Generate differential and test hypothesis with examination findings
Tips for Practice: Familiarize yourself with primary lesions by looking at real examples. The morphology is often pathognomonic. For example, "target lesions" are classic for erythema multiforme, and "vesicles on an erythematous base" is classic for varicella or herpes simplex.
🔴 Inflammatory Dermatoses & Acneiform Eruptions
Acne Vulgaris
Chronic inflammatory disorder of the pilosebaceous unit affecting adolescents and adults. Pathogenesis involves increased sebum production, follicular hyperkeratinization, colonization with Cutibacterium acnes, and inflammation.
Severity Classification: Mild (comedones/few papules), Moderate (papulopustules, few nodules), Severe (numerous nodules/cysts, risk of scarring).
Chronic inflammatory disorder presenting with flushing, persistent erythema, papules, pustules, and telangiectasia on central face. Triggers include alcohol, spicy foods, thermal extremes, stress.
First-Line Treatment: Sunscreen + gentle skincare. Metronidazole 0.75% topical or oral doxycycline (anti-inflammatory dose, lower than acne dosing).
Psoriasis
Chronic immune-mediated inflammatory disorder with thick, silvery, well-demarcated plaques. Often on extensor surfaces (elbows, knees, scalp, nails).
Classic Triad: Well-demarcated erythematous plaques with silvery scale. Auspitz sign (pinpoint bleeding when scale removed). Koebner phenomenon (lesions at sites of trauma).
Psoriasis Treatment
Mild/Localized: Topical corticosteroids, topical vitamin D analogs, topical retinoids
Chronic pruritic inflammatory condition with impaired skin barrier and immune dysregulation. Presents with intense pruritus, xerosis, and lichenified plaques.
Pruritus precedes rash: Patients scratch, then lesions develop. "The itch that rashes" is classic.
Lichenoid Reactions & Lichen Planus
Autoimmune inflammatory condition presenting with violaceous, polygonal, papules with lacy white reticular pattern (Wickham striae). May involve oral mucosa.
Medication-Induced Lichenoid Reaction: NSAIDs, ACE inhibitors, beta-blockers, thiazides, antimalarials can cause lichenoid lesions. Discontinue offending agent.
🦠 Bacterial & Fungal Skin Infections
Impetigo
Highly contagious superficial bacterial skin infection, most common in children. Non-bullous form (>70%) presents with honey-crusted pustules; bullous form is staph aureus.
Treatment: Topical antibiotics (mupirocin) for localized. Oral antibiotics (amoxicillin-clavulanate, cephalexin) for widespread. Avoid ineffective oral penicillin V.
Cellulitis & Erysipelas
Feature
Cellulitis
Erysipelas
Depth
Deeper dermis & subcutaneous
Superficial dermis only
Borders
Poorly demarcated, blend gradually
Well-demarcated, sharp borders
Appearance
Edema, warmth, erythema
Bright red, shiny, raised borders
Cause
Group A Strep, Staph, Gram-negatives
Group A Streptococcus (primarily)
Treatment
IV cefazolin or clindamycin (cover MRSA)
Penicillin V or amoxicillin
Abscesses & Folliculitis
Folliculitis: Staphylococcal infection of hair follicle. Treat with topical antibiotics (mupirocin) or drainage if needed.
Furuncles (boils): Deep folliculitis with abscess formation. Treat with warm compresses, drainage, and oral antibiotics if systemic signs.
Tinea (Dermatophyte Infections)
Type
Location
Presentation
Treatment
Tinea Pedis
Feet (web spaces)
Maceration, erythema, scale, pruritus
Topical azole or terbinafine
Tinea Cruris
Groin, inner thighs
Annular plaques with scale, spares scrotum
Topical azole, terbinafine, or oral terbinafine
Tinea Corporis
Trunk, extremities
Annular plaques with central clearing ("ring worm")
Topical azole; oral for extensive disease
Tinea Capitis
Scalp
Scaling, alopecia, pustules
Oral griseofulvin or terbinafine + antifungal shampoo
Diagnosis: KOH mount (potassium hydroxide preparation) of scale shows hyphae and spores under microscopy. Fungal culture if diagnosis uncertain.
Candidiasis
Yeast infection causing erythematous patches with satellite pustules, maceration in intertriginous areas (skinfolds). Treat with topical azoles or nystatin.
Oral Thrush: White plaques on tongue/palate. Risk factors: antibiotics, immunosuppression, HIV. Treat with nystatin suspension or fluconazole.
Onychomycosis (Nail Fungus)
Fungal infection of nails causing discoloration (yellow, white), thickening, and crumbling. Slower to treat than tinea corporis.
