A patient with myasthenia gravis on pyridostigmine develops profuse secretions, miosis, and bradycardia after a dose increase. The mechanism responsible for the muscarinic side effects of pyridostigmine but NOT for its therapeutic benefit involves which receptor subtype?

• A M2 receptors on cardiac pacemaker cells ✓
• B M1 receptors on gastric parietal cells
• C Nicotinic NMJ receptors on skeletal muscle
• D Alpha-1 adrenoceptors on vascular smooth muscle

Explanation

Pyridostigmine's therapeutic effect in myasthenia gravis is mediated through nicotinic NMJ receptor activation (enhancing ACh at the neuromuscular junction). Its muscarinic side effects — bradycardia, secretions, miosis — result from M2 receptor stimulation on cardiac pacemaker cells (bradycardia) and M3 receptors on glands/smooth muscle. The M2 cardiac receptor is the key subtype mediating the unwanted bradycardia. Nicotinic NMJ receptors mediate the therapeutic myasthenic benefit, while gastric M1 and vascular alpha-1 receptors are not primarily responsible for these specific side effects.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.