General Medicine

Scabies = intensely pruritic infestation by the mite *Sarcoptes scabiei* var. hominis ; transmitted by close personal (skin-to-skin) contact; household/institutional spread. Worldwide; all socioeconomic groups.

• Causative agent and transmission: Sarcoptes scabiei var. hominis - an obligate human mite; transmitted by prolonged skin-to-skin contact (sexual contact, household members); mites cannot survive off the host for more than 72 hours.
• Clinical features: intensely itchy papular rash worse at night (heightened immune response during sleep); classic sites - finger web spaces, wrists, anterior axillary folds, areolae, umbilicus, genitalia; burrows are pathognomonic (serpiginous tracks in the stratum corneum); face and scalp spared in adults (involved in infants and immunocompromised).
• Management: permethrin 5% cream (first-line) applied from neck down, left for 8-12 hours, washed off; repeat at 1 week; OR ivermectin 200 mcg/kg oral, repeated at 2 weeks; treat all household contacts simultaneously; wash clothing and bedding at > 60C; Norwegian (crusted) scabies in immunocompromised patients requires combined topical and oral therapy.
• Clinical features: Intense pruritus — worse at night (pathognomonic timing; mites more active in warm bedding); pruritus in multiple family members (virtually diagnostic )
• Distribution: Web spaces between fingers (most common site ); flexor wrists; periumbilical; genitalia (scrotum/penis in males ); axillary folds; infants/elderly — may involve scalp, palms, soles; spares face and scalp in adults (unlike infants)
• Burrows — pathognomonic; tiny (5–10 mm) grey-white linear wavy tracks in stratum corneum (mite tunnels); best seen at web spaces + wrists; found by dermoscopy ('jet with contrail' sign )
• Norwegian (crusted) scabies — immunocompromised (HIV, elderly, malnourished); millions of mites (vs 10–15 in classical); hyperkeratotic crusted plaques; highly contagious ; NOT intensely pruritic (due to impaired immune response)

▶ Permethrin 5% cream — first-line; apply to whole body (neck to toes; include scalp in infants/elderly ) + leave for 8–12 hrs then wash off; repeat in 1 week ; treat ALL household contacts simultaneously

▶ Ivermectin 200 μg/kg oral single dose — equally effective (WHO first-line for mass treatment); preferred for Norwegian scabies (oral + topical); repeat in 1–2 weeks

• Wash all clothing/bedding in hot water (> 50°C) OR seal in bag for 3 days; post-scabetic itch (due to dead mites — not re-infestation) can last 4–6 weeks after treatment → manage with antihistamines + topical steroid

Psoriasis = chronic immune-mediated inflammatory skin disease; Th1 + Th17 mediated ; ↑ TNF-α, IL-17, IL-23; keratinocyte hyperproliferation. Prevalence 2–3%; genetic predisposition (HLA-Cw6 ); triggers: streptococcal infection (guttate psoriasis), stress, drugs (lithium, beta-blockers, chloroquine, NSAIDs, IFN-α).

• Clinical features:

• Plaque psoriasis (most common, 80%): Well-demarcated erythematous plaques with silvery-white scales ; extensor surfaces (elbows, knees ); scalp; lower back (sacral region )
• Nail changes (50%): Pitting (pathognomonic); onycholysis (nail separation from bed — 'oil spot' ); subungual hyperkeratosis; splinter haemorrhages
• Guttate psoriasis: Small drop-like lesions following streptococcal throat infection (especially in children + young adults)
• Auspitz sign — pinpoint bleeding on removal of scale (exposure of dilated capillaries); Koebner (isomorphic) phenomenon — new lesions in areas of trauma (skin injury, scratch, surgery)

• Psoriatic arthropathy — 30% of psoriasis; DIP joints + asymmetric + nail disease; seronegative
• Emergency in Psoriasis — Erythrodermic Psoriasis + Pustular Psoriasis: Systemic illness; admission; hospitalise

