PH2.2 | PH2.2 | Cholinergic Drugs and Organophosphate Poisoning Management — SDL Guide — Summary & Reflection

KEY TAKEAWAYS

Cholinergic drugs act on muscarinic (M1–M5) and nicotinic (N_M, N_N) receptors. Agonists include direct-acting agents (pilocarpine, bethanechol) and AChE inhibitors divided into reversible (neostigmine, pyridostigmine, physostigmine — quaternary/no BBB vs tertiary/BBB; donepezil, rivastigmine for Alzheimer's) and irreversible (organophosphates — covalent phosphorylation). Cholinergic antagonists include atropine (non-selective, crosses BBB, prototype), ipratropium (quaternary, inhaled COPD), glycopyrrolate (quaternary, perioperative), and oxybutynin/solifenacin (bladder-selective).

Organophosphate poisoning management: decontaminate → secure airway → atropine 2–4 mg IV (repeated; titrate to secretions drying, NOT HR normalisation; doses >20 mg may be needed) → pralidoxime 1–2 g IV (within the ageing time window) → diazepam for seizures → ICU support. Pralidoxime is not needed for carbamate poisoning. The anticholinergic toxidrome (atropine overdose or tricyclics): dry/hot/flushed/confused/tachycardic — antidote is physostigmine (tertiary, crosses BBB).

REFLECT

Organophosphate poisoning is preventable — it arises from occupational exposures that can be mitigated with protective equipment and regulation. Yet it remains among the leading causes of toxicological death in low- and middle-income countries. As a future physician, you will likely encounter this presentation in your internship or early career. Think about what the atropine titration scenario in the hook demanded: clear pharmacological reasoning under pressure, with the evidence to resist stopping atropine prematurely because of tachycardia. What other clinical scenarios in your future career will require that same readiness to apply drug mechanisms — not just recall a protocol? How would you build that readiness before you are alone in the emergency department?