NAGELHOUT PHARMACOLOGY COMPLETE SET OF VERIFIED EXAM
QUESTIONS AND ACCURATE ANSWERS WITH A GUARANTEED PASS
PROMISE
1. Q: What is the primary neurotransmitter of preganglionic sympathetic
neurons? ANSWER Acetylcholine (ACh) acting on nicotinic receptors.
2. Q: What receptors do postganglionic sympathetic neurons primarily
stimulate? ANSWER Alpha and beta adrenergic receptors (except sweat
glands which use ACh on muscarinic receptors).
3. Q: What is the rate-limiting step in catecholamine synthesis? ANSWER
Conversion of tyrosine to DOPA by tyrosine hydroxylase.
4. Q: Which enzyme metabolizes catecholamines in the synaptic cleft?
ANSWER Catechol-O-methyltransferase (COMT) and monoamine oxidase
(MAO).
5. Q: What type of receptor is the nicotinic receptor? ANSWER Ligand-
gated ion channel (ionotropic receptor).
6. Q: What type of receptor is the muscarinic receptor? ANSWER G-
protein coupled receptor (metabotropic receptor).
7. Q: What are the five subtypes of muscarinic receptors? ANSWER M1,
M2, M3, M4, and M5.
8. Q: Which muscarinic receptor subtype causes bradycardia? ANSWER
M2 receptors in the heart.
9. Q: What happens when alpha-1 receptors are stimulated? ANSWER
Vasoconstriction, increased peripheral vascular resistance, mydriasis.
10. Q: What happens when beta-1 receptors are stimulated? ANSWER
Increased heart rate, contractility, and AV node conduction velocity.
11. Q: What happens when beta-2 receptors are stimulated? ANSWER
Bronchodilation, vasodilation, uterine relaxation, tremor.
12. Q: Where are dopamine-1 receptors primarily located? ANSWER
Renal, mesenteric, and coronary vascular beds.
, 13. Q: What effect does dopamine-1 receptor stimulation have? ANSWER
Vasodilation and increased renal blood flow.
14. Q: What is the mechanism of action of indirect-acting
sympathomimetics? ANSWER Release of stored norepinephrine from nerve
terminals (e.g., ephedrine, amphetamine).
15. Q: What is the mechanism of action of mixed-acting
sympathomimetics? ANSWER Both direct receptor stimulation and
norepinephrine release (e.g., ephedrine).
16. Q: Why is epinephrine more potent than norepinephrine at beta-2
receptors? ANSWER Epinephrine has higher affinity for beta-2 receptors due
to its chemical structure.
17. Q: What is the primary mechanism of norepinephrine reuptake
termination? ANSWER Uptake-1: neuronal reuptake into the presynaptic
terminal.
18. Q: What is tachyphylaxis with sympathomimetics? ANSWER
Decreased response with repeated administration due to depletion of
norepinephrine stores (seen with indirect agents).
19. Q: Which anticholinesterase crosses the blood-brain barrier?
ANSWER Physostigmine (tertiary amine, lipophilic).
20. Q: Why doesn't neostigmine cross the blood-brain barrier? ANSWER
It's a quaternary ammonium compound (charged, hydrophilic).
21. Q: What is the duration of action of edrophonium? ANSWER 5-15
minutes (shortest-acting anticholinesterase).
22. Q: What is the mechanism of organophosphate poisoning? ANSWER
Irreversible inhibition of acetylcholinesterase causing cholinergic crisis.
23. Q: What is the treatment for organophosphate poisoning? ANSWER
Atropine (muscarinic antagonist) and pralidoxime (2-PAM, reactivates
acetylcholinesterase).
24. Q: What are the muscarinic effects of anticholinesterase overdose
(SLUDGE)? ANSWER Salivation, Lacrimation, Urination, Defecation, GI
upset, Emesis.
25. Q: What is the mechanism of botulinum toxin? ANSWER Prevents ACh
release from presynaptic terminals by cleaving SNARE proteins.