▶ Mild-moderate (topical): Topical corticosteroids + Vitamin D analogues (calcipotriol — first-line combination ); coal tar; dithranol; topical tacrolimus (sensitive areas)

▶ Moderate-severe (systemic): Methotrexate 7.5–25 mg weekly (most used); Ciclosporin (rapid onset; renal toxicity); Acitretin (retinoid; teratogenic ); PUVA (psoralen + UVA)

▶ Biologic therapy: Anti-TNF (adalimumab, etanercept); IL-17 inhibitors (Secukinumab, Ixekizumab) — highest skin clearance rates; IL-23 inhibitors (Guselkumab, Risankizumab, Tildrakizumab ) — sustained long-term clearance; most effective biologics for psoriasis

• Classification (Ridley-Jopling): immunological spectrum Tuberculoid (TT) - Borderline tuberculoid (BT) - Borderline (BB) - Borderline lepromatous (BL) - Lepromatous (LL); TT = high cell-mediated immunity with few bacilli, LL = low immunity with abundant bacilli. WHO operational: Paucibacillary (<= 5 skin lesions, smear-negative) vs Multibacillary (> 5 lesions or smear-positive).
• Clinical features: hypopigmented or erythematous anaesthetic skin patches; thickened peripheral nerves (ulnar, common peroneal, great auricular, posterior tibial); sensory loss leading to trophic ulcers; motor loss causing claw hand, wrist drop, foot drop; lepromatous features - symmetrical nodules, leonine facies, madarosis (loss of eyebrows), saddle-nose deformity.
• Skin biopsy — essential for diagnosis; histopathology differentiates TT (granuloma with few/no bacilli ) from LL (no granuloma; foamy macrophages packed with AFB = Virchow cells ); Fite-Faraco stain for AFB in tissue
• Slit-skin smear — from earlobes + skin lesions; Ziehl-Neelsen stain; Bacterial Index (BI) (0–6+ scale based on bacillary load); > 0 = multibacillary
• Lepromin test (Mitsuda reaction) — NOT diagnostic; assesses CMI; strongly positive in TT (high immunity); negative in LL (absent immunity); given 4 weeks before reading
• MDT: PB = Rifampicin 600 mg monthly + Dapsone 100 mg OD × 6 months ; MB = Rifampicin 600 mg monthly + Clofazimine 300 mg monthly + Clofazimine 50 mg OD + Dapsone 100 mg OD × 12 months
• Reactions: Type 1 (reversal) — treat with prednisolone 40 mg/day; Type 2 (ENL) — thalidomide (most effective) or prednisolone + clofazimine; DO NOT stop MDT during reactions
• Borderline leprosy and reactions: the clinical spectrum is immunologically unstable; leprosy reactions (type 1 reversal and type 2 erythema nodosum leprosum) are acute inflammatory episodes that can occur before, during, or after treatment; they are the main cause of nerve damage and disability.
• Disability prevention: regular nerve function assessment (voluntary muscle testing and sensory testing) every month during treatment; steroids for reactions to prevent nerve damage; self-care for anaesthetic hands and feet (daily inspection, footwear, moisturising); surgery for deformity.

Acne vulgaris = chronic inflammatory disease of pilosebaceous unit. Pathogenesis: sebaceous hyperactivity (androgens ) + follicular obstruction + *P. acnes* colonisation + inflammation . Affects 85% of adolescents.

• Isotretinoin side effects: Dry lips (most common; universal); dry eyes; epistaxis; teratogenicity; depression (controversial); hypertriglyceridaemia; hepatotoxicity; arthralgia; avoid high-dose vitamin A supplements
• Pathogenesis in detail: four factors interact - sebaceous gland hyperactivity (driven by androgens), follicular hyperkeratosis (retention hyperkeratosis blocking the follicle), Cutibacterium acnes (C. acnes) colonisation, and inflammation triggered by C. acnes lipases and toll-like receptor activation.
• Pre-treatment counselling for isotretinoin: mandatory contraception for women (highly teratogenic - Pregnancy Prevention Programme), baseline LFTs and fasting lipids (hypertriglyceridaemia), mood assessment (monitor for depression), avoid waxing and UV exposure; usual course 4-6 months at 0.5-1 mg/kg/day.

