{"title": "Chapter 13: Dermatological Disorders", "flashcards": [{"q": "What is the ABCDE rule for melanoma and what was the later addition?", "a": "Asymmetry, Border irregularity, Colour variation (multiple colours within one lesion), Diameter >6 mm, Evolution (change over time). Later addition: EFG for nodular melanoma — Elevation (raised lesion), Firmness, Growth (rapid). Nodular melanoma lacks early ABCD features, presenting as a uniformly pink/red elevated firm nodule."}, {"q": "Name the Breslow thickness staging for melanoma and its clinical significance.", "a": "Breslow thickness (mm) determines primary tumour T-stage: T1a ≤0.8 mm (no ulceration); T1b ≤0.8 mm with ulceration or 0.8–1.0 mm; T2 1.0–2.0 mm; T3 2.0–4.0 mm; T4 >4.0 mm. Sentinel lymph node biopsy is recommended for T1b and above. Breslow thickness is the strongest single predictor of survival in primary melanoma."}, {"q": "What are the features of necrotising fasciitis and how is it distinguished from cellulitis?", "a": "Red flags for NF over cellulitis: disproportionate pain, skin necrosis/bullae/crepitus, rapid progression, systemic sepsis disproportionate to local findings, pain on gentle lateral skin tension ('finger test'). Laboratory Risk Indicator for Necrotising Fasciitis (LRINEC) score ≥6 suggests NF. CT shows fascial plane gas. Management: immediate surgical debridement + broad-spectrum antibiotics — mortality >40% without urgent surgery."}, {"q": "Define psoriasis Area and Severity Index (PASI) and at what score is systemic treatment indicated?", "a": "PASI scores erythema, scaling, and induration across four body regions (head, trunk, upper/lower limbs) weighted for area affected. Maximum score = 72. PASI ≥10 AND DLQI >10 (significant impact on quality of life) defines moderate-to-severe psoriasis warranting systemic therapy (methotrexate, ciclosporin, acitretin, or biologics). PASI 75/90/100 response rates are standard clinical trial endpoints."}, {"q": "What is the Stevens-Johnson Syndrome/TOXIC EPIDERMAL NECROLYSIS spectrum and how is severity defined?", "a": "SJS/TEN is a life-threatening immune-mediated mucocutaneous reaction. SJS: <10% BSA detachment; SJS-TEN overlap: 10–30%; TEN: >30%. SCORTEN score predicts mortality (6 risk factors: age >40, malignancy, HR >120, initial epidermal detachment >10%, blood urea >10 mmol/L, glucose >14 mmol/L, bicarbonate <20 mmol/L). Commonest cause: drugs (sulfonamides, allopurinol, carbamazepine, lamotrigine, NSAIDs)."}, {"q": "Name three cutaneous signs of systemic disease.", "a": "Acanthosis nigricans (insulin resistance, occult malignancy — gastrointestinal); erythema nodosum (sarcoidosis, IBD, TB, streptococcal infection, drugs); necrobiosis lipoidica (diabetes mellitus); pyoderma gangrenosum (IBD, RA, myeloproliferative disease); dermatomyositis rash (Gottron's papules, heliotrope rash — associated with malignancy); Cullen's sign (periumbilical bruising — acute haemorrhagic pancreatitis)."}, {"q": "What is the mechanism of action of dupilumab in atopic dermatitis?", "a": "Dupilumab is a fully human monoclonal antibody blocking the IL-4Rα subunit shared by IL-4 and IL-13 signalling. Blocking both IL-4 and IL-13 reduces Th2 immune skewing, decreases IgE production, reduces barrier gene suppression (filaggrin), and decreases pruritus via IL-31 pathway. It is licensed for moderate-to-severe atopic dermatitis in adults and children from age 6 months failing topical therapy."}, {"q": "Name the four most common skin cancers in order of frequency.", "a": "Basal cell carcinoma (BCC) — most common cancer overall (~80% of NMSC); squamous cell carcinoma (SCC) — second most common, with metastatic potential; melanoma — highest mortality; Merkel cell carcinoma (rare but aggressive). BCC rarely metastasises; SCC risk of metastasis ~5%, higher in immunosuppressed patients, ears, lips. Melanoma metastasises early via lymphatics."}, {"q": "What is the recommended treatment pathway for moderate-to-severe atopic dermatitis?", "a": "BNF/NICE NG190: Step 1 — emollients + mild topical corticosteroids (TCS); Step 2 — moderate/potent TCS; Step 3 — potent TCS + tacrolimus/pimecrolimus (TCI — steroid-sparing); Step 4 — phototherapy (narrowband UVB); Step 5 — systemic immunosuppressants (ciclosporin, methotrexate); Step 6 — dupilumab, JAK inhibitors (abrocitinib, baricitinib, upadacitinib) for inadequate response."