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USMLE Step 2 (Fach) / Dermatology (Lektion)

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• Sporotrichosis Risk factor: Traumatic injury to skin during gardening (eg, thorn) Clinical features:- Pustules and ulcers with ascending lymphangitis- Disseminated disease: pneumonia, meningitis Diagnostics:- Fungal culture showing dimorphic, cigar-shaped yeast- Septate hyphae, rosette-like clusters of conidia at the tips of the conidiophores Treatment:- Oral itraconazole or potassium iodide- Disseminated: Amphotericin B
• Intertrigo Dermatitis that primarily affects skin folds (e.g., submammary, inguinal, interdigital) Etiology:- Increased moisture in the skin folds- Obesity- Immunodeficiency- Friction- Lack of air circulation- Secondary infection Clinical features:- Erythematous plaques/papules → macerations, crusting, erosion, or fissures on an erythematous base- If infected with Candida → Satellite lesions Treatment:- Uncomplicated: topical protective and drying agents (eg, zinc oxide, talcum powder, aluminum sulfate)- If secondary infection is present: Candida → miconazole/clotrimazole/fluconazole; Strep A → mupirocin/erythromycin
• Erythrasma Skin infection caused by Corynebacterium minutissimum Risk factors:- Moist skin- Immunodeficiency- Diabetes- Advanced age Clinical features:- Location: Intertriginous areas (eg, toe webs, groin, axilla)- Well demarcated erythematous or brown patches with fine scaling and wrinkling- Pruritus usually absent Diagnostics:- Wood lamp examination: coral-red fluorescence- Gram stain of skin scrapings: gram-positive rods Treatment:- Improved skin hygiene- Localized disease: Topical antibiotic treatment (e.g., clindamycin, erythromycin)- Extensive disease: Systemic antibiotic treatment (e.g., erythromycin)
• Necrobiosis lipoidica Inflammatory granulomatous disorder of the skin; characterized by collagen degeneration and lipid accumulation in the surface of the skin. Epidemiology:- > 60% associated with diabetes mellitus- W >> M Clinical features:- Rash: Circumscribed, erythematous plaques with atrophic centers and irregular margins- Common sites: Pretibial region- Usually asymptomatic Treatment: Corticosteroids may be effective
• Infantile hemangioma = Strawberry hemangioma Natural history:- May present as a patch of telangiectasias at birth- Proliferation: Age 0-1, bright red raised nodule- Involution: Age 1-9, deeper red/violet, regression in size Management:- Observation- Topical beta blocker (eg, propanolol) for ulcerated or cosmetically sensitive areas (eg, face) Complications:- Ulceration/scarring- Vision impairment if near eye- Life-threatening if near airway
• Bed bugs Hide in old furniture and in the seams and folds of mattresses. Come out at night to feed on exposed skin. Clinical features:- Small, punctate lesions with surrounding erythema- Classically in linear tracks or clusters ("breakfast, lunch, and dinner" bites)- Uncommon on the palms and soles due to thickness of skin
• Epidermal inclusion cyst Discrete benign nodule lined with squamous epithelium that contains a semisolid core of keratin and lipid. Clinical features:- Slow-growth, firm, mobile, painless nodule- Dark colored punctum may be seen- Localized predominatly on the face, head, neck, back, or genital area- High probability of recurrence Treatment:- Excision performed for cosmetic reasons- Incision and drainage for infected and fluctuant cysts that are painful and erythematous
• Calciphylaxis Calcific uremic arteriolopathy Characterized by systemic arteriolar calcification and soft-tissue calcium deposition with local ischemia and necrosis. Epidemiology:- Patients with longstanding end-stage renal disease who are on hemodialysis- Patients with kidney transplants Clinical features:- Painful subcutaneous plaques and nodules that can be violaceous or purpuric- Nodules can progress to ischemic or necrotic ulcers- Most common in areas of adiposity (eg, trunk, thighs)- Intact peripheral pusles Lab findings:- High PTH- Hyperphosphatemia
• Lymphedema Etiology:- Obstruction (eg, malignancy)- Lymph node dissection- Chronic inflammation (eg, recurrent cellulitis)- Congenital (eg, Turner syndrome)- Parasitic infection (eg, filariasis) Clinical features:- Swelling, pain, heaviness- Early: Soft skin, pitting edema- Late: Firm & thickened skin, nonpitting edema- Stemmer sign: Inability to life the skin on the dorsum of the second toe Treatment:- Weight loss- Limb elevation & compression- Physiotherapy
