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Dermatology and Skin Disease Concepts - Practice Flashcards

Acneiform lesions

  • Acne vulgaris

    • Disease of the pilosebaceous unit
    • Key components: increased sebum, hyperkeratinization, Propionibacterium acnes (P. acnes) // sometimes written as C. acnes
    • Primary lesion type: comedones (hallmark feature)
    • Initial management for mild acne: topical retinoid; benzoyl peroxide (BP)
    • Do not use topical retinoids and benzoyl peroxide at the exact same time of day; they are started at different times of the day
    • Add topical antibiotic when needed; options include clindamycin or erythromycin; continue BP as well
    • Reassess strategy at 3 months for topical antibiotics
    • For moderate to severe acne: options include oral antibiotics, oral contraceptives, or oral spironolactone (based on acne features)
    • Continue topical retinoid and topical antibiotic with systemic therapy as needed
    • Isotretinoin (oral) is used after exhausting other therapies; highly effective but teratogenic
    • Terminology: “P. acnes” often appears in literature and lectures

  • Folliculitis (Leculitis)

    • Inflammation/infection of hair follicles; mainly bacterial
    • Common organism: Staphylococcus aureus; hot-tub folliculitis often due to Pseudomonas; fungal causes in refractory cases
    • Presentation: small papules and pustules around hair follicles
    • Initial management: benzoyl peroxide wash; topical antibiotics (bactroban/mupirocin or clindamycin)
    • If not improved: switch to oral antibiotics with anti-staph coverage; MRSA coverage as needed

  • Rosacea

    • Chronic disease of facial pilosebaceous unit
    • Risk factors: genetics, female gender; flushing is pathognomonic
    • Subtypes: flushing with or without papules/pustules; telangiectasia; Demodex mites are more numerous in rosacea
    • Extra facial symptoms: ocular symptoms in some patients; rhinophyma indicates glandular hyperplasia
    • Triggers: factors that inflame skin; Demodex mites
    • Management: avoid triggers; sunscreen; vasoconstrictor therapies for telangiectasia (topical formulations; example in slide: dramaticidin/dramotidine gel – note textbook naming varies; focus on vasoconstrictor effect)
    • Light-based therapies: pulse-dye lasers, lasers
    • Papules/pustules: topical metronidazole is first-line
    • Other approaches: systemic tetracyclines or isotretinoin for Phymid rosacea (rosacea with rhinophyma not specified in detail here)
    • Ocular symptoms: ocular lubricants, ocular cyclosporine, or tetracycline
    • Surgical/laser approaches for rhinophyma or persistent vascular changes

  • Desquamating conditions

    • Erythema multiforme (EM)
    • Immunologically mediated skin condition; target lesions commonly on hands/extremities; mucosal involvement possible but usually milder than SJS/TEN
    • Most common cause: herpes simplex virus (HSV)
    • Demographics: usually young adults; more common in males; can be recurrent (HSV association)
    • Management: mild cases observation; topical steroids; sedating oral antihistamines
    • Mucosal involvement: topical steroids (gel) and magic mouthwash; oral steroids if more severe; ophthalmology referral if eyes involved
    • Antiviral therapy considered for recurrence
    • Stevens–Johnson syndrome (SJS) / Toxic epidermal necrolysis (TEN)
    • On a continuum with EM; extent defined by % body surface area (BSA): SJS < 10% BSA; TEN > 30% BSA
    • Features: significant mucosal involvement (2+ sites); generalized target lesions with rapid confluence; bullae; skin sloughing; positive Nikolsky sign
    • Prodrome: upper respiratory-like symptoms; more common in females
    • Etiology: most commonly drug-induced (many medications); HSV as a cause in some contexts
    • Onset: drug eruptions can occur several weeks after starting a drug (not just 7–10 days; up to 8 weeks)
    • Management: discontinue offending agent; ICU/burn unit admission; systemic steroids; ophthalmology involvement
    • Staphylococcal scalded skin syndrome (SSSS)
    • Positive Nikolsky sign; often in very young children (2–3 years)
    • Cause: exfoliative toxins from Staphylococcus aureus
    • Distinguishing feature: mucous membranes relatively spared compared with SJS/TEN
    • Diagnosis: culture from primary infection site (nares/oropharynx often sampled); histology if needed
    • Management: inpatient IV antibiotics (e.g., oxacillin/nafcillin); aggressive supportive skin care; monitor for dehydration and secondary infection