}, {"q": "What is the tumbler test and what does a positive result indicate?", "a": "Press a transparent glass tumbler firmly against a non-blanching (petechial/purpuric) rash. If the rash persists (does NOT blanch) under pressure, it indicates red blood cells have extravasated outside vessels — suggesting vasculitis, thrombocytopaenia, or meningococcaemia. A blanching rash (erythema) indicates vascular dilation (inflammatory). CRITICAL: a blanching rash does not exclude meningococcaemia — treat on clinical suspicion."}], "quiz": [{"q": "What is the most important step in managing a patient presenting with a 2 mm petechial rash, fever, and confusion?", "opts": ["Take blood cultures and wait for results", "Administer IV benzylpenicillin (or ceftriaxone) immediately — do not delay for investigations if meningococcal disease is suspected", "Apply topical hydrocortisone", "Request urgent CT head"], "ans": 1, "exp": "Non-blanching petechial/purpuric rash + fever + altered consciousness = meningococcal septicaemia until proved otherwise. Immediate IM benzylpenicillin 1.2g (or ceftriaxone 2g IV) must NOT be delayed for investigations. Early antibiotics are the single most important intervention — mortality rises with every hour of delay. Call for emergency support and arrange urgent hospital transfer."}, {"q": "A patient on allopurinol for 6 weeks develops a widespread maculopapular rash, fever, and lymphadenopathy. What is the most likely diagnosis?", "opts": ["Urticaria from allopurinol", "Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS syndrome) — a severe delayed hypersensitivity reaction", "Contact dermatitis", "Psoriasis flare"], "ans": 1, "exp": "DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms) is a delayed (2–8 weeks after drug initiation), life-threatening drug hypersensitivity: widespread rash + fever + lymphadenopathy + eosinophilia ± atypical lymphocytes + organ involvement (hepatitis, pneumonitis, nephritis). Allopurinol and anticonvulsants are common triggers. Stop drug immediately; high-dose systemic corticosteroids."}, {"q": "What is the first-line topical treatment for mild-moderate plaque psoriasis on the body?", "opts": ["Calcineurin inhibitors (tacrolimus)", "Potent corticosteroid (betamethasone) + vitamin D analogue (calcipotriol) combination — e.g. Dovobet gel or ointment", "Salicylic acid alone", "Topical retinoids"], "ans": 1, "exp": "NICE NG94 recommends a corticosteroid + vitamin D analogue combination as first-line for trunk/limb psoriasis. Dovobet (calcipotriol + betamethasone dipropionate) is preferred over sequential application. Vitamin D analogues slow keratinocyte proliferation; corticosteroids reduce inflammation. Twice-daily applications for 4 weeks, then once daily maintenance for limited periods to avoid atrophy."}, {"q": "Which investigation is most important in a 50-year-old with new-onset widespread pruritus without rash?", "opts": ["Skin biopsy", "Full blood count, LFTs, renal function, TFTs, LDH, glucose, and CXR — to exclude systemic causes (haematological malignancy, cholestasis, uraemia, thyroid disease)", "Patch testing", "Serum IgE"], "ans": 1, "exp": "Pruritus sine materia (itch without primary skin lesions) in a middle-aged or older adult requires systemic investigation. Differential: iron deficiency, CKD, cholestasis (including PBC), hypothyroidism, polycythaemia vera (aquagenic pruritus), lymphoma (Hodgkin's B symptoms — night sweats, fever, weight loss), solid organ malignancy. Treat underlying cause."}, {"q": "What is the dermatological presentation of secondary syphilis?", "opts": ["Painless genital ulcer", "Generalised non-pruritic maculopapular rash including palms and soles, condylomata lata, mucous patches, generalised lymphadenopathy — 4–10 weeks after primary chancre", "Vesicular rash on trunk", "Purpuric rash"], "ans": 1, "exp": "Secondary syphilis results from haematogenous dissemination of Treponema pallidum. Rash: generalised coppery-red maculopapular rash, characteristically involving palms and soles (distinguishing it from most viral exanthems). Associated: condylomata lata (moist perianal/vulval plaques), mucous patches, patchy alopecia, generalised lymphadenopathy. Highly infectious. Serological tests (RPR + TPHA/TPPA) confirm; treat with benzathine penicillin."