• Tinea capitis Epidemiology:- Most common in African American children- Transmission via direct contact or from fomite (eg, shared combs) Etiology:- E.g. Microsporum canis Clinical features:- Scaly erythematous patch with hair loss on scalp- ± black dots in affected area- ± tender lymphadenopathy Management: Oral griseofulvin or terbinafine Complications: Kerion
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• Ichthyosis Chronic, inherited skin disorder characterized by diffuse dermal scaling. Epidemiology: Most common type of hereditary ichthyosis Etiology: Autosomal dominant inheritance; associated with atopic diseases Clinical presentation:- Onset usually between 3 and 12 months of age- Generalized fine, white scaling- Dry and coarse skin (xerosis): more common on extensor surfaces (skin folds are usually not affected)- Hyperlinearity of palms and soles (accentuated skin lines)- Symptoms generally worsen in winter and improve in summer Treatment:- Skin moisturizers (e.g., creams containing urea or panthenol), topical retinoids Prognosis: Good; lesions usually disappear during adolescence
• Perianal dermatoses Contact dermatitis- Most common cause in infants- Spares creases/skinfolds- Treatment: Topical barrier ointment or paste Candida dermatitis- Second most common cause in infants- Beefy-red rash involving skinfolds with satellite lesions- Treatment: Topical antifungal therapy Perianal Streptococcus pyogenes- School-aged children- Bright, sharply demarcated erythema over perianal/perineal area; pruritus and pain with stooling; perirectal fissues; blood-streaked stools- Treatment: Oral antibiotics
• Skin conditions & associated diseases Acanthosis nigricans:- Insulin resistance- GI malignancy Multiple skin tags:- Insulin resistance- Pregnancy- Crohn disease (perianal) Porphyria cutanea tarda, cutaneous leukocytoclastic vasculitis (palpable purpura) secondary to cryoglobulinemia:- Hepatitis C Dermatitis herpetiformis:- Celiac disease Sudden-onset severe psoriasis, recurrent herpes zoster, disseminated molluscum contagiosum:- HIV infection Severe seborrheic dermatitis:- HIV infection- Parkinson disease Explosive onset of multiple itchy, seborrheic keratoses:- GI malignancy Pyoderma gangrenosum:- Inflammatory bowel disease
• Acute febrile neutrophilic dermatosis (Sweet syndrome) Characterized by an abrupt onset of painful edematous papules, plaques, or nodules on the head, neck, and upper extremities - Associated with hematologic malignancies, upper respiratory and gastrointestinal infections, and inflammatory bowel disease
• Drug-induced acne Common triggers:- Glucocorticoids, androgens- Immunomodulators (eg, azothioprine, EGFR inhibitors)- Anticonvulsants (eg, phenytoin), antipsychotics- Antituberculous drugs (eg, isoniazid) Presentation:- Monomorphic papules or pustules- Lack of comedones, cysts & nodules- Location & age of onset may be atypical for age Management:- Discontinue offending medication- Standard acne therapy unlikely to be effective
• Psoriatic arthritis Definition: inflammation of joints (primarily on hands, feet, spine) that may occur with psoriasis Epidemiology: 5-30% of psoriasis patients affected Clinical features:- Psoriasis and psoriatic arthritis may occur independently or together - Oligoarthritis (most common, accounting for 70% of cases): typically with involvement of both the DIP and PIP- Spinal involvement (up to 40% of cases)- Enthesitis- Tenosynovitis- Dactylitis: inflammation and swelling of fingers or toes (“sausage digit”) ClASsification Criteria for Psoriatic ARthritis (CASPAR) (≥ 3 out of the 5 following points required). 1. Evidence of psoriasis2. Psoriatic nail dystrophy3. Negative rheumatoid factor (RF)4. Dactylitis5. Radiologic signs- Imaging studies: joint destruction, ankylosis- Fingers: pencil-in-cup deformity- Spine: syndesmophytes, and in particular asymmetric paravertebral ossification Treatment:- Mild disease: NSAIDs- Moderate to severe disease: disease-modifying antirheumatic drugs (DMARDs)- Physical therapy
