FM13.{1-10,21} | Toxicology: General Principles — Glossary

Highly porous charcoal that adsorbs organic compounds in the GI lumen, preventing absorption; dose 1 g/kg; ineffective for iron, lead, lithium, alcohols, acids, and alkalis.

Absorption, Distribution, Metabolism, Excretion — the four processes governing the fate of a poison (or drug) in the body; collectively termed toxicokinetics (or pharmacokinetics for therapeutic agents).

Chronic arsenic poisoning from prolonged exposure to arsenic-contaminated drinking water; characterised by skin melanosis, palmar keratosis, Mees lines, peripheral neuropathy, and elevated cancer risk (bladder, lung, skin).

A poison causing death by preventing oxygen delivery (CO — carboxyhaemoglobin) or cellular oxygen utilisation (cyanide — cytochrome oxidase inhibition); chemical asphyxiants are more toxic than simple asphyxiants.

Spectroscopic technique quantifying metallic elements using element-specific hollow cathode lamps; ground-state atoms absorb light at characteristic wavelengths; effective for arsenic, lead, mercury, thallium; cannot detect organic compounds.

Aggregated ribosomal RNA granules visible in erythrocytes on blood film; a haematological marker of lead poisoning (lead inhibits pyrimidine 5-nucleotidase).

Progressive increase in concentration of a persistent lipid-soluble substance (e.g., methylmercury, DDT) with each step up the food chain; results in top predators accumulating concentrations many times higher than ambient environmental levels.

Blue-black lead sulphide deposits at the gingival margin; a clinical sign of chronic lead poisoning visible on oral examination.

The unbroken documented record of who collected, handled, transferred, and analysed an evidentiary sample; essential for admissibility of forensic evidence in court.

Pathognomonic post-mortem skin colour in CO poisoning (carboxyhaemoglobin) and also seen in cyanide poisoning; indicates that deoxygenated haemoglobin has been replaced by a persistent bright-red compound.

Irreversible dealkylation of the organophosphate-cholinesterase bond, occurring 24-48 hours after exposure; after ageing, pralidoxime cannot reactivate the enzyme.

The medical specialty concerned with the diagnosis, management, and prevention of poisoning in living patients.

Multi-wavelength spectrophotometric analysis on an arterial blood gas analyser; distinguishes oxyhaemoglobin, deoxyhaemoglobin, carboxyhaemoglobin (HbCO), and methaemoglobin; required for accurate CO poisoning diagnosis (standard pulse oximetry is unreliable).

A poison that destroys tissue on contact through chemical necrosis; includes strong mineral acids (H₂SO₄, HCl, HNO₃) and strong alkalis (NaOH, KOH, phenol).

Central Pollution Control Board / State Pollution Control Board; statutory bodies under the Environment Protection Act 1986 that regulate industrial air and water discharge standards in India.

Section of the Code of Criminal Procedure 1973 under which a police officer holds an inquiry into sudden, suspicious, or unnatural deaths; triggers the medico-legal autopsy request.

Indian legislation providing mandatory compensation to employees for occupational injuries and diseases; Schedule III lists specific occupational diseases (including lead, mercury, and arsenic poisoning) compensable without proof of employer negligence.

Neuropsychiatric syndrome from inorganic mercury vapour poisoning; characterised by extreme irritability, timidity, social withdrawal, memory impairment, and progressive dementia; classically 'Mad Hatter' syndrome from felt-hat industry.

Bedside colorimetric urine test for salicylates; positive = purple/violet colour; false positive with phenothiazines and phenylpyruvic acid.

Hepatic metabolism of an orally absorbed substance before it reaches the systemic circulation via the portal route; reduces bioavailability but may also generate toxic metabolites (e.g., paracetamol → NAPQI).

Enhanced elimination technique using IV sodium bicarbonate to alkalinise urine (pH 7.5-8.5), trapping weak acids (salicylates, phenobarbital) in ionised form to prevent tubular reabsorption.

The application of toxicological principles and analytical methods to medico-legal investigations, answering legal questions about cause of death or impairment.

Formaldehyde solution (10% in water) used as histological fixative; ABSOLUTELY CONTRAINDICATED for toxicological FSL specimens — destroys volatile compounds and cross-links proteins.