}, {"q": "What is the DLQI score and what score indicates a severe impact on quality of life?", "opts": ["0–5 = severe", "11–20 = very large effect on quality of life", "21–30 = moderate effect", "0 = maximum impact"], "ans": 1, "exp": "Dermatology Life Quality Index (DLQI): 10 questions covering symptoms, daily activities, leisure, work, personal relationships, and treatment impact. Scoring: 0–1 = no effect; 2–5 = small; 6–10 = moderate; 11–20 = very large; 21–30 = extremely large effect. DLQI >10 is typically required alongside PASI ≥10 for biologic therapy eligibility in psoriasis."}, {"q": "Which organism most commonly causes impetigo in children?", "opts": ["Streptococcus pyogenes (GAS)", "Staphylococcus aureus (most common), or Streptococcus pyogenes — often mixed; bullous impetigo = S. aureus exfoliative toxin A/B", "MRSA exclusively", "Candida albicans"], "ans": 1, "exp": "Non-bullous (crusted) impetigo: caused by S. aureus, GAS, or both. Bullous impetigo: exclusively caused by S. aureus exfoliative toxin A/B, which cleaves desmoglein 1, causing superficial blistering. Treatment: topical fusidic acid or mupirocin for localised disease; oral flucloxacillin (or erythromycin if penicillin allergic) for extensive disease."}, {"q": "What is lichen planus and what are its characteristic features?", "opts": ["Autoimmune blistering disorder", "Immune-mediated T-cell attack on basal keratinocytes — characterised by the 4 Ps: Purple, Polygonal, Pruritic, Papules; also found in oral mucosa as reticular white striations (Wickham's striae)", "A fungal infection", "A bacterial folliculitis"], "ans": 1, "exp": "Lichen planus is a T-cell-mediated autoimmune lichenoid reaction. Skin: flat-topped, shiny, purple polygonal papules on flexural surfaces (wrists, ankles); Koebner phenomenon (lesions at trauma sites); intense pruritus. Oral: reticular white striations (Wickham's striae) on buccal mucosa — may progress to erosive oral LP with malignant potential. Nails: longitudinal ridging, pterygium. Treatment: potent TCS."}, {"q": "What is the investigation of choice for bullous pemphigoid?", "opts": ["Skin swab", "Perilesional skin biopsy for direct immunofluorescence (linear IgG/C3 at the dermoepidermal junction) + indirect immunofluorescence + ELISA for anti-BP180/BP230 antibodies", "Serum IgE", "Patch testing"], "ans": 1, "exp": "Bullous pemphigoid: autoantibodies against BP180 (type XVII collagen) and BP230 in the hemidesmosome. Perilesional biopsy for DIF: linear IgG and C3 at the DEJ (pathognomonic). Serum BP180 ELISA titres correlate with disease activity. Treatment: superpotent topical TCS (clobetasol propionate — BLISTER trial evidence), oral prednisolone, doxycycline (steroid-sparing), azathioprine, rituximab for refractory disease."}, {"q": "A 70-year-old on furosemide and amlodipine develops photosensitivity. Which drug class most commonly causes drug-induced photosensitivity?", "opts": ["Beta-blockers", "Thiazide diuretics, amiodarone, tetracyclines, fluoroquinolones, NSAIDs, and phenothiazines are the most common photosensitisers", "Calcium channel blockers", "ACE inhibitors"], "ans": 1, "exp": "Drug-induced photosensitivity occurs via phototoxic (more common — non-immune, dose-dependent, UVA-mediated, occurs on first exposure) or photoallergic (immune-mediated, requires sensitisation) reactions. Thiazides, tetracyclines, amiodarone, fluoroquinolones, NSAIDs, and sulphonamides are the most common causative drug classes. Management: identify and stop offending drug, sun protection, topical TCS for acute reactions."}, {"q": "What is Nikolsky's sign and which dermatoses cause it?", "opts": ["Blanching of purpuric rash on pressure", "Lateral pressure on normal-appearing skin or gentle rubbing causes epidermal separation/blistering — positive in pemphigus vulgaris, TEN, staphylococcal scalded skin syndrome, bullous pemphigoid (weakly); reflects loss of keratinocyte cohesion from desmoglein antibodies (pemphigus) or epidermal-dermal separation (TEN)", "Pitting of nails in psoriasis", "Dermographism in urticaria"], "ans": 1, "exp": "Nikolsky's sign: skin shearing with gentle lateral traction at the edge of a blister or on apparently normal skin. Strong positive in pemphigus vulgaris (IgG against desmoglein 3/1 on suprabasal keratinocytes) and TEN (full-thickness epidermal necrosis). Bullous pemphigoid (subepidermal blistering) may be weakly positive. Staphylococcal scalded skin syndrome in children also positive (exfoliatin A/B cleave desmoglein 1)."