Autonomic Nervous System Pharmacology Flashcards

Physostigmine crosses the blood-brain barrier while neostigmine does not. The structural reason is:

Answer: Physostigmine is a tertiary amine; neostigmine is a quaternary ammonium compound

Tertiary amines (physostigmine) are lipid-soluble and cross the BBB, while quaternary ammonium compounds (neostigmine) are permanently charged and cannot.

Mirabegron is a newer drug for overactive bladder. Its mechanism differs from oxybutynin because it:

Answer: Is a beta-3 adrenergic agonist that relaxes the detrusor

Mirabegron activates beta-3 receptors on bladder detrusor muscle, promoting relaxation and increasing bladder capacity without anticholinergic side effects.

Labetalol is useful in hypertensive emergencies in pregnancy because it:

Answer: Blocks both alpha-1 and beta receptors, lowering BP without causing reflex tachycardia

Labetalol's combined alpha-1 and non-selective beta blockade reduces peripheral resistance and prevents reflex tachycardia, making it effective and relatively safe in pregnancy.

Methacholine challenge testing is used to diagnose asthma. Methacholine acts by:

Answer: Directly stimulating muscarinic receptors causing bronchoconstriction

Methacholine is a synthetic muscarinic agonist that causes bronchoconstriction; asthmatic airways are hyperresponsive and show a ≥20% drop in FEV1 at low doses.

Reserpine depletes catecholamine stores by:

Answer: Inhibiting the vesicular monoamine transporter (VMAT), preventing storage of catecholamines

Reserpine irreversibly inhibits VMAT, so newly synthesized catecholamines cannot be packaged into vesicles and are degraded intraneuronally.

Which autonomic drug is used to treat neurogenic orthostatic hypotension by activating peripheral alpha-1 receptors?

Answer: Midodrine

Midodrine is an alpha-1 agonist prodrug that increases venous return and arterial resistance, raising standing blood pressure in orthostatic hypotension.

A patient develops a hypertensive crisis after stopping clonidine abruptly. This is due to:

Answer: Rebound increase in central sympathetic outflow

Abrupt clonidine withdrawal causes rebound sympathetic hyperactivity as the suppressed central alpha-2 receptors are no longer activated, leading to severe hypertension.