Government laboratory that performs chemical analysis of viscera, body fluids, and suspected substances in medico-legal investigations; India's first FSL was established in Calcutta in 1853.

Chromatographic separation using an inert carrier gas and a heated capillary column; separates compounds by volatility and stationary phase interaction; GC-MS combines separation with mass spectrometric detection for unique molecular fingerprinting.

GI decontamination technique using large-bore nasogastric tube and saline aliquots; most effective within 1 hour of ingestion; absolutely contraindicated for corrosive and petroleum distillate ingestions.

Gas chromatography coupled to mass spectrometry; gold standard for organic drug and poison identification; the mass spectrum provides a unique molecular fingerprint for each compound; used for confirmatory analysis.

Extracorporeal elimination technique removing small, water-soluble, low-protein-bound, low-Vd poisons across a semi-permeable membrane; effective for salicylates, methanol, ethylene glycol, and lithium.

Extracorporeal elimination technique passing blood through a charcoal or resin column to directly adsorb lipophilic or protein-bound poisons; more effective than dialysis for paraquat, theophylline, and carbamazepine.

Element-specific light source in AAS; emits at the exact characteristic absorption wavelength of the target element, providing the selectivity of the technique.

An abnormal, qualitatively different pharmacological response that is genetically determined; e.g., G6PD deficiency causing haemolysis after naphthalene (mothball) exposure.

Antibody-based detection method for drugs in urine or blood; rapid and sensitive but cross-reactive (false positives); results are presumptive only and require GC-MS or LC-MS confirmation before use as legal evidence.

Indian Penal Code provision making it an offence (up to 10 years imprisonment) to administer a poison or stupefying substance to another person with intent to commit or facilitate an offence.

A poison that causes inflammation and irritation at the contact site (local) or in systemic organs (remote); arsenic, antimony, and mercury are classic remote irritants.

The dose of a substance lethal to 50% of a defined test population under specified experimental conditions; always qualified by species, route of administration, age, and sex.

Chromatographic separation in liquid mobile phase coupled to mass spectrometric detection; used for non-volatile, thermally labile, high-molecular-weight compounds; LC-MS/MS (triple quadrupole) provides highest specificity and sensitivity for forensic analysis.

Spanish-born French chemist (1787–1853) and founder of modern forensic toxicology; first to systematically apply chemical analysis to medico-legal death investigations.

Any clinical case that has actual or potential legal implications — including poisoning, assault, sexual offences, road traffic accidents — requiring mandatory documentation and police notification.

Transverse white bands across all fingernails; a clinical marker of acute/subacute arsenic exposure; each line corresponds to a period of heavy exposure; nail growth (~1 mm/week) allows approximate timing.

Malignant tumour of the pleural or peritoneal mesothelium; pathognomonically associated with asbestos (particularly crocidolite) exposure; latency 20-40 years; no safe threshold of asbestos exposure.

Neurological syndrome from methylmercury poisoning; characterised by cerebellar ataxia, constriction of visual fields, circumoral paraesthesia, and sensorineural hearing loss; described in Minamata Bay, Japan, from industrial methylmercury discharge.

The hospital's medico-legal case register; the primary legal record for all MLC admissions including poisoning; must be contemporaneous, signed, and retained for a minimum of 10 years.

Mnemonic for causes of elevated anion gap metabolic acidosis in poisoning: Methanol, Uraemia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates.

Antidote for paracetamol overdose; replenishes glutathione, preventing NAPQI accumulation and hepatocellular necrosis; most effective within 8 hours; guided by the Rumack-Matthew nomogram.

Competitive opioid receptor antagonist; antidote for opioid overdose; dose 0.4-2 mg IV; shorter half-life than most opioids — re-narcotisation requires repeat dosing or infusion.

The Narcotic Drugs and Psychotropic Substances Act 1985; prohibits narcotic/psychotropic substances except under licence; Schedule I lists prohibited substances; Section 22 covers psychotropic offences; Section 27 covers personal consumption.

A poison acting primarily on the nervous system; subclassified as spinal (strychnine — tetanic convulsions), cerebral depressant (opioids, alcohol — sedation/coma), or peripheral (neuromuscular blockers).

