Brian McMichael Rob Klever Marjan Siadat
Samuel Lee Jeff McMenomy David Mishkin
Allison Loynd Scott Ottolini Devon Moore
Julie Nguyen Brian Kern Richard Gordon
The answer is c.
The patient drank insecticide, which is primarily composed of organophosphate compounds (e.g., Malathion). These compounds inhibit acetylcholinesterase, the enzyme responsible for the breakdown of acetylcholine. The patient is having a “cholinergic crisis.” Overstimulation of muscarinic and nicotinic receptors leads to his symptoms, commonly remembered by the mnemonics SLUDGE (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal [GI] upset, Emesis) or DUMBBELS (Defecation, Urination, Miosis, Bronchospasm, Bronchorrhea, Emesis, Lacrimation, Salivation). The treatment for organophosphate toxicity is atropine and pralidoxime (2-PAM). Atropine is an anticholinergic, therefore it competitively inhibits the excess acetylcholine. Pralidoxime works to regenerate acetylcholinesterase, therefore also limiting the amount of acetylcholine available in neuronal synapses.
(a) Pilocarpine is a non-selective muscarinic receptor agonist that is used in the treatment of chronic open-angle glaucoma and acute angle-closure glaucoma. Suxamethonium, also known as succinylcholine, is a depolarizing neuromuscular blocker. It imitates the action of acetylcholine at the neuromuscular junction, acting on muscle type nicotinic receptors, but it is not degraded by acetylcholinesterase, rather by butyrylcholinesterase, a plasma cholinesterase. (b) N-Acetylcysteine is used in APAP (Acetaminophen) overdoses. (d) Flumazenil reverses benzodiazepines (e.g., diazepam). (e) Physostigmine is a reversible cholinesterase inhibitor. Its effect is to increase acetylcholine in the pre- and postsynaptic junctions. This will worsen the patient’s condition by exacerbating the cholinergic syndrome.
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