FM13.11-20,FM14.{2-3,15-16} | Toxicology: Specific Poisons — Glossary

A bedside test for viper envenomation: 2 mL fresh venous blood in a clean, dry glass tube — if blood remains incoagulable after 20 minutes, significant viper (haemotoxic) envenomation is confirmed; the test is used both diagnostically and to monitor antivenom efficacy.

Note: the 20-Minute Whole Blood Clotting Test is a SNAKEBITE investigation tool, NOT a food poisoning test. In food poisoning, the investigations are stool culture, food sample microbiological analysis, and stool/blood PCR for organisms.

A ribosome-inactivating protein (RIP) toxin from Abrus precatorius (jequirity bean) seeds; the A-chain cleaves ribosomal RNA, blocking protein synthesis; toxic mechanism identical to ricin but from a different plant; causes multi-organ failure with delayed onset of 12–24 hours.

The enzyme that hydrolyses acetylcholine in the cholinergic synapse, terminating neurotransmission; irreversibly inhibited by organophosphates (via phosphorylation of the serine active site) and reversibly inhibited by carbamates.

The principal toxic alkaloid of Aconitum species (aconite/monkshood); permanently activates voltage-gated Na⁺ channels (prevents inactivation), causing sustained neuronal depolarisation — characterised by immediate oral burning/tingling and numbing, followed by cardiac arrhythmias; distinct mechanism from cardiac glycosides; no specific antidote.

The irreversible modification (dealkylation) of the organophosphate-AChE covalent complex that renders it no longer reactivatable by oximes (pralidoxime/PAM); occurs over 24–48 hours depending on the specific OP; after ageing, PAM is ineffective.

An enzyme in the haem biosynthesis pathway (converts delta-aminolaevulinic acid to porphobilinogen); among the most lead-sensitive enzymes in the body — inhibited at very low blood lead levels (<10 µg/dL), making blood ALA-D activity a sensitive biomarker of lead exposure.

The principal toxin of Amanita phalloides (death cap mushroom); a bicyclic octapeptide that specifically inhibits RNA polymerase II (the enzyme responsible for mRNA transcription in eukaryotic cells); most toxic to hepatocytes and renal tubular cells; responsible for 90% of fatal mushroom poisoning worldwide.

A post-synaptic nicotinic acetylcholine receptor blocker in cobra (Naja naja) venom; competitively blocks the NMJ nicotinic receptor; flaccid paralysis that may PARTIALLY respond to neostigmine (accumulated ACh can partially overcome competitive block).

A solid rodenticide (tablet form, brand names Celphos/Quickphos) that releases highly toxic phosphine gas (PH₃) on contact with moisture or gastric acid; phosphine inhibits cytochrome c oxidase; has NO specific antidote; one of the most lethal suicidal poisons in rural India.

A life-threatening type I IgE-mediated hypersensitivity reaction to bee or wasp venom proteins; characterised by urticaria, bronchospasm, hypotension, and angioedema within minutes of sting; first-line treatment is IM adrenaline (epinephrine) 0.5 mg.

The syndrome of muscarinic receptor blockade: 'dry as a bone, red as a beet, hot as a hare, blind as a bat, mad as a hatter, full as a flask' — anhidrosis, flushed skin, hyperthermia, mydriasis, delirium, urinary retention; seen in TCA, antihistamine, and atropine overdose.

Systemic poisoning from salicylate overdose; characterised by a biphasic acid-base disturbance — early respiratory alkalosis (respiratory centre stimulation) followed by high anion-gap metabolic acidosis (salicylate accumulation + uncoupling of oxidative phosphorylation).

The mass of ethanol per unit volume of blood, expressed in India as mg per 100 mL; the Indian Motor Vehicles Act legal threshold for driving impairment is 30 mg/100 mL (0.03%).

Coarse basophilic (blue) granules in red blood cells on Romanowsky-stained peripheral blood film, representing aggregated ribosomal RNA; characteristic of lead poisoning (ALA-dehydratase inhibition impairs haem synthesis and ribosomal RNA metabolism).

A pre-synaptic neurotoxin from krait (Bungarus caeruleus) venom that irreversibly destroys the ACh release mechanism at the neuromuscular junction; causes flaccid paralysis that does NOT respond to neostigmine (ACh cannot be released even if AChE is inhibited).

