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USMLE Step 2 (Subject) / Dermatology (Lesson)

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• Atopic dermatitis (eczema) Epidemiology:- About 10-15% of all children are affected- Onset of symptoms usually occurs between 3-6 months of age- Disease often improves with age Etiology:- Genetics (polygenic inheritance): Approx. 70% of patients have a family history of atopic disease - Triggers: Exposure to indoor dust, heat, extremely dry or humid climate, skin irritation Clincal features:- Main symptoms: intense pruritus and dry skin - Infantile AD (age < 2 years)→ Eczema: over the cheeks, face, head, and extensor surfaces of the extremities that usually spares the diaper area→ Dennie-Morgan fold: increased folds below the eye- Childhood AD (age 2 to 12 years)→ Eczema: flexural creases (antecubital and popliteal fossae), skin folds, extensor surface of hands→ Lesions usually become lichenified (lichenification is thickening of the skin with accentuated skin markings) - Adult/adolescent AD (age > 12 years)→ Lichenified lesions and pruritus of flexor surfaces of the extremities Diagnosis: Clinical- KOH prep can help distinguish eczema from tinea infection.- Mild eosinophilia and ↑ IgE may be seen in some patients, but these are not used to make the diagnosis. Treatment:- Avoid triggers- Mild ezcema: Emollients (↑ skin hydration by reducing evaporation); topical steroids - Moderate eczema: + Topical calcineurin inhibitors- Severe ezcema: + Phototherapy (narrow band UVB)
• Erythema toxicum neonatorum Benign eruption that typically begins 1-3 days after delivery and resembles ezcema, presenting with red papules, pustules, and/or vesicles with surrrounding erythematous halos. - ↑ eosinophils are present in the pustules or vesicles. - Usually resolves in 1-2 weeks with no treatment. 
• Contact dermatitis A type IV hypersensitivity reaction that results from contact with an allergen to which the patient has previously been exposed and sensitized. Etiology:- Poison ivy, poison oak, poison sumac (urushiol-induced contact dermatitis)- Nickel, cobalt, chromium- Perfumes, soaps, cosmetics- Latex or rubber gloves- Topical medications: hydrocortisone, topical antibiotics (e.g., neomycin), benzocaine Clinical features:- Intensely pruritic, erythematous, papular rash- Vesicles and serous oozing in severe cases- Can spread to other parts of the body through antigen transfer by the hands or in the circulationLatex allergy is not contact dermatitis - it is a type I hypersensitivity reaction. Diagnosis: Clinical- Patch testing can be used to establish the causative allergen.→ Allergen is fixed on a patch and then attached to the arm or back.→ Reaction is recorded at two times: The first assessment is after 48 hours, the second after 4-5 days.→ Positive result: erythema, papules, and vesicles under the area of contact Treatment:- Avoidance of the allergen- Mild to moderate cases: topical corticosteroids, oatmeal baths, soothing lotions (e.g., calamine), wet dressings (especially for oozing, crusting lesions), topical antihistamines- Severe cases: systemic corticosteroids, systemic antihistamines
• Seborrheic dermatitis A common chronic inflammatory skin disease that may be caused by hypersensitivity reaction to Malassezia furfur, a generally harmless yeast found in sebum and hair follicles. It has a predilection for areas with sebaceous glands.  Epidemiology:- Sex: M > F- Bimodal distribution: infants 2 weeks to 12 months; puberty and early adulthood. Predisposing factors:- Parkinson's disease- Immunodeficiency (e.g., HIV infection)- Oily skin (seborrhea)- Androgenetic alopecia- Familial history of seborrhoeic dermatitis, psoriasis Clinical features:- Ranges from erythematous plaques with patchy scaling → greasy yellow crusts. Seen around the ears, eyebrows, nasolabial fold, midchest, and scalp.- Dandruff and itching- Infants: Severe, red diaper rash with yellow scale, erosions, and blisters. Scaling and crusting ("cradle cap") may be seen on scalp.Atopic dermatitis: While seborrheic dermatitis typically presents during the first 3 months of life, atopic dermatitis tends to appear at a later stage. Diaper dermatitis: usually spares intertriginous areas (skin folds) Diagnosis: ClinicalConsider HIV or Parkinson's disease if there is a marked or unusual distribution of seborrheic dermatitis! Treatment:- Selenium sulfide or zinc pyrithione shampoos for the scalp.- Topical antifungals (ketoconazole cream) and/or topical corticosteroids for other areas.  Complications: - Exacerbation of seborrheic dermatitis may lead to generalized erythroderma- Secondary bacterial infection
• Stasis dermatitis Lower extremity dermatitis due to venous hypertension forcing blood from the deep to the superficial venous system. Venous hypertension is often a result of venous valve incompetence or flow obstruction. Risk factors:- Obesity- Advanced age- Varicose veins- History of DVT Clinical features:- Leg pain (achy, heavy)- Edema- Venous dilation (varicosities, telangiectasias)- Dermatitis: erythema, pruritus, scaling, weeping- Chronic woody induration and brown discoloration- Ulcers  Treatment: - Leg elevation, compression stockings, emollients, and topical steroids.
• Psoriasis Epidemiology:- Prevalence: ∼ 2% of the white population- Age of onset: 20-40 years Trigger factors:- Infectious: Infections caused by group A streptococci, staphylococcus, HIV- Mechanical irritation- Drugs (e.g., beta-blockers, chloroquine, lithium, interferon) Clinical features:- Course: relapsing, with symptom-free intervals- Well-demarcated, erythematous lesions and silvery-white scaling plaques- Mainly on scalp, back, elbows, and knees (extensor surfaces), but any other site may be involved- Pruritus in ∼ 80% of cases (typically mild, but may also be severe)- Involvement of nails (in ∼ 50% of cases)→ Nail pitting: small, round depressions in the nail→ Oil drop sign (or salmon spot): well-circumscribed, yellow-reddish discoloration of the nail→ Brittle nails: nail dystrophy with crumbling of the nail→ Onycholysis: partial and mostly distal separation of the nail plate- Less than 10% develop psoriatic arthritis→ Distal interphalangeal joints, arthritis mutilans (deforming & destructive)- Soft tissue involvement: Enthesitis, dacylitis, swelling of the hands or feet with pitting edema Cutaneous variants: Plaque psoriasis; Guttate psoriasis; Erythrodermic psoriasis; Inverse psoriasis Diagnosis: Clinical- Koebner phenomenon: Physical stimuli or skin injury (e.g., trauma, scratching, irritating clothing) lead to skin lesions typical of the underlying condition appearing on previously healthy skin ("isomorphic response"). - Auspitz sign: small pinpoint bleeding when scales are scraped off- Biopsy: Parakeratosis, Munro microabscess, acanthosis, spongiotic dermatitis Treatment: - Mild disease: Topical steroids (triamcinolone, fluocinonide, clobetasol), calcipotriene (vitamin D derivative), tar preparations (anthralin), and vitamin A derivatives- Moderate disease: Topical medication as combination therapy. Add systemic agents as needed (methotrexate, retinoid, cyclosporine)- Severe disease: Topical + systemic treatment. Phototherapy; Methotrexate or anti-TNF biologics (etanercept, infliximab, adalimumab)
• Urticaria (Hives) Results from the release of histamine and prostaglandins from mast cells in a type I hypersensitivity response. It is characterized by superficial, intense erythema and edema in a localized area. Can be acute or chronic (lasting >6 weeks). Etiology:- Infections (viral, bacterial, parasitic)- IgE mediated (antibiotics, insect bites, latex, food, blood products)- Direct mast cell activation (narcotics, muscle relaxers, radiocontrast medium)- NSAIDs- Idiopathic (up to 50% of patients) Clinical features:- Well-circumscribed, raised erythematous plaques- Lesions can be oval, round, or serpiginous up to several centimeters in diameter- Intense pruritus- Lesions can worsen over minutes to hours, then resolve within 24 hours Treatment: systemic antihistamines- Anaphylaxis requires epinephrine IM, antihistamines, IV fluids, and airway maintenance.