  • Androgenic alopecia

    • Most common non-scarring alopecia
    • Male onset: teens to 40s; female onset: later, typically later than men
    • Presentation: men with various patterns; women with wider part and vertex thinning
    • Diagnosis: mostly clinical; labs (hormones, thyroid function, vitamin D, CBC) for premenopausal women if indicated
    • Management: prevent progression; topical minoxidil (OTC) for newer onset
    • Finasteride can be added to minoxidil
    • Platelet-rich plasma (PRP) used variously
    • Premenopausal women: spironolactone or low-dose minoxidil

  • Alopecia areata

    • Autoimmune hair loss; strong genetic component; patches of smooth hairless skin
    • Exclamation point hairs can indicate regrowth; female and male involvement possible
    • Diagnosis: clinical; biopsy sometimes; check for associated autoimmune diseases (TSH, thyroid antibodies, etc.)
    • Management: first-line intralesional corticosteroids; potent topical steroids with minoxidil; oral JAK inhibitors in select cases; psychological support as needed; self-limiting in some cases

  • Onychomycosis

    • Fungal infection of nails; dermatophyte most common: Trichophyton rubrum
    • Not a clinical diagnosis alone; requires nail clipping or fungal culture; two tests (culture + KOH with calcofluor) increase sensitivity to ~96%
    • Management: topical antifungals long-term (e.g., terbinafine daily for ~12 weeks); post-clearance prophylaxis with topical antifungal (e.g., itraconazole weekly, etc.)
    • Risk factors: increasing age, immunosuppression, underlying skin conditions; occlusive footwear

  • Paronychia

    • Acute infection of lateral proximal nail fold; commonly Staph/Strep
    • Chronic paronychia: Candida commonly implicated
    • Management: warm compresses; hygiene; if abscess forms or no improvement: incision and drainage; oral antibiotics with anti-staph coverage; if chronic or fungal pattern: add antifungal and possibly topical steroids

  • Bites

    • Brown recluse bites
    • Skin reaction predominates; necrosis possible but uncommon
    • Typical lesions: red papules/plaques with a central blister or eschar
    • Management: immobilization, ice, elevation; anti-staphylococcal antibiotics; tetanus prophylaxis
    • Widow spider bites
    • Neurotoxic symptoms predominate: muscle pain/spasms, weakness, tremors, abdominal symptoms, tetany
    • Management: wound care and oral analgesics for mild cases; IV opioids and benzodiazepines for moderate/severe; antivenom for severe muscle pain/spasms; tetanus prophylaxis

  • Animal and human bites

    • Most common bites: dog bites; cat bites have higher risk of infection due to bite mechanics
    • Bites are polymicrobial; Pasteurella species particularly common in cat bites
    • Management: aggressive cleaning, irrigation, debridement; avoid suturing if infection present or if on hands; amoxicillin-clavulanate for cat/dog bites
    • Prophylaxis: cat/human bites; hand bites; immunocompromised patients; moxifloxacin or other broad agents may be used in selected cases
    • Tetanus and rabies prophylaxis as indicated

