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

(a)(i) Drowning

Medico-legally, drowning is death from asphyxia due to submersion (or immersion of the mouth and nose) in liquid; the WHO/Utstein 2002 definition describes it as the process of experiencing respiratory impairment from submersion or immersion in liquid, with outcomes of death, morbidity or no morbidity. It is a form of asphyxia 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 water inhalation (typical or wet drowning) or from laryngospasm (dry drowning); cardiac arrest from haemodilution and haemolysis with hyperkalaemia and ventricular fibrillation in fresh water, or from haemoconcentration and pulmonary oedema in salt water; vagal inhibition (cardiac inhibition or immersion syndrome) from cold water striking the face, nose or larynx; secondary (delayed) drowning from pulmonary oedema, pneumonia or ARDS hours to days after rescue; and exhaustion or coincidental injury (head injury, alcohol, epilepsy). In wet drowning, water enters the airways and lungs. Postmortem findings are external: fine, white, persistent froth at the mouth and nostrils (a vital sign, reappearing when wiped and on chest pressure), cutis anserina (goose skin), washerwoman's hands and feet (wrinkling after some hours in water), cadaveric spasm with weeds, sand or grass clutched in the hands, and abrasions on the forehead, knuckles and knees from the river bed; and internal: froth in the trachea and bronchi, voluminous, heavy, doughy, pitting lungs overlapping the heart (emphysema aquosum) with Paltauf's haemorrhages under the pleura, water, silt or weeds in the stomach and duodenum, fluid in the middle ear and sphenoid sinus (Svechnikov's sign), a distended right heart, and diatoms in bone marrow, brain and kidneys matching those in the water.

(a)(ii) Diatom test

Diatoms are unicellular algae with siliceous (acid-resistant) walls present in natural waters. In antemortem drowning, water with diatoms enters the lungs, crosses into the circulation while the heart is still beating, and lodges in distant organs; hence finding matching diatoms in the femoral bone marrow, brain, kidneys or liver is evidence of drowning while alive, whereas diatoms in lungs alone can enter after death. The 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. A sample of the water from the scene is examined to match species and concentration. Its limitations are laboratory contamination (glassware, reagents); false positives because diatoms can enter the body in life through ingestion, inhalation of air-borne diatoms or diet, and postmortem penetration into lungs; false negatives in dry drowning, rapid death, water poor in diatoms (tap water, swimming pools, bath tubs) and seasonal variation; unsuitability of heavily decomposed or skeletonised bodies without marrow; and the need for expert quantitative and qualitative analysis, since there is no universal cut-off.

(b)(i) Glomerulonephritis

Four major primary glomerulonephritides presenting with nephrotic syndrome are minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulonephritis. Post-infectious glomerulonephritis classically follows infection with nephritogenic strains of group A β-haemolytic streptococci, 1–4 weeks after pharyngitis or 3–6 weeks after skin infection (impetigo), and presents as acute nephritic syndrome (haematuria, oedema, hypertension, oliguria) with raised ASO or anti-DNase B titres and low C3. Streptococcal antigens (nephritis-associated plasmin receptor and streptococcal pyrogenic exotoxin B) are implanted in glomeruli or form circulating complexes. 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.

(b)(ii) 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. By the end of the first month, the scar is cellular connective tissue covered by intact epidermis, and wound strength reaches about 70–80% of normal skin by 3 months. 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.

(c)(i) 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, flushing, postural hypotension and syncope, reflex tachycardia, rarely methaemoglobinaemia, and tolerance with continuous use, which is prevented by a nitrate-free interval of 8–12 hours (for example, eccentric dosing of isosorbide mononitrate or removing patches at night). Nitrates are contraindicated within 24–48 hours of PDE-5 inhibitors such as sildenafil because of profound hypotension.

(c)(ii) Exenatide

Exenatide, a synthetic exendin-4 from the saliva of the Gila monster, is a GLP-1 receptor agonist resistant to DPP-4 degradation, given subcutaneously (5–10 µg twice daily, or 2 mg once weekly extended-release). It enhances glucose-dependent insulin secretion, suppresses glucagon, delays gastric emptying, and promotes satiety. Because its insulinotropic effect is glucose-dependent, hypoglycaemia is rare unless it is combined with sulfonylureas or insulin. It is used in type 2 diabetes mellitus, with metformin or other agents, and produces modest weight loss (it is not licensed for obesity alone, unlike liraglutide or semaglutide). The EXSCEL trial showed cardiovascular non-inferiority, but a reduction in cardiovascular events was not proven. Side effects are nausea, vomiting, injection-site reactions, and rarely pancreatitis and renal impairment; the weekly form carries a warning about medullary thyroid carcinoma.

(c)(iii) 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. The short-acting artemisinin also reduces the parasite biomass that the long-acting partner must clear, so each drug protects the other. ACTs are well tolerated and safe in the second and third trimesters (and, per WHO 2022, artemether–lumefantrine in the first trimester), and fixed-dose combinations aid adherence. India's national drug policy uses artesunate plus sulfadoxine–pyrimethamine (AS+SP) for P. falciparum, and artemether–lumefantrine in the north-eastern states where SP resistance exists, with single-dose primaquine. The emergence of partial artemisinin resistance (kelch13 mutations) in the Greater Mekong and Africa makes combination therapy, and never monotherapy, essential.