URTICARIA

Urticaria (Hives) = transient well-demarcated wheals (raised, erythematous, intensely pruritic skin lesions; < 24 hrs at any site; skin returns to normal when weal resolves) ± angioedema (deeper; involves dermis/subcutaneous; eyelids, lips, tongue, throat). Chronic urticaria = > 6 weeks duration.

• Urticaria: wheals (hives) - transient (< 24 h) itchy raised erythematous lesions with central pallor; acute (< 6 weeks) usually IgE-mediated (foods, drugs, infection); chronic (> 6 weeks) - 80% chronic spontaneous urticaria (CSU, autoimmune in many), 20% inducible (cold, pressure, exercise); angioedema = swelling of deeper dermis and subcutis, may be without wheals.
• Management of urticaria: identify and avoid triggers; 2nd-generation non-sedating antihistamines (cetirizine, loratadine, fexofenadine) are first-line; dose can be increased up to 4x; omalizumab (anti-IgE) for refractory CSU; short courses of prednisolone for severe acute episodes; adrenaline for anaphylaxis.
• Impetigo: superficial bacterial skin infection; S. aureus (#1), GAS; two forms - non-bullous (honey-coloured crusted erosions, face and extremities) and bullous (S. aureus exfoliative toxin, intact blisters); treat with mupirocin or fusidic acid topically for localised disease; flucloxacillin or amoxicillin-clavulanate orally for extensive disease.
• Causes: Food allergy (peanuts, shellfish, egg, milk ); drugs (penicillin, aspirin, NSAIDs, ACEi); infections (viral — Hep B, EBV; parasitic); physical (dermographism — stroking skin produces wheal; cold; cholinergic; pressure); chronic idiopathic/autoimmune (autoantibodies to FcεRI; most common cause of chronic urticaria )

▶ Non-sedating antihistamines (H1 blockers) (first-line): Cetirizine 10 mg OD; Fexofenadine 180 mg OD; Loratadine 10 mg OD; up to 4× dose in chronic urticaria (BSACI guideline )

▶ Omalizumab (anti-IgE) 300 mg SC monthly — for antihistamine-refractory chronic urticaria; highly effective; biological option

IMPETIGO

Impetigo = superficial bacterial skin infection; most common skin infection in children; two forms:

• Non-bullous (crusted) impetigo (#1; 70%) — *S. aureus* ± *S. pyogenes*; honey-coloured crusts over erythematous base; face (around nose + mouth ); contagious
• Bullous impetigo — *S. aureus* (phage type II; exfoliative toxins A + B ); flaccid bullae → rupture → thin brown crust; trunk + axillae; infants; ecthyma = deep form (ulcerating through dermis; violaceous border)

▶ Localised: Topical fusidic acid cream 2% TDS × 7 days OR mupirocin 2% TDS × 5 days

▶ Extensive/bullous/systemic: Oral flucloxacillin 500 mg QDS × 7 days; clarithromycin if penicillin allergy; MRSA: oral co-trimoxazole

• Antifungal agents: Terbinafine (allylamine; squalene epoxidase inhibitor — most fungicidal ); Azoles (clotrimazole, miconazole, fluconazole, itraconazole — inhibit ergosterol synthesis via CYP51/P450 ); Griseofulvin (microtubule disruption; only dermophytes )
• Diagnosis: clinical - annular scaly plaque with active border; confirmed by skin scraping/nail clipping for KOH preparation (hyphae) and fungal culture; Wood lamp shows green fluorescence for Microsporum (not Trichophyton).
• Treatment duration: tinea corporis/cruris - 2-4 weeks topical; tinea capitis - systemic griseofulvin 6-8 weeks or terbinafine 4 weeks (griseofulvin for Microsporum); tinea unguium (onychomycosis) - terbinafine 12 weeks for nails, or itraconazole pulse therapy.
• Complications and prevention: secondary bacterial infection; Majocchi granuloma (fungal folliculitis from topical steroid use on tinea - avoid using steroid-antifungal combinations); avoid sharing towels, well-ventilated footwear for tinea pedis.