  • Other infectious diseases

    • Cellulitis vs parasyphilitis (paraphrased from transcript as a differentiated cellulitis variant)
    • Cellulitis: infection of dermis and subcutaneous tissue; borders are ill-defined; common cause: beta-hemolytic streptococcus (GAS)
    • Parapsoriasis-like variant described; generally superficial with well-defined borders; both can have systemic symptoms
    • Assessment: clinical diagnosis; incisional drainage if abscess present
    • Treatment: mild cases dicloxacillin or cephalexin; severe cases parenteral antibiotics; MRSA coverage if suspected
    • Impetigo: superficial epidermal infection; non-bullous type with honey-colored crusts; bullous type with bullae; eczema herpeticum-like variants uncommon but noted
    • Non-bullous impetigo treatment: topical mupirocin; extensive lesions or ulcerative/exudative involvement: cephalexin or dicloxacillin
    • Abscess (revisited): clinical diagnosis; culture if severe or recurrent; USPOCUS often used to evaluate for retained foreign bodies or to guide drainage
    • Abscess management by severity: drainable abscess → incision and drainage; mild disease → may avoid antibiotics; moderate disease → oral antibiotics with MRSA coverage; severe disease → IV antibiotics (MRSA coverage)

  • Necrotizing soft tissue infections (NSTIs)

    • Rapidly progressive; disproportionate pain; skin changes progress quickly to necrosis
    • Pathophysiology: vasculitis and thrombosis contributing to necrosis and bronze/brown discoloration; crepitus possible; high fever, hypotension, tachycardia; bacteremia common
    • Diagnosis: high suspicion; MRI with contrast provides best sensitivity; do not delay surgical consultation
    • Common pathogens: polymicrobial; Group A Streptococcus is common; other pathogens as well
    • Management: emergent surgical consultation; aggressive fluid resuscitation; blood transfusion as needed; broad-spectrum antibiotics with triple coverage: penicillin, clindamycin, metronidazole plus an aminoglycoside

  • Candidal infections

    • Candida albicans causes mucocutaneous infections; risk with warm, moist environments, immunocompromise, antibiotic/steroid use
    • Clinical progression: papules/pustules on an erythematous base with erosions and satellite lesions; mucosal involvement common
    • Vulvovaginitis: single-dose fluconazole; recurrent use a weekly regimen; topical azoles also used
    • Esophageal candidiasis: fluconazole (oral or IV depending on severity)
    • Thrush: nystatin oral suspension
    • Invasive candidiasis: IV echinocandins (e.g., caspofungin), micafungin, anidulafungin
    • Clinical reminder: evaluate for underlying immunosuppression (e.g., diabetes, HIV)

  • Dermatophytes (tinea infections)

    • Fungi infect nonviable keratinized skin structures
    • Risk factors: history of atopic dermatitis; topical immunosuppression; friction
    • Classic presentation: pruritic annular patches with peripheral scaling and central clearing
    • Common dermatophyte: Trichophyton rubrum
    • Diagnosis: KOH microscopy to identify hyphae; fungal culture if needed
    • Management
    • Tinea corporis, cruris, pedis, manum: start with topical antifungals (e.g., terbaniphin? [transcript mentions tirpanophine], topical itraconazole, tolnaptate)
    • Tinea capitis and barbae: systemic therapy (e.g., griseofulvin/ crisoflavin, terbanifine, itraconazole, or fluconazole as per transcript)

  • Pediculosis capitis (head lice)

    • Infestation with Pediculus humanus capitis; live lice plus many nits near scalp
    • Symptoms: intense nocturnal itching
    • Diagnosis: presence of live lice; nit inspection; wet combing technique can help reveal nits
    • Treatment: topical permethrin 1% (often first-line; resistance reported)
    • Additional measures: mechanical removal with fine-toothed combs; treat with nit combs
    • Refractory cases: oral ivermectin

  • Scabies

    • Infestation with Sarcoptes scabiei
    • Transmission: close skin-to-skin contact
    • Classic distribution: wrists, web spaces between fingers, ankles; can be subtle and present with nocturnal itch; burrows may be seen
    • Diagnosis: visualization of mites, eggs, or feces on microscopy; presumptive diagnosis acceptable
    • Treatment: permethrin 5% cream; alternatives: lindane 1% lotion/cream; oral ivermectin; treat close contacts

