1) A drug that selectively blocks β3-adrenergic receptors is most likely to affect which of the

following processes?
A) Vasoconstriction in the skin and mucous membranes.
B) Lipolysis in adipose tissue.
C) Heart rate and contractility.
D) Bronchodilation in the lungs.
E) Glucose uptake in skeletal muscles.
2) Which of the following best explains why non-selective β-blockers can worsen
hypertension in patients receiving epinephrine?
A) They enhance β2 receptor activity, leading to increased peripheral resistance.
B) They prevent β2-mediated vasodilation, leaving α1-mediated vasoconstriction unopposed.
C) They increase norepinephrine release, causing excessive vasoconstriction.
D) They prolong the half-life of epinephrine by inhibiting its metabolism.
E) They block α2 receptors, increasing norepinephrine synthesis.
3) Which of the following is the rate-limiting step in norepinephrine (NE) synthesis?
A) Hydroxylation of tyrosine to DOPA.
B) Decarboxylation of DOPA to dopamine.
C) Hydroxylation of dopamine to norepinephrine.
D) Methylation of norepinephrine to epinephrine.
E) Reuptake of norepinephrine by the presynaptic neuron.
4) Which of the following explains why β1-receptor stimulation increases cardiac output?
A) Increased intracellular cAMP leads to inhibition of phospholipase C.
B) Activation of Gq protein increases intracellular Ca²⁺, enhancing contractility.
C) Increased cAMP activates protein kinase A (PKA), increasing Ca²⁺ influx.
D) β1 receptors inhibit Na⁺/K⁺ ATPase, leading to depolarization.
E) Stimulation of β1 receptors causes vasodilation, reducing cardiac afterload.
5) A 50-year-old man undergoes a minor surgical procedure. To minimize bleeding, the
surgeon administers a local anesthetic combined with epinephrine. What is the primary
role of epinephrine in this setting?
A) To enhance anesthesia by blocking sodium channels in nerve cells.
B) To decrease systemic absorption of the anesthetic by vasoconstriction.
C) To stimulate β1 receptors, increasing cardiac output during the procedure.
D) To inhibit norepinephrine reuptake, prolonging the anesthetic effect.
E) To prevent histamine release, reducing inflammation at the surgical site.
6) A 45-year-old woman with chronic nasal congestion has been using a topical nasal
decongestant containing phenylephrine for several weeks. She notices that her congestion
worsens when she skips a dose. What is the most likely explanation for this phenomenon?
A) Phenylephrine has a direct toxic effect on nasal mucosa.
B) Prolonged use has caused receptor downregulation, leading to rebound congestion.
C) The drug has accumulated in the nasal tissues, requiring higher doses over time.
D) α1 receptor overstimulation has led to increased norepinephrine release.
E) Phenylephrine has blocked β2 receptors, reducing nasal blood flow.
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7) A patient with chronic hypertension is prescribed prazosin. What is a common side effect
of the first dose?
A) Reflex bradycardia.
B) Severe orthostatic hypotension.
C) Bronchoconstriction.
D) Hyperkalemia.
E) Cardiac arrhythmia

