Diseases you are expected to have a general understanding of by the end of your rotation:



Acne Vulgaris

Moderate mixed comedonal & inflammatory acne with scarring

Clinical Presentation

– Affects areas of abundant sebaceous glands (e.g., face, neck, upper trunk, upper arms) 

– Classification based on morphology: comedonal (open – “blackheads” vs closed – “whiteheads”), inflammatory (papules & pustules), nodulocystic (nodules & cysts)

– Also classify by severity & presence of scarring

– Post-inflammatory hyperpigmentation: macules that persist after inflammation, more common in darker skin types

– Hormonal acne: normal serum hormone levels, often perioral lesions or along jaw line, commonly post-adolescent women w/premenstrual flare-up


– Disorder of pilosebaceous follicles that begins with “clogged pores” (comedones)

– Contributing factors: androgens, excess sebum production, P. acnes activity, follicular hyperkeratinization 

Treatment: Target pathogenesis, treat cystic or scarring acne aggressively to prevent scarring!


– Topical retinoids (ex: tretinoin/Retin-A, adapalene/Differin): vit A derivatives; normalize desquamation of follicular epi (corrects hyperkeratinization), increase skin turnover rate 

Benzoyl peroxide (BP): antibacterial & comedolytic, free radicals oxidize P. acnes cell wall 

– Topical abx: e.g., clindamycin 1%; controls C. acnes; use w/BP to prevent abx resistance 


– Oral abx: controls C. acnes colonization of skin & follicles; 1st line = doxy, minocycline (SE: vertigo, dizziness, hyper-pigmentation), TCN (SE: GI, photosensitivity), ; 2nd line = Macrolide; use w/BP to prevent abx resistance

– Oral isotretinoin (Accutane): retinoic acid derivative; for severe, nodulocystic acne failing other therapies; SE: xerosis, cheilitis, LFT abnormalities, hypertriglyceridemia; teratogenic (contraindicated in pregnancy, females on 2 forms of contraception, monthly pregnancy test); never use w/TCN (increases pseudotumor cerebri risk)

– Hormonal therapies: spironolactone (androgen-receptor blocker, inhibits 5-alpha reductase) or oral contraceptives (FDA-approved for acne: Yaz, Ortho Tri-cyclen, Estrostep)

– Topical agents take 2-3 mo to see effect; continue therapy for at least 8wks before eval tx response (counsel patients on this)

Treatment approach based on subtype:

Atopic dermatitis (AD)


Clinical Presentation:

– More common in children 

– May progress from AD in early infancy to developing allergic rhinitis, food allergy and asthma (atopic march)

– Appearance and distribution varies based on age:

  • Infants: erythematous papules + vesicles on face + head, diaper area, extensor surfaces

  • Older children and adults: erythematous and scaly or lichenified plaques on neck, face, upper chest, and flexor surfaces (esp. antecubital and popliteal fossa), may have fissuring and hemorrhagic crust

– Primary sx = pruritus → scratching can lead to “itch-scratch” cycle that exacerbates the disease

– Thickening of epidermis with accentuated skin lines due to chronic scratching = lichenified

– May be complicated by skin infections

  •  E.g., Eczema herpeticum (widespread vesiculopustular eruption due to HPV infxn of atopic dermatitis affected skin) 

  • Also increased risk of secondary bacterial infections (staph and group A strep)

Pathogenesis: disruption of skin barrier and immune dysfunction, food allergy can contribute


– Moisturize (esp. after bathing), avoid irritants (soaps, cleansers)

– To target inflammation: topicals (steroids, tacrolimus, pimecrolimus)

  • Start with lower potency, increase potency if needed (more cautious for children)

– To target itch: antihistamines

– Bleach baths can help reduce severity

– Avoid food allergens if applicable (triggers 20-30% of patients with moderate to severe AD)

– If topicals inadequate, systemic therapies include: phototherapy, immunomodulators (azathioprine, cyclosporine, mycophenolate mofetil, methotrexate), dupilumab

Clinical Pearls:

– Hx questions: hx of atopic conditions?

– Eczema = nonspecific term for inflammatory skin conditions with pruritus, erythema and scaling, AD is a type of eczema

Contact dermatitis 

Allergic Contact Dermatitis (ACD)

Rhus Dermatitis

Irritant Contact Dermatitis (ICD

Contact dermatitis types: allergic contact dermatitis (ACD), irritant contact dermatitis (ICD), 

Clinical Presentation

– Acute = erythema, vesiculation, pruritus

– Chronic = dryness, scaling, lichenification, fissuring, pruritus  

ACD: pruritic, erythematous, scaly edematous plaques w/vesicles/bullae (common ex: Rhus dermatitis aka poison ivy) 

ICD: causes eruption in most people who come in contact with substance; may be from severely toxic substances or repeated application of mildly irritating substances (soaps, detergents); high risk areas include face, neck, scrotum, dorsal hands; erythema, chapped skin, dryness & fissuring; if severe → edema, exudate, tenderness, painful bullae  