  • Warts

    • Verruca vulgaris (common warts): HPV types 2 and 4
    • Presentation: papules/plaques; hands and feet common; plantar warts may resemble calluses and look different
    • Management: lesion destruction methods; over-the-counter salicylic acid; cryotherapy (liquid nitrogen) in office or OTC; extensive lesions or resistant lesions may require laser, surgical excision
    • Condyloma acuminata (genital warts): HPV types 6 and 11
    • Presentation: fleshy papules in anogenital region; may be asymptomatic; pruritus or tenderness possible initially
    • Management: observation for spontaneous clearance; topical therapies (imiquimod, cryotherapy); surgical excision for extensive lesions
    • Molluscum contagiosum
    • Cause: poxvirus
    • Presentation: waxy, umbilicated papules; common in children; sites on neck, face, trunk, axillae
    • Course: usually self-limiting over ~18 months; cosmetic concern
    • Management: curettage, liquid nitrogen, chemical therapy

  • HSV-1 and HSV-2

    • HSV-1 (more common): gingivostomatitis/pharyngitis; fever, malaise, systemic symptoms in primary infection; herpes labialis (cold sores) with recurrences; genital HSV-1 less common with bilateral ulcers and lymphadenopathy
    • Diagnosis: PCR or viral culture
    • Treatment: antivirals; treat primary infection if within 72 hours; for recurrences, topical anesthetic for symptoms
    • HSV-2: primary infection can range from asymptomatic to painful genital ulcers; recurrences common but typically less severe; dysuria, inguinal lymphadenopathy, systemic symptoms possible
    • Diagnosis: clinical or HSV DNA detection via PCR
    • Treatment: antivirals; oral therapy 7–10 days; episodic or suppressive therapy depending on recurrence frequency

  • Shingles (Herpes zoster)

    • Reactivation of latent varicella-zoster virus (VZV) in dorsal root ganglia
    • Demographics: common in patients ≥50 years
    • Presentation: prodrome with acute neuritis; unilateral dermatomal vesicular rash; severe neuropathic pain
    • Diagnosis: clinical; Zank’s smear can show multinucleated giant cells (not specific to VZV)
    • Treatment: antivirals for 5–7 days; supportive care

  • Hand, foot, and mouth disease

    • Etiology: Coxsackievirus (nonpolio enteroviruses; peak in late summer/fall)
    • Presentation: stomatitis with vesicular rash on hands/feet; may involve nails; fever common
    • Diagnosis: clinical; supportive care
    • Notable visual: vesicles on hands, feet, mouth

  • Keratotic disorders

    • Actinic keratosis (AK)
    • Precancerous lesions that may progress to squamous cell carcinoma
    • Risk factors: fair skin, sun exposure history
    • Appearance: rough, crusty lesions; may be white or red
    • Management: cryotherapy; field therapy with fluorouracil or imiquimod for area of multiple AKs; biopsy for atypical features
    • Seborrheic keratosis (SK)
    • Common, benign, “stuck-on” waxy papules; often appear after age 30
    • Management: observation; cryotherapy, curettage, flat excision for cosmetic or symptomatic reasons
    • Sign of Lesser-Trello: a sudden eruption of many SKs can be a red flag for malignancy