8) A patient with open-angle glaucoma is prescribed timolol eye drops. How does this drug
help lower intraocular pressure?
A) By blocking β1 receptors in the ciliary muscle, reducing aqueous humor production.
B) By inhibiting α1 receptors in the iris, improving aqueous humor drainage.
C) By blocking β2 receptors in the ciliary epithelium, decreasing aqueous humor secretion.
D) By reducing norepinephrine release from sympathetic nerve terminals in the eye.
E) By inhibiting muscarinic receptors, decreasing intraocular pressure.
9) A 50-year-old man is diagnosed with essential hypertension and started on propranolol.
After several weeks, he experiences episodes of hypoglycemia, despite no changes in his
diet or medication. What is the most likely explanation?
A) Propranolol inhibits insulin secretion from pancreatic β-cells.
B) Propranolol blocks β2 receptors, decreasing glycogenolysis and glucagon secretion.
C) Propranolol increases insulin sensitivity, lowering blood glucose levels.
D) Propranolol inhibits α1 receptors, reducing hepatic glucose production.
E) Propranolol blocks α2 receptors, causing increased insulin release.
10) A 65-year-old woman with heart failure is prescribed carvedilol. What is the main
advantage of carvedilol over other β-blockers in heart failure treatment?
A) It selectively blocks β1 receptors, improving cardiac contractility.
B) It has intrinsic sympathomimetic activity, reducing heart rate fluctuations.
C) It also blocks α1 receptors, reducing peripheral vascular resistance.
D) It inhibits norepinephrine synthesis, reducing sympathetic activity.
E) It has a shorter half-life, allowing more flexible dosing.
11) Which of the following is a major consequence of β-blockers on the metabolic system?
A) Increased glycogenolysis.
B) Increased insulin secretion.
C) Masking of hypoglycemia symptoms.
D) Increased lipolysis.
E) Increased free fatty acid metabolism.
12) Which of the following β-blockers has the shortest half-life and is used in emergency
settings?
A) Atenolol.
B) Metoprolol.
C) Esmolol.
D) Propranolol.
E) Nadolol.
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13) A patient receives rocuronium for muscle relaxation during surgery. Near the end of the
procedure, the anesthesiologist wants to rapidly reverse its effects. Which of the following
agents would be the most appropriate choice?
A) Neostigmine.
B) Atropine.
C) Sugammadex.
D) Edrophonium.
E) Physostigmine.
14) A 29-year-old man with a history of malignant hyperthermia is undergoing surgery.
Which neuromuscular blocker should be avoided in this patient?
A) Cisatracurium.
B) Rocuronium.
C) Succinylcholine.
D) Vecuronium.
E) Mivacurium.
15) A patient receiving aminoglycoside antibiotics is scheduled for surgery and is given
vecuronium as a neuromuscular blocker. Which of the following best explains why
aminoglycosides enhance the effect of vecuronium?
A) They inhibit acetylcholine synthesis in motor neurons.
B) They block the release of calcium-dependent acetylcholine vesicles.
C) They directly inhibit nicotinic receptors at the neuromuscular junction.
D) They block acetylcholinesterase, increasing acetylcholine levels.
E) They stimulate presynaptic muscarinic receptors, reducing acetylcholine release.

16) A 60-year-old man is given tropicamide eye drops for an ophthalmic examination. Which
of the following best explains its mechanism of action?
A) Activation of α1 receptors, leading to pupil dilation.
B) Blockade of M3 receptors, causing mydriasis and cycloplegia.
C) Inhibition of nicotinic receptors, preventing pupillary constriction.
D) Increased acetylcholine release at the iris sphincter muscle.
E) Direct stimulation of β2 receptors, enhancing aqueous humor outflow.

17) A patient receives a high dose of atropine and develops hallucinations, agitation, and
delirium. Which of the following drugs can reverse these central toxic effects?
A) Neostigmine.
B) Physostigmine.
C) Pralidoxime.
D) Edrophonium.
E) Pilocarpine.

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18) Which of the following correctly describes the difference between atropine and
scopolamine?
A) Atropine has greater CNS penetration than scopolamine.
B) Scopolamine has more pronounced central effects and is more sedating than atropine.
C) Atropine is more effective in preventing motion sickness than scopolamine.
D) Scopolamine causes significant bradycardia, while atropine does not.
E) Atropine has a longer duration of action than scopolamine.
19) A patient receives an excessive dose of neostigmine after surgery. Which of the following
symptoms is most indicative of cholinergic toxicity?
A) Mydriasis and tachycardia.
B) Urinary retention and dry mouth.
C) Diaphoresis, bradycardia, and muscle fasciculations.
D) Hypertension and hyperthermia.
E) Constipation and blurred vision.
20) Which of the following correctly differentiates neostigmine from physostigmine?
A) Neostigmine is a tertiary amine and crosses the blood-brain barrier.
B) Physostigmine is a quaternary amine and cannot enter the CNS.
C) Physostigmine can be used for atropine toxicity, while neostigmine cannot.
D) Neostigmine is used for glaucoma, while physostigmine is not.
E) Neostigmine is more potent than physostigmine in reversing neuromuscular blockade.
21) A scientist working in a laboratory accidentally inhales a nerve agent. Which of the
following symptoms would most likely be seen first in this patient?
A) Bronchodilation and tachycardia.
B) Diarrhea, salivation, and miosis.
C) Hypertension and hyperthermia.
D) Dry skin and urinary retention.
E) Muscle rigidity and spasticity.
22) Which of the following best explains why atropine should be avoided in patients with
narrow-angle glaucoma?
A) Causes cycloplegia and increases aqueous humor production.
B) Reduces tear production leading to dry eyes.
C) Increases intraocular pressure by reducing aqueous humor drainage.
D) Stimulates ciliary muscle causing accommodation.
E) Enhances parasympathetic tone.
23) Which antimuscarinic agent is preferred for retinal examination due to its short duration
of action?
A) Atropine.
B) Tiotropium.
C) Cyclopentolate.
D) Tropicamide.
E) Scopolamine.