QUESTIONS AND ACCURATE ANSWERS WITH A GUARANTEED PASS
PROMISE
1. Q: What is the primary neurotransmitter of preganglionic sympathetic
neurons? ANSWER Acetylcholine (ACh) acting on nicotinic receptors.
2. Q: What receptors do postganglionic sympathetic neurons primarily
stimulate? ANSWER Alpha and beta adrenergic receptors (except sweat
glands which use ACh on muscarinic receptors).
3. Q: What is the rate-limiting step in catecholamine synthesis? ANSWER
Conversion of tyrosine to DOPA by tyrosine hydroxylase.
4. Q: Which enzyme metabolizes catecholamines in the synaptic cleft?
ANSWER Catechol-O-methyltransferase (COMT) and monoamine oxidase
(MAO).
5. Q: What type of receptor is the nicotinic receptor? ANSWER Ligand-
gated ion channel (ionotropic receptor).
6. Q: What type of receptor is the muscarinic receptor? ANSWER G-
protein coupled receptor (metabotropic receptor).
7. Q: What are the five subtypes of muscarinic receptors? ANSWER M1,
M2, M3, M4, and M5.
8. Q: Which muscarinic receptor subtype causes bradycardia? ANSWER
M2 receptors in the heart.
9. Q: What happens when alpha-1 receptors are stimulated? ANSWER
Vasoconstriction, increased peripheral vascular resistance, mydriasis.
10. Q: What happens when beta-1 receptors are stimulated? ANSWER
Increased heart rate, contractility, and AV node conduction velocity.
11. Q: What happens when beta-2 receptors are stimulated? ANSWER
Bronchodilation, vasodilation, uterine relaxation, tremor.
12. Q: Where are dopamine-1 receptors primarily located? ANSWER
Renal, mesenteric, and coronary vascular beds.
, 13. Q: What effect does dopamine-1 receptor stimulation have? ANSWER
Vasodilation and increased renal blood flow.
14. Q: What is the mechanism of action of indirect-acting
sympathomimetics? ANSWER Release of stored norepinephrine from nerve
terminals (e.g., ephedrine, amphetamine).
15. Q: What is the mechanism of action of mixed-acting
sympathomimetics? ANSWER Both direct receptor stimulation and
norepinephrine release (e.g., ephedrine).
16. Q: Why is epinephrine more potent than norepinephrine at beta-2
receptors? ANSWER Epinephrine has higher affinity for beta-2 receptors due
to its chemical structure.
17. Q: What is the primary mechanism of norepinephrine reuptake
termination? ANSWER Uptake-1: neuronal reuptake into the presynaptic
terminal.
18. Q: What is tachyphylaxis with sympathomimetics? ANSWER
Decreased response with repeated administration due to depletion of
norepinephrine stores (seen with indirect agents).
19. Q: Which anticholinesterase crosses the blood-brain barrier?
ANSWER Physostigmine (tertiary amine, lipophilic).
20. Q: Why doesn't neostigmine cross the blood-brain barrier? ANSWER
It's a quaternary ammonium compound (charged, hydrophilic).
21. Q: What is the duration of action of edrophonium? ANSWER 5-15
minutes (shortest-acting anticholinesterase).
22. Q: What is the mechanism of organophosphate poisoning? ANSWER
Irreversible inhibition of acetylcholinesterase causing cholinergic crisis.
23. Q: What is the treatment for organophosphate poisoning? ANSWER
Atropine (muscarinic antagonist) and pralidoxime (2-PAM, reactivates
acetylcholinesterase).
24. Q: What are the muscarinic effects of anticholinesterase overdose
(SLUDGE)? ANSWER Salivation, Lacrimation, Urination, Defecation, GI
upset, Emesis.
25. Q: What is the mechanism of botulinum toxin? ANSWER Prevents ACh
release from presynaptic terminals by cleaving SNARE proteins.