• Lichen sclerosus Lichen sclerosus is a chronic inflammatory disease with characteristic white, atrophic plaques. Etiology: unknown; but genetic, immunological and hormonal factors likely play a role Epidemiology: rare disease; more common in women (postmenopausal) Localization:- Anogenital: vulvar and perianal area in women → classic “figure eight” appearance; glans penis in males- Extragenital: most commonly on back, shoulders, neck, wrists, thighs and under the breast Lesions:- Initially: papules and plaques that are white, polygonal, well-demarcated, and may be surrounded by an inflammatory halo- Later: lichenification and erosive scarring Clinical presentation:- Severe pruritus, pain/soreness, anal fissure, painful defecation - Dyspareunia in women, and phimosis in men Diagnosis:- Punch biopsy: confirms diagnosis and rules out squamous cell carcinoma Complications:- Increased risk of cancer (vulvar carcinoma; squamous cell carcinoma)- Destructive scarring Treatment:- High potency topical steroids (clobetasol, sometimes betamethasone) or calcineurin inhibitors (tacrolimus)- If necessary, surgical excision
• Common acquired melanocytic nevi (“mole”) Epidemiology: common, regardless of age, gender, or ethnicity Etiology:- Genetics (parents with many moles)- Fair skin and red hair- Intense sun exposure during childhood Clinical features:- Generally, all types have a uniform color, border, and surface.- Junctional nevi (epidermal): flat, well-demarcated brownish macules - Compound nevi: arising from a junctional nevus → elevated lesion- Intradermal nevi (dermal): elevated lesion that may be hard (fibrotic) and grow hair Diagnosis: Dermoscopy shows well-nested melanocytic proliferations at the dermal-epidermal junction. Treatment: usually not required; biopsy or excision if nevi appear atypical Prognosis: may undergo dysplastic changes into precursor lesions for melanoma → then called dysplastic nevus (atypical mole)
• Bowen's disease Definition: squamous cell carcinoma in situ of the skin Etiology:- Exposure to sun- Often associated with human papillomavirus (HPV) types 16 and 18- May be related to arsenic exposure Lesions:- Irregularly shaped and sharply defined borders- Erythematous and scaly- Lesions are usually isolated- Most common site: commonly occurs on skin that is exposed to sun Prognosis: May progress to invasive squamous cell carcinoma. If treated, however, the prognosis is excellent. Treatment:- 5-FU, imiquimod, or photodynamic therapy- Surgical excision with a margin
• Erythroplasia of Queyrat (= Bowen's disease of the glans penis) Definition: squamous cell carcinoma in situ of the penile mucosa Associated with:- Chronic irritation or infection- Lack of circumcision- HPV types 16 and 8 Lesion: single or multiple sharply demarcated, nonhealing lesions (e.g., plaques or red papules) that may ulcerate and bleed easily Most common site: preputium, glans penis Treatment:- 5-FU, imiquimod, or photodynamic therapy- Surgical excision with a margin
• Albinism Congenital disorders of melanin synthesis resulting in hypopigmentation. Epidemiology:- Affects all races and both sexes- Most types of albinism are congenital and are noticed early in life (e.g., newborns, toddlers) Classification:- Ocular albinism (OA): only the visual system (e.g., eyes, optic nerve) is affected.- Oculocutaneous albinism (OCA): absence of melanin in the skin, hair, and the visual system (e.g., eyes, optic nerve).- May be associated with Chédiak-Higashi syndrome Pathophysiology: impaired melanin production - Due to dysfunctional tyrosinase activity, or impaired transport of tyrosine or melanin.- Normal melanocyte number, decreased or absent melanin production. Clinical features:- Translucent, hypopigmented, blue, grey, or green irides- Photophobia, decreased visual acuity- Strabismus, nystagmus, amblyopia- Abnormalities of the optic nerve- Skin and hair: milky, white color, photosensitivity, sunburns.- Associated with increased risk of skin cancer Treatment: only supportive treatment, no curative treatment available.- Treatment of strabismus: eye-patching , eye surgery- Sunscreen, avoidance of sunburns, regular screening for skin cancer- Dark, tinted glasses- Nitisinone: used for hereditary tyrosinemia type 1
• Androgenic alopecia Progressive, nonscarring alopecia that affects the regions of the scalp with the most androgen-sensitive hair follicles, resulting in a characteristic pattern of balding (bitemporal scalp in men and vertex and frontal scalp in women). Epidemiology:- Most common type of alopecia- Prevalence: Increases with age- Sex: ♂ > ♀ (but very common in women as well)- Age at onset: puberty in males; menopause in females- Ethnicity: more common in white populations Etiology:- Increased androgen sensitivity of hair follicle in genetically predisposed individuals - Congenital adrenal hyperplasia- Androgen-producing tumors: Leydig cell tumor, arrhenoblastoma Pathophysiology: Androgen shortens the anagen phase of hair growth → vellus hair formation (thin, short hair) Treatment: Males- First-line treatment: finasteride or 5% minoxidil Treatment: Females:- 2% Minoxidil: first-line treatment- Spironolactone