Treatment: Oral terbinafine (fastest) or fluconazole. Nail lacquer (amorolfine) as adjunct. Requires 3-6 months therapy. Topical therapy alone has low cure rates.
Pityriasis Versicolor
Malassezia furfur infection causing hypo- or hyperpigmented patches on trunk. KOH mount shows "spaghetti and meatballs" appearance (hyphae and yeast).
Treatment: Topical azole or selenium sulfide shampoo. Oral fluconazole for extensive disease. May recur.
🦠 Viral & Parasitic Skin Infections
Herpes Simplex Virus (HSV)
Recurrent viral infection presenting with grouped vesicles on erythematous base. HSV-1 (orolabial), HSV-2 (genital).
Prodrome → Vesicles → Pustules → Crust → Healing. Systemic symptoms (fever, malaise) may occur during primary infection.
HSV Treatment
Localized: Topical acyclovir cream (early in course)
Systemic/Severe: Oral acyclovir, valacyclovir, or famciclovir
Prophylaxis: Long-term acyclovir or valacyclovir for frequent recurrences
Varicella (Chickenpox) & Herpes Zoster (Shingles)
Primary VZV infection (chickenpox) presents with fever and vesicular rash in successive crops. Reactivation (shingles) presents with vesicles in dermatomal distribution, often preceded by neuralgic pain.
Shingles Complications: Postherpetic neuralgia (chronic pain after rash resolves), ophthalmic zoster (risk of blindness), disseminated disease in immunocompromised.
VZV Treatment
Chickenpox: Mainly supportive; antivirals if severe or immunocompromised
Shingles (early): Acyclovir, valacyclovir, or famciclovir within 72 hours of rash onset
Prevention: Varicella and zoster vaccines reduce risk and severity
Molluscum Contagiosum
Poxvirus infection causing umbilicated papules in clusters. Autoinoculation is common. Often self-limited but can spread.
Treatment Options: Curettage, cryotherapy, imiquimod (immune modifier), or observation (spontaneous resolution in weeks to months).
Warts (HPV)
Human papillomavirus infection causing verrucous lesions. Common warts on hands/feet; plantar warts can be painful.
Wart Treatment
Topical salicylic acid (keratolytic)
Cryotherapy (liquid nitrogen)
Laser therapy for resistant warts
Many warts resolve spontaneously; treatment is optional
Scabies (Sarcoptes scabiei)
Mite infestation causing intense pruritus, especially at night. Burrows and nodules appear on wrists, finger webs, axillae, genitals. Highly contagious via skin-to-skin contact.
Diagnosis: Clinical history + exam. Burrow ink test or microscopy of burrow contents shows mite/eggs/feces.
Scabies Treatment
First-line: Permethrin 5% cream (apply neck-down, leave 8-14 hours, repeat in 1 week). Alternative: Ivermectin (especially for crusted scabies in elderly/immunocompromised).
Important: Treat all household/close contacts simultaneously to prevent re-infestation. Wash all clothing and bedding in hot water.
Pediculosis (Lice)
Pediculus humanus capitis (head lice), P. h. corporis (body lice), Phthirus pubis (pubic lice). Present with pruritus, nits (eggs) visible on hair shafts, and excoriations.
Treatment: Permethrin 1% shampoo or lotion for head/pubic lice. Ivermectin for resistant cases. Comb out nits. Wash bedding/clothing.
Cutaneous Larva Migrans
Hookworm larvae penetrating skin, creating serpentine burrows. Common in tropical/subtropical areas after contact with contaminated soil. Self-limited but highly pruritic.
Treatment: Ivermectin (systemic) or topical thiabendazole. Scratching may lead to secondary bacterial infection.
🔬 Skin Neoplasms
Actinic Keratosis (AK)
Premalignant lesion from chronic sun exposure. Rough, scaly papules/plaques on sun-exposed skin. Risk of progression to squamous cell carcinoma (0.6-2.6% per year).
Treatment: Topical 5-FU, imiquimod, or diclofenac for multiple lesions. Cryotherapy, curettage, or chemical peels for individual lesions.
Basal Cell Carcinoma (BCC)
Most common skin cancer. Usually on sun-exposed skin (face, neck). Presents as pearly nodule with central ulceration and rolled borders ("rodent ulcer").
Risk of Metastasis: <1%. Excellent prognosis if caught early. Treatment by dermatology or oncology.
