Inflammatory Skin Diseases
Psoriasis
Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by epidermal hyperproliferation (turnover 3β4 days vs. normal 28β30 days). Pathophysiology: T-helper cell (Th1/Th17) activation β TNF-Ξ±, IL-17, IL-23 β keratinocyte proliferation + inflammation. Genetic component (HLA-Cw6 association). Triggers: stress, infection (strep throat β guttate psoriasis), medications (lithium, beta-blockers, NSAIDs, antimalarials), alcohol.
| Type | Features |
|---|---|
| Plaque (most common, 80β90%) | Well-demarcated, salmon-pink plaques with silvery-white scale; extensor surfaces (knees, elbows), scalp, lumbosacral area; Auspitz sign (pinpoint bleeding when scale removed) |
| Guttate | Small drop-shaped lesions; triggered by strep pharyngitis; young patients; good prognosis |
| Pustular | Sterile pustules; can be generalized (von Zumbusch β systemic toxicity) or palmoplantar |
| Erythrodermic | Diffuse erythema covering >90% BSA; life-threatening; risk of fluid loss, infection, hypothermia |
| Inverse | Smooth, shiny plaques in skin folds (axilla, groin, inframammary) |
π₯ Psoriasis Treatment β Severity-BasedMild (BSA <3%): topical steroids (1st line), vitamin D analogues (calcipotriene), topical calcineurin inhibitors, salicylic acid. Moderate-severe (BSA >10% or DLQI >10): phototherapy (NBUVB), methotrexate, cyclosporine, acitretin. Biologics: TNF-Ξ± inhibitors (adalimumab, etanercept, infliximab), IL-17 inhibitors (secukinumab, ixekizumab), IL-23 inhibitors (guselkumab, risankizumab) β most effective. Psoriatic arthritis affects ~30%: treat with DMARDs (methotrexate) or biologics.
Atopic Dermatitis (Eczema)
Chronic, relapsing inflammatory skin disease characterized by pruritus and dry skin. Pathophysiology: filaggrin gene mutations (FLG) β impaired skin barrier β transepidermal water loss + allergen penetration β Th2-driven inflammation β IL-4, IL-13, IgE elevation β mast cell and eosinophil activation. Associated with atopic triad: asthma, allergic rhinitis, atopic dermatitis.
| Age | Location | Features |
|---|---|---|
| Infants (0β2y) | Face (sparing nasal tip), scalp, extensor surfaces | Weeping, crusting; often first manifestation of atopic march |
| Children/adults | Flexural areas (antecubital, popliteal fossae, neck, wrists, ankles) | Lichenification (skin thickening); excoriations; Dennie-Morgan lines; xerosis |
π― Boards PearlHanifin-Rajka criteria (major): pruritus, chronic relapsing course, typical distribution, personal/family history of atopy. Emollients are cornerstone of management. Topical corticosteroids (acute flares). Topical calcineurin inhibitors (tacrolimus, pimecrolimus) for face/skin folds. Dupilumab (IL-4/IL-13 biologic) for moderate-severe AD β highly effective. Avoid: hot baths, harsh soaps, known triggers. Secondary bacterial infection (S. aureus) is common β mupirocin or oral antibiotics.
