A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 46-year-old man presents after he accidentally got splashed with a liquid insecticide that was stored in a bucket in the storeroom one hour ago. He says that he can’t stop coughing and is having problems breathing. He also says he has a pain in his thighs which is unbearable, and his vision is blurry. His temperature is 36.7°C (98.1°F), the pulse is 130/min, the blood pressure is 144/92 mm Hg, and the respiratory rate is 20/min. On physical examination, the patient shows mild generalized pallor, moderate respiratory distress, excessive salivation, and diaphoresis. Cough is non-productive. Pupils are constricted (pinpoint). The cardiopulmonary exam reveals bilateral crepitus. The patient is administered atropine and pralidoxime, which help improve his symptoms. Which of the following is most likely to improve in this patient with the administration of atropine?
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A
BronchospasmCorrect. bronchospasm is a muscarinic effect of acetylcholine excess; atropine directly antagonizes muscarinic receptors and improves it.
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B
TachycardiaIncorrect. Tachycardia in OP poisoning reflects nicotinic ganglionic sympathetic stimulation; atropine does not target nicotinic receptors and may worsen tachycardia.
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C
Muscle crampsIncorrect. Muscle cramps and fasciculations are NICOTINIC effects at the neuromuscular junction; atropine does not block nicotinic receptors. Pralidoxime addresses these.
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D
PallorIncorrect. Pallor here is due to nicotinic sympathetic vasoconstriction, which atropine does not antagonize.
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E
FasciculationsIncorrect. Describes a nicotinic neuromuscular effect of acetylcholine accumulation; atropine does not block nicotinic receptors and pralidoxime is needed to regenerate acetylcholinesterase for these symptoms.
↑ Tap an answer to reveal the reasoning
Answer: A. This is acute organophosphate (insecticide) poisoning — the classic cholinergic toxidrome from irreversible inhibition of acetylcholinesterase, causing acetylcholine accumulation at both muscarinic and nicotinic synapses. Muscarinic effects are summarized by SLUDGE/DUMBBELS: Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis; or Diarrhea, Urination, Miosis, Bronchospasm/Bronchorrhea, Bradycardia, Emesis, Lacrimation, Salivation. Nicotinic effects include muscle fasciculations, weakness, and (paradoxically) tachycardia and pallor from sympathetic ganglion stimulation.
Atropine is a competitive muscarinic antagonist. It REVERSES the MUSCARINIC effects: bronchospasm and bronchorrhea, salivation, lacrimation, sweating, miosis, bradycardia, and GI hypermotility. The most clinically critical and life-threatening of these is bronchospasm/bronchorrhea, which is why atropine is dosed to dry secretions and reverse bronchoconstriction.
Atropine does NOT reverse nicotinic effects (muscle fasciculations, cramps, weakness). For nicotinic and overall reactivation of cholinesterase, pralidoxime (2-PAM) is used, ideally before aging of the enzyme-OP complex occurs.
Additionally, the tachycardia and pallor here reflect nicotinic (sympathetic) stimulation, so atropine won't fix those — and the muscle cramps from nicotinic muscle activation also won't respond to atropine.
**Why each option:**
**A.** Correct — bronchospasm is a muscarinic effect of acetylcholine excess; atropine directly antagonizes muscarinic receptors and improves it.
**B.** Tachycardia in OP poisoning reflects nicotinic ganglionic sympathetic stimulation; atropine does not target nicotinic receptors and may worsen tachycardia.
**C.** Muscle cramps and fasciculations are NICOTINIC effects at the neuromuscular junction; atropine does not block nicotinic receptors. Pralidoxime addresses these.
**D.** Pallor here is due to nicotinic sympathetic vasoconstriction, which atropine does not antagonize.