Question
A 52-year-old man is brought to the emergency department 30 minutes after his farmhand found him on the ground sweating profusely. On arrival, he is lethargic and unable to provide any history. His temperature is 37.5°C (99.5°F), pulse is 42/min, and blood pressure is 95/60 mm Hg. Physical examination shows diaphoresis and excessive salivation. The pupils are constricted. There is scattered expiratory wheezing throughout both lung fields. His clothes are soaked with vomit, urine, and feces. A drug with which of the following mechanisms of action is most appropriate for this patient?
| A. |
ß2 adrenergic receptor agonism
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| B. |
Muscarinic acetylcholine receptor antagonism
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| C. |
Acetylcholinesterase enzyme inhibition
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| D. |
Nicotinic acetylcholine receptor agonism
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Show Answer
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Correct Answer � B
Explanation
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Answer B) Muscarinic acetylcholine receptor antagonism
This man’s symptoms (fecal and urinary incontinence, miosis, bronchospasm, bradycardia, salivation, diaphoresis) suggest organophosphate poisoning.
Muscarinic acetylcholine receptor antagonism
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Atropine is a muscarinic acetylcholine receptor antagonist that is considered the antidote of choice for organophosphate poisoning, which is likely given this patient’s symptoms of cholinergic crisis and history of farm work.
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Organophosphates are commonly used pesticides that cause irreversible inhibition of acetylcholinesterase, resulting in increased acetylcholine levels and both muscarinic and nicotinic receptor activation.
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Atropine competitively inhibits the effects of organophosphates at the muscarinic receptors.
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Because atropine does not act on nicotinic receptors, it cannot reverse any neuromuscular dysfunction caused by organophosphate poisoning.
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Pralidoxime, a cholinesterase reactivator, is also effective in treating the nicotinic effects of organophosphates and should be given in addition to atropine.
ß2 adrenergic receptor agonism
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Beta-2 receptor agonists (e.g., albuterol) are commonly used to treat bronchospasm (e.g., due to asthma, COPD).
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While wheezing was heard during this patient’s pulmonary examination, use of a beta-2 receptor agonist would not address his other life-threatening symptoms, nor the underlying etiology of his cholinergic crisis.
Acetylcholinesterase enzyme inhibition
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Acetylcholinesterase enzyme inhibition is the mechanism of action of cholinomimetic drugs such as neostigmine and physostigmine.
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These agents function similarly to organophosphates and would lead to increased levels of acetylcholine and exacerbation of his cholinergic crisis.
Nicotinic acetylcholine receptor agonism
- Nicotinic acetylcholine receptor agonism is the mechanism of action of nicotine (e.g., in cigarettes) and neuromuscular-blocking agents such as succinylcholine. Drugs that cause acetylcholine receptor agonism would further exacerbate the cholinergic crisis seen in this patient, and are therefore contraindicated.
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