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24) Which of the following antimuscarinic drugs is preferred for treating overactive bladder
in elderly patients with dementia?
A) Oxybutynin.
B) Solifenacin.
C) Tolterodine.
D) Darifenacin.
E) Trospium.
25) Which of the following is most likely to cause urinary retention as a side effect?
A) Bethanechol.
B) Pilocarpine.
C) Scopolamine.
D) Oxybutynin.
E) Nicotine.
26) Which effect is NOT typical of cholinergic antagonists?
A) Mydriasis.
B) Decreased GI motility.
C) Bradycardia.
D) Urinary retention.
E) Dry mouth.
27) Which of the following effects is most likely with Bethanechol administration?
A) Mydriasis and cycloplegia.
B) Constipation and dry mouth.
C) Bronchodilation and urinary retention.
D) Bronchospasm and increased urinary voiding.
E) Increased heart rate and AV conduction.
28) What would most likely occur following the administration of black widow spider venom?
A) Inhibition of ACh release.
B) Permanent receptor blockade.
C) Massive ACh release into synapse.
D) Decreased intracellular calcium.
E) Enzymatic degradation of nicotinic receptors.

29) Which of the following drugs is used in the treatment of xerostomia associated with
Sjögren syndrome?
A) Carbachol.
B) Bethanechol.
C) Cevimeline.
D) Neostigmine.
E) Tropicamide.

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30) Which of the following cholinergic agonists is not hydrolyzed by acetylcholinesterase and
stimulates both nicotinic and muscarinic receptors?
A) Acetylcholine.
B) Bethanechol.
C) Carbachol.
D) Methacholine.
E) Pilocarpine.
31) A 60-year-old man with a history of benign prostatic hyperplasia (BPH) is experiencing
urinary retention after surgery. He is given bethanechol. What is the primary reason for
using this drug?
A) It activates nicotinic receptors, increasing bladder contraction.
B) It inhibits norepinephrine release, relaxing the bladder sphincter.
C) It selectively stimulates M3 receptors, increasing detrusor muscle contraction.
D) It blocks muscarinic receptors, preventing urinary retention.
E) It enhances dopamine release, improving urinary function.

32) Which of the following correctly differentiates muscarinic and nicotinic receptors?
A) Muscarinic receptors mediate fast excitatory responses, while nicotinic receptors mediate
slower responses.
B) Nicotinic receptors are G-protein coupled, while muscarinic receptors are ion channels.
C) Muscarinic receptors are primarily found at autonomic ganglia, while nicotinic receptors are
found at effector organs.
D) Nicotinic receptors function as ligand-gated ion channels, while muscarinic receptors use
second messengers.
E) Muscarinic receptors require direct acetylcholine binding, while nicotinic receptors do not.

33) A 65-year-old man is admitted for severe bradycardia (HR = 42 bpm). The physician
administers atropine. Which of the following best explains the mechanism by which
atropine increases heart rate?
A) Inhibition of β1 receptors, leading to increased heart rate.
B) Stimulation of α1 receptors, causing vasoconstriction and increased cardiac output.
C) Blockade of M2 receptors in the sinoatrial node, reducing vagal inhibition.
D) Inhibition of acetylcholinesterase, increasing acetylcholine at the synapse.
E) Direct activation of nicotinic receptors at autonomic ganglia.
34) How does activation of α2 receptors reduce norepinephrine release?
A) Increased intracellular cAMP leading to enhanced feedback inhibition.
B) Stimulation of potassium channels, leading to neuronal hyperpolarization.
C) Blockade of voltage-gated calcium channels, reducing neurotransmitter exocytosis.
D) Direct inhibition of tyrosine hydroxylase, reducing catecholamine synthesis.
E) Increased sodium influx, preventing norepinephrine reuptake.

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35) What is the primary role of the parasympathetic nervous system?
A) Activation of fight-or-flight responses.
B) Regulation of metabolic rate and energy mobilization.
C) Maintenance of homeostasis and promotion of rest-and-digest functions.
D) Increasing cardiac output and skeletal muscle perfusion.
E) Direct control of voluntary muscle movement.
36) Which of the following adrenergic agonists is classified as a mixed-acting agent?
A) Epinephrine.
B) Phenylephrine.
C) Amphetamine.
D) Ephedrine.
E) Isoproterenol.

37) Which adrenergic effect contributes to epinephrine-induced hyperglycemia?

