Pediatrics EOR (2026): Dermatologic (Smarty PANCE)

What is acne vulgaris?

A chronic inflammatory disorder of the pilosebaceous unit that is the most common skin condition of adolescence.

What are the four pathogenic factors in acne vulgaris?

Follicular hyperkeratinization, increased sebum production (androgen-driven), Cutibacterium acnes proliferation, and inflammation.

What lesion type defines comedonal acne?

Non-inflammatory open comedones (blackheads) and closed comedones (whiteheads) without papules or pustules.

What is first-line therapy for mild comedonal acne?

Topical retinoid (tretinoin, adapalene), with benzoyl peroxide added for inflammatory lesions.

What is first-line therapy for moderate inflammatory acne in an adolescent?

Topical retinoid plus benzoyl peroxide plus a topical or oral antibiotic (doxycycline; avoid tetracyclines under age 8).

What are the key adverse effects and monitoring requirements of isotretinoin?

Teratogenicity (iPLEDGE, two forms of contraception, monthly pregnancy tests), hypertriglyceridemia, transaminitis, xerosis/cheilitis, and mood changes; monitor lipids and LFTs.

What should acne with hirsutism, irregular menses, and rapid virilization in an adolescent girl prompt?

Evaluation for PCOS or an androgen-secreting tumor (check total/free testosterone, DHEA-S, 17-OH progesterone).

What is neonatal acne (neonatal cephalic pustulosis)?

Benign papulopustular eruption on the face at 2–4 weeks of age from maternal androgens/Malassezia; resolves spontaneously without treatment.

What are drug eruptions?

Cutaneous adverse reactions to medications, ranging from benign morbilliform rashes to life-threatening reactions like SJS/TEN and DRESS.

What is the most common type of drug eruption?

Morbilliform (exanthematous) eruption — symmetric pink macules and papules starting on the trunk 7–14 days after starting the drug.

Which drug classes most commonly cause pediatric drug eruptions?

Antibiotics (penicillins, cephalosporins, sulfonamides), anticonvulsants (lamotrigine, phenytoin, carbamazepine), NSAIDs, and allopurinol.

What red-flag features suggest a severe cutaneous adverse reaction rather than a simple morbilliform rash?

Fever, mucosal involvement, skin pain, blistering/Nikolsky sign, facial edema, lymphadenopathy, eosinophilia, and transaminitis.

What is DRESS syndrome?

Drug Reaction with Eosinophilia and Systemic Symptoms — fever, morbilliform rash, facial edema, lymphadenopathy, eosinophilia, and internal organ involvement (liver most common) 2–8 weeks after drug exposure.

What is a fixed drug eruption?

A well-demarcated round dusky/violaceous plaque that recurs at the same site with each re-exposure, classically from sulfonamides, NSAIDs, or tetracyclines.

What is the mainstay of management for a drug eruption?

Immediate discontinuation of the offending drug; supportive care with antihistamines and topical steroids for mild cases, systemic steroids and admission for severe reactions.

What is urticaria?

Transient, pruritic, well-circumscribed edematous wheals caused by mast cell histamine release in the superficial dermis.

How long does an individual urticarial wheal last?

Individual lesions last less than 24 hours and resolve without residual skin changes; lesions persisting >24 hours with bruising suggest urticarial vasculitis.

What distinguishes acute from chronic urticaria?

Acute lasts less than 6 weeks (usually infection or drug/food trigger in children); chronic lasts 6 weeks or longer and is most often idiopathic/autoimmune.

What is the most common cause of acute urticaria in children?

Viral infection, followed by medications and foods.

What is angioedema and how does it differ from urticaria?

Deeper dermal/subcutaneous swelling involving the lips, eyelids, tongue, and airway; it is often non-pruritic and painful, and carries risk of airway compromise.

What is first-line treatment for urticaria?

Second-generation H1 antihistamines (cetirizine, loratadine), uptitrated as needed; add H2 blocker or short-course steroids for refractory cases.

What is the immediate treatment when urticaria occurs with airway compromise or hypotension?

Intramuscular epinephrine 0.01 mg/kg (1:1000) into the anterolateral thigh — this is anaphylaxis.

What is acanthosis nigricans?

Velvety, hyperpigmented, thickened plaques in flexural areas (neck, axillae, groin) that most often signal insulin resistance.

What is the most common underlying cause of acanthosis nigricans in children?

Obesity with insulin resistance, prediabetes, or type 2 diabetes mellitus.