A clostridial neurotoxin that cleaves presynaptic SNARE proteins (specifically SNAP-25), preventing acetylcholine vesicle fusion and release at the NMJ and autonomic junctions; causes DESCENDING flaccid paralysis (cranial nerves first) and autonomic dysfunction (dry mouth, constipation); countered by trivalent botulinum antitoxin.

A blue-black line of lead sulphide at the margin of the gingiva, seen in lead poisoning in individuals with poor dental hygiene (oral bacteria convert absorbed lead to lead sulphide); a pathognomonic clinical marker of plumbism.

The connecting peptide co-secreted equimolarly with endogenous insulin from pancreatic beta cells (proinsulin is cleaved to insulin + C-peptide); absent from all exogenous insulin preparations; the forensic marker for insulin homicide: elevated insulin with absent C-peptide indicates exogenous insulin administration, not endogenous hypersecretion.

A cardiac glycoside-like compound from Calotropis procera (madar/crown flower) plant latex; has local irritant, cardiac, and CNS effects; the milky sap has been used in India to inject into cadavers to alter or accelerate post-mortem changes; forensically detected by LC-MS/MS of post-mortem tissue.

The passage of dark green or black urine following carbolic acid (phenol) poisoning; due to urinary excretion of phenol metabolites and oxidised quinones after systemic absorption.

Haemoglobin with CO bound to the haem iron instead of O₂; formed because CO has 200–300 times greater affinity for haemoglobin than O₂; cherry-red in colour; cannot transport O₂ and causes functional anaemia plus leftward shift of the O₂ dissociation curve (Haldane effect).

The 'suicide tree' or 'pong-pong tree' native to coastal Kerala and Tamil Nadu; its kernel contains cerberin, a cardiac glycoside more potent than digoxin; one of the most common causes of plant-related suicidal death in South India; detected by specific LC-MS/MS analysis of blood and gastric contents.

The documented sequence of collection, handling, analysis, and storage of forensic evidence (including biological samples) that ensures its integrity and admissibility in court; every person who handles the specimen must sign the custody record.

Bright red post-mortem skin staining in dependent areas; characteristic of CO poisoning (HbCO is bright red) and cyanide poisoning (tissues retain HbO₂ because O₂ cannot be extracted); distinguished from normal post-mortem lividity (blue-purple) and from the dark lividity of other causes.

Multi-wavelength spectrophotometric analysis of blood to directly measure HbO₂, HbCO, metHb, and deoxyHb fractions; essential for CO poisoning diagnosis — standard pulse oximetry cannot distinguish HbCO from HbO₂ and gives falsely normal readings in CO poisoning.

A form of tissue death in which the protein structure of cells is preserved but cell function is abolished; proteins denature and form a firm, opaque coagulum or eschar, typical of acid injuries.

Gastric lavage solution containing 0.1% copper sulphate used in phosphorus poisoning; Cu²⁺ reacts with phosphorus to form insoluble, non-absorbable copper phosphide, reducing further absorption and providing a diagnostic colour reaction.

The specific chelating agent for acute iron toxicity; forms water-soluble ferrioxamine complex excreted in urine, which turns a distinctive pink-orange ('vin rosé') colour confirming active chelation; do NOT substitute BAL.

Digoxin-specific antibody fragments that bind free cardiac glycoside (digoxin and cross-reactive plant glycosides including oleandrin and cerberin); the complex is renally excreted; the specific antidote for serious cardiac glycoside toxicity from both pharmaceutical and plant sources.

British Anti-Lewisite; a dithiol chelating agent that forms stable complexes with arsenic, lead, mercury, and gold; given IM; CONTRAINDICATED in iron and cadmium poisoning as it redistributes these metals to sensitive tissues.

The neuropsychiatric syndrome of inorganic/elemental mercury poisoning: pathological shyness, social withdrawal, emotional instability, impaired memory, and insomnia; classically described in hat-makers who used mercuric nitrate in the felting process ('Mad Hatter').

The firm, leathery or charred tissue formed at the site of acid contact due to protein coagulation; acts as a partial barrier limiting deeper tissue penetration.

Phase 2 of amatoxin mushroom poisoning (days 1–4 post-ingestion): apparent clinical improvement after the initial GI phase, while hepatocyte destruction from RNA pol II inhibition silently progresses; misinterpretation as recovery leads to dangerous premature discharge before fulminant hepatic failure in Phase 3.

