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FM13.11-20,FM14.{2-3,15-16} | Toxicology: Specific Poisons — Practice Quiz
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A 28-year-old man deliberately ingests a mouthful of concentrated sulphuric acid (H₂SO₄). The type of injury caused to the oesophagus and stomach is:
Correct. Strong mineral acids cause coagulative necrosis (protein denaturation forming a hard, leathery eschar). Alkalis cause liquefactive (colliquative) necrosis which is deeper and more dangerous.
Acid burns: coagulative necrosis — eschar limits depth. Alkali burns: liquefactive necrosis + saponification of fats — deeper, more dangerous, higher oesophageal perforation risk.
Acids → coagulative necrosis (eschar limits penetration). Alkalis → liquefactive necrosis (saponification, deeper penetration). This distinction determines injury severity.
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A 40-year-old smelter worker presents with abdominal colic, constipation, peripheral motor neuropathy affecting the wrists, and a blue-black gingival line (Burton's line). The most likely diagnosis is:
Correct. Burton's line (blue-black line at gum margin from lead sulphide deposition) + lead colic + wrist drop (extensor motor neuropathy) = classic chronic lead poisoning. Basophilic stippling on blood film confirms.
Lead poisoning triad: Lead colic (severe abdominal pain, constipation) + Peripheral motor neuropathy (wrist drop, foot drop) + Burton's line. Basophilic stippling on peripheral blood film.
Burton's line (blue gum line) is pathognomonic for lead poisoning. Arsenic has Mees' lines (transverse white nail bands). Mercury causes erethism (mad hatter syndrome).
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Under the Motor Vehicles Act (India), the legal blood alcohol concentration (BAC) limit for driving is:
Correct. The Indian Motor Vehicles Act specifies 30 mg/100 mL (0.03%) as the legal driving limit. This is stricter than the 80 mg/100 mL limit used in the UK and many other countries.
India BAC limit: 30 mg/100 mL (Motor Vehicles Act). Widmark formula for back-calculation: C = A/(r × W) where r=0.7 (male) or 0.6 (female). Blood for alcohol analysis in NaF/oxalate (prevents fermentation).
India's MV Act limit is 30 mg/100 mL (0.03%) — NOT 0.08% (UK/USA). This is a critical Indian law fact for the MBBS forensic medicine examination.
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A 32-year-old man presents with confusion, visual disturbance, and metabolic acidosis after consuming 'country liquor' (hooch). The most toxic metabolite responsible for his visual symptoms is:
Correct. Methanol is oxidised by alcohol dehydrogenase → formaldehyde → formic acid (formate). Formate inhibits cytochrome c oxidase in the retinal ganglion cells and optic nerve, causing blindness.
Methanol toxicity pathway: Methanol → (ADH) → Formaldehyde → (ALDH) → Formic acid. Formate is the end-organ toxin. Antidote: ethanol (competitive ADH inhibitor) or fomepizole.
Methanol's toxic metabolite is formic acid (NOT formaldehyde). Formate causes optic nerve toxicity and high anion gap metabolic acidosis. Acetaldehyde is ethanol's toxic metabolite.
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A patient is admitted after agrochemical poisoning. Blood work shows low plasma cholinesterase. The patient develops intermediate syndrome on day 4 — proximal limb weakness, neck flexor weakness, and respiratory failure. This syndrome is:
Correct. Intermediate syndrome (IMS) occurs 24-96 hours after apparent recovery from the acute cholinergic phase. It is caused by prolonged AChE inhibition at nicotinic (NMJ) receptors. Respiratory muscle paralysis is the life-threatening feature.
OP poisoning timeline: Acute cholinergic crisis (hours) → Intermediate syndrome (1-4 days, nicotinic NMJ failure) → OPIDN (2-5 weeks, distal neuropathy). IMS needs ventilatory support — atropine and PAM do NOT help IMS.
IMS ≠ OPIDN (which appears weeks later with distal sensorimotor neuropathy). IMS = proximal weakness + respiratory failure at day 1-4, due to persistent NMJ AChE inhibition.
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Pulmonary oedema occurring hours after exposure to a war gas (chemical warfare agent) with no immediate irritation is most characteristic of:
Correct. Phosgene is the classic 'delayed pulmonary toxicant' — minimal immediate irritation (smell of fresh cut hay), followed by 4-24 hour latent period, then severe pulmonary oedema. 85% of WWI gas deaths were due to phosgene.
War gas classification: Choking agents (phosgene, chlorine — lungs), Blister agents (mustard, lewisite — skin/lungs), Blood agents (HCN — cellular respiration), Nerve agents (tabun, sarin — AChE inhibition).
Phosgene hallmark: minimal immediate irritation + delayed (4-24h) pulmonary oedema. Chlorine: immediate irritation. HCN: rapid collapse. H₂S: 'knockdown' at high concentrations.