What workup should a child with acanthosis nigricans receive?

Fasting glucose or HbA1c, fasting lipid panel, and BMI assessment; consider PCOS evaluation in adolescent girls.

What syndromes and medications are associated with acanthosis nigricans?

PCOS, Cushing syndrome, hypothyroidism, acromegaly; drugs include systemic corticosteroids, niacin, and oral contraceptives.

When should malignancy be suspected with acanthosis nigricans?

Abrupt onset, extensive/rapidly progressive involvement, mucosal or palmar involvement (tripe palms), and weight loss — classically gastric adenocarcinoma (rare in children).

What is the mainstay of treatment for acanthosis nigricans?

Treat the underlying cause — weight loss, exercise, and insulin sensitizers (metformin); topical retinoids or keratolytics for cosmesis.

What is alopecia?

Loss of hair from areas where it normally grows, categorized as scarring (permanent) or non-scarring (potentially reversible).

What is the most common cause of patchy hair loss with scale in a school-aged child?

Tinea capitis — scaly patches with broken hairs ("black dots") and occipital/posterior cervical lymphadenopathy.

What is the treatment for tinea capitis?

Oral antifungal therapy (griseofulvin or terbinafine) for 6–8 weeks — topical agents alone are inadequate; adjunctive selenium sulfide or ketoconazole shampoo reduces spread.

What is alopecia areata and its classic exam finding?

Autoimmune non-scarring hair loss producing smooth, round patches of complete hair loss with "exclamation point" hairs at the margins and nail pitting.

What is trichotillomania?

Compulsive hair pulling producing irregular patches with hairs of varying lengths and no scale or inflammation.

What is telogen effluvium?

Diffuse non-scarring shedding 2–4 months after a physiologic stressor (illness, surgery, severe febrile illness, major weight loss); it is self-limited with full regrowth.

What is a kerion and how is it managed?

A boggy, tender, inflammatory mass from an intense host response to tinea capitis; treat with oral antifungals plus systemic corticosteroids to reduce scarring alopecia.

What is atopic dermatitis?

A chronic, relapsing, intensely pruritic inflammatory skin disease caused by skin barrier dysfunction (filaggrin mutations) and immune dysregulation.

What is the classic distribution of atopic dermatitis in infants versus older children?

Infants: face, scalp, and extensor surfaces (diaper area spared); older children and adolescents: flexural surfaces (antecubital and popliteal fossae), neck, wrists, and ankles.

What is the "atopic triad"?

Atopic dermatitis, asthma, and allergic rhinitis.

What is the cardinal symptom of atopic dermatitis?

Pruritus — "the itch that rashes"; without itch, the diagnosis should be questioned.

What is the cornerstone of atopic dermatitis management?

Liberal emollients, lukewarm bathing followed immediately by moisturizer ("soak and smear"), trigger avoidance, and topical corticosteroids for flares.

What non-steroidal topicals are used for sensitive areas like the face and eyelids?

Topical calcineurin inhibitors (tacrolimus, pimecrolimus) and crisaborole.

What is eczema herpeticum?

Disseminated HSV superinfection of eczematous skin — monomorphic punched-out vesicles/erosions with fever and malaise; a dermatologic emergency treated with systemic acyclovir.

What is the most common bacterial superinfection of atopic dermatitis?

Staphylococcus aureus — presents with honey-colored crusting, weeping, and pustules; dilute bleach baths reduce colonization.

What is erythema multiforme?

An acute, immune-mediated hypersensitivity reaction producing symmetric targetoid lesions, most often triggered by infection.

What is the most common trigger of erythema multiforme in children?

Herpes simplex virus; Mycoplasma pneumoniae is the second most common, especially in children.

What is the classic lesion of erythema multiforme?

A "target" or iris lesion with three zones — a dusky/bullous center, a pale edematous ring, and an erythematous outer rim — favoring the acral extremities and palms/soles.

How does EM major differ from EM minor?

EM major involves at least one mucosal surface; EM minor has no significant mucosal involvement.

How is erythema multiforme distinguished from SJS?

EM has typical raised target lesions with acral distribution and less than 10% BSA with minimal skin detachment; SJS has atypical flat targets, truncal predominance, prominent mucosal disease, and is drug-triggered.

What is the treatment for erythema multiforme?

Supportive care (antihistamines, topical steroids, oral rinses); treat the underlying trigger and consider suppressive acyclovir for HSV-associated recurrences.