• Erythema multiforme A rare, acute hypersensitivity reaction most commonly triggered by herpes simplex virus (HSV) infections. Etiology:- Infections (most common): herpes simplex virus (HSV), Mycoplasma pneumoniae, and fungal infections - Drugs: e.g., barbiturates, phenytoin, NSAIDs, penicillins, and sulfonamides- Immunizations (rare): e.g., after diphtheria, tetanus, influenza, hepatitis B vaccination Clinical features:- Acute onset, with progression from erythematous macules to papules to target lesions (“bull’s-eye lesions”)- Symmetrical distribution- Affects backs of hands and feet first → spreads proximally and can affect the entire body, including palms and soles- EM minor: no/minimal involvement of mucus membranes- EM major: painful ulcers of the oral (most common), ocular, genital mucosa It is a distinct entity from SJS, and there is no risk of progression to TEN.- Further symptoms: fever, myalgia, and arthralgia in cases of EM major Diagnosis: Clinical- Should be suspected (especially) if there is a history of recurrent labial herpes, recent drug intake, or immunizations.- Serology (PCR testing): in patients with suspected HSV/M. pneumoniae infections - Skin biopsy: indicated only in doubtful cases (e.g., no target lesions, recurrent EM)- As opposed to SJS or TEN, in EM the Nikolsky sign is negative. Treatment: - Symptomatic; systemic corticosteroids are of no benefit.- Severe cases (EM major): hospitalize and treat as thermal burns- Recurrent EM: oral acyclovir for 4 months
• Stevens-Johnson syndrome/Toxic epidermal necrolysis SJS and TEN constitute two different points on the spectrum of life-threatening exfoliative mucocutaneous diseases that are often caused by a drug-induced immunologic reaction.< 10% = SJS10-30% = SJS/TEN overlap> 30% = Toxic epidermal necrolysis (severe SJS) Etiology:- Drugs (most common trigger, ∼ 80% of cases): Antibiotics (sulfonamides, aminopenicillins, rifampicin), corticosteroids, antiretrovirals (e.g., nevirapine), antiepileptics (phenytoin, phenobarbital, lamotrigine, valproic acid, carbamazepine, ethosuximide), NSAIDs (e.g., piroxicam), allopurinol, sulfasalazine- Infections: Mycoplasma pneumoniae, CMV, herpes- Vaccinations- Graft-versus-host disease Risk factors: HIV infection Clinical features:- Begins 1-3 weeks after the intake of medication- Acute influenza-like prodrome- Mucocutaneous lesions appear 1-3 days after the onset of prodromal symptoms- Painful, erythematous/purpuric macules→ May have a targetoid appearance (cockade lesions)→ Typically seen over the face and trunk- Lesions form bullae and/or vesicles; positive Nikolsky's sign- Extensive, full-thickness epidermal necrosis and sloughing (resembling large superficial burns)- Healing by re-epithelialization: begins 1-2 weeks after epidermal sloughing and is completed within a few weeks- Mucosal membranes: almost always involved- Shock may develop Diagnosis:- SJS: Biopsy shows degeneration of the basal layer of the epidermis.- TEN: Biopsy shows full-thickness eosinophilic epidermal necrosis. Differential diagnosis: Erythema multiforme, SSSS, GvH reaction, radiation therapy, burnsUnlike SJS and TEN, mucous membranes are typically not involved in SSSS. In SSSS the split is intradermal, while the split appears to be subepidermal in the case of TEN and SJS. Treatment: - Discontinuation of ALL medications including steroids- Patients have the same complications as burn victims: Thermoregulatory and electrolyte disturbances and 2° infections, so cover the skin and manage fluids and electrolytes.
• Erythema nodosum An inflammation of subcutaneous fat caused by a delayed hypersensitivity reaction. Epidemiology:- Sex: F > M- Peak incidence: 18-34 years Etiology: - Idiopathic (most common)- Infection (e.g. streptococcal pharyngitis, histoplasmosis, coccidioidomycosis, TB, leprosy)- Autoimmune diseases (e.g. sarcoidosis, Crohn's disease, ulcerative colitis, Behcet's syndrome)- Drugs (oral contraceptives, sulfonamides, iodide)- Pregnancy- Malignancy Clinical features:- Non-specific symptoms: fever, arthralgia, malaise, hilar lymphadenopathy- Painful, subcutaneous nodules appear on the patient's anterior shins 1. Firm, erythematous (1st week)2. Fluctuant (without suppuration) and bluish (2nd week)3- Progressively fades (i.e., yellow or brown hue), turning brown or gray Diagnosis: Clinical- CBC, ESR- Antistreptolysin-O titer; throat or blood culture- Chest x-ray: hilar lymphadenopathy (e.g., in sarcoidosis, tuberculosis)- VDRL- Inflammatory bowel disease workup- Skin biopsy if diagnosis is uncertain Treatment: - Symptomatic: Bed rest, leg raise, cold compresses, NSAIDs, potassium iodide- Treat underlying disease.