The chelate complex of iron + deferoxamine; water-soluble and renally excreted; the pink-orange urine colour in a child receiving deferoxamine treatment is ferrioxamine and confirms the chelator is binding free iron effectively.

A competitive antagonist at the benzodiazepine binding site of the GABA-A receptor; reverses benzodiazepine-induced sedation; short half-life (~1 h) vs BZD half-lives → monitor for re-sedation; contraindicated in chronic BZD users (may precipitate withdrawal seizures).

A blood collection tube containing sodium fluoride (prevents enzymatic/microbial fermentation of glucose and ethanol) and potassium oxalate (anticoagulant); the standard tube for ethanol (BAC) analysis and glucose (blood sugar) in forensic blood specimens — fluoride preserves ethanol and glucose integrity.

A specific inhibitor of alcohol dehydrogenase (ADH); used as antidote for methanol and ethylene glycol poisoning to block their metabolism to toxic acids (formic acid and oxalic acid respectively); preferred over ethanol where available due to predictable dosing and absence of ethanol side-effects.

The central Indian statute regulating food safety, food standards, and food businesses; established FSSAI as the regulatory authority; replaced the Prevention of Food Adulteration Act 1954; governs civil and regulatory liability for food poisoning negligence; criminal provisions for deliberate adulteration remain under IPC §272–273.

The primary toxic metabolite of methanol (produced via formaldehyde intermediate from ADH + ALDH metabolism); inhibits cytochrome c oxidase (Complex IV, mitochondrial electron transport chain) → metabolic acidosis and selective optic nerve/retinal degeneration → blindness.

Injuries defined by IPC as grievous, including permanent loss of vision or hearing, permanent disfigurement of face or head, fracture of bone, and permanent loss of limb use; acid attacks almost invariably constitute grievous hurt under items 7 (permanent disfigurement) and/or 1 (emasculation).

Enhanced elimination by extracorporeal blood purification; most effective for small (<500 Da), water-soluble, protein-unbound drugs; indicated for lithium toxicity (small, unbound), severe salicylate poisoning (salicylate >350 mg/L), severe methanol/ethylene glycol poisoning, and barbiturate-induced renal failure.

Extracorporeal blood purification that removes small, non-protein-bound toxins across a semipermeable membrane; indicated in severe aspirin poisoning (salicylate >350 mg/L) to rapidly reduce total body salicylate load.

Forensic analysis of hair for drugs and their metabolites; hair grows at approximately 1 cm per month; drugs are incorporated into the hair shaft as it forms; a 1-cm segment of proximal hair represents the preceding month's exposure; allows reconstruction of drug use history over months to years from a single sample.

In CO poisoning, CO binding to one haem subunit increases the O₂ affinity of the remaining subunits (left shift of the O₂-Hb dissociation curve), meaning the small amount of O₂ still carried is held too tightly and not released to tissues; compounds the tissue hypoxia beyond what HbCO level alone predicts.

A form of cellular hypoxia in which oxygen is delivered to tissues but cells cannot utilise it; caused by inhibitors of the mitochondrial electron transport chain (cytochrome c oxidase inhibitors — cyanide, CO); characterised by paradoxically high venous PO₂ because tissues do not extract O₂.

Illicitly produced liquor (country liquor); forensically significant because inadequate distillation or deliberate methanol addition produces methanol-contaminated alcohol; responsible for periodic mass-casualty poisoning events (hooch tragedies) in India.

A cobalt-containing compound (vitamin B12 analogue) used as a cyanide antidote; the cobalt centre directly binds CN⁻ to form cyanocobalamin, which is renally excreted; preferred in fire victims with suspected CO+CN co-poisoning because it does not cause methaemoglobinaemia (unlike sodium nitrite).

A belladonna alkaloid (anticholinergic) from Datura stramonium (dhatura); blocks muscarinic acetylcholine receptors → anticholinergic toxidrome (dry, hot, red, blind, mad, full); the primary toxin responsible for dhatura's criminal-incapacitation use; distinguished from atropine by greater CNS sedation and amnesia.