Pemphigus vulgaris (PV) = autoimmune intraepidermal blistering disease; IgG anti-desmoglein 3 (Dsg3) antibodies (and sometimes Dsg1) target desmosomes → acantholysis (loss of cell cohesion) → intraepidermal suprabasal split → flaccid blisters. Fatal without treatment (historically 75% mortality ).

• Clinical: Oral mucosa FIRST (90%) — painful erosions (oral blistering → erosions → dysphagia; first and last to heal ); then skin (trunk, head, neck); flaccid (not tense) blisters that rupture easily → painful erosions; Nikolsky sign positive (lateral pressure on normal skin → epidermal separation )
• Diagnosis: Skin biopsy (H&E) → intraepidermal split above basal layer; DIF (Direct Immunofluorescence) — IgG + C3 in intercellular 'fishnet' pattern (chicken wire pattern ) = pathognomonic; serum anti-Dsg3 ELISA

▶ Prednisolone 1–1.5 mg/kg/day — cornerstone; ↓ antibody production; taper slowly as titres fall

▶ Rituximab (anti-CD20) — now first-line in many centres ; B-cell depletion → ↓ anti-Dsg3 Ab; achieves remission in 90%; dramatically reduces steroid requirements

▶ Azathioprine 1–3 mg/kg/day OR Mycophenolate mofetil (steroid-sparing); IVIg; Dapsone (adjunct)

• Bullous pemphigoid (BP) comparison: subepidermal blisters (tense, intact because the split is below the epidermis); mostly elderly; skin first (mucosal rarely); IgG and C3 at dermoepidermal junction on DIF (linear band); treat with topical or oral steroids; anti-BP180/BP230 antibodies.
• Monitoring: anti-desmoglein antibody titres correlate with disease activity; reduce treatment as titres fall; watch for steroid complications and infections (main cause of mortality in pemphigus); oral hygiene is essential for mucosal disease.

• SJS: < 10% BSA epidermal detachment; mucosal involvement; mortality < 10%
• SJS/TEN overlap: 10–30% BSA; mortality 10–30%
• TEN: > 30% BSA; mortality 30–40%; burns unit; SCORTEN score
• Key drugs: Allopurinol (#1 overall cause ); Carbamazepine + HLA-B*1502 (Asian patients); Lamotrigine; Phenytoin; Co-trimoxazole; Nevirapine
• Management: Stop drug IMMEDIATELY (most critical step — earlier withdrawal = better prognosis ); burns unit/ICU; IV fluids; wound care (Biobrane/cadaveric skin); Cyclosporin 3–5 mg/kg/day OR IVIg 3 g/kg (controversial); ophthalmology (ocular involvement → blindness)
• SCORTEN criteria (mortality predictor for TEN): Age > 40; HR > 120; malignancy; BSA > 10%; urea > 10; bicarbonate < 20; glucose > 14; score 0–1 = 3% mortality; score ≥ 5 = 90% mortality
• Pathogenesis: delayed hypersensitivity (Type IV) with cytotoxic T-cell-mediated keratinocyte apoptosis; HLA associations explain why only certain individuals develop SJS/TEN with specific drugs.
• Management in detail: stop the causative drug immediately (most critical step); burn unit care (skin is functionally like a burn - fluid balance, infection prevention, wound care); ophthalmology review urgently (conjunctival involvement can cause blindness); systemic cyclosporin or etanercept have emerging evidence for TEN; IVIg and steroids are controversial.
• Nikolsky sign: lateral pressure on apparently normal skin causes the epidermis to shear off; positive in pemphigus (intraepidermal blister) and SJS/TEN (necrotic epidermis); helps clinically distinguish from erythema multiforme and urticaria.
• Eye involvement: acute conjunctivitis progressing to pseudomembrane formation, conjunctival scarring, and symblepharon (adhesion of palpebral and bulbar conjunctiva); late sequelae include dry eye (scarring of lacrimal ducts), trichiasis, and corneal scarring causing visual impairment; urgent ophthalmology input is mandatory.
• Nutritional support: patients with extensive mucositis cannot eat; nasogastric feeding is essential; pain management with opioids and mouthwashes; intensive wound care with non-adherent dressings; monitor for sepsis (the main cause of death in TEN).