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• Bullous pemphigoid Epidemiology:- Peak incidence: > 60 years of age- Most common bullous autoimmune disease Etiology: Autoantibodies directed against hemidesmosomes  Clinical features:- Prodromal phase characterized by pruritic eczematous, papular, or urticarial lesions- Large, tense, subepidermal blisters on normal, erythematous, or erosive skin- Intensely pruritic lesions, possibly hemorrhagic, heal without scar formation- Distributed on palms, soles, lower legs, groin and axillae- Oral involvement rare Diagnostics:- Tzanck test: Negative- Nikolsky's sign (= the formation of a cutaneous blister upon stroking the skin): Negative- Histology and immunohistochemistry→ Subepidermal clefting and blistering→ Deposition of linear IgG and C3 along the dermoepidermal junction Treatment:- First-line: High-dose topical steroids (clobetasol, betamethasone)- Second-line: Systemic glucocorticoids and immunosuppressants (e.g., methotrexate, azathioprine) Prognosis: Benign disease, usually responds well to treatment
• Dermatitis herpetiformis Epidemiology:- Peak incidence: 15-40 years- ♂ > ♀ Etiology:- Most likely genetic predisposition to autoimmune reaction (associated with HLA-DR3 and HLA-DQ2)- Associated with celiac disease; sensitivity to potassium iodide (e.g., contrast medium) Clinical features:- Tense, grouped subepidermal vesicles (herpetiform appearance)- Intense pruritus- Bilateral, symmetrical distribution, commonly over elbows, knees, buttocks, shoulders, scalp- No mucosal involvement Diagnostics:- Autoantibodies: Tissue transglutaminase, epidermal transglutaminase (most sensitive), endomysium- Histology and immunohistochemistry→ Subepidermal vesicle formation→ Neutrophilic papillary microabscesses→ Deposition of granular IgA in dermal papillae Treatment: Dapsone and gluten-free diet
• Molluscum contagiosum A poxvirus infection that is most common in young children and in AIDS patients. It is spread by direct skin-to-skin contact (sport, sex) or sharing infected clothing or towels. Risk factors: immunosuppression, active atopic dermatitis (in children), hot and humid climates, crowded living conditionsSuspect AIDS if large, persistent, widespread lesions appear on an adult! History/PE:- Presents as tiny flesh-colored dome-shaped waxy papules, frequently with central umbilication. In children, lesions are found on the trunk, extremities, or face. In adults, they are most commonly found on the genitalia and in the perineal region. Typically spares palms and soles.- Lesions are asymptomatic. Diagnosis: Clinical Treatment:- Spontaneous remission usually happens within 6-9 months (thus treatment often unnecessary).- Consider treatment for sexually transmitted cases, immunocompromised individuals, and/or to reduce autoinoculation or transmission.- Cryotherapy is often the first-line treatment for adolescents and adults as it is better tolerated than in children.- Curettage
• Verrucae (warts) Hyperkeratosis and hyperplasia of epidermis commonly caused by human papillomavirus. Epidemiology: more frequent in children and young adults Etiology: Human papillomavirus infection (HPV) 1, 2, 4; transmitted by direct skin contact Clinical features- Common warts (verruca vulgaris)→ Localization: elbows, knees, fingers, palms→ Appearance: skin-colored or whitish, rough, scaly papules or plaques (sometimes with a cauliflower-likeappearance)- Flat warts (verruca plana)→ Localization: face, back of the hand, legs→ Appearance: flesh-colored, smooth papules, flat surface- Plantar wart (verruca plantaris)→ Localization: soles of the feet→ Appearance: flesh-colored, hyperkeratotic surface Histology:- Irregular hyperkeratosis (thickening of the stratum corneum)- Papillomatosis: elongated rete ridges of the epidermis that point towards the center of the wart- Acanthosis Diagnosis: Clinical Treatment- Indications: Pain, functional impairment, cosmetic reasons, immunosuppression- First-line treatment: salicylic acid; daily application for a few weeks- Alternatives: 5-fluorouracil cream or topical retinoic acid for flat warts- Surgery: Cryotherapy with liquid nitrogen; Surgical excision
• Impetigo Local infection of the epidermis that primarily occurs in children and is caused by both group A streptococcal and staphylococcal orgnaisms.  Epidemiology:- Age: primarily affects children (especially between 2-6 years of age)- Prevalence: high in developing countries and underprivileged populations- Impetigo is highly contagious and can cause epidemics in preschools or schools. Predisposing factors:- Atopic dermatitis and other skin conditions- Diabetes mellitus- Immunodeficiency (e.g., HIV, post-organ transplantation, systemic corticosteroids) Clincial features:- Pustules and honey-colored crusts on erythematous base, often on the face around the mouth, nose, or ears. - Localization: Face (most common), especially around the nose and mouth; extremities- May be pruritic but is rarely painful- Regional lymphadenopathy- Ecthyma: ulcerative impetigo that extends into the dermis (coin-sized, superficial ulcer, with a 'punched-out' appearance) - Systemic signs: possible in severe cases (e.g., fever, malaise, weakness) Diagnosis: Clinical Treatment: - Wound cleansing with antibacterial washes (e.g., chlorhexidine)- Mild localized disease: Topical antibiotics (mupirocin)- Severe disease (non-MRSA): Oral cephalexin (1st generation cephalosporin), dicloxacillin- Severe disease (MRSA likely): Oral trimethoprim-sulfamethoxazole Complications:- Acute poststreptococcal glomerulonephritis (PSGN)- Very rarely: staphylococcal scalded skin syndrome (SSSS)- Superinfection
• Folliculitis Inflammation and/or infection of a hair follicle. Typically caused by infection with Staphylococcus, Streptococcus, and gram - bacteria. Occasionally can be caused by yeast such as Candida albicans or Malassezia furfur. Can occur on any body area with follicles.Pseudomonas aeruginosa infection leads to "hot tub folliculitis." History/PE:- Presents as a tiny pustule at the opening of a hair follicule with a hair penetrating it. When the infection is deeper, a furuncle, or hair follicle abscess, develops. Furuncles may disseminate to adjacent follicles to form a carbuncle.- Patients with diabetes or immunosuppression are at ↑ risk. Eosinophilic folliculitis can occur in AIDS patients, in whom the disease is intensely pruritic and resistant to therapy. Diagnosis: Clinical Treatment: Topical antibiotics (muriprocin) treat mild superficial disease. More severe disease is treated with cephalexin or cloxacillin orally, escalating to clindamycin if MRSA is suspected.