• Cutaneous larva migrans Pathogen: - Human hookworms (Ancylostoma duodenale and Necator americanus)- Zoonotic hookworms, i.e., cat and dog hookworms that can also infect humans (Ancylostoma braziliense and Ancylostoma caninum) Mode of transmission: percutaneous penetration of larvae (primarily via the feet)- Human hookworm life cycle: soil contaminated with human feces containing hookworm eggs → eggs hatch into larvae → penetration of larvae into skin (usually the feet) → larvae migrate to lungs via blood and lymphatic vessels → migration via the bronchi and trachea to the larynx → larvae are expectorated and swallowed back into the intestine→ larvae mature into adult worms that colonize the intestinal tract → female hookworms lay eggs in the intestines that are eliminated with the feces - Zoonotic hookworms are usually unable to break through the basement membrane after entering the human epidermis (humans are accidental intermediate hosts) → migration through the epidermis for several weeks Clinical features:- Cutaneous entry: pruritus, erythema, maculopapular rash, occasionally with serpiginous marks representing larval tracks→ In zoonotic hookworm infections, only cutaneous symptoms are present, which is termed cutaneous larva migrans (CLM)- Respiratory tract: dry cough, wheezing → Löffler syndrome- Intestine: abdominal pain, weight loss, nausea, vomiting, diarrhea- Anemia Diagnosis:- Initial test: complete blood cell (CBC) count may show eosinophilia and microcytic anemia- Confirmatory test: consecutive stool examination for eggs or worms Treatment:- For human hookworms: bendazoles or pyrantel pamoate- For CLM: bendazoles, ivermectin
• Type I hypersensitivity reaction Course:- Immediate reaction: allergic reaction within minutes of contact with the antigen- Late-phase reaction: occurs hours after immediate reaction for a duration of 24-72 hours Main symptoms: pruritus, edema, rash, rhinitis, bronchospasm, and abdominal cramping Treatment:- Urticaria: avoid offending agent (if known), H1-receptor blocker (e.g., cetirizine), glucocorticoids- Drug reactions→ Mild reactions (mild urticaria/angioedema) may be treated by removing the offending drug and monitoring ± antihistamines.→ Moderate reactions (more pronounced urticaria/angioedema) should be treated with withdrawal of the offending drug and antihistamines ± glucocorticoids.→ Severe reactions require emergency resuscitation (see anaphylaxis).- Allergen immunotherapy (desensitization)
• DRESS syndrome Drug rash with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome) Delayed hypersensitivity reaction to a drug (within 1-8 weeks following administration) Etiology:- Allopurinol- Antiepileptic drugs (e.g., lamotrigine, phenytoin, carbamazepine)- Antibiotics (e.g., sulfonamide) Clinical features:- Fever- Pruritic morbilliform rash- Facial edema- Hepatomegaly- Diffuse lymphadenopathy- Possible multiorgan failure Laboratory tests:- Eosinophilia- Thrombocytopenia- Atypical lymphocytosis Treatment:- Drug withdrawal- Symptomatic: Corticosteroids are often used, but their effect is disputed. Prognosis: fatal in ∼ 10% of cases
• Pyoderma gangrenosum Associated with various conditions, including Crohn disease, UC, rheumatoid arthritis, and trauma Most common site: extensor side of the lower limbs Clinical features: very painful, rapidly-progressive, red spots that can change into purulent pustules or deep ulcerated lesions with central necrosis Therapy: immunosuppressants (corticosteroids, cyclosporine A)
