummular eczema?

Aggressive moisturization (thick emollients), mid-to-high potency topical corticosteroids, topical calcineurin inhibitors, oral antihistamines; treat secondary infection if present.

What is Pilonidal Disease?

A chronic inflammatory condition of the natal cleft (sacrococcygeal area) caused by ingrown hairs that lead to abscess and sinus tract formation; most common in young hirsute males.

What are the risk factors for pilonidal disease?

Young males (15-30), obesity, hirsutism, prolonged sitting (truck drivers, soldiers — "Jeep disease"), poor hygiene, family history.

What is the treatment for an acute pilonidal abscess?

Incision and drainage (off-midline incision preferred); no routine antibiotics unless cellulitis, immunocompromise, or systemic signs; wound packing and follow-up.

What is the definitive treatment for chronic/recurrent pilonidal disease?

Surgical excision of sinus tracts with primary closure, marsupialization, or flap repair (Bascom, Karydakis, Limberg); hair removal (laser) and meticulous hygiene for prevention.

What is Pityriasis Rosea?

A self-limited papulosquamous eruption, likely viral (HHV-6/7 associated), starting with a single "herald patch" followed by a generalized "Christmas tree" pattern.

What is the classic presentation of pityriasis rosea?

Single 2-5 cm oval salmon-colored "herald patch" on trunk, followed 1-2 weeks later by smaller similar lesions in "Christmas tree" distribution along skin tension lines (Langer lines).

What is a critical "do-not-miss" diagnosis to consider with pityriasis rosea?

Secondary syphilis — can mimic pityriasis rosea exactly but typically involves palms and soles; always check RPR in sexually active patients with PR-like rash.

What is the treatment for pityriasis rosea?

Self-limited (resolves 6-8 weeks); symptomatic — antihistamines, topical steroids for pruritus; UV light or short-course oral acyclovir may shorten duration if started early.

What is Seborrheic Dermatitis?

A chronic relapsing inflammatory skin condition of sebum-rich areas, associated with Malassezia furfur (yeast), presenting with greasy yellow scales on erythematous patches.

What is the classic distribution of seborrheic dermatitis?

Scalp ("dandruff"/cradle cap in infants), eyebrows, nasolabial folds, ears, chest, beard area, intertriginous areas.

What conditions are associated with severe or refractory seborrheic dermatitis?

HIV/AIDS (severe, refractory cases), Parkinson disease, neurologic disorders, immunosuppression — consider HIV testing in severe presentations.

What is the treatment for seborrheic dermatitis?

Antifungal shampoos (ketoconazole 2%, selenium sulfide, zinc pyrithione, ciclopirox); low-potency topical steroids for inflammatory flares; topical calcineurin inhibitors for facial involvement.

What is Seborrheic Keratosis?

A common benign epidermal neoplasm of older adults, appearing as well-demarcated waxy "stuck-on" papules or plaques with variable pigmentation.

What is the classic description of seborrheic keratosis?

Well-circumscribed, waxy, "stuck-on" appearance, brown to black, with comedone-like openings/horn cysts; commonly on trunk, face, neck in older adults.

What is the Leser-Trélat sign?

Sudden eruption of multiple seborrheic keratoses — potential paraneoplastic sign of internal malignancy (especially gastric adenocarcinoma); workup for underlying cancer.

How do you differentiate seborrheic keratosis from melanoma?

SK: stuck-on, waxy, well-demarcated, horn cysts, no change over years; Melanoma: ABCDE criteria (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolution), dermoscopy/biopsy if uncertain.

What is the treatment for seborrheic keratosis?

No treatment needed (benign); cosmetic removal via cryotherapy (liquid nitrogen), curettage, electrodessication, or topical hydrogen peroxide 40% (Eskata).

What is Tinea Versicolor?

A superficial fungal infection caused by Malassezia furfur (formerly Pityrosporum), characterized by hypopigmented or hyperpigmented patches with fine scale on the trunk and shoulders.

What is the classic presentation of tinea versicolor?

Hypopigmented (more common in dark skin) or hyperpigmented oval macules with fine scale on upper trunk, shoulders, neck; worsens in summer/humidity; more apparent after sun exposure.

What is the diagnostic test for tinea versicolor?

KOH prep showing "spaghetti and meatballs" appearance (short hyphae + spores); Wood's lamp shows yellow-gold fluorescence.

What is the treatment for tinea versicolor?

Topical: selenium sulfide 2.5% shampoo, ketoconazole shampoo, terbinafine; Oral: itraconazole or fluconazole for extensive disease; counsel pigment changes take months to resolve and recurrence is common.

What is Toxic Epidermal Necrolysis (TEN)?

A life-threatening mucocutaneous reaction (>30% BSA epidermal detachment) with full-thickness epidermal necrosis, almost always drug-induced, on the spectrum with Stevens-Johnson Syndrome (SJS).

How is the SJS/TEN spectrum classified by BSA?

SJS: <10% BSA epidermal detachment; SJS/TEN overlap: 10-30% BSA; TEN: >30% BSA. All involve mucous membranes.

What are the most common drug triggers for SJS/TEN?

Sulfonamides (TMP-SMX), allopurinol (highest risk), anticonvulsants (lamotrigine, carbamazepine, phenytoin), NSAIDs (oxicams), nevirapine; HLA-B*15:02 increases risk with carbamazepine in Asians.

What is the classic clinical course of SJS/TEN?

Prodrome (fever, flu-like symptoms) 1-3 days, then painful erythematous/dusky macules → blistering and full-thickness epidermal detachment with POSITIVE Nikolsky sign; mucosal involvement (oral, ocular, genital).

What is SCORTEN and what does it predict?

Severity of Illness Score for TEN — 7 prognostic factors (age >40, malignancy, HR >120, BSA >10%, BUN >28, glucose >252, bicarb <20); predicts mortality (score ≥5 = >90% mortality).