A 60-year-old man is administered a drug that causes sweating, salivation, and miosis but NO bradycardia, and the effects are NOT reversed by atropine. The most likely mechanism is:
- A Activation of muscarinic M3 and M4 receptors only, sparing M2
- B Direct muscarinic agonism with higher selectivity for M3 than M2
- C Blockade of acetylcholinesterase, increasing ACh at nicotinic and muscarinic sites ✓
- D Blockade of neuronal uptake of norepinephrine
Explanation
An anticholinesterase drug like physostigmine or neostigmine prevents ACh breakdown, raising ACh at all cholinergic synapses—both muscarinic and nicotinic. The clinical picture of sweating (muscarinic), salivation (muscarinic), and miosis (muscarinic) with partial nicotinic activation is classic. If atropine were given, it would reverse the muscarinic effects; the question states effects are not reversed by atropine, suggesting a compound scenario of organophosphate poisoning where nicotinic effects (muscle fasciculation, sweating) persist. However, among the options, anticholinesterase action is the mechanism that explains all three muscarinic signs simultaneously. Selective M3/M4 agonism would not spare the heart entirely under all doses.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.