Administration of 100% O₂ at supra-atmospheric pressure (2–2.5 atm); shortens HbCO half-life to ~20 minutes (vs ~60–90 min on normobaric 100% O₂); also reverses CO binding to cytochrome c oxidase; indicated for severe CO poisoning (LOC, HbCO >25%, pregnancy, cardiac arrhythmia).

Serum calcium below 2.1 mmol/L (or ionised Ca²⁺ <1.15 mmol/L); in oxalic acid poisoning, caused by chelation of serum calcium by absorbed oxalate ions forming insoluble calcium oxalate, leading to tetany and cardiac arrhythmia.

A delayed complication of organophosphate poisoning occurring 24–96 hours after the cholinergic crisis; characterised by proximal limb weakness, respiratory muscle paralysis, and cranial nerve palsies; not responsive to atropine or PAM — requires mechanical ventilatory support.

Chronic toxicity from excessive iodide intake; manifests as coryza-like symptoms (runny nose, excessive salivation, lacrimation), iodide rash (acneiform eruption), metallic taste, and transient hypothyroidism (Wolff-Chaikoff effect); distinct from acute iodine ingestion.

A pharmacokinetic principle by which a drug in its ionised (charged) form cannot cross lipid membranes and is therefore retained in a body compartment; urinary alkalinisation traps salicylate as its ionised form in tubular lumen, increasing renal clearance.

Section 326A of the Indian Penal Code (inserted 2013): voluntarily causing grievous hurt by use of acid, carrying a minimum sentence of 10 years imprisonment (may extend to life); enacted specifically for acid attack cases following judicial direction.

Potassium channels that normally allow K⁺ to flow into cells at rest; barium ions (Ba²⁺) block these channels, trapping K⁺ inside cells and creating severe extracellular hypokalaemia despite normal total body potassium — the mechanism of barium-induced paralysis and arrhythmia.

The infusion of a lipid emulsion (Intralipid 20%) IV during cardiac arrest from highly lipophilic drugs (bupivacaine, TCA); the lipid phase acts as a 'sink' sequestering the lipophilic drug out of cardiac tissue; the first-line resuscitation intervention for bupivacaine cardiac arrest.

The property of being soluble in fat/oil; yellow phosphorus is highly lipophilic, meaning fats and oils dramatically increase its gastrointestinal absorption — hence oil-based preparations (castor oil, milk fat) are contraindicated in phosphorus poisoning management.

A form of tissue death in which enzymes dissolve cell components, producing a liquid-filled cavity; characteristic of alkali injuries (not acids) — alkaline saponification of fat and protein dissolution allows deeper tissue penetration than acid coagulation necrosis.

The classic qualitative analytical chemistry test for arsenic, developed in 1836; arsenious compound in test material reduced to arsine gas (AsH₃) by zinc + H₂SO₄, which passes over a heated glass tube depositing a black arsenic mirror; foundational to forensic toxicology.

A formal medical document prepared by a registered doctor at the request of a legal authority (police, magistrate, court) recording the findings of a medical examination, the specimens collected, and the doctor's expert opinion on the medicolegal significance; admissible as documentary evidence in legal proceedings.

Transverse white bands (striae) running across the full width of the fingernail, each representing a discrete episode of arsenic (or occasionally other heavy metal) exposure. The nail grows approximately 3 mm/month, so the distance of a Mees' line from the nail fold can date the exposure episode.

The Indian statute that replaced the Mental Health Act 1987; Section 115 presumes that a person who attempts suicide is under severe mental stress and must receive care and treatment — not prosecution; effectively decriminalised attempted suicide under IPC §309.

An extremely reactive isocyanate compound used in carbamate pesticide synthesis; released in the Bhopal disaster (1984); mechanism: alkylation of biological molecules (proteins, DNA) in respiratory epithelium causing chemical ARDS, pulmonary oedema, and systemic injury; no specific antidote.

Section 185 of the Motor Vehicles Act 1988 (India) that defines drunken driving as driving with a blood alcohol concentration exceeding 30 mg per 100 mL of blood (0.03%); the basis for police-requested drunkenness medical examinations.

The primary receptor mediating opioid analgesia, euphoria, miosis, constipation, and — critically — respiratory depression; the target of morphine, heroin, fentanyl, codeine, and naloxone (antagonist).

The specific antidote for paracetamol (acetaminophen) overdose; replenishes hepatic glutathione stores and provides sulphydryl groups to conjugate NAPQI; most effective within 8 hours of ingestion but should be given up to 24+ hours if LFTs are rising.