  • Neoplasms

    • Basal cell carcinoma (BCC)
    • Most common skin cancer; strongly linked to UV exposure
    • Classic appearance: pearly papule, translucent, waxy, firm; rolled border; may have central ulceration and telangiectasias
    • Common sites: head and neck; often in older adults
    • Diagnosis: biopsy
    • Management: excisional biopsy with margins; electrodesiccation and curettage; Mohs surgery in select anatomic areas; topical 5-fluorouracil (5-FU) or imiquimod for certain cases
    • Metastasis: very low risk
    • Squamous cell carcinoma (SCC)
    • Keratinocytes invading dermis or deeper; risk factors include UV exposure plus others (transplant, HPV, arsenic, radiation, chronic inflammation)
    • Types: differentiated (keratotic crusty type) and undifferentiated (soft, vegetative, papillomatous; can bleed easily)
    • Bowen disease (SCC in situ)
    • Scaly plaque limited to epidermis; can be misdiagnosed as dermatitis or psoriasis
    • Diagnosis: biopsy to depth of dermis
    • Management: full-thickness excision or Mohs; electrodesiccation and curettage in select high-risk areas
    • Melanoma
    • Types: de novo melanomas; precursor lesions include dysplastic nevi and congenital melanocytic nevi
    • Epidemiology: fifth most common cancer in men and women; median age at diagnosis in the 50s
    • Risk factors: white adults >50, many nevi (>50), dysplastic or atypical nevi, family history, immunosuppression, Fitzpatrick types I-II
    • Precursor lesions: dysplastic nevi; features include ABCDEs; “fried egg” appearance; asymmetry and color variegation
    • Types: superficial spreading (radial growth phase; better prognosis), nodular (rapid depth increase; poorer prognosis), lentigo maligna (older patients, face), acral lentiginous (palms/soles, more common in darker-skinned individuals)
    • Diagnosis: complete full-thickness excisional biopsy with adequate margins; sentinel lymph node biopsy; staging based on tumor depth, nodal involvement, metastasis
    • Management by stage: stage I–II (excision +/- adjuvant therapy); stage III (regional metastasis) with immunotherapy; stage IV (metastatic) with immunotherapy/chemotherapy and possibly surgical/radiation approaches
    • Prognostic factor: Breslow depth (depth of invasion) is the best prognostic factor
    • Secondary cancer risk: about 10x increased risk of a second primary melanoma; lifelong surveillance
    • Kaposi sarcoma
    • Cancer of lymphatic/blood vessel lining; most common in immunocompromised patients (HIV-associated KS)
    • Etiology: HHV-8 infection in the setting of immunosuppression
    • Clinical presentation: non-tender violaceous to brown/black macules, plaques, nodules; may ulcerate and bleed; can occur internally
    • Diagnosis: biopsy; management depends on immune status and extent; options include observation, surgery, chemotherapy, injections, retinoids, radiation

  • Papulosquamous disorders

    • Differentiating irritant vs allergic contact dermatitis
    • Irritant contact dermatitis (ICD)
    • Mechanism: epidermal disruption and inflammation due to irritant exposure
    • Common sites: hands (occupational skin disease)
    • Symptoms: redness, fissuring, oozing, tenderness; itching present but less dominant
    • Management: identify/avoid offending agent; emollients; topical steroids as needed
    • Allergic contact dermatitis (ACD)
    • Mechanism: sensitization; initial sensitization phase lasts ~10–14 days; re-exposure causes reaction within ~24 hours
    • Presentation: vesicular rash with linear patterns; more itching than ICD
    • Management: identify/remove allergen; topical steroids; antihistamines; patch testing if needed
    • Exanthematous drug eruptions (morbilliform)
    • Most common drug eruption; onset 7–10 days after starting drug
    • Presentation: measles-like eruption or maculopapular/eczematous rash
    • Management: discontinue offending drug; topical steroids and/or antihistamines
    • Fixed drug eruptions
    • Eruptions recur at the same site with re-exposure; round/oval macules or plaques; may have vesicles or bullae; violaceous evolution with hyperpigmentation
    • Common causes: tetracyclines, metronidazole, sulfonamides, antibiotics, NSAIDs, salicylates
    • Management: discontinue offending drug; if non-eroded, potent topical steroids; if eroded, antimicrobial ointment and possibly oral prednisone