• Acne vulgaris Etiology:- Genetic predisposition- Hormonal factors: Sebum production, menstrual cycle- Follicular hyperkeratosis- Bacterial colonization with Cutibacterium acnes (formerly known as Propionibacterium acnes) - External factors: Climate, drugs (e.g. corticosteroids), or food Clinical features:1. Comedonal acne: Open ("blackheads") or closed ("whiteheads") comedones2. Inflammatory: The comedones rupture, creating inflammatory papules, pustules, nodules, and cysts.3. Scar Diagnosis: Clinical Treatment:- Mild acne: Topical benzoyl peroxide OR topical retinoids. - Moderate acne: Topical benzoyl peroxide AND topical retinoids / antibiotics- Severe acne: Oral isotretinoin; oral antibiotics (tetracycline-class) AND topical combination therapy
• Pilonidal cyst A skin condition caused by local inflammation of the superior midline gluteal cleft, which may progress to a local abscess or fistula. Epidemiology:- Sex: ♂ > ♀ (∼ 3:1)- Peak incidence: 15-25 years Risk factors: - Young men with excessive body hair- Obesity- Deep gluteal cleft- Poor anal hygiene/local irritation- Sedentary lifestyle- Family history Clinical features:- Possible history of trauma or surgery for pilonidal cyst- May be asymptomatic- Simple sinus tract opening in sacrococcygeal region, ∼ 5 cm from the anal verge- Acute inflammation (e.g., abscess)→ Possible purulent discharge and fever→ Can be very painful→ Fluctuant, erythematous swelling- Chronic inflammation→ Discharge (purulent, mucoid, or blood‑stained) from abscess or fistula opening→ Localized pain in sacrococcygeal region or at fistula opening Treatment:  Incision and drainage of the abscess followed by sterile packing of the wound
• Tinea versicolor Epidemiology:- Occurs worldwide, with a higher incidence in tropical climates- More prevalent in healthy individuals of 15-24 years of age Pathogen: Malassezia globosa and furfur (part of normal skin flora) Risk factors:- Warm and humid climates- Excessive sweating, seborrhea, and oily skin- Immunosuppression- Cushing syndrome Pathophysiology: pathogens infect the stratum corneum → degrade lipids → produce acids that damage melanocytes and cause inflammation → hypopigmentation or hyperpigmentation of skin, respectively Clinical features:- Round, well-demarcated macules that reveal a fine, subtle scale with gentle scraping → can coalesce into patches (which may have irregular shapes)- Colors vary from hypopigmentation (pityriasis versicolor alba) to hyperpigmentation (pityriasis versicolor rubra) - Mild pruritus- Common sites are the trunk and chest, but the neck, abdomen, upper arms, and thighs may also be affected.Patients often become more aware of the lesions after exposure to sunlight because the surrounding skin tans while the lesions do not! Diagnosis: Clinical. - Confirmatory test: potassium hydroxide (KOH) preparation of skin scrapings demonstrates the "spaghetti and meatballs" pattern - Ultraviolet light (Wood's lamp) may reveal a coppery-orange or yellow fluorescence (∼ 30% of cases) Treatment: - Topical antifungals (first-line therapy)→ Selenium sulfide lotion or shampoo→ Azoles (miconazole or ketoconazole) or allylamines (terbinafine)- Oral antifungals→ Reserved for disease that is severe, widespread, or unresponsive to topical therapy to reduce the possible risks of systemic medication (not typically used in children)→ Oral fluconazole or itraconazole are the preferred oral agents.
• Candidiasis Pathogen: Candida albicans (most common) Risk factors:- Immunosuppression is the main risk factor for infection: HIV, diabetes mellitus, certain patient groups (e.g., ICU, transplant patients, surgical patients, and neonates)- Medications: antibiotics, steroids, cytostatic agents, immunosuppressive therapy- ↑ Estrogen levels during pregnancy- Hematologic malignancies (e.g., acute myeloid leukemia, multiple myeloma)- Compromised skin: Excessive moisture, local lesions (e.g., elderly with dentures, burns)- Smoking cigarettes Oropharyngeal (oral thrush)- Pseudomembranous candidiasis→ White plaque in the oral cavity that can be scraped off, giving way to red, inflamed, or bleeding areas.→ Cottony feeling in the mouth, loss of taste, and in some cases pain while eating- Skin and nail infections: erythematous patches and satellite lesions→ Intertriginous areas→ Digital web spaces (erosio interdigitalis blastomycetica)→ Paronychia and onychomycosis- Diaper dermatitis: typically in infants→ Peak incidence: 3-4 months of age→ Develops as a result of prolonged wetness and diaper occlusion→ Chronic candidal diaper dermatitis should raise suspicion of diabetes mellitus type 1- Candida esophagitis → AIDS-defining illness and in patients with hematologic malignancies→ Often presents together with oral thrush (but may occur on its own)→ Retrosternal pain on swallowing (odynophagia) Diagnosis: - KOH test (potassium hydroxide smear) on a wet mount preparation of scrapings or smears (best initial test): budding yeasts, hyphae, and pseudohyphae- Blood or tissue culture (best confirmatory test)→ Candida spp. form yeast cells and pseudohyphae at 20-25°C→ Candida albicans forms germ tubes at 37°C Treatment:- Oral candidiasis: Oral fluconazole tablets, nystatin swish and swallow- Superficial (skin) candidiasis: Topical antifungals, keep skin clean and dry- Diaper rash: Topical nystatin
• Dermatophyte infections Dermatophyte infections, also known as tinea, are the most common fungal infections of the skin, hair, and nails. Pathogen: Trichophyton (most common), Microsporum, and Epidermophyton Risk factors:- Diabetes mellitus- Immune compromise (e.g., HIV)- Poor circulation, peripheral arterial disease- Maceration of skin (e.g., in athletes) Location:- Tinea corporis: Scaly, pruritic eruption with a sharp, irregular border, often with central clearing.- Tinea pedis/manuum: Foot, hand- Tinea cruris ("jock itch"): Inguinal (typically sparing the scrotom)- Tinea capitis: Scalp. A large inflammatory boggy mass caused by tinea capitis is called a keroin. Diagnosis: - Best initial test: KOH preparation, possibly with fungal stain, showing segmented hyphae- Confirmatory test: fungal culture- Wood's light: yellow-green fluorescence of Microsporum species Treatment: - Topical antifungals: → Indication: dermatophyte infections other than tinea capitis→ Agents: e.g., terbinafine 1% for 1 week, azoles - Systemic antifungal therapy indications: → Tinea capitis→ Failed topical treatment→ Immunocompromised patients→ Extensive spread→ Some cases of tinea unguium→ Agents: terbinafine, itraconazole, fluconazole, and griseofulvin
• Lice Lice live off blood and on specific parts of the body, depending on their species (head lice, body lice, public lice). Lice are spread through body contact or by the sharing of bedclothes and other garments or hair accessories. They secrete local toxins that lead to pruritus. History/PE:- Patients with lice often experience severe pruritus, and 2° bacterial infection of the excoriations is at risk. - Body lice are seen in people with inadequate hygiene or in those with crowded living coniditions. Public lice contain anticoagulant in their saliva, so their bites often turn blue. Diagnosis: Lice and their eggs (nits) can be seen with the naked eye. Treatment:- Head lice: Topical permethrin, pyrethrin, benzyl alcohol, and mechanical removal.- Body lice: Wash body, clothes, and bedding thoroughly.- Public lice: Treat with the same medications as for head lice.
