(a) A 40-year-old male who was bedridden for the last two months following a fracture in the lower limb developed sudden…

(a)(i) Diagnosis

Acute pulmonary embolism from deep vein thrombosis, after two months of immobilisation (Virchow's triad: stasis, endothelial injury and hypercoagulability).

(a)(ii) Investigations

• Pre-test probability by Wells or revised Geneva score.
• Plain tests: ECG (sinus tachycardia; right heart strain, right bundle branch block, S1Q3T3 in a minority); arterial blood gas (hypoxaemia, hypocapnia); chest X-ray (Westermark sign, Hampton hump, effusion).
• D-dimer is useful only to exclude PE when probability is low or intermediate.
• CT pulmonary angiography is the investigation of choice; V/Q scan when CT is contraindicated (renal failure, contrast allergy, pregnancy).
• Echocardiography for right ventricular dilatation and dysfunction (McConnell sign); troponin and NT-proBNP for risk stratification.
• Compression ultrasound of the leg veins for residual DVT.

(a)(iii) Management

1. Resuscitation: oxygen to keep SpO2 above 90%; cautious fluids (avoid right ventricular overload); norepinephrine for hypotension.
2. Start anticoagulation at once if suspicion is high: low molecular weight heparin (enoxaparin 1 mg/kg twice daily), fondaparinux or unfractionated heparin.
3. High-risk (massive) PE with shock: systemic thrombolysis (alteplase 100 mg over 2 hours, or tenecteplase or streptokinase where affordable) unless contraindicated; otherwise catheter-directed therapy or surgical embolectomy.
4. Long-term anticoagulation: apixaban or rivaroxaban (loading phase of higher dose), or warfarin overlapped with heparin for at least 5 days until INR is 2–3 for 24 hours; at least 3 months for a provoked event.
5. IVC filter when anticoagulation is contraindicated or PE recurs despite it.
6. Prevention: early mobilisation and thromboprophylaxis in future immobilisation.

(b)(i) Clinical severity of jaundice

Jaundice before 24 hours of age is pathological. Kramer's rule assesses cephalocaudal spread: jaundice reaching palms and soles (zone 5) suggests serum bilirubin above about 15 mg/dL, though this is only a rough guide. Confirm by serum bilirubin. Excessive (high-pitched) cry and convulsions at 20 hours indicate acute bilirubin encephalopathy, graded by the BIND score (hypotonia, irritability, retrocollis or opisthotonus, setting-sun sign, seizures).

(b)(ii) Key investigations

• Total and direct serum bilirubin, repeated to see the rate of rise.
• Blood group and Rh of mother and baby; direct Coombs test on the baby; maternal indirect Coombs titre.
• Haemoglobin, haematocrit, reticulocyte count and peripheral smear (spherocytes, nucleated red cells).
• Albumin, G6PD, sepsis screen and thyroid function where indicated.

Diagnosis: Rh haemolytic disease of the newborn (or ABO incompatibility, as the mother is group O).

(b)(iii) Management

• Emergency admission to NICU; start intensive phototherapy immediately (blue light, 460–490 nm, irradiance at least 30 µW/cm²/nm, covering maximal skin surface), keeping hydration and feeding.
• Prepare for double-volume exchange transfusion (about 170 mL/kg) with Rh-negative, group O blood cross-matched against the mother, because seizures signal encephalopathy. Give albumin before exchange if indicated. Monitor glucose, calcium and electrolytes.
• Intravenous immunoglobulin 0.5–1 g/kg over 2 hours if bilirubin keeps rising despite phototherapy.
• Treat convulsions (phenobarbitone), correct acidosis, anaemia and hypoalbuminaemia.
• Follow-up: hearing (BERA), neurodevelopment, and counselling the mother on anti-D immunoglobulin within 72 hours of delivery in future Rh-positive pregnancies.

(c)(i) Clinical findings by site in lichen planus

• Nails: nail-plate thinning, longitudinal ridging and splitting, onycholysis, subungual hyperkeratosis, dorsal pterygium and, in severe disease, permanent nail loss; twenty-nail dystrophy in children.
• Scalp (lichen planopilaris): perifollicular erythema and scale, follicular papules and scarring alopecia; Graham-Little-Piccardi-Lassueur syndrome and frontal fibrosing alopecia are variants.
• Mucosa: Wickham's striae (lacy white lines) on the buccal mucosa, tongue and gums; erosive, atrophic, plaque and bullous forms; genital annular lesions.
• Palms and soles: violaceous or yellowish keratotic papules and plaques, sometimes with punctate keratoses; erosive painful lesions on soles.

(c)(ii) Histopathology of oral lichen planus

Parakeratosis or hyperkeratosis with absent or thin granular layer, saw-tooth rete ridges, liquefactive degeneration of the basal layer, a dense band-like subepithelial lymphocytic infiltrate in the lamina propria, Civatte (colloid) bodies in the lower epithelium, and artefactual clefts at the junction (Max-Joseph spaces).

(c)(iii) Management of oral lichen planus

• Reassurance, removing triggers (sharp teeth, amalgam, drugs, tobacco, alcohol and spicy food), good oral hygiene and treating candidiasis.
• First-line: high-potency topical corticosteroid (clobetasol 0.05% or triamcinolone 0.1% in an adhesive base); intralesional triamcinolone for focal lesions.
• Second-line: topical tacrolimus 0.1% or pimecrolimus.
• Severe or erosive disease: short course of oral prednisolone; hydroxychloroquine, acitretin, methotrexate or ciclosporin in refractory cases.
• Follow up every 6–12 months because of a small risk of malignant transformation; biopsy any non-healing ulcer or plaque.