Pharmacology Autonomic Nervous System Pharmacology 3 — Questions and Answers
Question 1: Clonidine is used to treat hypertension. What is its primary mechanism?
- Blocks peripheral alpha-1 receptors
- Stimulates central alpha-2 receptors reducing sympathetic outflow (Correct answer)
- Inhibits ACE
- Blocks beta-1 receptors in the heart
Correct 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.
Question 2: A patient receives organophosphate poisoning. Which drug reverses the muscarinic effects?
- Neostigmine
- Physostigmine
- Atropine (Correct answer)
- Pralidoxime alone
Correct answer: Atropine
Atropine competitively blocks muscarinic receptors and reverses bronchospasm, excessive secretions, and bradycardia in organophosphate poisoning.
Question 3: Which effect distinguishes norepinephrine from epinephrine at clinical doses?
- Norepinephrine causes more bronchodilation
- Norepinephrine has no beta-2 effect and causes reflex bradycardia (Correct answer)
- Norepinephrine lowers diastolic pressure
- Norepinephrine stimulates beta-1 more than epinephrine
Correct 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.
Question 4: Ipratropium is preferred over atropine for COPD bronchodilation because it:
- Crosses the blood-brain barrier more readily
- Is inhaled and poorly absorbed systemically, reducing side effects (Correct answer)
- Has a longer half-life than atropine
- Stimulates beta-2 receptors
Correct 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.
Question 5: Cocaine blocks the reuptake of norepinephrine. This causes:
- Hypotension and bradycardia
- Vasodilation and miosis
- Hypertension, tachycardia, and mydriasis (Correct answer)
- Bronchospasm and lacrimation
Correct answer: Hypertension, tachycardia, and mydriasis
By blocking norepinephrine reuptake, cocaine increases sympathomimetic tone, causing hypertension, tachycardia, and pupil dilation.
Question 6: Hexamethonium blocks ganglionic transmission. Its primary clinical use historically was:
- Treating asthma
- Managing hypertensive emergencies (Correct answer)
- Treating urinary retention
- Reversing neuromuscular blockade
Correct answer: Managing hypertensive emergencies
Hexamethonium was a ganglionic blocker used to treat severe hypertension by blocking both sympathetic and parasympathetic ganglia.
Question 7: A patient on a MAO inhibitor eats tyramine-rich food. What occurs?
- Severe hypotension
- Hypertensive crisis due to excess norepinephrine release (Correct answer)
- Cholinergic crisis
- Bradycardia and miosis
Correct 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.
Pharmacology Autonomic Nervous System Pharmacology 3
Clonidine is used to treat hypertension.
What is its primary mechanism?