Mohs micrographic surgery (preferred due to subclinical extension)
Squamous Cell Carcinoma (SCC)
Second most common skin cancer. Risk factors: chronic sun exposure, immunosuppression, actinic keratosis, chronic wounds. Presents as scaly nodule or ulcer on sun-exposed skin.
Risk of Metastasis: ~5% overall; higher risk with depth >4mm, poor differentiation, ear/lip location, immunosuppression. Monitor lymph nodes.
SCC Treatment
Excision with adequate margins (4-6mm for low-risk, up to 10mm for high-risk)
Mohs micrographic surgery for high-risk features, head/neck, recurrent SCC
Adjuvant radiation if advanced or high-risk features
Melanoma
Most lethal skin cancer. Presents as asymmetric, irregular-bordered, variegated-color (>3 colors) macule/patch/nodule. ABCDE criteria help identify suspicious lesions.
Metastatic: Immunotherapy (checkpoint inhibitors), targeted therapy (BRAF/MEK inhibitors if BRAF+), or chemotherapy
Benign Nevi (Moles)
Common benign lesions. Junctional, compound, and intradermal nevi are variants. Dysplastic nevi (atypical moles) are risk factor for melanoma.
Red Flags for Dysplastic Nevi: Irregular borders, mixed colors, diameter >5mm, evoking appearance. Monitor with photography/dermoscopy.
Seborrheic Keratosis
Common benign lesion in middle-aged/older adults. "Stuck-on" appearance with waxy, scaly surface. Often multiple, brown to black color.
Benign, no malignant potential. Remove if irritated, cosmetic concern, or diagnostic uncertainty. Cryotherapy or curettage.
🎨 Pigment Disorders
Melasma
Chronic hyperpigmentation disorder. Affects women of reproductive age. Light-brown to dark-brown patches on face (malar, mandibular, forehead, chin, upper lip).
First-Line: Hydroquinone 4% cream (once or twice daily for 2-6 months)
Second-Line: Combination therapy (hydroquinone + tretinoin + fluocinolone), chemical peels (glycolic acid, salicylic acid, TCA), or laser (low-fluence Q-switched)
Note: Incomplete response common; frequent relapses with UV/hormonal exposure
Vitiligo
Acquired depigmentation disorder causing well-demarcated, milk-white macules and patches. Autoimmune destruction of melanocytes. Affects 0.1-2% of population equally across ethnicities.
Segmental vs. Non-Segmental: Segmental progresses rapidly then stabilizes; non-segmental spreads slowly over time.
Self-Limited: Usually resolves within 6 months. Reassurance and optimization of nutrition/stress management.
Onychomycosis (Nail Fungus)
Already covered in Fungal Infections tab. Fungal infection causing discoloration, thickening, crumbling of nails.
Psoriasis of Nails
Nail changes in psoriasis include pitting (punctate depressions), onycholysis (nail separation), subungual hyperkeratosis, and nail discoloration.
Difficult to treat. Topical corticosteroids, vitamin D analogs, or intralesional corticosteroid injections. Systemic therapy for extensive involvement.
Nail Infections & Paronychia
Acute paronychia: Bacterial (often Staph) infection of nail fold. Chronic paronychia: Often Candida, associated with frequent water exposure/nail biting.
Paronychia Treatment
Acute: Warm soaks, topical antibiotics (mupirocin), or drainage if abscess
Chronic: Avoid water/irritants, topical antifungal (nystatin, azole), or systemic antifungal if severe
🩸 Vascular Skin Abnormalities
Port-Wine Stain (Nevus Flammeus)
Congenital vascular malformation. Pink to dark red patch present at birth, typically on face/neck. Darkens and thickens with age.
Risk of Sturge-Weber Syndrome: If involving V1 distribution (ophthalmic), screen for CNS involvement (seizures, glaucoma).
Port-Wine Stain Treatment
Pulsed dye laser (gold standard) in childhood is most effective. Multiple sessions required. Early treatment prevents progression and darkening.
Hemangiomas
Benign vascular tumors. Infantile hemangiomas appear within first weeks of life. Rapid growth phase (0-12 months), then plateau, then involute over years (most resolve by age 5-7).
Most Are Self-Limited: Observation often appropriate. Intervene if: airway compromise, visual obstruction, ulceration, or significant functional impairment.
Hemangioma Treatment
Observation (most cases)
Propranolol (first-line if intervention needed)
Topical timolol for superficial lesions
Corticosteroids (intralesional or systemic)
Laser therapy for residual telangiectasia
Telangiectasia
Dilated capillaries visible on skin surface. May be inherited (hereditary hemorrhagic telangiectasia/Osler-Weber-Rendu), acquired (from sun damage, rosacea, liver disease), or medication-induced.