What is lichen planus?

A T-cell mediated inflammatory disorder of the skin and mucosa producing pruritic, purple, polygonal, planar papules with fine white lines.

What are the "6 P's" of lichen planus?

Pruritic, Purple, Polygonal, Planar, Papules, and Plaques.

What are Wickham striae?

Fine, lacy, white reticular lines overlying lichen planus papules or on the buccal mucosa — a classic diagnostic clue.

What is the Koebner phenomenon and which conditions show it?

New lesions appearing at sites of trauma or scratching; seen in lichen planus, psoriasis, vitiligo, and verrucae.

What systemic infection is associated with lichen planus?

Hepatitis C — screening is reasonable, particularly with oral lichen planus.

What is the treatment for lichen planus?

High-potency topical corticosteroids and antihistamines for pruritus; systemic steroids or phototherapy for widespread disease. It is usually self-limited over 1–2 years.

What is pityriasis rosea?

A benign, self-limited papulosquamous eruption thought to be triggered by HHV-6/HHV-7 reactivation, most common in older children and young adults.

What is the herald patch?

A single, larger (2–10 cm) salmon-colored oval plaque with a trailing collarette of scale that precedes the generalized eruption by 1–2 weeks.

What is the classic distribution of the pityriasis rosea eruption?

Oval, scaly plaques along the skin cleavage lines of the trunk producing a "Christmas tree" or "fir tree" pattern; the face, palms, and soles are typically spared.

What critical diagnosis must be excluded in a patient with a pityriasis rosea–like rash?

Secondary syphilis — check RPR/VDRL, especially in sexually active adolescents or when the palms and soles are involved.

What is the treatment and prognosis of pityriasis rosea?

Reassurance; it self-resolves in 6–8 weeks. Antihistamines, topical steroids, or emollients relieve pruritus.

What is seborrheic dermatitis?

A chronic inflammatory dermatitis of sebaceous-rich areas associated with Malassezia species, producing greasy yellow scale on an erythematous base.

What is seborrheic dermatitis called in infants and when does it occur?

"Cradle cap" — greasy, yellow, adherent scale on the scalp appearing in the first 3 months of life; it is typically non-pruritic and self-limited.

What is the classic distribution of seborrheic dermatitis?

Scalp, eyebrows, nasolabial folds, retroauricular areas, chest, and intertriginous/diaper areas.

How is infantile seborrheic dermatitis distinguished from atopic dermatitis?

Seborrheic dermatitis is non-pruritic, greasy, involves the diaper area, and appears earlier (

What is the treatment of infantile seborrheic dermatitis?

Emollients/mineral oil with gentle scale removal and frequent shampooing; low-potency topical hydrocortisone or topical ketoconazole for persistent cases.

What is the treatment of adolescent seborrheic dermatitis?

Antifungal shampoos (ketoconazole, selenium sulfide, zinc pyrithione) plus low-potency topical corticosteroids for flares.

What is Stevens-Johnson syndrome?

A severe, drug-induced mucocutaneous reaction with epidermal necrosis and detachment involving less than 10% of body surface area plus at least two mucosal surfaces.

What BSA percentages define SJS, SJS/TEN overlap, and TEN?

SJS <10% BSA detachment;

SJS/TEN overlap 10–30%;

TEN >30%.

What are the most common drug triggers of SJS in children?

Sulfonamides, anticonvulsants (lamotrigine, phenytoin, carbamazepine, phenobarbital), NSAIDs, and allopurinol; Mycoplasma pneumoniae is a key infectious trigger in children.

What is the classic prodrome and skin finding of SJS?

1–3 days of fever, malaise, sore throat, and painful/burning eyes, followed by dusky macules with atypical flat targets that blister, plus painful erosions of the oral, ocular, and genital mucosa.

What is Nikolsky sign?

Lateral pressure on skin causes the epidermis to shear off — positive in SJS/TEN and staphylococcal scalded skin syndrome.

What is the management of SJS?

Immediate withdrawal of the offending drug, admission to a burn/ICU unit, aggressive fluid and electrolyte management, wound care, pain control, and ophthalmology consultation to prevent ocular sequelae.

What is tinea versicolor?

A superficial fungal infection caused by Malassezia furfur producing hypo- or hyperpigmented scaly macules on the trunk and upper arms.

What is the classic clinical presentation of tinea versicolor?

Well-demarcated oval macules with fine scale on the chest, back, and shoulders that fail to tan, becoming more noticeable in summer; usually asymptomatic or mildly pruritic.

