(a) Classify the various types of poisons. Enumerate the features of Plumbism. Discuss the tests which will show/establish the…

Toxicology Poisons are classified by chemical nature and source: corrosives (sulphuric acid, alkali, kerosene), metallic (lead, arsenic, mercury), gaseous (carbon monoxide, hydrogen sulphide), organic (organophosphates, carbon tetrachloride), vegetable (aconite, datura), animal (snake venom, scorpion venom) and mechanical (foreign bodies). They may also be grouped by route—ingestion, inhalation, injection or skin absorption—and by target organ, as neurotoxins, haematotoxins, hepatotoxins and nephrotoxins. Plumbism is chronic lead poisoning. Features include abdominal colic, constipation, Burtonian blue-black gingival line, wrist drop or peripheral neuropathy, hypertension, renal tubular dysfunction, microcytic or normocytic anaemia with basophilic stippling, and encephalopathy in severe cases. Lead colic may mimic acute abdomen; renal Fanconi syndrome and optic neuritis may occur. Early biochemical tests are more sensitive than symptoms: raised urinary delta-aminolevulinic acid and coproporphyrin, raised blood zinc protoporphyrin in µg/dL, raised urinary lead, and raised blood lead level in µg/dL; these reflect inhibition of ALA dehydratase and ferrochelatase and establish early stages before overt neuropathy or colic.

Haematology The bleeding, fever, anaemia, very high WBC count and 75% blasts with fine azurophilic granules and Auer rods point to acute promyelocytic leukaemia, AML-M3. APL often presents with DIC and bleeding, and Auer rods may form faggot cells; bone marrow confirms the diagnosis. Cytochemical stains useful are myeloperoxidase and Sudan black B, both positive in myeloid blasts; non-specific esterase is negative, helping exclude monocytic leukaemia, and PAS may show block positivity. Favourable cytogenetic findings in APL are t(15;17)(q24;q21) producing PML-RARA and an isolated/simple karyotype without additional rearrangements; the translocation is diagnostic and predicts response to ATRA. Unfavourable findings are complex karyotype and the alternative t(11;17)(q23;q21) PLZF-RARA translocation, which is associated with poorer response to ATRA.

Rheumatic heart disease Rheumatic heart disease follows untreated group A streptococcal pharyngitis. Molecular mimicry between streptococcal M protein and cardiac antigens triggers type II hypersensitivity and autoimmune injury, with immune-complex and T-cell mediated damage, producing pancarditis. Microscopically, the early lesion is the Aschoff body: a perivascular granuloma with fibrinoid necrosis, macrophages, lymphocytes and Anitschkow cells; Aschoff bodies are pathognomonic, and pericardial inflammation may cause effusion. In the mitral valve, early verrucous vegetations form along the line of closure; later the valve thickens, fibroses and calcifies, chordae shorten and fuse, producing commissural fusion, retraction, doming and stenosis, often with regurgitation.

Malaria and insulin Complicated P. falciparum malaria is a medical emergency, with cerebral malaria, severe anaemia, respiratory distress, shock, renal failure, jaundice, hypoglycaemia or acidosis. First-line treatment is intravenous artesunate, 2.4 mg/kg at 0, 12 and 24 hours, then 2.4 mg/kg daily, followed by a full oral course. If artesunate is unavailable, quinine is given as a 20 mg/kg loading dose, then 10 mg/kg every 8 hours, with caution for hypoglycaemia and QT prolongation. Supportive care includes ICU monitoring of airway, glucose, renal function, haemolysis and electrolytes; severe anaemia may need transfusion, and ARDS is managed with lung-protective ventilation. Parenteral benzodiazepines are used for malarial seizures as abortive therapy, not prophylaxis. Exchange transfusion is not routinely recommended; it may be considered case-by-case in selected severe cases, for example very high parasitaemia, often >10% or >5% with severe organ dysfunction, when rapid parasite reduction is needed. Prevention of blackwater fever includes avoiding oxidant drugs, correcting acidosis and monitoring urine for haemoglobinuria.

Insulin is indicated in type 1 diabetes, diabetic ketoacidosis, hyperosmolar hyperglycaemic state, gestational diabetes, perioperative hyperglycaemia and severe insulin resistance. Basal-bolus regimens are commonly used. Adverse effects are hypoglycaemia, weight gain, lipodystrophy at injection sites, local or systemic allergic reactions, insulin resistance, and oedema.

Preventive measures include lead-safe housing and food handling, prompt streptococcal prophylaxis, malaria vector control, and structured diabetes education.