  • Dermatitis and eczema spectrum

    • Atopic dermatitis (eczema)
    • Classic itch-scratch disease with early onset; majority by age 1; 90% by school age
    • Associated with eczema, allergies, asthma; pruritic, papules, plaques, scaling, lichenification
    • Distribution changes with age: <2 years often extensor surfaces, face, diaper area; older children/adults tend to involve flexural areas (antecubital, popliteal fossae); hands/feet involvement in older ages
    • Management: education and trigger identification; avoid hot water; emollients as first-line therapy; topical anti-inflammatories (steroids, calcineurin inhibitors, phosphodiesterase inhibitors, coal tar); phototherapy; systemic therapy for severe disease (biologics, methotrexate, cyclosporine, systemic steroids as needed)
    • Secondary infections may require systemic antibiotics
    • Perioral dermatitis
    • Benign eruption around mouth; sparing of upper vermilion border; often involves nose and sometimes eyes
    • Predisposing factors: prior facial steroid use or intranasal steroids; new facial products
    • Management: avoid steroids; topical antibiotics (metronidazole, clindamycin, erythromycin); topical sulfur or azelaic acid; topical calcineurin inhibitors if needed; consider oral antibiotics if persistent
    • Nummular (nummular) eczema
    • Chronic, very pruritic; discoid plaques on extremities; flares in winter; often in adults
    • Management: hydration with emollients; topical steroids; calcineurin inhibitors; coal tar; phototherapy (PUVA); others as needed
    • Dyshidrotic eczema
    • Characterized by microvesicles on hands/feet; palm/ finger involvement with vesicles; intense pruritus
    • Triggers: stress, contact irritants; dry skin
    • Management: high-potency topical steroids; intralesional steroids for focal lesions; phototherapy; calcineurin inhibitors; systemic agents (cyclosporine, methotrexate) for severe cases; botulinum injections in refractory cases
    • Seborrheic dermatitis
    • Affects high-sebum areas; phase: infantile (cradle cap) and adults
    • Appearance: erythematous patches with yellow greasy scales
    • Management: adults with selenium sulfide, tar, ketoconazole shampoo; low-potency topical steroids on sensitive areas (face)
    • Alternatives: topical calcineurin inhibitors for dermatitis; maintenance with medicated shampoos; infant management often starts with olive oil/oil-based methods
    • Lichen planus
    • Idiopathic T-cell mediated; classic “five P’s”: Pruritic, Purple, Polygonal, Planar, Papules/Placks
    • Common sites: wrists, forearms, legs; mucosal involvement common (oral cavity in >50% of patients)
    • Koebner phenomenon can occur; Wickham striae on mucosa; can cause scarring alopecia if scalp involved
    • Management: topical steroids for limited skin disease; oral steroids for extensive disease; topical steroids for mucosal lesions; consider inclusive dressing for better penetration; antifungal prophylaxis if mucosal involvement
    • Additional associations: hepatitis C testing; oral LP increases risk of squamous cell carcinoma in the mouth; potential HIV and Parkinsonism associations

  • Pigment and pigmentary disorders

    • Pityriasis rosea
    • Acute exanthem; likely HHV-6 or HHV-7 etiology
    • Herald patch precedes widespread eruption by ~1–2 weeks; salmon-colored oval plaques with fine peripheral scaling in a Christmas-tree distribution
    • Self-limited; usually resolves in 8–12 weeks; supportive care
    • Important to rule out syphilis (RPR) in sexually active patients
    • Melasma
    • Hyperpigmentation of the face, typically in women; associated with pregnancy or oral contraceptives; sun exposure exacerbates
    • Management: strict sun protection; epidermal vs dermal melasma; epidermal melasma treated with hydroquinone, tretinoin, and topical steroids
    • Vitiligo
    • Autoimmune destruction of melanocytes; symmetric depigmented macules/patches; periorificial predominance common; autoimmune associations
    • Diagnosis: clinical; skin biopsy sometimes; patch testing generally not needed
    • Management: topical calcineurin inhibitors for localized disease; narrowband UV therapy for widespread disease; PUVA; topical steroids; sunscreen; consider phototherapy; sometimes combined topical steroids with phototherapy; skin protection is essential
    • Tinea versicolor (pityriasis versicolor)
    • Yeast infection with Malassezia furfur; often in sebaceous-rich areas (face, neck, upper chest, upper back)
    • Presentation: round/oval patches with fine scaling; patch color may be hypo- or hyperpigmented depending on baseline skin
    • Diagnosis: KOH prep showing hyphae with thick-walled budding spores
    • Treatment: two-dose oral fluconazole 14 days apart; topical selenium sulfide lotion or ketoconazole shampoo as adjuncts
    • Counseling: pigmentation normalization may take months; avoid expectation of complete rapid repigmentation

