Autonomic Nervous System Pharmacology Flashcards

Clonidine is used to treat hypertension. What is its primary mechanism?

Answer: Stimulates central alpha-2 receptors reducing sympathetic outflow

Clonidine activates alpha-2 receptors in the brainstem (locus coeruleus), reducing sympathetic outflow and lowering blood pressure.

A patient receives organophosphate poisoning. Which drug reverses the muscarinic effects?

Answer: Atropine

Atropine competitively blocks muscarinic receptors and reverses bronchospasm, excessive secretions, and bradycardia in organophosphate poisoning.

Which effect distinguishes norepinephrine from epinephrine at clinical doses?

Answer: Norepinephrine has no beta-2 effect and causes reflex bradycardia

Norepinephrine lacks significant beta-2 activity, so it raises both systolic and diastolic pressure without vasodilation, triggering a baroreceptor-mediated reflex bradycardia.

Ipratropium is preferred over atropine for COPD bronchodilation because it:

Answer: Is inhaled and poorly absorbed systemically, reducing side effects

Ipratropium is a quaternary ammonium compound that is poorly absorbed after inhalation, providing local bronchodilation with minimal systemic anticholinergic effects.

Cocaine blocks the reuptake of norepinephrine. This causes:

Answer: Hypertension, tachycardia, and mydriasis

By blocking norepinephrine reuptake, cocaine increases sympathomimetic tone, causing hypertension, tachycardia, and pupil dilation.

Hexamethonium blocks ganglionic transmission. Its primary clinical use historically was:

Answer: Managing hypertensive emergencies

Hexamethonium was a ganglionic blocker used to treat severe hypertension by blocking both sympathetic and parasympathetic ganglia.

A patient on a MAO inhibitor eats tyramine-rich food. What occurs?

Answer: Hypertensive crisis due to excess norepinephrine release

Without MAO to metabolize tyramine, it triggers massive norepinephrine release from nerve terminals causing a dangerous hypertensive crisis.