The mechanism shared by all cardiac glycoside agents (digoxin, oleander, Cerbera, digitalis): inhibition of the cardiomyocyte sodium-potassium pump causes intracellular Na⁺ accumulation → reversal of the Na⁺/Ca²⁺ exchanger → Ca²⁺ overload → triggered ventricular arrhythmias and AV block.

A pure competitive opioid receptor antagonist that reverses opioid-induced respiratory depression, sedation, and miosis; short duration of action (30–90 min) — shorter than most opioids; re-narcotisation may occur requiring repeat dosing or infusion.

The reactive hepatotoxic metabolite of paracetamol formed by CYP2E1; at therapeutic doses neutralised by glutathione; in overdose, glutathione is depleted and NAPQI accumulates, covalently binding to cellular macromolecules and causing centrilobular hepatic necrosis.

The Narcotic Drugs and Psychotropic Substances Act 1985 (India); schedules narcotic substances including morphine, heroin, opium, codeine, and their derivatives; criminalises possession, sale, manufacture, and trafficking; governs prosecution of narcotic-related deaths.

A rare but life-threatening idiosyncratic reaction to antipsychotics (typicals > atypicals); characterised by hyperthermia, generalised rigidity, autonomic instability (labile BP, diaphoresis), and altered consciousness; treated with dantrolene (muscle relaxant) and bromocriptine (D2 agonist).

A class of halogenated organic insecticides (examples: DDT, BHC, endosulfan, lindane) that prolong voltage-gated sodium channel opening, causing excitatory CNS toxicity (tremor, seizures); highly lipophilic and bioaccumulating; most banned from agricultural use in India but legacy exposure continues.

A bipyridinium herbicide that undergoes intracellular redox cycling to generate superoxide radical; preferentially accumulated by alveolar type II pneumocytes via the polyamine transport system, causing progressive pulmonary fibrosis; oxygen is contraindicated as it accelerates radical generation.

A colourless, highly toxic gas with a characteristic garlic/rotten-fish smell; released from aluminium and zinc phosphide tablets on contact with moisture; mechanism of toxicity is cytochrome c oxidase inhibition (similar to cyanide) causing cellular hypoxia and direct cardiac toxicity.

The emission of faint visible light by a substance without requiring a heat source; in forensic toxicology, yellow/white phosphorus in hepatic tissue produces a characteristic greenish glow in the dark, pathognomonic of phosphorus poisoning at post-mortem.

Indian polyvalent antivenom covering the four Big Four snakes (Russell's viper, cobra, krait, saw-scaled viper); dosed at 10 vials IV regardless of patient weight; repeated every 6 hours until 20WBCT normalises or neurotoxic features resolve.

An oxime (nucleophilic agent) that reactivates acetylcholinesterase by displacing the organophosphate from the enzyme's serine active site; effective only within 24–48 hours of OP exposure, before ageing of the OP-AChE complex; treats both muscarinic and nicotinic effects.

An alpha-1 adrenoceptor blocker; the specific evidence-based treatment for Indian red scorpion (Mesobuthus tamulus) envenomation; counteracts the catecholamine-mediated alpha-adrenergic cardiovascular toxicity (hypertension → cardiomyopathy).

Prolongation of the QRS complex on ECG (>100 ms) caused by tricyclic antidepressant blockade of fast (phase 0) sodium channels in the cardiac conduction system; a predictor of ventricular arrhythmia; treated with IV sodium bicarbonate (sodium loading overcomes the channel block).

A characteristic cutaneous finding of chronic arsenic poisoning: alternating hyperpigmented and hypopigmented macules over the trunk and extremities, giving the appearance of raindrops on dusty skin; associated with arsenical keratosis of palms and soles.

A decrease in serum (extracellular) potassium caused by shift of K⁺ into cells, not by actual K⁺ loss from the body; seen in barium poisoning, insulin therapy, beta-agonist use, and alkalosis. Total body K⁺ is normal; treatment is IV K⁺ replacement to restore extracellular level.

A screening test for arsenic, mercury, bismuth, and antimony; a copper strip placed in acidified test material is coated with a grey/silver deposit if these metals are present; less specific than Marsh test but a useful screen.