Atopic dermatitis (AD/Eczema) = chronic relapsing-remitting pruritic inflammatory skin disease; associated with atopy (asthma, allergic rhinitis); filaggrin gene mutation (impaired skin barrier) → sensitisation; IgE-mediated (Type I) + Type IV hypersensitivity.

• Pathogenesis: filaggrin (FLG) gene mutations (loss-of-function) disrupt the skin barrier, allowing allergen entry and sensitisation; Th2-mediated inflammation with IL-4, IL-13, and IL-31 (pruritus mediator); IgE elevation and peripheral eosinophilia; part of the atopic march (eczema -> allergic rhinitis -> asthma).
• Management ladder: emollients liberally and regularly (cornerstone of all management); mild-moderate - topical corticosteroids (hydrocortisone 1% for face/flexures, moderate-strength for body) or topical calcineurin inhibitors (tacrolimus, pimecrolimus - for face and sensitive sites); moderate-severe - dupilumab (anti-IL-4Ra) has transformed treatment; narrow-band UVB for extensive disease; systemic immunosuppression (ciclosporin, azathioprine, methotrexate) for refractory cases.
• Complications: eczema herpeticum (Kaposi varicelliform eruption) - widespread HSV superinfection in eczema; treat urgently with systemic aciclovir; secondary bacterial infection (S. aureus colonises in > 90%, treat with antibiotics if frank infection); psychological impact and reduced quality of life.
• Clinical: Intense pruritus (hallmark; worse at night ); infants (face, scalp, extensor surfaces); children/adults (flexural surfaces — antecubital fossa, popliteal fossa — 'lichenification' from chronic rubbing → thickened leathery skin with accentuated skin markings)
• Diagnostic criteria (Hanifin & Rajka): Major: pruritus; typical morphology + distribution; chronic/relapsing; personal/family history of atopy; Minor: ↑ IgE; xerosis; early age onset; elevated TEWL (transepidermal water loss)

▶ Moisturisers (emollients) — first-line; restore skin barrier; apply liberally and frequently; cornerstone of ALL eczema management

▶ Topical corticosteroids — low-potency (hydrocortisone 1%) for face + folds; moderate-potency (betamethasone valerate) for body; short courses (flares); avoid long-term face/fold use

▶ Topical calcineurin inhibitors (Tacrolimus 0.03–0.1%; Pimecrolimus 1%) — steroid-sparing; safe for face/folds; no skin atrophy; 'steroid phobia' management; avoid in infection

▶ Dupilumab (anti-IL-4Rα mAb) — SC biweekly; for moderate-severe uncontrolled AD; dramatically reduces pruritus + skin lesions; best biologic for AD; conjunctivitis as SE

• Oral antihistamines (sedating — chlorphenamine — for sleep disturbance); phototherapy (narrowband UVB); systemic immunosuppression (ciclosporin, methotrexate, dupilumab )