Pathogenesis: reaction to externally applied substance

– ACD is a delayed hypersensitivity rxn


– Avoid offending substance

– Mostly supportive care (topical steroids, antihistamines, oatmeal soaks/calamine lotion)

– In mild-to-moderate cases, topical steroids of medium to strong potency for limited course

– Severe cases may require oral steroids

– In chronic cases, may need patch testing to ID allergen 

– For face: class 6 & 7 steroids (e.g., desonide) can safely be used intermittently during flares

– Chronic cases or dermatitis involving >10% of BSA should be referred to dermatologist 

Clinical Pearls:

– Shape, configuration & location of dermatitis are useful clues in ID-ing allergen (e.g., linear streaks in Rhus dermatitis are from linear contact of plants)

Geometric shape of rash often points to contact dermatitis

– Hx questions: daily skin care routine, topical products, occupation/hobbies, regular & occasional exposures (e.g., lawn products, animal shampoos)

Seborrheic dermatitis

Clinical Presentation:

– Very common

– Patient may complain of dandruff

– Description: fine white scale of the scalp +/- erythema, poorly defined patches and plaques with mild to moderate erythema and yellowish, greasy scaling

– Distribution: scalp, eyebrows, face, ears (areas with hair + numerous sebaceous glands), can also affect intertriginous areas, axilla, groin, inframammary folds


–  Inflammatory reaction to Malassezia yeast (part of natural skin flora)


– OTC: Head and Shoulders, Nizoral, Selsun Blue

– Prescription strength shampoos: ketoconazole, zinc pyrithione, selenium sulfide

– If extremely itchy, can also give clobetasol solution for scalp, hydrocortisone cream, tacrolimus

Clinical Pearls:

Ddx: tinea capitis, atopic dermatitis, psoriasis, rosacea, perioral dermatitis

– Consider checking HIV status if very severe


Verruca vulgaris

Verruca plana 

Palmoplantar verruca

External genital warts

Many different types (depending on type of HPV)

verruca vulgaris (common wart): hyper-keratotic, exophytic, dome-shaped papules/nodules; commonly on fingers, dorsal hands, knees/elbows; punctate black dots represent thrombosed capillaries; may spread w/trauma

verruca plana (flat wart): skin-colored or pink; smooth-surfaced, slightly-elevated, flat-topped papules; commonly on dorsal hands, arms, face (exposed surfaces)

palmoplantar verruca: thick, endophytic papules; mosaic warts (plantar warts coalescing into large plaques); can develop thick callus over & around wart; may be painful   

external genital warts: not hard & hyper-keratotic (unlike common warts); papillomatous or sessile, exophytic papules or large confluent plaques


– HPV – infects basal keratinocytes of cutaneous & mucosal epi. Transmitted by skin-to-skin contact or contaminated surfaces/objects. 


– Mechanism often destructive &/or stimulates immune system, no specific HPV therapy

– Almost always need multiple txs for any modality, chance of spontaneous resolution at 2yrs > 75%

Common therapies:

– Cryotherapy: liquid nitrogen; in clinic may first pare down lesion with scalpel, then treat with liquid nitrogen

– Salicylic acid 17-40%: chemically irritating, destructive; apply under occlusion; change every 1-2d; takes several weeks, OTC formulations available

DCNB = dinitrochlorobenzene

IL = intra-lesional

– HPV vaccination can reduce genital warts & HPV-associated malignancies but does not prevent or treat common warts (different HPV types)

Fungal infections – Tinea Aka “ringworm


Clinical presentation:

Different names based on location on body:

  • tinea corporis: body

  • tinea capitis: scalp

  • tinea barbae: beard area

  • tinea cruris: inguinal folds

  • tinea pedis: feet

  • hands (palms primarily): tinea manuum

  • majocchi granuloma: follicle

  • onychomycosis: nails

– Annular erythematous, scaling plaques, may have erythematous border (+/- papules, vesicles and crusting, indicates active disease) with central clearing 

– May be macerated in intertriginous areas

– May be itchy

Pathogenesis: dermatophyte infection


– For limited, localized disease – topical terbinafine, clotrimazole, econazole

– Extensive disease, tinea capitis and onychomycosis – may require oral antifungals

Clinical Pearls:

– Can be particularly severe for immunosuppressed

– DDx: nummular eczema, granuloma annulare, fixed drug eruption, tinea versicolor, lyme disease, contact dermatitis, psoriasis, lichen planus, seborrheic dermatitis, scabies, mycosis fungoides, and more

– Dx: scrape the scaly, active border, put on glass slide, place drop of KOH solution and look under microscope for branching fungal hyphae

Fungal infections – candida intertrigo

Clinical presentation:

Intertrigo = inflammation of the skin folds (inframammary folds, gluteal cleft, inguinal creases, under pannus), can be complicated by candida yeast infection

– Sx: burning

Classic description: sharply defined beefy red plaques involving the skin folds with surrounding satellite macules


