Review Question - QID 101704

The patient's clinical presentation is consistent with organophosphate poisoning, likely from fertilizer used on his farm.

Normally, AChE rapidly converts acetylcholine (ACh) into the inactive metabolites choline and acetate in the synaptic cleft. In organophosphate poisoning, over-stimulation of the post-junctional acetylcholine receptor occurs due to irreversible inhibition of AChE by organophosphate compounds. The cholinergic toxicity associated with this poisoning is managed by administering atropine and pralidoxime. Atropine prevents cholinergic activation by competing with acetylcholine at muscarinic receptors, and not nicotinic receptors. Pralidoxime reactivates cholinesterase, thus having a favorable effect at the level of nicotinic and muscarinic receptors. These medications are given concurrently.

Incorrect Answers:
Answer 1: Various medications, such as atropine and scopolamine, antagonize ACh at nicotinic, muscarinic, and neuromuscular receptors to selectively block ACh activity.

Answer 2: ACh agonists such as pilocarpine and cevimeline are used for the treatment of open angle glaucoma and Sjogren's syndrome, respectively.

Answer 3: Inhibition of presynaptic exocytosis of ACh vesicles is the mechanism of botulinum neurotoxin. It results in decreased activity of ACh.

Answer 5: Reversible inhibition of AChE is the mechanism employed by many medications including those used to treat Alzheimer's disease (donepezil) and myasthenia gravis (pyridostigmine). The danger of organophosphates is their IRREVERSIBLE inhibition of AChE.