}, {"q": "What is the first-line investigation for a 2 cm pigmented lesion on the back with irregular border?", "opts": ["Photography and review in 6 months", "Excision biopsy with 2 mm margin (for histological diagnosis and Breslow thickness measurement) — dermoscopy should be performed first by a trained clinician to guide decision to excise", "Punch biopsy of the most pigmented area", "Shave biopsy"], "ans": 1, "exp": "Any suspicious pigmented lesion should be referred via 2WW suspected skin cancer pathway. Excision biopsy with narrow margin (2 mm) provides definitive histological diagnosis and Breslow thickness — which then guides re-excision margin (0.5–2 cm depending on T stage) and sentinel lymph node biopsy consideration. Incisional biopsy (punch) is used for large lesions where complete excision is impractical. Dermoscopy improves diagnostic accuracy."}, {"q": "What are the main adverse effects of systemic corticosteroids used in dermatology?", "opts": ["Only skin thinning", "Weight gain, cushingoid features, hyperglycaemia, hypertension, osteoporosis (HPA axis suppression, osteoblast inhibition), adrenal suppression, GI ulceration, susceptibility to infection, cataracts, glaucoma, avascular necrosis (femoral head), psychiatric effects (steroid psychosis/euphoria/depression), skin thinning and striae (topical TCS)", "Only GI adverse effects", "Only relevant with IV steroids"], "ans": 1, "exp": "Systemic corticosteroids suppress HPA axis (may cause adrenal insufficiency on withdrawal), reduce bone formation (prescribe bisphosphonate prophylaxis for courses >3 months), impair glucose metabolism (hyperglycaemia), elevate BP, reduce immune surveillance, cause cataracts and glaucoma with long-term use. Topical TCS adverse effects: skin atrophy, telangiectasia, striae, perioral dermatitis, contact sensitisation, adrenal suppression (high-potency TCS on large body surface areas)."}, {"q": "What is dermatitis herpetiformis (DH) and how is it treated?", "opts": ["Herpes simplex infection of the skin", "Intensely pruritic vesicular rash on extensor surfaces (elbows, knees, buttocks, scalp) associated with coeliac disease (gluten sensitivity) — caused by IgA deposits at dermal papillae; treated with gluten-free diet (definitive) ± dapsone (rapid symptom control)", "A variant of bullous pemphigoid", "A form of eczema caused by detergent contact"], "ans": 1, "exp": "DH is a chronic blistering dermatosis occurring in patients with coeliac disease (gluten-sensitive enteropathy) — may have subclinical gut disease. Direct immunofluorescence of uninvolved perilesional skin: granular IgA at dermal papillae (pathognomonic). Anti-tTG IgA serology positive. Strict GFD leads to gradual rash resolution over 2 years; dapsone provides rapid but symptomatic relief only. Regular skin and gut surveillance required."}, {"q": "What is the management of a patient with generalised urticaria and angioedema without anaphylaxis?", "opts": ["Adrenaline IM immediately", "Non-sedating antihistamine (e.g. cetirizine 10 mg or loratadine 10 mg OD — first-line); escalate to higher antihistamine doses (up to 4× licensed dose per BSACI guidelines) if inadequate; add montelukast or H2 antagonist; omalizumab (anti-IgE) for chronic spontaneous urticaria refractory to antihistamines", "Oral prednisolone alone without antihistamines", "Diphenhydramine (sedating antihistamine) as first-line"], "ans": 1, "exp": "Chronic spontaneous urticaria (CSU — urticaria >6 weeks without identifiable trigger) management ladder: Step 1: second-generation non-sedating antihistamine OD; Step 2: increase to 4× dose; Step 3: add omalizumab 300 mg SC 4-weekly (ASTERIA, GLACIAL trials — response in ~60%); Step 4: ciclosporin for refractory CSU. Avoid ACE inhibitors (bradykinin-mediated angioedema) and NSAIDs (exacerbate urticaria in aspirin-sensitive patients)."}, {"q": "What is a 'herald patch' in pityriasis rosea?", "opts": ["The last lesion to resolve", "The initial large (2–10 cm), oval, salmon-pink scaly plaque appearing 1–2 weeks before the generalised secondary eruption of smaller 'daughter' lesions — classically following skin cleavage lines in a 'Christmas tree' pattern on the trunk", "The most inflamed lesion", "The perianal involvement"], "ans": 1, "exp": "Pityriasis rosea is a self-limiting papulosquamous disorder (probable HHV-6/7 reactivation trigger). Herald patch: solitary oval, slightly raised, annular scaly plaque (collarette scale pointing inward) appears 1–2 weeks before disseminated eruption. Generalised eruption follows cleavage lines ('Christmas tree' pattern on back). Resolves spontaneously in 6–8 weeks. Pruritus treated with emollients and antihistamines; UV phototherapy for extensive/persistent disease."