Any substance that, when introduced into or applied to a living organism in sufficient quantity by any route, causes harm, disease, or death by its own chemical or physiological action.

Indian legislation empowering state governments to regulate the import, possession, manufacture, sale, and transport of scheduled poisons.

Phenomenon where lipophilic drugs diffuse from organs into adjacent cardiac blood post-mortem, falsely elevating apparent concentrations; femoral blood is preferred to avoid this artefact.

Diffusion of lipophilic drugs from high-concentration tissue depots into adjacent blood post-mortem; causes overestimation of antemortem blood concentration; mitigated by collecting femoral (peripheral) blood and vitreous humour.

Cholinesterase reactivator; antidote for organophosphate poisoning; must be given within 24-48 hours of exposure before irreversible ageing of the OP-cholinesterase bond; does not replace atropine.

90% ethanol solution; acceptable preservative for solid viscera for non-volatile poison analysis; must NOT be used when ethanol itself is the suspected poison.

Distance migrated by compound ÷ distance migrated by solvent front; a reproducible characteristic under standard TLC conditions; not unique — different compounds can share the same Rf on the same system.

Log-linear graph plotting serum paracetamol level against time post-ingestion; the 'treatment line' identifies patients at risk of hepatotoxicity who require NAC; serum level measured at 4 hours post-ingestion.

Preferred preservative for solid viscera (liver, kidney, brain) in toxicological analysis; does not interfere with volatile compound analysis; required when ethanol is the suspected poison.

Progressive nodular pulmonary fibrosis from inhalation of crystalline silica; upper-lobe predominance on chest X-ray; predisposes to tuberculosis; Group 1 carcinogen for lung cancer.

Osteosclerosis and ligament calcification from chronic fluoride ingestion above 4 mg/L; causes progressive spinal rigidity ('poker spine') and joint pain; endemic in several Indian states.

Mnemonic for muscarinic cholinergic toxidrome: Salivation, Lacrimation, Urination, Defaecation, GI cramps, Emesis — produced by organophosphate/carbamate poisoning (acetylcholinesterase inhibition).

Preservative added to blood collection tubes for toxicological analysis; inhibits glycolysis (prevents spurious post-mortem ethanol generation) and is bacteriostatic; used in grey-top tubes.

Combined effect of two agents that exceeds the sum of individual effects; clinically relevant in polypharmacy poisonings (e.g., alcohol + benzodiazepine — potentiated respiratory depression).

The ratio LD50/ED50; quantifies the margin of safety between a toxic and a therapeutic dose. Drugs with a narrow TI (e.g., digoxin, lithium, warfarin) require tighter monitoring.

Chromatographic separation on silica plate using a liquid mobile phase; compounds identified by Rf value and visualisation reagent colour; screening tool — Rf values are not unique identifiers; confirmatory method required for legal proceedings.

Reduced pharmacological response to the same dose following repeated exposure, requiring higher doses for the same effect; underlies opioid dependence and explains why chronic users tolerate potentially lethal doses.

The scientific study of the adverse effects of chemical substances on living organisms, encompassing their detection, mechanisms of harm, treatment, and prevention.

A cluster of clinical signs produced by a specific pharmacological mechanism, allowing identification of poison class before laboratory results; key toxidromes include cholinergic (OP), anticholinergic, opioid, and sympathomimetic.

A poison produced by a living organism (bacterial, plant, or animal), such as botulinum toxin or ricin.

A toxin of biological origin that is actively injected into another organism via a specialised anatomical apparatus (fang, sting, spine); all venoms are toxins but not all toxins are venoms.

Fluid from the posterior chamber of the eye; preferred specimen for alcohol quantification and electrolyte analysis as it is protected from post-mortem redistribution and decomposition-related changes.

The apparent volume (L/kg) into which a poison distributes if evenly distributed at the plasma concentration. Low Vd = confined to plasma (haemodialysis effective); high Vd = extensive tissue binding (haemodialysis ineffective).

Bowel clearance using polyethylene glycol electrolyte solution (PEG-ELS) by NGT at 1-2 L/hour; indicated for iron, sustained-release preparations, and body-packed drug concealment.