  • Skin integrity and wounds

    • Burns
    • Depth categorization: superficial (erythema, intact capillary refill); superficial partial thickness (blisters, pink/wet); deep partial thickness (white, wet, bleeds on poke; preserved sensation); full thickness (white/yellow, charred; loss of adnexa; hard, inelastic; no sensation)
    • Important time window: first 48 hours critical for progression and infection risk
    • Rule of nines (body surface area estimates): head/neck 9%; each arm 9%; anterior trunk 18%; posterior trunk 18%; each leg 18%; genital area 1%
    • Parkland formula for fluid resuscitation in first 24 hours:
      ext{Fluids in first 24h} = 4 \, ext{mL} imes ext{kg} imes ext{ ext{% TBSA burned}}.
      Half of this volume is given in the first 8 hours from time of burn, with the remainder over the next 16 hours
    • Management: ABCs; avoid infection; rapid debridement and skin grafting for deep or full-thickness burns; analgesia (NSAIDs, opioids, ketamine); wound care with topical antibiotics; prevent hypothermia; monitor urinary output; nutrition
    • Frostbite
    • Degree progression on frostbite depth; rewarming in 40–42°C moving water bath
    • Pharmacologic options: intra-arterial thrombolytics considered within first 24 hours
    • Management: wound care; tetanus; infection prevention; digital dressings between digits
    • Non-freezing cold injuries
    • Trench foot: prolonged cold exposure; pale, numb, sluggish; management includes dry, warming, elevation, rest, vasodilators (limaprost) in some cases
    • Chilblains (pernio): inflammatory lesions due to cold exposure; rest and warmth; prevention with proper clothing
    • Lacerations
    • Considerations: tetanus status; mechanism; foreign body risk; cosmetic significance; neurovascular status
    • Evaluation: imaging (X-ray, ultrasound) for foreign bodies
    • Repair timing: primary closure within ~12–18 hours if clean; delayed closure at day 3–4 for contaminated wounds or higher risk of poor outcome
    • Wound care: hemostasis, debridement, irrigation, anesthesia; close wounds with topical antibiotics; dressings kept for ~24 hours
    • Pressure ulcers
    • Risk factors: immobility, decreased sensation, incontinence, poor nutrition, friction and shear
    • Management: pressure-relieving devices (air mattresses), wound debridement, skin grafting for significant ulcers; appropriate dressings
    • Diabetic ulcers
    • Prevalence: up to 25% of diabetics may develop ulcers
    • Characteristic ring around the ulcer with callus; risk of deeper infection to joints/bone
    • Vascular assessment crucial: pedal pulses; vascular referral if poor pedal pulses
    • Management: offloading, wound care, infection monitoring, glycemic control, foot care; assess for coexisting conditions (onychomycosis, vascular disease)
    • Stasis dermatitis
    • Combination of dermatitis and venous insufficiency; edema and inflammation
    • Management: leg elevation; compression stockings; emollients; topical steroids for inflammation

  • Vascular abnormalities

    • Cherry angioma
    • Benign vascular proliferation; bright red dome-shaped papules; trunk and proximal extremities; typically in 30s–40s
    • Usually asymptomatic; clinical diagnosis; observation; treatment for cosmetic purposes via shave excision, electrocautery, laser, or cryotherapy
    • Abrupt multiple new lesions may prompt evaluation for internal malignancy (less common)
    • Telangiectasia
    • Superficial dilated vessels in skin/mucous membranes; face and lower extremities common
    • Associated with rosacea, steroid use, pregnancy, autoimmune disease; usually benign
    • Management: laser therapy or electrocautery if bothersome

  • Vesiculobullous diseases

    • Pemphigus vulgaris
    • Autoimmune; younger adults (30–60 typical); mucosal involvement common; flaccid bullae that rupture easily; high risk of infection
    • Nikolsky sign positive
    • Diagnosis: immunofluorescence
    • Management: steroids and immunosuppressives; requires close monitoring for infection
    • Pemphigoid
    • Usually older individuals; less mucosal involvement; fewer ruptures; Nikolsky sign negative
    • Diagnosis: immunofluorescence
    • Management: steroids/immunosuppressants; often more self-limiting than pemphigus vulgaris