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A 19-year-old student intentionally ingests 30 tablets of paracetamol 500 mg (total 15 g) approximately 8 hours ago. She now appears well but has right upper quadrant tenderness. The MOST important investigation and treatment at this point is:
Correct. At 8 hours post-ingestion, plot serum paracetamol on the Rumack-Matthew nomogram. If above the treatment line, IV NAC is the antidote — it replenishes glutathione stores, preventing NAPQI-mediated hepatocellular necrosis. Activated charcoal is only effective <4 hours post-ingestion.
Paracetamol overdose: toxic metabolite = NAPQI (N-acetyl-p-benzoquinone imine). Glutathione normally neutralises NAPQI. Overdose depletes glutathione → centrilobular hepatic necrosis. NAC = glutathione precursor.
At 8 hours: AC is ineffective. Nomogram + NAC is the correct answer. NAC is the specific antidote for paracetamol hepatotoxicity — works via glutathione replenishment.
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A 22-year-old man in rural India is brought in 30 minutes after being bitten on the foot by a snake. He has local swelling extending to the knee, a coagulation screen showing non-clotting blood, and gingival bleeding. He is conscious with stable vitals. The most appropriate immediate management is:
Correct. This is a haemotoxic (viper) envenomation. Management: immobilise limb (reduces lymphatic spread), IV access, and POLYVALENT ASV after sensitivity test (intradermal test). Tourniquets and incision/suction are harmful and contraindicated.
Indian Big 4: Russell's viper (haemotoxic), Saw-scaled viper (haemotoxic), Common krait (neurotoxic), Indian cobra (neurotoxic). Haemotoxic → coagulopathy + local swelling. Neurotoxic → descending paralysis, ptosis.
Snake bite management: immobilise (NOT tourniquet), IV access, ASV if indicated. Tourniquet causes ischaemia. Incision/suction is ineffective and causes wound infection.
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A patient presents with MDMA (Ecstasy) intoxication at a music concert. His vital signs show temperature 40.2°C, HR 140 bpm, BP 170/100 mmHg. Sodium is 118 mEq/L. The most likely mechanism for the hyponatraemia is:
Correct. MDMA causes SIADH (inappropriate ADH secretion) AND promotes polydipsia. Combined with the common practice of drinking large volumes of water, this produces dilutional hyponatraemia — a major cause of MDMA-related deaths.
MDMA (Ecstasy) toxicity: 3H syndrome — Hyperthermia, Hyponatraemia (SIADH+polydipsia), Haemorrhagic complications. Management: careful fluid restriction for hyponatraemia, NOT aggressive free water replacement.
MDMA hyponatraemia = SIADH + polydipsia + dilution. NOT simple dehydration/excess sweating. Severe hyponatraemia causes cerebral oedema and herniation.
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In a medico-legal examination of a person suspected of drunkenness, the doctor notes the smell of alcohol, slurred speech, and unsteady gait. To establish intoxication scientifically, the BEST single test is:
Correct. Blood alcohol concentration (BAC) by gas chromatography (GC) is the gold standard forensic test for proving intoxication. Breath tests are screening tools, admissible in traffic cases but not the gold standard for medico-legal purposes.
Drunkenness examination: Clinical + BAC. BAC by GC is admissible court evidence. Collect blood into NaF/oxalate tube. Skin sterilised with non-alcoholic antiseptic (iodine/povidone-iodine — NOT spirit).
GC of blood alcohol is the forensic gold standard. Breath analysers are used for roadside screening (Motor Vehicles Act) but blood BAC is definitive for medico-legal evidence.
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A young adult presents with a toxidrome of miosis, respiratory depression, bradycardia, and decreased bowel sounds. The most appropriate reversal agent is:
Correct. Miosis + respiratory depression + decreased gut motility = opioid toxidrome. Naloxone is the specific opioid antagonist (μ-receptor). Give IV/IM, titrate carefully to avoid precipitating acute withdrawal.
Opioid vs benzodiazepine coma distinction: Both cause CNS depression. Opioids → miosis + respiratory depression. Benzodiazepines → normal pupils + respiratory depression less severe. Naloxone for opioids; flumazenil for benzodiazepines.
Opioid toxidrome = 'OD triad': miosis, respiratory depression, decreased consciousness. Antidote = naloxone (NOT flumazenil which reverses benzodiazepines).
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Mees' lines (Aldrich-Mees' lines) — transverse white bands on nails — are characteristically seen in poisoning with:
Correct. Mees' lines are horizontal white bands on the nails in chronic arsenic poisoning (also seen in thallium). They represent disruption of nail growth during a toxic episode and appear ~4-6 weeks after exposure.
Arsenic chronic poisoning signs: Mees' lines, arsenical keratosis (raindrop pigmentation), Mees' lines, peripheral neuropathy (glove-and-stocking), and Aldrich-Mees' lines on nails. Garlic smell = breath in acute arsenic poisoning.
Mees' lines = arsenic (and thallium). Lead = Burton's line (gums). Mercury = tremor, erethism, acrodynia. Copper = Kayser-Fleischer rings (Wilson's disease) or haemolysis.
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