 – Candida infection


– To prevent: keep intertriginous areas dry, clean and cool, weight loss if obese, loose cotton clothing

– Topical antifungals: imidazole (miconazole, clotrimazole, econazol) – more effective than nystatin but can burn, also treats dermatophytes; nystatin – has powder (good for keeping dry) and ointment formulation

– Low strength topical steroids or tacrolimus can be used if itchy and burning

Tinea versicolor


Pityriasis versicolor

Clinical Presentation:

– Asymptomatic

– Description: hyperpigmented or hypopigmented macules and patches with fine scale, particularly on the trunk and arms

– May fluoresce under wood’s lamp

Pathogenesis: benign superficial fungal infection due to Malassezia (yeast)


– First line: topicals – shampoo (ketoconazole, selenium sulfide, or zinc pyrithione) to body, or imidazole creams (clotrimazole, econazole) for 1-4 weeks 

– For widespread disease: oral antifungals (fluconazole, itraconazole)

– Skin color changes may resolve within 1-2 months of tx, but pts with darker skin may have post inflammatory hyperpigmentation

– Commonly recurs – can use antifungal shampoos on body several times a month, oral antifungals 1x/month for maintenance

Clinical pearls:

– Ddx: confluent and reticulated papillomatosis, tinea, atopic dermatitis, pityriasis rosea, guttate psoriasis

– Dx: Skin scraping – scrape the scale, put on glass slide and cover with coverslip, add KOH to edge of coverslip, looks for Malassezia hyphae and spores (spaghetti and meatballs”)

Herpes simplex

Clinical presentation: 2 strains: HSV-1 (favors mouth and nose) and HSV-2 (favors genitalia and buttocks)

– Primary HSV-1 usually occurs in children and is generally subclinical, but 10% have acute gingivostomatitis: fever, malaise, bleeding, painful gums, pain w/eating, pharyngitis, malodor

– Primary HSV-2 occurs most often through sexaul contact; primary genital herpes: headache, fever, malaise, pain, dysuria

– Prodrome: itching, burning, tingling, pain preceding skin lesion 

– Painful, grouped vesicles on erythematous base → vesicles become pustules → rupture (may only see erosions with bright red border)

– Tends to recur in the same place

– Herpetic whitlow = HSV on fingers

– In patients with HIV or immunosuppression, can get severe perianal HSV


HSV-1 and HSV-2 (herpes simplex virus)

– Spread by contaminated body fluids during viral shedding 

– Lifelong latency in dorsal root ganglia; reactivation spontaneous or triggered (by trauma, UV exposure, illness, immunosuppression, etc)


– Oral acyclovir or valacyclovir – start immediately at first sign of recurrence or prodromal sx

Clinical pearls:

– HSV erosions often have a “punched out” appearance

– Neonatal HSV acquired in utero, perinatally or postnatally can cause CNS and disseminated infections (high mortality rate)

Varicella zoster

Clinical presentation:

– Grouped vesicles on erythematous base in a dermatomal distribution (unilateral)

– Prodrome: vesicles preceded by pain, burning and/or itching

– More common in adults

– If immunocompetent: usually occurs only once (unlike HSV, which tends to recur)

– Some may develop postherpetic neuralgia: persistent pain after skin sx have resolved 


– Recrudescence of latent varicella zoster virus (VZV) in pts previously infected w/VZV (i.e had chicken pox)


– Can prevent with Zostavax vaccine (indicated if >60 years old)

– Acyclovir (can decrease risk of postherpetic neuralgia)

Clinical pearls:

– Rarely bilateral!

If on face/head, ask about sensory involvement and examine tip of nose (may indicate involvement of cranial nerve V1, which can cause scarring of cornea and conjunctiva)


– Common bacterial infection of the soft tissues (deep dermis and subcutaneous tissue)

Clinical presentation

– Unilateral erythema, pain, warmth and swelling with poorly demarcated borders, if severe, may have vesicles, bullae, ecchymoses and petechiae

– Can also have fevers, chills, and malaise

– Most commonly affects the extremities in adults


– Immunocompetent adults: S. aureus and strep pyogenes

– Immunocompetent kids: S. aureus

– Immunocompromised, including DM: mix of gram + and gram – aerobes and anaerobes

– Spread: direct inoculation for immunocompetent; hematogenous for immunocompromised

– Risk factors: skin trauma, piercings, IV drug use, tinea pedis, peripheral vascular disease and venous stasis, immunosuppression, lymphatic damage (e.g. s/p lymph node dissection, vein harvest for CABG)


– First assess for purulence → dictates empiric bugs to cover

1. Purulent (cover for staph)

– Oral: Empiric MSSA and MRSA or if known MRSA: bactrim, doxycycline or clindamycin x 5-10 days; Definitive MSSA: dicloxacillin or keflex (cephalexin) x 5-10 days

– IV: Empiric (covers MRSA): vancomycin or linezolid; Definitive MSSA: Ancef or clindamycin

