FM13.3 | Poisons: Classification, Toxicokinetics & Diagnosis — Summary & Reflection

KEY TAKEAWAYS

Poisons are classified by two complementary axes used in Indian forensic medicine. By origin: animal (venoms, toxins), vegetable (alkaloids, glycosides — aconitine, strychnine, abrin, ricin), mineral (metals, acids, alkalis — arsenic most important in India), and synthetic (OPs, carbamates, solvents). By action: corrosive (strong acids/alkalis — tissue necrosis on contact), irritant (local or remote/systemic — arsenic, antimony), neurotic (spinal = strychnine; cerebral depressant = opioids/alcohol; peripheral = curare), cardiac (digitalis, aconitine), and asphyxiant (CO, cyanide, CO₂).

Toxicokinetics follows the ADME framework: absorption (route determines speed — inhalation fastest, oral slowest with first-pass effect modifying bioavailability), distribution (Vd — low Vd = dialysable; high Vd = tissue-sequestered), metabolism (Phase I CYP450 — may generate toxic metabolites like NAPQI from paracetamol; Phase II conjugation), and excretion (renal — pH manipulation is the basis of forced diuresis). Toxicodynamics involves dose-response relationships, receptor mechanisms, tolerance (chronic exposure), idiosyncrasy (genetic — G6PD), synergism (alcohol + benzodiazepines), and antagonism (basis of antidote therapy).

Clinical diagnosis uses toxidromes: cholinergic (OP — miosis, bradycardia, SLUDGE, fasciculations), anticholinergic (mydriasis, tachycardia, dry hot skin), opioid (miosis, respiratory depression, coma), sympathomimetic (mydriasis, tachycardia, agitation). Post-mortem diagnosis relies on: cherry-red lividity (CO), perioral burns (corrosive), yellow liver (phosphorus, paracetamol), garlic odour (OP/arsenic), bitter almond odour (cyanide). Poison classification determines medicolegal inference, applicable IPC section, and FSL analytical protocol.

REFLECT

Consider the two patients from the opening scenario. Using the classification and toxicokinetic framework you have now acquired: which specific post-mortem viscera would you preserve for the housewife who ingested toilet cleaner (strong alkali), and which analytical method would confirm the diagnosis? For the drowsy student at the party, what toxidrome do you suspect and which antidote would you reach for first? Finally, reflect on this: organophosphate pesticides are the leading cause of poisoning deaths in rural India. They are legally available, cheap, and effective as agricultural agents. What regulatory or public health measures, grounded in the classification and toxicokinetic knowledge from this module, might reduce their lethality in deliberate self-poisoning?