Skin Infections
| Infection | Organism | Features | Treatment |
|---|---|---|---|
| Impetigo | S. aureus (most common), Group A Strep | Superficial; honey-colored crusts over erosions; non-bullous vs. bullous (S. aureus toxin); highly contagious; face/extremities in children | Mupirocin (topical) for limited; oral cephalexin or dicloxacillin for extensive. MRSA: TMP-SMX or doxycycline |
| Cellulitis | S. aureus, GAS (S. pyogenes) | Non-purulent: diffuse erythema, warmth, swelling, tenderness; no fluctuance; usually lower extremities; fever/leukocytosis in severe | Non-purulent: cephalexin or dicloxacillin Γ 5β7 days; MRSA concern: TMP-SMX or doxycycline. IV antibiotics (cefazolin) if systemic signs. Mark borders with pen to track progression |
| Erysipelas | Group A Strep (primarily) | Superficial cellulitis involving upper dermis/lymphatics; sharply demarcated raised border (unlike cellulitis); bright red; typically face or lower legs; systemic symptoms common | Penicillin (drug of choice); amoxicillin or cephalexin for oral |
| Folliculitis/Furuncle/Carbuncle | S. aureus | Folliculitis: pustules at hair follicles; Furuncle (boil): deeper nodule with fluctuance; Carbuncle: confluence of furuncles with multiple sinus tracts | Folliculitis: topical antibiotics or antiseptic wash. Furuncle/carbuncle: incision & drainage (I&D) is cornerstone; add antibiotics (TMP-SMX or doxycycline) if systemic signs, multiple lesions, or immunocompromised |
| Tinea (Dermatophytosis) | Trichophyton, Microsporum, Epidermophyton (fungi) | Tinea pedis (athlete's foot); tinea corporis (ringworm); tinea cruris (jock itch); tinea capitis (scalp β children); tinea unguium (onychomycosis β nails). KOH prep: hyphae and spores | Topical azoles (clotrimazole, miconazole) for body/feet/groin. Oral terbinafine or griseofulvin for scalp, nails, or extensive. Nail: terbinafine Γ 6β12 weeks |
| Herpes Zoster (Shingles) | VZV reactivation | Dermatomal distribution; prodrome of pain β vesicular rash; resolves in 2β4 weeks; post-herpetic neuralgia (PHN) in elderly. Disseminated if immunocompromised | Acyclovir, valacyclovir, or famciclovir Γ 7 days (start within 72 hours of rash onset). Steroids: controversial, some use for ophthalmic zoster. PHN: gabapentin, TCAs, lidocaine patch, capsaicin. Prevention: Shingrix vaccine (recombinant, preferred, 2 doses β all adults β₯50) |
Skin Cancers
| Cancer | Cell Origin | Risk Factors | Appearance | Management |
|---|---|---|---|---|
| Basal Cell Carcinoma (BCC) | Basal cell layer of epidermis | UV radiation, fair skin, Gorlin syndrome (PTCH mutation), arsenic, ionizing radiation | Pearly/translucent papule with rolled borders and telangiectasias ("rodent ulcer"); rarely metastasizes; most common skin cancer; nodular, superficial, morpheaform subtypes | Surgical excision (Mohs micrographic surgery for high-risk/cosmetically sensitive areas); electrodesiccation and curettage; vismodegib (hedgehog inhibitor) for advanced/inoperable |
| Squamous Cell Carcinoma (SCC) | Keratinocytes | UV, smoking, HPV (genital/oral SCC), immunosuppression, chronic wounds, arsenic, actinic keratosis (precursor) | Erythematous, scaly, keratotic plaque or nodule; may ulcerate; more aggressive than BCC; can metastasize (especially on ear, lip, immunosuppressed patients); actinic keratosis = premalignant | Surgical excision; Mohs for high-risk; radiation; cemiplimab/pembrolizumab (anti-PD1) for advanced/metastatic |
| Melanoma | Melanocytes | UV exposure, fair skin/light eyes, numerous nevi, dysplastic nevi, family history, CDKN2A mutation, BRAF V600E mutation (50β60% of melanomas) | ABCDE criteria; thin melanoma = excellent prognosis (5-year survival >95%); Clark level/Breslow thickness determine staging and prognosis; subtypes: superficial spreading (most common), nodular (most aggressive, blue-black), lentigo maligna (elderly, sun-damaged), acral lentiginous (palms/soles/nails, AA patients) | Wide local excision; sentinel lymph node biopsy if Breslow >0.8mm; adjuvant therapy for high-risk; metastatic: BRAF inhibitors (vemurafenib, dabrafenib) + MEK inhibitor if BRAF-mutated; immunotherapy: pembrolizumab, nivolumab (PD-1 inhibitors), ipilimumab (CTLA-4) |
π§ Mnemonic β Melanoma ABCDEAsymmetry Β· Border irregularity Β· Color variation (multiple colors) Β· Diameter >6mm (size of pencil eraser) Β· Evolution (changing over time)
π― Boards PearlBCC vs. SCC: BCC rarely metastasizes; SCC can (lymph nodes, lung). Actinic keratosis: sun-damaged, scaly, rough precursor to SCC; treat with liquid nitrogen, 5-fluorouracil (5-FU) cream, imiquimod, photodynamic therapy. Keratoacanthoma: rapidly growing, dome-shaped nodule with central keratin plug; some consider variant of SCC; excise. Seborrheic keratosis: benign, "stuck-on" waxy appearance; Leser-TrΓ©lat sign = sudden eruption of multiple SK β possible internal malignancy.