Spider Angiomas
Central arteriole with radiating capillaries ("spider legs"). Associated with liver disease, pregnancy, estrogen excess. Blanch with pressure over central vessel.
Treatment: Usually asymptomatic; treat if cosmetically bothersome. Laser or electrocautery of central vessel. Address underlying cause.
Cherry Angiomas
Small (1-5mm) red papules on trunk, arms. Benign, common with aging. Do not blanch with pressure.
No treatment needed unless cosmetically concerning. Cryotherapy or laser removal available if desired.
✨ Other Dermatological Conditions
Acanthosis Nigricans
Velvety, hyperpigmented plaques in intertriginous areas (neck, axillae, groin). Associated with insulin resistance, obesity, diabetes, or malignancy (especially gastric cancer in adults).
Workup: Fasting glucose, HbA1c, insulin level. Screen for malignancy in adults with sudden onset or extensive involvement.
Acanthosis Nigricans Management
Treat underlying insulin resistance: metformin, weight loss
Topical tretinoin or ammonium lactate for cosmetic improvement
Chronic inflammatory condition with recurrent nodules, abscesses, sinus tracts, and scarring in apocrine gland-bearing areas (axillae, groin, inframammary, perianal).
Significant Morbidity: Painful, draining lesions; scarring; depression. Requires early aggressive treatment to prevent progression.
HS Treatment
Mild: Good hygiene, antiseptic washes, topical antibiotics
Severe: TNF-α inhibitors (adalimumab, infliximab), surgical drainage, wide excision of affected areas
Photosensitivity Reactions
Polymorphic light eruption (PMLE): pruritic papules/plaques on sun-exposed skin within hours to days of UV exposure. More common in temperate climates, females.
Antimalarial drugs (hydroxychloroquine) for prophylaxis
Keloids & Hypertrophic Scars
Hypertrophic scars: Raised, red, stay within original wound boundaries; often improve over time. Keloids: Fibroproliferative lesions that extend beyond original wound; don't regress.
Risk Factors for Keloids: African or Asian ancestry, age 10-30, locations: chest, shoulders, earlobes. Often triggered by piercing, tattoo, surgery, acne.
Surgical excision (risk of recurrence; combine with other modalities)
Silicone gel sheeting for prevention after injury
Pilonidal Disease
Chronic abscess or sinus tract in sacrococcygeal region. Presents with painful cysts, drainage, or hair protruding from pit. More common in males, hairy individuals.
Treatment: Poor hygiene/hair removal increases risk. Acute abscess requires drainage. Definitive treatment is surgical excision of sinus tract, often with midline closure or flap procedures.
🚨 Dermatologic Emergencies
Toxic Epidermal Necrolysis (TEN)
Life-threatening mucocutaneous reaction with >30% body surface area epidermal detachment. Mortality 25-35%. Usually drug-induced (NSAIDs, antibiotics, anticonvulsants, allopurinol).
Management: IMMEDIATE admission to ICU/burn unit. Discontinue offending drug. Supportive care (fluid management, temperature control, wound care). Consider IVIG or corticosteroids (controversial). Treat secondary infections.
Stevens-Johnson Syndrome (SJS)
Severe mucocutaneous reaction with <10% body surface area epidermal detachment (10-30% is overlap SJS/TEN). Fever, malaise, oral/genital ulcers, target lesions on extremities.
Erythema Multiforme (EM)
Acute inflammatory reaction to infection (HSV, mycoplasma) or medications. Classic "target lesions" with three zones: red center, pale ring, erythematous outer ring.
First-generation (diphenhydramine) if sedation acceptable
Corticosteroids if severe or systemic involvement
For angioedema: consider ACE inhibitor as trigger (if relevant)
Necrotizing Fasciitis
Rapidly spreading deep soft-tissue infection (bacterial). Severe pain out of proportion to skin findings, skin becomes dusky/hemorrhagic, systemic toxicity evident early.
Medical Emergency: Requires surgical debridement + aggressive antibiotics. High mortality if delayed. Clinical diagnosis; imaging (MRI, ultrasound) supportive.
Pressure Ulcers (Decubitus Ulcers)
Preventable wounds from prolonged pressure over bony prominences. Staged I-IV by depth. Common in immobile, elderly patients.
Pressure Ulcer Prevention & Management
Prevention: Frequent repositioning, pressure relief, skin care, nutrition
Stage I: Continue prevention, skin protection
Stage II-IV: Wound cleansing, debridement, moist dressings, infection management, consider surgical intervention for deep ulcers
📝 Practice Questions
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