– Drain any abscesses

2. Non-Purulent (most likely strep or MSSA)

– Oral: dicloxacillin, augmentin (amoxicillin clavulanate), keflex (cephalexin), penicillin (or clindamycin if penicillin allergy), x 5-10 days

– IV (if inpatient and SIRS): Ancef (cefazolin) or clindamycin

Clinical Pearls:

– If bilateral, it is not cellulitis! (common inpatient consult)

– Important to differentiate from necrotizing fasciitis (surgical emergency) → look for pain out of proportion on exam, erythema evolving to dusky gray, “dirty dishwater” discharge, crepitus, edema beyond erythematous areas, rapid progression despite abx treatment

  • If you suspect necrotizing fasciitis, get a surgical and/or ID consult!

– Mark edge of erythema and monitor q4-6 hours for progression or unresponsiveness

– Hx of risk factors to assess for: immune status, comorbidities, hx or possible causes of skin barrier disruption, hx of cellulitis, MRSA risk factors (long term care, IVDU, hx of MRSA, indwelling catheter, recent admission, prisoners, military service)

– Exam: check vitals (evidence of sepsis), evidence of port of entry such as a wound, lymphangitis (red streaking), palpable lymph nodes, crepitus and other evidence of nec fasc

– Labs: CBC, blood cultures (esp. for immunocompromised), wound culture of any drainage (assess for MRSA, but otherwise swab of superficial skin not helpful)


– Superficial skin infection common in children and teenagers

Clinical presentation:

– Starts as erythematous vesicles or pustules (won’t see this usually) → superficial erosions with a “honey-colored” crust 

– Description: honey-colored crusted papules and plaques, sometimes with small inflammatory halo

– Bullous impetigo: exotoxin from the bacteria (usually staph) targets desmosomes, causing fragile, clear or cloudy bullae that rupture and form papules with thin, varnish-like crust and erosions. More frequently in children.


– Usually staph, but can also be caused by strep


– If localized: warm soaks and topical mupirocin 

– If widespread: systemic antibiotics to target MSSA (kids: 7 days of cephalexin or erythromycin; adults: same as kids or dicloxacillin) or if MRSA risk factors (kids: 7 days of clindamycin; adults: same as kids or doxycycline or bactrim)

Clinical pearls:

– Hx questions: Fevers, chills? In contact with anybody else with these sx? (can be very infectious)

– Dx: Consider wound culture

Alopecia areata


Clinical Presentation

– Round, patchy areas of nonscarring hair loss (usually limited to 1 or 2 small patches) of usually scalp, but can also affect eyebrows, eyelashes, beard, etc.

– Alopecia universalis: loss of all scalp and body hair

– Sudden onset

– Higher incidence if have Down syndrome or other autoimmune diseases (esp. thyroid)


– T-cell mediated autoimmune disease of hair follicles → non-scarring hair loss


– In most, hair will eventually spontaneously regrow, but unpredictable course, recurrences common

– Mild: topical mid-to-high potency steroids

– Mild-to-moderate (<25% involvement): intralesional corticosteroids to the scalp

– Alternative: topical steroids and anthralin cream; topical immunotherapy with squaric acid or diphencyprone (induces contact dermatitis)

Clinical pearls: 

– DDx: other non-scarring alopecias: trichotillomania, telogen effluvium, tinea capitis, androgenetic alopecia

– On exam, may see exclamation point hairs – hairs that are broad and ragged proximally with tapering base, positive hair pull test (gently pulling hair with fingers) indicates disease is active


Pustular Psoriasis

Inverse/Flexural Psoriasis

Guttate Psoriasis

Palmoplantar Psoriasis

Psoriatic Erythroderma

Plaque Psoriasis

Psoriatic Arthritis

Chronic immune-mediated multisystem disease w/predominantly skin & joint manifestations

Clinical presentation:

– Bimodal age distribution: (20-30, 50-60)

– Waxes & wanes; few spontaneous remissions

– Classified by morphology (diff. types may require diff. tx): 

  • Plaque: most common; scaly, erythematous patches, papules, plaques with silvery scale; may Koebnerize

  • Inverse or flexural: erythematous patches in skin folds

  • Guttate: dew drop-like, 1-10mm salmon-pink papules w/fine scale; can be triggered by streptococcal pharyngitis

  • Erythrodermic: generalized erythema of nearly the entire body w/scaling; assoc. w/fever, chills, malaise; may need hospitalization

  • Pustular: pustules often triggered by corticosteroid withdrawal, can be life-threatening if generalized + should be hospitalized

Psoriatic Arthritis (PsA): arthritis of joints & surrounding ligaments & tendons (dactylitis, enthesitis); psoriasis; nail changes

Psoriatic onychodystrophy: possible in all psoriasis types, but greater risk in PsA; nail pitting, splitting, subungual hyperkeratosis, oil drop sign


