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PH9.2 | PH9.2 | Common Toxicology Emergencies — SDL Guide — SDL Guide (Part 3)
Self-Assessment
Test your understanding of toxicology pharmacology with the following questions.
- Name the antidote and its mechanism of action for: (a) paracetamol poisoning, (b) opioid overdose, (c) organophosphate poisoning (give two antidotes and explain the role of each), (d) benzodiazepine overdose, (e) haemotoxic snake bite.
- A rural patient arrives in shock with confusion, sweating, and a HR of 120/min after working in a pesticide-sprayed field. His pupils are pinpoint and there is pronounced bronchorrhoea. Is this OP or anticholinergic poisoning? State the antidote and endpoint of treatment.
- The 20WBCT is performed on a suspected snake bite victim and blood does not clot at 20 minutes. Which snake types are likely, and what treatment is indicated?
- Why is pralidoxime less useful if given late in organophosphate poisoning? What is the molecular basis for this limitation?
- When is flumazenil contraindicated in a patient with sedation in the emergency department? Name two scenarios.
SELF-CHECK
In organophosphate poisoning, atropine is given to control the muscarinic effects. Which of the following features of OP toxicity will atropine NOT reverse?
A. Bronchospasm and bronchorrhoea
B. Profuse salivation and lacrimation
C. Muscle fasciculations and weakness at the neuromuscular junction
D. Bradycardia and urinary incontinence
Reveal Answer
Answer: C. Muscle fasciculations and weakness at the neuromuscular junction
Atropine is a muscarinic receptor antagonist — it blocks only the muscarinic effects of acetylcholine accumulation: bronchospasm, bronchorrhoea, salivation, lacrimation, bradycardia, miosis, urinary incontinence, GI hypermotility, and sweat secretion. Muscle fasciculations and weakness at the neuromuscular junction are NICOTINIC effects (acetylcholine acting on nicotinic receptors at the neuromuscular junction). Atropine has no effect at nicotinic receptors. Pralidoxime (by reactivating AChE before aging) reduces acetylcholine at ALL synapses including nicotinic ones, and thus addresses the fasciculations and weakness. This distinction is the pharmacological rationale for combining atropine + pralidoxime in OP poisoning.