What is the KOH finding in tinea versicolor?

"Spaghetti and meatballs" — short hyphae with clusters of round yeast spores.

What does a Wood's lamp show in tinea versicolor?

Yellow-gold or coppery-orange fluorescence (present in only a minority of cases).

What is the treatment of tinea versicolor?

Topical selenium sulfide, ketoconazole shampoo, or topical azoles; oral fluconazole or itraconazole for extensive or refractory disease. Pigment changes take months to normalize.

Why is oral terbinafine ineffective for tinea versicolor?

It does not achieve adequate concentrations in the stratum corneum against Malassezia — use azoles instead.

What is toxic epidermal necrolysis?

The most severe form of the SJS/TEN spectrum, with full-thickness epidermal necrosis and detachment of greater than 30% of body surface area.

What is the primary cause of TEN?

Medications — sulfonamides, anticonvulsants, NSAIDs, allopurinol, and antiretrovirals.

What is the SCORTEN score?

A validated mortality prediction tool for TEN based on age, malignancy, heart rate, BSA detached, BUN, bicarbonate, and glucose.

What are the major causes of death in TEN?

Sepsis (S. aureus and Pseudomonas), massive fluid and electrolyte loss, and multiorgan failure.

How is TEN distinguished from staphylococcal scalded skin syndrome (SSSS)?

TEN involves the mucous membranes, shows full-thickness epidermal necrosis on biopsy, and is drug-induced; SSSS spares mucosa, splits at the granular layer, affects infants/young children, and is toxin-mediated.

What is the management of TEN?

Stop the offending drug, transfer to a burn unit, provide meticulous supportive/wound care, fluid resuscitation, and ophthalmology consult; adjunctive IVIG, cyclosporine, or etanercept may be considered. Avoid prophylactic systemic antibiotics.

What is a cutaneous abscess?

A localized collection of pus within the dermis or subcutaneous tissue, presenting as a fluctuant, erythematous, tender nodule.

What is the most common organism causing skin abscesses in children?

Staphylococcus aureus, with MRSA being a leading cause of community-acquired abscesses.

What is the definitive treatment for a simple cutaneous abscess?

Incision and drainage — antibiotics alone are inadequate.

When should antibiotics be added after incision and drainage?

Systemic symptoms/SIRS, surrounding cellulitis, immunosuppression, extremes of age, abscess >2 cm, failure of initial drainage, or high-risk location (face, hand, genitalia).

Which oral antibiotics cover community-acquired MRSA?

Trimethoprim-sulfamethoxazole, clindamycin, or doxycycline (age ≥8 years).

What imaging modality helps distinguish an abscess from cellulitis when the exam is equivocal?

Point-of-care ultrasound — shows an anechoic/hypoechoic fluid collection with posterior acoustic enhancement.

What is cellulitis?

An acute bacterial infection of the deep dermis and subcutaneous tissue producing poorly demarcated erythema, warmth, swelling, and tenderness.

What are the most common pathogens causing cellulitis?

Beta-hemolytic streptococci (especially Group A Strep) and Staphylococcus aureus.

How does erysipelas differ from cellulitis?

Erysipelas involves the superficial dermis and lymphatics with sharply demarcated, raised borders and is almost always caused by Group A Streptococcus.

What is the empiric outpatient treatment for non-purulent cellulitis?

Cephalexin or another beta-lactam targeting streptococci; add MRSA coverage (TMP-SMX or clindamycin) if purulence, abscess, or risk factors are present.

What red flags suggest necrotizing fasciitis rather than cellulitis?

Pain out of proportion to exam, rapid progression, systemic toxicity, crepitus, bullae, skin anesthesia, and dusky/necrotic skin — a surgical emergency.

What organism should be considered in periorbital or facial cellulitis in an unimmunized child?

Haemophilus influenzae type b; also evaluate for orbital cellulitis with CT if there is proptosis, pain with EOM, or vision change.

What is impetigo?

A highly contagious superficial bacterial skin infection of the epidermis, most common in preschool and school-aged children.

What are the causative organisms of impetigo?

Staphylococcus aureus (most common) and Streptococcus pyogenes.

What is the classic appearance of non-bullous impetigo?

Honey-colored, golden crusted erosions, typically around the nose and mouth.

What causes bullous impetigo?

Staphylococcus aureus exfoliative toxin, producing flaccid bullae that rupture leaving a collarette of scale.