• Scabies Scabies is a parasitic skin infestation caused by the Sarcoptes scabiei mite. Clinical features:- Incubation period: approximately 3-6 weeks following infestation- Intense pruritus at night - Burning sensation- Elongated, erythematous papules- Burrows of 2-10 mm in length- Scattered vesicles filled with clear or cloudy fluid- Excoriations, pustules, and secondary infection - Predilection sites: Wrists (flexor surface); medial aspect of fingers, interdigital folds (hands and feet); male genitalia (e.g., scrotum, penis) Diagnosis:  Detection of mites, larvae, ova, or mite feces- Revealed in dermoscopy- Microscopic examination of the skin- Skin scraping and histology  Treatment:- Drug of choice: 5% permethrin lotion→ Should be applied to every area of the body.→ Patients should leave cream on overnight (>8 to 10 hours) and wash it off the next morning.- Oral ivermectin: especially indicated in large outbreaks or severe forms of scabies
• Acanthosis nigricans A condition in which the skin in the intertriginous zones (neck folds, genitals, axillae) is hyperkeratotic and hyperpigmented with a velvet appearance. Etiology:- Endocrinal: diabetes mellitus type 2, PCOS, Cushing syndrome- Obesity: pseudoacanthosis nigricans- Familial causes: autosomal dominant inheritance- Drug-related causes: glucocorticoids, oral contraceptives etc.-  May also be a paraneoplastic sign of underlying adenocarcinoma (usually GI) Clinical findings:- Brown to black, intertriginous and/or nuchal hyperpigmentation that can turn into itching, papillomatous, poorly-defined efflorescence- Localization: axilla, groin, neck Treatment: Encourage weight loss.
• Lichen planus A self-limited, recurrent, or chronic inflammatory disease affecting the skin, oral mucosa, and genitalia.- Associated with HCV infection.- Drug-induced: ACE-inhibitors, thiazides, furosemide, beta-blockers Clinical features:- Purple papules, well-demarcated- Planar (flat-topped)- Polygonal, irregular borders- Pruritic, often severe- Wickham's striae: pattern of white lines on the lesion's surface- Affects the extremities, especially the ankles and flexor wrists; trunk- Lesions arranged in linear or circular groups; may coalesce into larger plaques- Bilateral, symmetrical distribution- Koebner phenomena = lesions appear at the site of trauma Genital lichen planus:- Papules on glans penis, or vulva and vagina- Pruritus, burning sensation, dyspareunia Diagnostics:- Punch biopsy: Hyperkeratinization, wedge-shaped hypergranulosis, irregular acanthosis (saw-tooth appearance), band-like lymphocytic infiltrate at the dermal-epidermal junction- Dermoscopy: detection of Wickham's striae- Endoscopy: detection of esophageal involvement (erosions, plaques, inflamed mucosa) Treatment: - First-line therapy: High-potency topical corticosteroids (e.g., betamethasone)- Second-line therapy: Oral corticosteroids (e.g., prednisone); phototherapy (UVB and PUVA)
• Rosacea Epidemiology:- Sex: F > M- Age range: 30-60 years Etiology: The cause of rosacea is not entirely understood, but is especially associated with triggers that increase body temperature. Trigger factors:- Hot weather, hot drinks, spicy food- Stress, alcohol, nicotine, caffeine 1. Erythematotelangiectatic rosacea- Facial flushing- Persistent erythema of the face (together with telangiectasia)- Burning discomfort 2. Papulopustular rosacea- Papules and pustules resembling acne 3. Phymatous rosacea- Skin and sebaceous glands thicken- Inflammatory, widespread nodules- Rhinophyma: enlarged, bulbous nose (almost exclusively in males)- Similar changes may occur on the chin, forehead, cheeks, and ears 4. Ocular rosacea- Conjunctival hyperemia (most common)- Involvement of the cornea, conjunctiva, and lids- Blepharitis (inflammation of the eyelid margin), stye (hordeolum externum)- Dry eyes and foreign-body sensation- Keratitis- Recurrent chalaziaIn contrast to acne, comedones are NOT present! Treatment: - Topical metronidazole for palpulopustular type- Laser or topical brimonidine (vasoconstrictive α-2 agonist) for erythematotelangiectatic type
• Pityriasis rosea An acute dermatitis of unknown etiology that has been hypothesized to represent a reaction to a viral infection with human herpesvirus (HHV) 7 because it tends to occur in mini-epidemics among young adults. Epidemiology:- Age range: 10-35 years of age- Sex: F > M Clinical features:- Prodrome (1-2 weeks prior to rash onset): flu-like symptoms (e.g., malaise, fever, pharyngitis)- Initial eruption (∼ 90% of cases): Herald patch that is erythematous and surrounded by a collarette- Secondary eruption (2-21 days later): Bilateral diffuse, oval-shaped, salmon-colored papules and plaques (< 1.5 cm) with scaly collarette; Papules appear along Langer's lines, which align on the back like the branches of a Christmas tree (Christmas tree appearance)- Pruritus may occur in 25-75% of cases.- Postinflammatory hypopigmentation or hyperpigmentation Diagnosis: Clinical- KOH preparation: to exclude tinea- RPR or VDRL: to exclude secondary syphilis Treatment: Spontaneous resolution within 6-8 weeks
• Vitiligo Vitiligo is a common skin condition in which a patchy loss of epidermal melanocytes results in depigmentation. Epidemiology:- Prevalence: 1-2% of the general population- Peak incidence: 20-30 years; can occur in any age group Etiology:- Genetic predisposition- Autoimmune destruction of melanocytes- Oxidative stress (free radicals) Clinical features:- Well demarcated, depigmented (white) macules or patches- Unilateral or bilateral distribution, with stable or slowly progressive lesions- Commonly on the face (e.g., perioral and periocular regions), neck, scalp, acral surfaces (e.g., hands), extensor surfaces, or genitalia- Leukotrichia: depigmented hair (indicator of poor prognosis)- Coexisting autoimmune diseases (∼ 20% of patients): Hashimoto thyroiditis, Graves disease, type 1 diabetes, psoriasis, inflammatory bowel disease, alopecia areata Diagnosis: Clinical- Wood's lamp examination: well defined blue-white areas- Dermoscopy: perilesional hyperpigmentation and telangiectasia- Skin biopsy and histology: Melanocytes are absent, perilesional lymphocytes may be observed. - Serological markers of autoimmune disease (e.g., thyroid function tests and antithyroid antibodies) once vitiligo is confirmed Therapy: - Limited disease: Topical steroids; topical calcineurin inhibitors (tacrolimus, pimecrolimus)- Progressive or refractory disease: Oral steroids; narrow band ultraviolet B phototherapy; PUVA phototherapy
• Eyelid lesion Xanthelasma: Soft and yellow plaques seen on the medial aspects of the eyelids bilaterally, associated with hyperlipidemia and 1° biliary cirrhosis. Hordeolum: Painful acute eyelid gland infection (stye), usually due to S aureus and located on the edge of the lid. Chalazion: Chronic inflammatory painless cyst due to a blocked eyelid gland.