A) Decreased cortisol secretion.
B) Inhibition of insulin receptors.
C) Increased insulin release via α2.
D) β2-mediated stimulation of glycogenolysis.
E) β1-mediated inhibition of glucagon.
38) In which scenario is the use of epinephrine contraindicated or used with caution?
A) Type I hypersensitivity.
B) Cardiac arrest.
C) Nasal mucosal bleeding.
D) Patients with hyperthyroidism.
E) Local anesthesia for dental surgery.

39) What is the primary mechanism of irreversible anticholinesterases?

A) Competitive inhibition of acetylcholinesterase.
B) Covalent phosphorylation of acetylcholinesterase, leading to permanent inactivation.
C) Direct activation of muscarinic receptors, increasing acetylcholine effects.
D) Inhibition of muscarinic receptors, reducing parasympathetic activity.
E) Blockade of voltage-gated sodium channels, preventing neurotransmission.

40) Which of the following is most likely to occur if norepinephrine is given after atropine
administration?
A) Reflex bradycardia.
B) Inhibition of α1 receptors.
C) Unopposed parasympathetic tone.
D) Direct tachycardia due to blocked vagal tone.
E) Severe hypotension.

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41) Which of the following sympathomimetic drugs is most likely to increase both systolic
pressure and heart rate while lowering diastolic pressure due to β2 vasodilation?
A) Norepinephrine.
B) Epinephrine.
C) Isoproterenol.
D) Phenylephrine.
E) Dopamine.

42) A major cardiovascular action of non-selective α-blockers like phentolamine is:

A) Decrease in heart rate due to β1 blockade.
B) Increased peripheral resistance due to α2 stimulation.
C) Reflex tachycardia due to vasodilation from α1 blockade.
D) Bradycardia due to presynaptic α2 inhibition.
E) Long-term suppression of renin release.

43) Which α1-selective blocker has the longest duration of action and is primarily excreted in
feces?
A) Prazosin.
B) Terazosin.
C) Alfuzosin.
D) Doxazosin.
E) Tamsulosin.

44) Which of the following β-blocker is known for its nitric oxide–mediated vasodilatory
properties?
A) Timolol.
B) Nadolol.
C) Nebivolol.
D) Esmolol.
E) Propranolol.

45) Which of the following β-blocker has the longest half-life?

A) Propranolol.
B) Atenolol.
C) Nadolol.
D) Metoprolol.
E) Esmolol.

46) Which of the following β-blocker is commonly used to manage hypertension during
pregnancy?
A) Bisoprolol.
B) Nebivolol.
C) Esmolol.
D) Labetalol.
E) Timolol.
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47) Which statement is TRUE regarding tamsulosin?
A) It significantly lowers blood pressure due to α1B blockade.
B) It selectively blocks β1 receptors.
C) It blocks α1A receptors in the prostate and bladder neck with minimal effect on BP.
D) It is a non-selective α-blocker used in Raynaud’s syndrome.
E) It is only used for hypertension.
48) Which of the following best explains why pralidoxime (2-PAM) must be administered
quickly in organophosphate poisoning?
A) To prevent irreversible aging of the phosphorylated enzyme.
B) To directly block muscarinic receptors, reversing symptoms.
C) To stimulate acetylcholine release, counteracting receptor desensitization.
D) To inhibit dopamine reuptake, improving autonomic function.
E) To prevent glutamate-induced excitotoxicity in the CNS.
49) Why do patients exposed to irreversible anticholinesterases develop muscle paralysis
despite an initial period of muscle twitching?
A) Acetylcholine accumulation leads to sustained depolarization and receptor desensitization.
B) The toxin blocks calcium release from the sarcoplasmic reticulum.
C) Muscarinic receptor activation causes excessive inhibition of motor neurons.
D) The toxin enhances norepinephrine release, depleting acetylcholine stores.
E) The toxin inhibits GABAergic transmission, causing loss of inhibitory control.
50) Both systolic and diastolic blood pressures are increased after the administration of which
ONE of the following drugs?
A) Clonidine.
B) Isoprenaline.
C) Salbutamol
D) Norepinehrine.
E) Dobutamine.
51) Which of the following is NOT a cardiovascular effect of an IV infusion of norepinephrine?
A) An increase in systolic and diastolic blood pressure.
B) An increase in peripheral resistance.
C) A small increase in the rate and force of contraction of the heart.
D) Reflex tachycardia.
E) Reflex bradycardia.
52) Several children at a summer camp were hospitalized with symptoms thought to be due to
ingestion of food containing botulinum toxin. Which one of the following signs or
symptoms is consistent with the diagnosis of botulinum poisoning?
A) Bronchospasm.
B) Urinary retention.
C) Diarrhea.
D) Skeletal muscle spasm.
E) Bradycardia.

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