(a) (i) Define 'drowning'. Enumerate the different modes of death in a case of drowning. List the postmortem findings in a case…

Drowning is death from asphyxiation due to submersion in liquid, in which water or airway obstruction prevents adequate gas exchange. The liquid may be fresh or salt water, but the essential mechanism is airway obstruction and hypoxia. The modes of death are asphyxia from laryngospasm or water inhalation, syncope from hypoxia, vagal inhibition, and exhaustion. In wet drowning, water enters the airways and lungs. Postmortem findings include fine froth in the mouth and airways, heavy oedematous and emphysematous lungs, water in the stomach, silt or sand in the gastric contents, washerwoman’s hands, cadaveric spasm, and possible diatoms in tissues.

Diatom test. The diatom test is based on acid digestion of lung, liver, bone marrow or other tissues, followed by microscopic identification of siliceous diatoms. The acid digestion dissolves organic tissue and leaves the siliceous shells, which are counted in lung, liver, bone marrow or other organs. Their presence in appropriate organs supports antemortem inhalation of water. Its limitations are contamination, false positives from postmortem putrefaction or water entry, false positives from water ingestion, false negatives in dry drowning, seasonal variation, and the need for quantitative analysis.

Glomerulonephritis. Four major primary glomerulonephritides presenting with nephrotic syndrome are minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulonephritis. Post-infectious glomerulonephritis usually follows streptococcal infection. Immune complexes deposit in the glomeruli, activate complement, recruit neutrophils, and cause mesangial and endothelial proliferation. Circulating or in situ immune complexes fix complement, causing neutrophilic infiltration and capillary loop obstruction. Light microscopy shows enlarged, hypercellular glomeruli with neutrophils and endocapillary proliferation. Immunofluorescence shows granular “starry sky” deposits of IgG and C3 along capillary loops and in the mesangium. Electron microscopy shows subepithelial electron-dense “humps” and mesangial deposits.

Wound healing by first intention. In clean, well-approximated wounds, the edges are closely held together, so tissue loss is minimal and granulation tissue is scant. Haemostasis is followed by an inflammatory phase with neutrophils and macrophages. The inflammatory phase lasts about 1–3 days, proliferation 3–14 days, and remodelling continues for weeks to months. Epithelial cells migrate from the wound margins within the first 24 hours. Granulation tissue forms around days 3–5, followed by collagen deposition, remodelling, and scar formation. A labelled diagram would show wound edges, migrating epithelium, granulation tissue, and collagen. Factors influencing repair include local infection, foreign body, blood supply, wound tension, age, nutrition, diabetes, steroids, and smoking. Infection and foreign bodies prolong inflammation, poor blood supply delays repair, age reduces fibroblast activity, protein deficiency impairs collagen, diabetes impairs microcirculation, steroids inhibit fibroblasts, and smoking reduces oxygen delivery.

Nitrates in angina. Nitrates are converted to nitric oxide, increase cGMP, and cause venodilation, reducing preload; coronary vasodilation relieves angina. They reduce myocardial oxygen demand by reducing preload and wall stress, while coronary vasodilation improves blood flow to ischaemic areas. Routes include sublingual, buccal, oral, transdermal, and intravenous. Sublingual nitrate is used for acute attacks, oral and transdermal forms for prophylaxis, and intravenous nitrate in hospital. Side effects include headache due to cerebral vasodilation, hypotension, reflex tachycardia, and tolerance with continuous use.

Exenatide. Exenatide is a GLP-1 receptor agonist. It enhances glucose-dependent insulin secretion, suppresses glucagon, delays gastric emptying, and promotes satiety. It is used in type 2 diabetes mellitus and for weight reduction; cardiovascular safety/non-inferiority data are available, but reduction in long-term cardiovascular mortality is not proven.

Artemisinin-based combination therapies. ACTs offer rapid parasite clearance, reduced gametocyte carriage, delayed resistance emergence, shorter treatment courses, and efficacy against multidrug-resistant Plasmodium falciparum. Artemisinin rapidly clears asexual parasites, while the partner drug suppresses residual parasites and prevents resistance. This reduces transmission by reducing gametocyte carriage, shortens treatment, improves compliance, and is effective against multidrug-resistant P. falciparum. Thus, the described mechanisms, findings and clinical applications establish the diagnostic, pathological and therapeutic principles asked.