The calculation of blood alcohol concentration at a past time point (e.g., time of the alleged offence) from a measured current BAC, using the known ethanol elimination rate (10–15 mg/100 mL/h); a forensic calculation used in traffic offence proceedings.

An endogenous enzyme in hepatic mitochondria that detoxifies cyanide by transferring sulfur from thiosulphate to CN⁻, producing relatively non-toxic thiocyanate (SCN⁻), which is renally excreted; the basis of sodium thiosulphate as a cyanide antidote.

A graph plotting serum paracetamol concentration against time since ingestion; levels plotting above the treatment line predict significant hepatotoxicity and mandate N-acetylcysteine treatment regardless of clinical symptoms; the standard decision tool for paracetamol overdose management.

A characteristic complication of Russell's viper (Daboia russelii) envenomation: acute renal failure caused by direct renal tubular toxicity of venom PLA2, haemoglobinuria (from haemolysis), and myoglobinuria (from rhabdomyolysis); requires dialysis in severe cases.

A drug-induced syndrome of excessive serotonergic activity; triad of cognitive effects (agitation, confusion), autonomic dysfunction (hyperthermia, tachycardia, diaphoresis), and neuromuscular abnormalities (clonus, hyperreflexia, tremor); caused by MDMA, MAOIs, SSRIs, tramadol — serotonin excess; key distinguishing sign from NMS is clonus.

A clinical mnemonic for the muscarinic features of cholinergic excess: Salivation, Lacrimation, Urination, Defaecation, GI distress, Emesis; plus B for Bradycardia and Bronchospasm; characteristic of organophosphate and carbamate poisoning.

An alkaloid from Strychnos nux-vomica seeds; blocks glycine receptors (inhibitory neurotransmitter) in spinal cord interneurons, removing inhibitory control of motor neurons; produces generalised convulsions with opisthotonus (arched back), risus sardonicus (fixed grin), and respiratory arrest; no specific antidote.

The characteristic progression of phosphorus poisoning: Phase 1 (GI symptoms, 0–24 h) → Phase 2 (latent/asymptomatic period, 24–48 h — deceptively improved) → Phase 3 (hepatorenal failure, arrhythmia, 48–96 h+).

A syndrome of signs and symptoms characteristic of a class of toxic substances; the nine main toxidromes (cholinergic, anticholinergic, sympathomimetic, sedative-hypnotic, opioid, serotonergic, hallucinogenic, excitatory/convulsant, and mixed) allow clinical identification of the poison class before analytical results are available.

Elevation of urine pH to 7.5–8.0 using IV sodium bicarbonate to increase the ionised fraction of a weak acid (e.g., salicylate) in urine, enhancing its renal elimination; the specific enhanced-elimination strategy for aspirin overdose.

The coagulopathy caused by Russell's viper and saw-scaled viper venom: venom proteases and PLA2 activate and consume clotting factors (prothrombin, fibrinogen, Factor X) producing a DIC-like state; detected at the bedside by the 20WBCT (incoagulable blood).

The pharmacokinetic equation C = A / (r × W) used to calculate blood alcohol concentration (C) from the total alcohol consumed (A, in grams), the Widmark distribution factor (r — 0.7 for males, 0.6 for females), and body weight (W, in kg); also used for retrograde extrapolation to estimate BAC at an earlier time.

A chemical reaction between nitric acid and aromatic amino acids (notably tyrosine) in skin proteins producing yellow/orange nitrated chromogens; pathognomonic of nitric acid exposure.

Note: the xanthoproteic reaction is specific to NITRIC ACID, not iodine. Iodine's mucosal marker is blue-black iodo-protein staining (iodine reacts with glycoproteins in mucus to form a blue-black chromogen, distinct from iodine-starch's blue colour).

The toxic allotrope of phosphorus (yellow and white refer to the same form) — pyrophoric (spontaneously flammable in air), garlic-smelling, phosphorescent in the dark; the form found in rat poisons and relevant to forensic toxicology (red phosphorus is non-toxic).

A pharmacokinetic elimination pattern in which a fixed amount of drug (not a fixed fraction) is eliminated per unit time, regardless of concentration; ethanol exhibits zero-order kinetics because ADH becomes saturated at blood concentrations above approximately 10–20 mg/100 mL, eliminating approximately 10–15 mg/100 mL/hour.