– Rapid proliferation in keratinocytes + activated immune system (mostly T-cell mediated)

– Triggered by environment in patients with genetic disposition


– For localized psoriasis (<5% body surface area): topical steroids

– First line agents: high potency topical steroids (clobetasol, halobetasol, betamethasone dipropionate), then maintenance therapy w/topical VitD analog (calcipotriene, calcitriol)

– For thin sites (face, neck, skin folds): low potency topical steroid (desonide, hydrocortisone, triamcinolone)

– Local cutaneous SEs w/topical steroid overuse: skin atrophy, telangiectasia, striae distensae, acne, folliculitis, purpura

– For moderate-to-severe disease, supplement topical w/systemic tx: oral meds (methotrexate, acitretin, cyclosporine, apremilast), biologic agents (TNF-a inhibitor, IL 12/23 inhibitor, IL-17 inhibitor), UVA/UVB phototherapy

– AVOID oral steroids as they can severely flare psoriasis once discontinued 

– If psoriatic arthritis is suspected, refer to rheumatologist 

Clinical pearls:

– Hx questions: (1) Cardiovascular comorbidities, health-related behaviors (smoking, alcohol); (2) How psoriasis affects daily living and their experiences with previous treatments, (3) Screen for psoriatic arthritis – joint pain, morning stiffness >1 hour

– Exam: examine joints, tendons (for enthesitis), dactylitis, nails for pitting

– If remove scale, can get pinpoint bleeding = Auspitz sign

Lichen planus (LP)

Wickham striae

Clinical Presentation:

– 6 P’s: planar, polygonal, pruritic, purple papules and plaques

– Most commonly on volar wrists and flexural surfaces, but can also involve other areas on body, mucous membranes, nails

– May have fine grayish white steaks = Wickham striae

– Can Koebnerize (lesions induced by trauma) – more commonly distributed in high trauma/friction areas

– Oral LP: white, lacy plaques with violaceous base on tongue or buccal mucosa, may also have Wickham striae (white reticular plaques)

– Lichen planopilaris (follicular LP) = follicle-based scalp papules, can cause scarring alopecia


– Autoimmune T-cell attack of basal keratinocytes 

– Can be drug induced


– Most will self resolve in 1-2 years

– Oral LP needs to be followed because can increase risk of oral SCC

– For itch: oral antihistamines, topical antipruritic like Sarna lotion

– First line: topical steroids 

– If drug-induced, stop the medication

Clinical Pearls:

– Exam: if you think you see LP, check mouth for Wickam striae

– If suspect drug-induced, obtain drug hx. Can occur several months to years after offending drug is started

Pityriasis rosea

Clinical presentation:

– Cutaneous eruptions lasting days to weeks mostly in adolescents & young adults 

– Close f/u in pregnant women recommended

– Starts as solitary scaly, pink or flesh-colored plaque (“herald patch”) 1st on trunk usually, then eruption of multiple discrete oval, erythematous, scaly plaques & patches along skin cleavage lines (esp. trunk & upper extremities); usually asymptomatic, but occasionally pruritic  

– Constitutional symptoms before eruption (e.g., fever, headache, cough, arthralgia)

– Drug-related pityriasis rosea-like lesions appear red-violet in color w/o “herald patch”


– Unknown, but possibly associated w/systemic reactivation of HHV-6 & HHV-7


– Assess hx of the following drugs: captopril, clonidine, omeprazole, NSAIDs, metronidazole, terbinafine, lamotrigine → cause eruptions that resemble pityriasis rosea 

– Typically self-limiting (w/in 8wks), recurrence rare 

Actinic keratosis (AK) 

Clinical presentation:

Gritty, erythematous papules distributed on sun-exposed areas

– May be symptomatic (tender)


Etiology: UV-induced p53 tumor suppressor mutations

Risk factors: age, fair skin/eyes/hair, immunosuppression, genetic syndromes 

– Part of a disease spectrum: photo-damaged skin → AK → SCC in situ (Bowen’s disease) → invasive SCC 

– Precancerous – potential to transform into cancer (almost always SCC), but not all AKs progress to SCC 


Factors to consider for tx: # & thickness of lesions, anatomic location, individual tolerance of specific tx, skin type (> dyspigmentation in skin of color), capability & likelihood of compliance, ability to cover cost  

Therapy types: localized (individual lesions) vs. field (multiple AKs over anatomic area)

Localized: liquid nitrogen cryotherapy, curettage +/- electrocautery

Field: topical 5-fluorouracil, imiquimod, ingenol mebutate gel, diclofenac gel, photodynamic therapy (PDT)

– Due to increased risk of skin cancers, should have regular skin exams every 6-12mo

Clinical pearls:

– Dx cautiously in >6mm lesions (may be SCC in situ or superficial BCC)

– On exam, helpful to feel lesions for gritty texture

Squamous cell carcinoma

– Second most common skin cancer in the world

Clinical Presentation:

– Can start as actinic keratosis that progresses in dysplasia

– Rate of metastasis: low, 4% (usually to regional lymph nodes)

Hyperkeratotic papule or nodule, may be smooth or plaquelike, exophytic or papillomatous

– May have secondary changes like scale, crust, erosion and ulceration. May be painful or tender.