• Seborrheic keratosis Benign growths of immature keratinocytes Epidemiology: most common benign skin tumor in the elderly population Etiology: incompletely understood, genetic predisposition Clinical features:- Multiple darkly pigmented papules/plaques, sharply demarcated, and soft- Greasy, wax-like, and 'stuck-on' appearance- May become irritated by external trauma or spontaneously; may be pruritic or bleed easily- Increase in number and size with time- Localization: trunk, back of the hands, face and neck, and forearms Diagnosis: Lesions are usually easily recognized. If in doubt, a shave or excisional biopsy can be performed to rule out malignancy. Treatment:- Not necessary- Cryotherapy, laser therapy, or surgical excision if desired for cosmetic reasons or if symptomatic
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• Actinic keratosis A UV-induced precancerous skin lesion that may progress to skin cancer. Epidemiology: occurs especially in individuals with light skin who are over the age of 50 Etiology: sun exposure (e.g., from working outdoors) Clinical features:- Initially: small lesion with rough surface → sandpaper-like texture- Later: lesions grow and become erythematous and scaly- Occurs on areas of sun-exposed skin Diagnosis: Clinical Treatment:- Single lesions: cryotherapy with liquid nitrogen- Multiple lesions: 5-fluorouracil (5-FU), imiquimod, photodynamic therapy
• Cutaneous squamous cell carcinoma Epidemiology: Second most common form of skin cancer after basal cell carcinoma Risk factors:- Sun exposure (especially among fair-skinned individuals)- Exposure to ionizing radiation- Exposure to chemical carcinogens (e.g., coal tars through smoking, arsenic)- Chronic scars/wounds/burn injuries- Chronic immunosuppression (e.g., HIV, transplant patients who receive immunosuppressive therapy)- Precancerous skin lesions (especially actinic keratosis and Bowen's disease) Clinical features:- Initial appearance may be plaque-like, nodular, papillomatous, and/or verrucous- All forms eventually ulcerate.→ The ulcer typically has everted edges.→ The floor of the ulcer resembles granulation tissue and bleeds easily.→ The skin around the ulcer is inflamed and indurated.- Most commonly on the face and neck; a typical location is the lower lip.- Locally invasive but grows slowly.- The overall rate of metastasis is 2%. Subtype: Marjolin's ulcer = an aggressive form of cSCC that typically develops from areas of chronically damaged skin such as ulcers (e.g., pressure ulcers, osteomyelitis) and scars (e.g., burn scars) Diagnosis: Clinical, confirm with shave biopsy Treatment: - Surgical excision or Mohs microscopic surgery- Radiotherapy- Chemotherapy (e.g., 5-fluorouracil, epidermal growth factor inhibitors)
• Basal cell carinoma Epidemiology:- Most common malignant skin tumor- Sex: ♂ > ♀ (∼ 2:1) Etiology:- Sun exposure- Skin types I and II (people with light complexions, red hair, and who sunburn easily)- Nevoid basal-cell carcinoma syndrome (Gorlin syndrome) Clinical features- Localization: Eyelid, nose- Pearly, indurated and nodular lesion with rolled border that is usually nontender- Central depression (crater) with ulceration- Slowly growing over months to years; Very rarely metastasizes Subtypes: Nodular and superficial Diagnostics: - Dermoscopy: initial clinical evaluation of suspected BCC lesions- Excisional biopsy (full-thickness biopsy): Most accurate assessment of the histologic subtype of the tumor Treatment: - Surgical excision of BCC with a safety margin of surrounding healthy tissue- Mohs micrographic surgery: The tumor is removed layer by layer, and each layer is examined for tumor cells.
• Melanoma The most common life-threatening dermatologic disease. Etiology:- UV radiation exposure- Light skin- Numerous nevi, giant congenital nevi, or inherited skin conditions (e.g., dysplastic nevus syndrome, familial atypical mole, melanoma syndrome, xeroderma pigmentosa) - Immunosuppression Clinical features:- Pruritic, persistently bleeding skin lesion- Dermoscopy should be used to examine lesions for ABCDE criteriaA = AsymmetryB = Border (irregular border with indistinct margins)C = Color (new changes in pigmentation or variations in pigmentation within the same lesion)D = Diameter > 6 mmE = Evolving (new lesion or a lesion that changes in size, shape, or color over time) Diagnosis:- Full-thickness excisional biopsy (best diagnostic test)→ S100-protein positive, epithelioid cells with fine granules in cytoplasm- Staging tests (e.g., ultrasound or MRI) once diagnosis confirmed: to determine tumor thickness, spread to lymph nodes, or distant metastasis Types:- Superficial spreading- Nodular- Acral lentiginous- Lentigo maligna- Amelanotic Treatment:- Excision with margins according to Breslow's depth. I: ≤ 1.0 mm → 1 cmII: 1.01–2 mm → 1-2 cmIII: 2.01–4 mm → 2 cmIV: ≥ 4 mm- If tumor thickness > 1 mm (Breslow stage ≥ II): perform sentinel lymph node biopsy- Chemotherapy, biologic therapy (e.g., intravenous interferon therapy), and radiation therapy are recommended for recurrent or widespread diseas
• Kaposi sarcoma A vascular proliferative disease that has been attributed to a herpesvirus HHV-8. History/PE:- Presents with multiple red to violaceous macules, papules, or nodules that can progress to plaques on the lower limbs, back, face, mouth, and genitalia.- Plaques can also be found in the GI tract and lung.- HIV-associated KS is an aggressive form of the disease, it remains the most common HIV-associated malignancy. Diagnosis: History, clinical impression, and histology. Treatment: - Start HAART therapy- Small local lesions can be treated with radiation or cryotherapy- Widespread or internal disease is treated with systemic chemotherapy (doxorubicin, paclitaxel, or IFN-α).