  • Other derm disorders

    • Acanthosis nigricans
    • Hyperpigmented, velvety, thickened flexural skin
    • Associations: obesity, hyperinsulinemia, diabetes; potential drug/malignancy associations
    • Hidradenitis suppurativa (HS)
    • Chronic, scarring inflammatory disease of apocrine glands
    • Strong associations: diabetes, PCOS, metabolic syndrome; smoking is a major risk factor
    • Common sites: axillae, anogenital regions; more common in women (female:male ~4:1)
    • Clinical: painful nodules, abscesses, sinus tracts; scarring; double comedones are pathognomonic
    • Management: topical or oral antibiotics; surgical drainage/tissue removal; TNF inhibitors; other biologics; lifestyle modifications and smoking cessation
    • Lipomas
    • Benign subcutaneous fat tumors; soft, round, mobile, non-tender; slow-growing
    • Common sites: neck, trunk, extremities
    • Management: observation; liposuction or surgical excision if symptomatic or changing
    • Epidermal inclusion cysts
    • Benign growths from hair follicle; common on face/trunk; central punctum
    • Characteristics: fluctuant; may drain foul-smelling cheesy material when ruptured
    • Management: inflamed lesions may need incision and drainage with possible steroid injection; watch for recurrence
    • Photosensitivity reactions
    • Phototoxic vs photoallergic reactions
    • Phototoxic: non-immune; rapid, localized to sun-exposed areas; common with antibiotics
    • Photoallergic: immune-mediated; delayed onset (24–48 hours) and can extend beyond sun-exposed areas; commonly caused by hydrochlorothiazide, amiodarone, chlorpromazine
    • Management: stop offending agent; UV protection; topical or oral steroids as indicated
    • Pilonidal disease
    • Pilonidal abscesses at the superior aspect of the gluteal fold with pits or tracts
    • Higher risk: teenage/young adult males; overweight or sedentary; long periods of sitting
    • Common pathogens: Staph/Strep; anaerobes and Gram-negatives also possible due to location
    • Management: incision and drainage with local packing; oral antibiotics; wound care; possible surgery for recurrent cases
    • Urticaria
    • Acute vs chronic; most cases are self-limited and acute
    • Common triggers: foods, infections (viral/URI), medications; insect bites in some seasons
    • Presentation: evanescent wheals; pruritus; angioedema may accompany
    • Diagnosis: clinical
    • Management: second-generation H1 antihistamines (cetirizine, loratadine) as first line; escalate doses if refractory; add first-generation antihistamines if needed; systemic steroids and epinephrine for angioedema/anaphylaxis

  • Pearls and quick references (from the end of the lecture)

    • Conditions with positive Nikolsky sign include SJS/TEN continuum, staphylococcal scalded skin syndrome, and pemphigus vulgaris
    • Hand, foot, and mouth disease etiologies include Coxsackie; other conditions that can mimic acral lesions include syphilis, Rocky Mountain spotted fever, Kawasaki disease, measles, meningococcemia, reactive arthritis, and toxic shock syndrome
    • Most common drug eruption: exanthematous (morbilliform) in about 90% of cases
    • Lichen planus associations to check for hepatitis C; HIV association noted; oral LP has a higher risk of squamous cell carcinoma in the mouth
    • HSV-1 primary gingivostomatitis may present with fever and oral ulcers; recurrences common in the lips (herpes labialis)
    • HSV-2 primarily causes genital herpes with recurrences; diagnosis via HSV DNA PCR is most sensitive
    • Eruption types and etiologies summarized for quick reference (e.g., pityriasis rosea linked to HHV-6/7; pityriasis rosea’s herald patch and Christmas-tree pattern; psoriasis triggers include streptococcal infections and Koebner phenomenon)
    • Melanoma prognosis: depth of invasion (Breslow depth) is the best prognostic factor
    • Strategies for field therapy and management emphasize treating the underlying condition, patient education, and long-term surveillance where applicable

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