– Growth and progression varies – some grow slowly while others progress rapidly

– Usually on sun-exposed areas (head, neck, forearms, top of scalp, dorsal hands)


– Photo-damaged skin → AK → SCC in situ (Bowen’s disease) → invasive SCC

Risk factors: lighter skin types, red hair, hx of sun/UV exposure, smoking, solid organ transplantation and other reasons for immunosuppression (HIV/AIDS), can also develop in chronic non-healing wounds + dermatoses such as discoid lupus, lichen planus, lichen sclerosus and HPV


– First need to dx (perform shave biopsy)

– Tx depends on tumor characteristics and patient

Generally surgical treatment – excision, Mohs (if high risk features or cosmetically sensitive area), curettage and electrodessication (small, low-risk primary SCC)

– If surgery contraindicated, radiation is an option but lower cure rates, possibility for long term sequelae

Prevention of SCC in pts prone to many SCCs: photodynamic therapy, oral nicotinamide, celecoxib, oral retinoids (esp. in transplant patients)

– Follow-up: total body skin exams regularly, patient at higher risk of other cutaneous malignancies

Clinical pearls:

– DDX: Hypertrophic actinic keratosis, Bowen’s disease, BCC, verruca vulgaris, condyloma acuminatum, keratoacanthoma, amelanotic melanoma, irritated seborrheic keratosis, lymphoma cutis, prurigo nodularis

– Hx questions: Assess for risk factors such as previous hx of skin cancer, lots of sun exposure, immunosuppression

Basal cell carcinoma (BCC)

Nodular BCC 

Superficial BCC

– Most common skin cancer worldwide

Clinical presentation: 

– Common clinical traits: pink/white color, central ulceration, rolled border, telangiectasias 

– Different subtypes: (1) morpheaform/infiltrative/sclerotic (white plaque w/scar-like areas), (2) nodular (most common; pearly papule/nodule; head & neck), (3) nodular, ulcerated (can result in scab), (4) pigmented (globules of pigment or maple leaf structures on dermoscopy), (5) superficial (pink patch w/fine scales) 

– Dermoscopy: pigment, arborizing telangiectasias

– Locally invasive; rarely metastasizes; increased risk of developing other skin cancers


– Arises from basal layer of epidermis

– Etiology: UV damage; PTCH1 (tumor suppressor gene) loss of function mutation

– Risk factors: fair skin (types I, II), severe sun damage, male, age >60, immunosuppression, genetics


Surgical tx options: curette & desiccation (small superficial & nodular BCC on trunk or extremities), cryosurgery w/liquid nitrogen, excision (3-4mm margins), Mohs (complete histologic analysis of 100% of tumor margins, maximal tissue conservation; lower recurrence rates; best for aggressive subtypes, large tumors, ill-defined margins, recurrent tumors)

Non-surgical tx options (superficial or nodular subtypes): Imiquimod 5% cream, 5-Fluorouracil 5% cream, photodynamic therapy, radiation

– Most agree f/u every 6-12 mo for 2 yrs after positive dx

– Ask patients to do regular skin self-exams for following warning signs: open sore, reddish patch/irritated area, shiny bump/nodule, pink growth, scar-like area

Pigmented lesions (nevi)

Congenital Nevus

Acquired Nevus

Atypical Nevus

– Melanocytic nevi = moles

Clinical presentation:

Congenital nevus: dome-shaped; mammillated (small protuberances); hypertrichosis (increase in density and coarseness of hair); if small, then benign

Acquired nevus: mostly in early childhood in sun-exposed areas; appearance differs by age (early childhood = brown macules & papules; late childhood = brown papules; adults = skin-colored soft papules); change doesn’t necessarily indicate malignancy; if >100 common acquired nevi, then higher risk for melanoma 

Atypical nevus: 3 of 5 criteria: poorly defined borders, irregular borders, irregular pigment (tan, brown, black, pink; “fried egg” appearance), background erythema, >5mm 

Spitz nevus: melanocytic nevus in pediatric patients; mostly benign; commonly on face; may have surface telangiectasias; may be pigmented 

Congenital nevi: small & medium-sized <1% risk of melanoma (excision is not standard); large-sized have slightly higher risk (<5%) & should be referred

Atypical nevi: higher risk of melanoma; biopsy when suspicious; refer for periodic evals  


– Biopsy if: pigment changes, changes in diameter/border, bleeding, persistent pruritus, new lesion at >50yo, “ugly duckling”

Clinical pearls:

– To evaluate concerning pigmented lesions, ask: (1) Has it remained about the same for the last year or so? (2) Is it symmetric, with distinct borders & primarily 1 color? (3) Is it relatively similar to other moles on the patient? (if yes to all 3, then likely benign)