• Mycosis fungoides Chronic, low-grade, malignant, CD4+ T-cell non-Hodgkin lymphoma that presents on the skin. Epidemiology: - Uncommon: only 4% of non-Hodgkin lymphoma cases- Age: mostly middle-aged or elderly patients- Mycosis fungoides and Sézary syndrome are the two most common cutaneous T-cell lymphomas. Clinical features: - Initially, pruritic cutaneous plaques and patches appear that develop brownish nodules.- Subsequently, systemic spread occurs, including lymphadenopathy and hepatosplenomegaly. Diagnostics:- Atypical CD4+ T-cells with cerebriform nuclei (from clumped chromatin) infiltrating the dermis and epidermis- Pautrier microabscesses: aggregates of atypical CD4+ T-cells within the epidermis that are indicative of the disease Treatment: - Early stage disease:→ Topical corticosteroids (1st line)→ Topical nitrogen mustard (2nd line)- Moderate to late stage disease:→ Total electron skin beam therapy→ Systemic chemotherapy (e.g., bexarotene)
• Cherry angiomas (hemangiomas) Epidemiology: incidence increases with age (most common acquired cutaneous vascular anomaly) Pathophysiology: proliferation of dilated mature capillaries Clinical features:- Bright cherry red, dome-shaped papules or macules → may appear purple with time - Usually on the trunk and upper extremities; but may occur all over the body- Usually multiple lesions Diagnosis: based on clinical appearance of lesion Treatment- Intervention is not necessary unless bleeding occurs or for cosmetic reasons- Options: electrocauterization, vascular laser therapy
• Keratocanthoma Low-grade tumor, more common in the elderly - Associated with Muir-Torre syndrome (variant of Lynch syndrome) Characteristic features:- Rapid growth (within 2-3 months) in areas of skin exposed to the sun (e.g., the ears)- Lesion: round erythematous nodule with central crater- Histology: central, hyperkeratotic crater surrounded by squamous epithelium Treatment: The tumor usually heals without treatment. Nonetheless, surgical removal is preferred because keratoacanthoma histologically resembles a cSCC, which is malignant.
• Pemphigus vulgaris Epidemiology: - Peak incidence: 40-60 years of age Etiology:- IgG antibodies directed against desmoglein 3 and desmoglein 1 in desmosomes - Exacerbating factors: drugs, viruses, UV radiation, diet Clinical features:- Spontaneous onset of painful flaccid, intraepidermal blisters → lesions rupture and become confluent → erosions and crusts → re-epithelialization with hyperpigmentation but without scarring- Pruritus is typically absent- Lesions typically first present on the oral mucosa (> 50% of cases), then on body parts exposed to pressure (e.g., intertriginous areas) Diagnostics:- Tzanck test: Positive- Nikolsky's sign: Positive- Histology and immunohistochemistry→ Intradermal suprabasal clefting and blistering just above the basal layer of the epidermis ("tombstome effect")→ Separated standing acantholytic cells on the floor of the blister, similar in appearance to a row of tombstones→ Acantholysis seen in biopsy→ Deposition of IgG in the intercellular spaces of the epidermis Treatment:- First-line: High-dose systemic steroids (prednisone)- Immunosuppression (e.g., azathioprine, IVIG, rituximab)- Topical treatment Prognosis: Often fatal without treatment!
• Porphyria cutanea tarda Epidemiology:- Most common porphyria- Peak incidence: 40-70 years- Sex: M > F Etiology: Defective uroporphyrinogen III decarboxylase (UROD)- Type I: acquired insufficiency of UROD in the context of hepatic damage→ Mainly occurs in older men with chronic alcoholism and hepatic cirrhosis- Type II: inherited (autosomal dominant) defective UROD Susceptibility factors:- Increased hepatic iron stores, hemochromatosis- Alcohol, smoking- Hepatitis C- HIV- Estrogen therapy- Sunlight exposure Clinical findings:- Increased fragility of sun-exposed skin → blistering and impaired healing (blistering photosensitivity)- Healing results in scarring and milia formation- Hypertrichosis- Hyperpigmentation- Scleroderma-like changes (especially forehead and scalp)- Commonly occurs on: Dorsum of the hand, face and neck, extensor surface of the forearm Diagnosis:- Urinary tests: ↑ uroporphyrin (tea-colored urine) - Blood tests: ↑ porphyrins, possibly abnormal LFTs Therapy:- Avoid susceptibility factors and excessive sunlight- Phlebotomy- Hydroxychloroquine or chloroquine
• Alopecia Classification:1. Cicatricial (scarring) alopecia- Brocq pseudopelade→ Seen in women 30-55 years of age→ Irregular areas of irreversible hair loss, which become scarred areas at a later stage- Lichen planopilaris- Frontal fibrosing alopecia- Skin conditions causing scarring alopecia: ichthyosis, dyskeratosis, discoid lupus erythematosus- Acquired scarring alopecia (e.g., via viral diseases, mycoses, burns, chemical burns)2. Nonscarring alopecia- Alopecia areata- Telogen effluvium Diagnostics:- The diagnosis is often clear from the patient history and physical examination. - Hair pull test: About 50 strands of hair are lightly tugged away from the scalp; if > 5 strands can be pulled out, the test is positive. - Dermoscopy: examination of the scalp skin, follicle size and hair shaft diameter by magnification- Microscopic examination of hair follicles and shaft: to determine the phase of hair growth (anagen, telogen) and structural abnormalities of the shaft- Scalp biopsies from sites of active disease: to confirm diagnosis of cicatricial alopecia- Trichograms (∼ 50 hairs are pulled out and microscopically examined to assess the presence of dystrophic hairs): aids diagnosis and prognosis of nonscarring alopecia
• Telogen effluvium The telogen (resting) phase of hair growth predominates → premature shedding of the resting hair follicles → diffuse, nonscarring hair loss Triggers:- Severe illness, fever, surgery- Pregnancy, childbirth- Emotional distress- Endocrine & nutritional disorders Clinical features:- Acute, diffuse, noninflammatory hair loss- Scalp & hair fibers appear normal- Hair shafts easily pulled out (hair pull test)- Hair density reduces by < 50%- Does not progress to complete baldness Diagnosis:- Clinical; scalp biopsy if uncertain (rarely necessary)- Hair-pluck test: ∼ 50% of hairs are in the telogen phase (normal: < 10%). - Tests to determine underlying condition Treatment: reassurance and manage underlying condition