• Chickenpox (varicella) Chickenpox (varicella) is a primary infection caused by the varicella-zostervirus (VZV) that occurs most frequently during childhood. Clinical features:- Incubation period: 2 weeks - Prodromes: 1-2 days prior to the onset of exanthem- Presents with constitutional symptoms (e.g., fever, malaise)- Exanthem phase- Duration: ∼ 6 days- Widespread rash starting on the trunk, spreading to the face, scalp, and extremities- Simultaneous occurrence of various stages of rash: erythematous macules → papules → vesicles filled with a clear fluid on an erythematous base → eruption of vesicles → crusted papules → hypopigmentation of healed lesions- Severe pruritus- Fever, headache, and muscle or joint pain Diagnostics:- Clinical diagnosis - Best initial test: Tzanck smear: Smear of vesicle fluid shows multinucleated giant epithelial cells with eosinophilic bodies.- Best confirmatory test: PCR Treatment:Symptomatic- Pruritus: topical applications (e.g., calamine lotion or pramoxine gel) and, in more severe cases, oral antihistamines (e.g., cetirizine) Antiviral therapy- Indication: Immunosuppressed individuals, primary infection in adults and in unvaccinated adolescents ≥ 13 years, individuals on long-term salicylate therapy (e.g., aspirin)- Administration: within 24 hours of onset of rash- Drug of choice: acyclovir (or also: valacyclovir, famciclovir)
• Warfarin-induced skin necrosis Warfarin inhibits all vitamin K-dependent coagulation factorsAnticoagulants protein C and protein S are depleted more quickly than procoagulants factors II, IX, and X → increased factor V and VIII activity → initial hypercoagulable state → vascular occlusion, tissue infarction, and blood extravasation Increased risk in patients with underlying hereditary protein C deficiency Presentation: painful purpura, hemorrhagic blisters, and large areas of necrosis; mostly affects subcutaneous adipose tissue Immediate management: discontinue warfarin, administer IV vitamin K, unfractionated heparin, and source of protein C (protein C concentrate, FFP); surgical debridement and grafting in therapy-refractory cases Prevention: temporary bridging therapy with heparin for immediate anticoagulation until warfarin has started to act
• Keloid Definition:- Skin lesions caused by high fibroblast proliferation and collagen production as excessive tissue response to typically small skin injuries- Grows beyond the boundaries of the original lesion- Does not regress spontaneously- Recurs after resection Etiology: imbalance in wound healing processes due to local factors and genetics   Clinical features:- Scar tissue of varying consistency (soft or hard) that may be brownish-red in color- Pruritus- Pain Localization: earlobes, face (especially cheeks), upper extremities, chest, and neck Diagnosis: based on clinical appearance of lesion and patient history of trauma or surgery Treatment:- First-line treatment: intralesional steroid injection → decreases scar thickening, and, if present, relieves pain and pruritus- Silicone gel sheets- Compression therapy- Surgery: Cryotherapy, Laser treatment, Surgical excision; may be combined with radiotherapy
• Shingles (herpes zoster) Treatment:- Treatment of skin lesions (e.g., wet dressings with 5% aluminum acetate)- Anti-inflammatory and analgesic therapy  - Antiviral therapy:acyclovir, valacyclovir or famciclovir  → Immunocompromised patients and/or those with disseminated disease should receive IV acyclovir.- Consider hospitalization if:→ The patient is immunocompromised→ Symptoms are atypical and/or severe (e.g., pain that requires strong medication, involvement of more than two dermatomes or dissemination)→ Signs of myelitis, meningoencephalopathy, ophthalmic involvement or severe bacterial superinfection
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• Post-herpetic neuralgia Timeframe: Persists > 4 months from onset Epidemiology:- Occurs in ∼ 10-15% of overall herpes zoster cases- Strong association with age   Clinical features: attacks of acute, intense pain, persisting for at least 3 months in the area previously affected by the rash Treatment:- First choice: tricyclic antidepressants (e.g., amitriptyline)→ Relative contraindications: patients with heart disease, epilepsy, or glaucoma→ Should be used in caution with elderly- Alternatives: gabapentin, pregabalin  - Second-line: topical capsaicin, opioids, intrathecal glucocorticoid injections Prognosis: Chronic pain develops in approximately 25-50% of affected individuals if remission does not occur within 12 months
• Sunburn Clinical features:- Symptoms begin hours after exposure, resolve by day 3-7- Mild-Moderate: Erythema, tenderness- Severe: As above + blistering, systemic symptoms (e.g. fever, vomiting, headache) Treatment:- Mild-moderate:→ Topical: Cold compresses, calamine lotion, aloe vera→ Oral: NSAIDs- Severe:→ Hospitalization→ IV fluids & analgesia→ Wound care

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