– Assess ABCDEs: asymmetry, borders irregular, color varies with multiple shades, diameter > 6mm, evolving

Malignant melanoma

Clinical presentation:

– Patient may report new (most develop de novo), growing, bleeding, itching lesion, but usually asx

– Various types: superficial spreading, lentigo maligna, nodular, acral lentiginous, subungual, amelanotic

– Description: irregularly shaped pigmented macule, papule or plaque

– ABCDEs: asymmetry, borders irregular, color varies with multiple shades, diameter >6mm, evolving

-“Ugly duckling” sign: “nevus” that looks different from others, increased suspicion for malignancy

– Risk factors: older age, fair skin, blue eyes, red or blond hair, > 25 acquired nevi &/or >5 atypical nevi; 2/+ 1st degree relatives w/melanoma hx, personal hx of melanoma, UV exposure (blistering sunburns, indoor tanning), immunosuppression


– Cancer of melanocytes and nevus cells

– UVA and/or UVB exposure

– Some familial/genetic basis


– Dx with biopsy (excisional or deep shave)

– Prognosis correlated with depth of invasion/tumor thickness (Breslow thickness: measures tumor thickness) 

– Ulceration + metastasis confer worse prognosis

– Definitive treatment: wide surgical excision (if not metastatic)

– For metastatic: chemotherapy, radiation, immunotherapy, etc.

– Follow-up interval with dermatologist based on stage of melanoma

Clinical Pearls: 

– DDX: benign nevus, SK, lentigo, pigmented BCC

– Hx questions: (1) FH of melanoma, other skin cancers, other neuroendocrine cancers such as pancreatic CA; (2) Risk factors? 

– Educate patients about self skin exams

Seborrheic keratosis

– Common benign neoplasm of epidermis

Clinical presentation

– Waxy, “stuck on” papules or plaques, usually well-circumscribed

– May look verrucous (“wart like”)

– Color can be variable 

– Asx, but if irritated or traumatized may become itchy or painful


– Benign with no malignant potential – no need to treat

– If inflamed, can treat with cryotherapy

Clinical Pearls:

– DDX: melanoma, pigmented BCC, melanocytic nevus, lentigo, wart, acrochordon (skin tag), other nevi

– Rapid onset of numerous SKs can be paraneoplastic (sign of Leser-Trélat), especially GI adenocarcinoma

Urticaria (hives)

Clinical Presentation:

– Wheals surrounded by red halo or flare (surrounding erythema blanches w/pressure)

Cardinal symptom: pruritus

Acute (<6wks; common causes: idiopathic, infxn, food rxn, drug rxn [penicillin & related abx, aspirin/NSAID], IV admin) vs. chronic (common causes: idiopathic [>50%], physical factors, autoimmune)  

– Most common cause in kids is viral 

– Most urticaria is acute & resolves; most chronic urticaria is episodic and self-limiting (2-5yrs)


– Vascular skin rxn (swelling of upper dermis)


– Don’t usually need lab testing for acute, or allergy testing for chronic 

– 1st-line tx (acute & chronic) = oral H1 antihistamines (e.g., Hydroxyzine, Loratadine; caution: sedative effects, glaucoma, prostatic hyperplasia, respiratory disease)

– Refer to dermatologist & biopsy if: persists >48hrs, painful/burning, petechial traits, systemic symptoms, unresponsive to antihistamines, pigmentation changes upon resolution → may signal systemic disease such as urticarial vasculitis

Clinical Pearls:

–  Ask about symptoms of anaphylaxis, obtain vitals & eval for respiratory distress & hypotension

Drug Reaction

-Many different drug reactions!

Immediate (<1 hour from last dose): Urticaria and/or angioedema

-Delayed (after 1 hour but can be weeks to months after start of a med): exanthematous drug eruption, fixed drug eruption, AGEP, DRESS, SJS/TEN, vasculitis

Management (general)

– STOP THE DRUG IF POSSIBLE (and document in allergy list with description of reaction)

– Topical steroids (very high potency, such as betamethasone), emollients, antihistamines for pruritis

– See below for reaction-specific

Clinical pearls

– Get a thorough med history (going back as far as 6 weeks), not only new Rx, but also new supplements, OTC meds, herbal meds, etc. 