• Classification of hypersensitivity: Type I (IgE-mediated, immediate - urticaria, anaphylaxis); Type II (cytotoxic - drug-induced haemolytic anaemia, thrombocytopenia); Type III (immune complex - serum sickness, vasculitis); Type IV (delayed/T-cell mediated - contact dermatitis, SJS/TEN, DRESS, FDE).
• Fixed drug eruption (FDE): round/oval well-demarcated erythematous-violaceous plaque that recurs at exactly the same site on re-exposure; most common culprits - NSAIDs, tetracyclines, phenolphthalein; heals with post-inflammatory hyperpigmentation.
• DRESS syndrome: Drug Reaction with Eosinophilia and Systemic Symptoms; delayed onset 2-6 weeks after starting drug; morbilliform rash + facial oedema + lymphadenopathy + systemic involvement (hepatitis, nephritis, pneumonitis, myocarditis); eosinophilia and atypical lymphocytes; treat with systemic steroids and stop the drug.
• Approach to a patient with suspected drug eruption: establish the timeline - most drug rashes occur 7-14 days after first exposure or within hours on re-exposure; identify all drugs (including OTC and herbal medicines); classify the morphology (maculopapular, urticarial, blistering, pustular); assess severity (face, mucosal involvement, systemic features).
• Stopping the drug: always stop the most likely causative drug immediately for serious reactions (SJS/TEN, DRESS, HSS); for mild rashes in patients on essential drugs, a risk-benefit decision is needed with close monitoring; drug re-challenge is absolutely contraindicated for SJS/TEN.

ERYTHEMA MULTIFORME (EM)

Erythema multiforme (EM) = acute immune-mediated hypersensitivity reaction affecting skin ± mucous membranes. NOT the same spectrum as SJS/TEN.

• Cause: HSV (#1 cause ) — herpes-associated EM; sulfonamides; mycoplasma (pneumonia ); drugs
• Target lesion (pathognomonic): 3 concentric zones — central dusky red area (may blister) → pale oedematous ring → outer erythematous ring; distribution: dorsa of hands , palms, feet, extensor extremities; EM minor (no mucosal); EM major (mucous membrane involvement )
• Treatment: Mild — supportive; identify cause; aciclovir (if HSV-related) ; topical steroids; severe or recurrent — systemic antivirals; systemic steroids (controversial)
• EM vs SJS distinction: EM has true target lesions (three concentric zones), is mostly HSV-triggered, predominantly affects the extremities and is usually self-limiting; SJS has flat atypical target lesions and is drug-triggered with mucosal involvement and epidermal detachment - the two conditions are now considered distinct entities.
• Recurrent EM: continuous suppressive aciclovir 400 mg BD is the treatment for HSV-associated recurrent EM.
• Kaposi sarcoma - staging and treatment: limited cutaneous KS in HIV responds to ART alone; advanced KS (visceral, oedema, rapid spread) needs systemic liposomal doxorubicin or paclitaxel; classic KS in elderly is slow-growing and may need radiotherapy or vinblastine.

KAPOSI'S SARCOMA (KS)

KS = vascular tumour associated with HHV-8 (Human Herpesvirus 8 / KSHV) ; 4 epidemiological types: Classic (elderly Mediterranean); Endemic (Africa); Transplant-related; AIDS-related (epidemic) (most common — CD4 < 200 ).

• Clinical: Violaceous (purple-brown) papules/plaques/nodules; hard palate (pathognomonic site ); skin; GI tract (lower endoscopy for staging); lung; lymph nodes; AIDS-KS spreads aggressively
• Treatment: ART (for AIDS-KS — immune reconstitution often clears KS ); Liposomal doxorubicin (advanced or ART-unresponsive); Paclitaxel; Radiotherapy (localised); Intralesional vinblastine

• Lupus hair and oral features: non-scarring alopecia (diffuse, often at hairline - "lupus hair" - fragile, breaks easily); scarring alopecia in discoid lupus; painless oral ulcers (hard palate) are a SLICC criterion.
• Management of cutaneous lupus: sun protection (SPF 50+) is the single most important intervention; hydroxychloroquine for all cutaneous manifestations; topical steroids or tacrolimus for localised lesions; add systemic steroids, methotrexate, dapsone or thalidomide for refractory disease.
• Photosensitivity: UV light triggers cutaneous and systemic flares; advise sun avoidance, protective clothing and broad-spectrum sunscreen year-round; photosensitising drugs should be avoided.