}, {"q": "What investigations should be performed for a new diagnosis of psoriasis?", "opts": ["Skin biopsy alone", "Clinical diagnosis (biopsy only if atypical); investigate for metabolic syndrome (BMI, BP, glucose, lipids) and cardiovascular risk; screen for psoriatic arthritis (joints, nails — pitting/onycholysis); DLQI for QoL impact; hepatitis B/C serology if systemic therapy (particularly biologics) planned", "CBC, LFT, U&E as routine", "No investigations needed — clinical diagnosis only"], "ans": 1, "exp": "Psoriasis has significant systemic associations: cardiovascular disease (risk equivalent to DM), metabolic syndrome, PsA (30% of psoriasis patients), depression. Baseline investigations before biologics: FBC, LFT, renal function, HbA1c, lipids, HBV/HCV serology (risk of reactivation with immunosuppression), TB screening (IGRA). Annual cardiovascular risk review is recommended for all moderate-severe psoriasis patients."}, {"q": "What are the characteristic nail findings in psoriasis?", "opts": ["Longitudinal ridging (beading)", "Pitting (most common), onycholysis (nail-plate separation from nail-bed), subungual hyperkeratosis, oil-drop (salmon patch) discolouration, splinter haemorrhages, leukonychia, nail bed pustules — nail psoriasis is a strong predictor of psoriatic arthritis", "Terry's nails", "Koilonychia (spoon-shaped nails)"], "ans": 1, "exp": "Nail psoriasis affects up to 90% of patients with plaque psoriasis. Pitting (matrix disease — focal parakeratosis) is the most common finding. Oil-drop/salmon patch (bed disease — characteristic reddish-brown discolouration seen through the nail plate). Nail psoriasis correlates with: psoriatic arthritis (especially DIP involvement), longer disease duration, severity. Nail NAPSI (Nail Area Psoriasis Severity Index) scores involvement."}, {"q": "What is contact dermatitis and what distinguishes irritant from allergic type?", "opts": ["They are identical and treated the same way", "Irritant CD: non-immune-mediated direct skin damage from irritants (detergents, solvents, water — hands most common); immediate onset; severity proportional to dose/duration. Allergic CD: type IV (delayed) hypersensitivity requiring prior sensitisation; presents 24–72 hours after re-exposure; distribution may spread beyond contact area; diagnosed by patch testing", "Allergic is more common than irritant", "Only allergic CD responds to topical steroids"], "ans": 1, "exp": "Patch testing (British Standard Series ± supplementary panels specific to occupation/exposure) is the gold standard for diagnosing allergic contact dermatitis, identifying causative allergens (most common: nickel, fragrance mix, methylisothiazolinone — in wet wipes/cosmetics, rubber chemicals, hair dyes — PPD). Irritant CD: barrier restoration (emollients) + avoidance of irritants; glove use. Allergic CD: avoidance of allergen + TCS for acute phase."}, {"q": "What is the 'erythroderma' syndrome and what are its causes?", "opts": ["A mild sunburn reaction", "Generalised erythema and scaling affecting >90% of the body surface area, causing physiological instability (hypothermia from excess heat loss, high-output cardiac failure, hypoalbuminaemia from protein loss, infection through disrupted barrier); causes: psoriasis (most common — psoriatic erythroderma), eczema (atopic erythroderma), drug reaction (DRESS), mycosis fungoides (Sézary syndrome), pityriasis rubra pilaris", "Localised erythema from cellulitis", "Telangiectasia from rosacea"], "ans": 1, "exp": "Erythrodermic psoriasis is a dermatological emergency: widespread erythema, scaling, itch, and potential haemodynamic instability. Triggers: abrupt withdrawal of systemic steroids, TNF inhibitors, infection, stress. Management: admission, temperature and fluid management, Sézary syndrome exclusion (lymph node biopsy, flow cytometry), skin biopsy to confirm underlying diagnosis. Ciclosporin or infliximab for rapid control of erythrodermic psoriasis."}]}