– 7’s I’s: instilled (eye or ear drops), inhaled (inhalers), ingested (capsules, tablets, syrups), inserted (suppositories), injected (IM, IV), incognito (herbs, non-traditional medicine, homeopathic, vitamins, OTC), intermittent (pts often won’t mention unless specifically asked)

VisualDx has list of meds that have been linked to each reaction

– Common suspect drugs: antibiotics, anti-epileptics, NSAIDS

– Consider making a drug timeline

– Labs: CBC + diff, CMP, LFTs to assess for systemic involvement

Exanthematous drug eruption

symmetric, confluent erythematous macules and papules on trunk and extremities

Clinical presentation:

– Most common

– Skin-limited, erythematous macules and papules on trunk, spreads to extremities symmetrically

– Rash appears 7-10 days after drug started if 1st episode, 24-48 hours if repeat

– Often described as “morbilliform” (measles-like)


– Should resolve after medication is stopped

– Can “treat through” (continue the med) safely if not too severe and no other med options

– Can get extensive desquamation as it resolves

– Tx: topical steroids and oral antihistamines

Clinical pearls:

– Hx: ask about recent viral illness (DDX includes viral exanthem)

Fixed drug eruption (FDE)

oval erythematous plaque with central bulla

Clinical presentation:

– One or more round or oval patches or plaques, can evolve into bullae and erosions

– Recurs at SAME site if re-exposed

– Can involve mucous membranes


– Should resolve days to weeks after drug is stopped, but can get postinflammatory hyperpigmentation

– For eroded FDE, apply protective or antimicrobial ointment and dressing until site is re-epithelialized

– For non-eroded, tx with topical steroid

Acute generalized exanthematous pustulosis (AGEP)

pinhead-sized sterile pustules with surrounding erythema

Clinical presentation:

– Onset within 2 weeks to 2 days after exposure to med, Hg exposure or viral infection

– Starts on face or groin and armpits then spreads, may also have oral involvement

– Pinhead-sized sterile pustules with surrounding erythema

– Persistent high fevers and marked neutrophilia 

– Lasts 1-2 weeks then skin desquamates as it resolves

– 10% have organ dysfunction (lungs, blood, kidney, liver)


Rash generally peels off and resolves spontaneously in about 10 days

– Discontinue new meds (culprit is often abx)

– Tx with topical steroids, oral antihistamines, analgesics

Drug reaction with eosinophilia and systemic symptoms (DRESS) aka Drug-induced hypersensitivity reaction (DIH)

facial edema, diffuse erythematous macules and plaques on trunk and extremities

Clinical presentation:

– Exanthem, erythematous centrofacial swelling, fever, malaise, lymphadenopathy, involvement of organ (systemic rxn), 10% fatality rate

– Systemic sx: fever, lymphadenopathy, heme (leukocytosis, eosinophilia, atypical lymphocytes), liver (elevated LFTs), renal (elevated BUN/Cr), CNS (encephalopathy, meningitis), lungs (resp. distress), thyroiditis (assoc. with hypothyroid afterwards)

– Starts ~3 weeks (range: 1-12 weeks) after start of med or increase in dose

– Can have persistent signs and symptoms even after stopping drug for many weeks


– Assess severity of reaction and organ systems involved

– Labs: CBC + diff (look for elevated eosinophils, leukocytosis), CMP (esp. BUN/Cr for renal involvement), LFTs, UA

– Do a thorough drug timeline and evaluate likely culprits (consult VisualDx, consider timeline)

– Stop culprits, discontinue anything non-essential

– Can use topical steroids if mild, systemic steroids if severe and taper as able, trend labs

Clinical pearls:

– Suspect in patients with rash and facial edema

– Suspect drugs for DRESS: allopurinol, antibiotics, anti-TB drugs, anti-epileptics (phenytoin, carbamazepine, lamotrigine), NSAIDS, abacavir

Stevens-Johnson syndrome/Toxic epidermal necrolysis (SJS/TEN)

Widespread erosions on the face, upper trunk and arms

erythematous macules on bilateral palms

Mucosal involvement

Clinical presentation:

– Systemic and acute life-threatening mucocutaneous reaction

– Extensive necrosis and detachment of the epidermis and mucosal surfaces

– SJS: <10% of BSA involved; SJS/TEN: 10-30%; TEN >30% 

– SJS mortality rate of 5-12%, TEN >20%

– ~8 weeks after starting med, may have preceding fever/headache/rhinitis/myalgias → mucocutaneous eruptions, initially erythematous irregularly shaped, dusky red to purpuric macules (atypical targets) → progressively coalesce, very painful, symmetric and distributed on the face, upper trunk and proximal extremities → flaccid blisters (break easily), epidermis that discharges with lateral pressure, extensive necrosis revealing large areas of exposed, red and oozing dermis

– Can get painful mucous membrane involvement of oral and genital mucosa, eyes 

– Complications include corneal damage, GU damage, pulmonary damage, fluid and electrolyte disturbances, nutritional requirements, secondary infection → sepsis


– Withdraw offending drug + supportive care, stop all non-life sustaining drugs, consult derm

– May required burn unit treatment if a lot of BSA involvement, ophthalmology consult for ocular sx

– Various protocols using IVIG, cyclosporine, steroids, etanercept (ongoing research about this)

Clinical pearls:

If suspect SJS/TEN, check for mucous membrane involvement

– Suspect drugs = SATANN: Sulfa antibiotics + sulfasalazine, allopurinol, tetracyclines + thiacetazone, anticonvulsants (carbamazepine, lamotrigine, phenobarbital, phenytoin), NSAIDS, nevirapine