• Alopecia areata Nonscarring hair loss in well demarcated patches due to immune mediated inflammation of hair follicles Epidemiology:- Prevalence: 1 in 1000 people- Age: mostly in people < 30 years- Sex: ♂ = ♀ Etiology:- Immune mediated inflammation and disruption of anagen phase hair follicles → well defined patches of nonscarring hair loss- A trigger factor (emotional stress, infections, pregnancy, etc.) may precede some cases - Family history in up to 20% of cases Clinical features:- Abrupt onset (within weeks)- Smooth, circular, well defined patches of hair loss without scarring (Bland scalp)- Exclamation point hairs- Various patterns of distribution- Nail involvement (up to 40% of cases): nail pitting, onycholysis, Beau lines, etc. Diagnostics: usually clinical, biopsy rarely necessary + histology, trichogram Differential diagnosis:- Trichotillomania: Compulsive pulling out of one's own hair → ill defined patchy hair loss and hairs of different lengths. - Tinea capitis: The affected areas of scalp are scaly compared to the smooth hair loss of alopecia- Secondary syphilis: patchy hair loss → moth-eaten appearance of scalp- Brocq pseudopelade: scarring Treatment:- Intralesional steroids (triamcinolone)- Topical immunotherapy: DCP (diphenylcyclopropenone) or SADBE (squaric acid dibutyl ester)- PUVA treatment (Psoralen + UVA)
• Burns 1st degree (superficial burn): Superficial layers of the epidermis- Pain- Erythema- Swelling- The burn wound blanches on applying pressure and refills rapidly- Healing within 3-6 days without scarring 2nd degree→ 2a (superficial partial-thickness burn): Epidermis and upper layers of the dermis; dermal appendages (hair follicles, sweat, and sebaceous glands) are spared.- Pain- Erythema- Vesicles/bullae- The burn wound blanches on applying pressure and refills slowly.- Healing within 1-3 weeks with hypopigmentation/hyperpigmentation but without scarring→ 2b (deep partial-thickness burn): Deeper layers of the dermis.- Minimal pain- Mottled skin with red and/or white patches- Vesicles/bullae- The burn wound does not blanch on applying pressure.- Healing takes 3 weeks or longer and results in scar formation 3rd degree (full thickness burn): Epidermis, dermis, and subcutaneous tissue.- No pain- Tissue necrosis with black, white, or gray leather-like skin (eschar)- No vesicles/bullae- The burn wound does not blanch on applying pressure.- The burn does not heal by itself. 4th degree: Deeper structures (muscles, fat, fascia, and bones)- Charred tissue- The tissue is dead and requires amputation 1st and 2nd-degree burns:- Irrigation- Topical moisturizers (e.g., calamine lotion) or aloe vera-based gels: relieve symptoms of 1st-degree burns- Consider antiseptic ointments (e.g., silver sulfadiazine, mafenide) or topical antibiotics (bacitractin; triple antiobitic ointments are a combination of bactracin neomycin, polymyxin B)- Dressing is indicated in partial thickness (2nd-degree) burns. 3rd and 4th-degree burns:- Early debridement of burnt, necrotic tissue- Method of tissue coverage varies depending on the specific burn characteristics. Options include:→ Free skin grafts (split-thickness or full-thickness)→ Flap reconstruction with free or pedicled flaps- Topical antibiotics (e.g., silver sulfadiazine, bacitracin, neomycin)
• Staphylococcal scaled skin syndrome (SSSS) Pathogen: Staphylococcus aureus strains that produce exfoliative toxins that cleave desmoglein-1 in the granular layer of the epidermis, thereby disrupting keratinocyte attachments. Clinical features:- Fever, malaise, and irritability- Skin tenderness- Diffuse or localized erythema, often beginning periorallyAfter 24-48 hours- Flaccid, easily ruptured blisters that break to reveal moist, red skin beneath (i.e., with a “scalded” appearance) → widespread sloughing of epidermal skin- Nikolsky's sign- No mucosal involvement- Cracking, and crusting is common- Signs of shock (hypotension, tachycardia) Diagnostics:- History: localized staphylococcal infection (e.g., pharyngitis, bullous impetigo)- Laboratory tests: for confirming the diagnosis: ↑ WBCs, ↑ ESR- Cultures of potential sites of preceding infection - Biopsy: Intraepidermal blistering; lack of inflammatory cell infiltrate Treatment:- IV antibiotics→ Penicillinase-resistant penicillins are the drug of choice: nafcillin, oxacillin→ In areas with high community-acquired MRSA prevalence: vancomycin- Supportive care: Fluid rehydration as indicated - Supportive skin care: emollients, covering denuded areas- NSAIDs as indicated for pain and fever
• Methotrexate Folic acid antagonist (antimetabolite) → purine nucleotide and thereby ↓ DNA synthesis Clinical use:- Treatment of severe psoriasis and rheumatoid arthritis- In neoplastic diseases like gestational choriocarcinoma, chorioadenoma, and hydatidiform mole Side effects:- Pancytopenia and/or macrocytic anemia- Mucositis (particularly stomatitis, enteritis), susceptibility to infection- Hepatotoxicity, nephrotoxicity- Nausea and vomiting, diarrhea- Pulmonary fibrosis and toxicity- Hair loss
• Sézary syndrome Cutaneous T-cell lymphoma with leukemic dissemination of mutated T cells.Can be an advanced form of mycosis fungoides or arise de novo. Characteristic triad of symptoms:1. Systemic skin lesions- Erythroderma accompanied by palmar and plantar hyperkeratosis- Intense pruritus2. Generalized lymphadenopathy3. Atypical T cells (Sézary cells) in peripheral blood The leukemic dissemination present in Sézary syndrome distinguishes it from mycosis fungoides.
• Hidradenitis suppurativa Chronic inflammatory condition that involves recurrent occlusion of hair follicles in intertriginous regions (e.g., groin, axilla). Epidemiology: Women aged 20-40 Risk factors: obesity, smoking, family history Clinical presentation:- Localization: in folded skin areas (most commonly the axillae, groin, inner thigh, and perineal area)- Formation of abscesses, fistulas, and keloids- Formation of draining sinuses with scarring and foul odor Treatment:- Antibiotics, retinoids- Reduce body weight, stop smoking- If insufficient: incision, surgical removal
• Dermatofibroma Fibroblast proliferation resulting in small, fibrous benign dermal growth. Epidemiology: ♀ > ♂ Etiology: sometimes related to insect bites or trauma, may have unknown cause Clinical features:- Asymptomatic- Slowly growing, skin-colored or brownish nodules of ∼ 3-10 mm diameter- Localization: most common on lower extremities; can be found anywhere on the body Diagnosis: dimple sign (Fitzpatrick's sign) → pinching of lesion produces central dimple (characteristic sign of dermatofibroma!) Treatment:- Usually no treatment required- Indications for excision: cosmetic reasons, symptomatic lesion, or suspicion of malignancy
• Pyogenic granuloma Benign vascular tumor  Etiology: cause unknown, associated with trauma and pregnancy Clinical features:- Soft, round, bright red tumor that bleeds easily- Localization: usually develops at a site of skin injury on the face or hands Diagnosis: based on clinical appearance of lesion and history of rapid growth and easily injured/bleeding surface Treatment: surgical excision    

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