Acne Vulgaris & Rosacea
Acne Vulgaris
Pathophysiology: 4 key factors β (1) excess sebum production (androgens stimulate sebaceous glands), (2) follicular hyperkeratinization (plugging of pilosebaceous duct), (3) Cutibacterium acnes (formerly P. acnes) colonization, (4) inflammation. Comedones β papules/pustules β nodules/cysts.
| Grade | Lesions | Treatment |
|---|---|---|
| Mild | Comedones, few papules/pustules | Topical retinoids (tretinoin, adapalene) Β± topical antibiotics (clindamycin, erythromycin) Β± benzoyl peroxide |
| Moderate | More papules/pustules, some nodules | Add oral antibiotics (doxycycline, minocycline β 3 months max); consider combined OCP or spironolactone (women) |
| Severe/Cystic | Nodules, cysts, risk of scarring | Isotretinoin (oral vitamin A derivative β most effective; requires iPLEDGE program; teratogenic; monitor LFTs/lipids) |
Rosacea
Chronic inflammatory skin disease of the central face. Subtypes: erythematotelangiectatic (flushing, persistent erythema, telangiectasias), papulopustular ("acne rosacea" β papules/pustules on erythematous background), phymatous (skin thickening, rhinophyma), ocular (eye involvement β blepharitis, conjunctivitis). Triggers: alcohol, spicy food, heat, sun, exercise, emotional stress.
π₯ Rosacea ManagementSun protection (SPF 30+). Topical: metronidazole (1st line), azelaic acid, ivermectin (for Demodex mites). Oral: doxycycline 40mg (sub-antimicrobial dose) or standard dose for severe. Laser for telangiectasias. Rhinophyma: surgical removal. Avoid triggers. Unlike acne: no comedones; no isotretinoin for rosacea (not standard treatment).
Other Common Dermatoses
| Condition | Mechanism | Features | Treatment |
|---|---|---|---|
| Contact Dermatitis (allergic) | Type IV hypersensitivity (T-cell mediated); common allergens: nickel (jewelry), poison ivy/oak (urushiol), latex, fragrances, neomycin | Pruritic vesicular rash confined to contact area; may take 24β72h to appear; linear/geometric distribution with poison ivy | Identify and avoid allergen; topical steroids; systemic steroids for severe/widespread; patch testing for identification |
| Contact Dermatitis (irritant) | Direct chemical/physical damage to skin; not immune-mediated; most common type | Burning/stinging (vs. itching in allergic); erythema, dryness, cracking; hands most commonly affected; healthcare workers, cleaning staff | Barrier protection, emollients, avoidance of irritant; topical steroids for acute inflammation |
| Seborrheic Dermatitis | Malassezia yeast overgrowth + abnormal inflammatory response in sebum-rich areas; worsens with stress, cold, neurological disease (Parkinson's, HIV) | Greasy, yellowish scales on erythematous base; scalp (dandruff), nasolabial folds, eyebrows, chest; non-contagious | Scalp: selenium sulfide, zinc pyrithione, or ketoconazole shampoo. Face: topical ketoconazole, low-potency steroid, calcineurin inhibitors. Treat Parkinson's/HIV as contributing factors |
| Urticaria (Hives) | IgE-mediated (type I) or non-IgE mast cell degranulation β histamine release β vascular leak; acute (<6 weeks) vs. chronic (>6 weeks, often idiopathic) | Transient, pruritic wheals (each lesion <24h); angioedema if deeper dermis involved; anaphylaxis if systemic symptoms | Antihistamines (cetirizine, loratadine) first line; systemic steroids for severe; omalizumab for chronic spontaneous urticaria; epinephrine for anaphylaxis |