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NURS 5334 / NURS5334 Exam 2 – Advanced Pharmacology Review Actual Exam 2026/2027 with Detailed Rationales | 100% Verified | Pass Guaranteed – A+ Graded

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NURS 5334 / NURS5334 Exam 2 – Advanced Pharmacology Review Actual Exam 2026/2027 – Real‑Style Exam Questions | 100% Correct Answers | Pharmacokinetics & Pharmacodynamics | Autonomic & CNS Agents | Cardiovascular & Renal Drugs | Anti‑Infectives & Endocrine Therapies | Detailed Rationales | Graded A+ Verified | Pass Guaranteed – Instant Download

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NURS 5334 / NURS5334 Exam 2 – Advanced
Pharmacology Review Actual Exam 2026/2027 with
Detailed Rationales | 100% Verified | Pass Guaranteed –
A+ Graded


SECTION 1: AUTONOMIC NERVOUS SYSTEM PHARMACOLOGY – SYMPATHETIC &
PARASYMPATHETIC AGENTS (Questions 1–25)

Q1: A patient with acute anaphylaxis presents with hypotension, bronchospasm, and
urticaria. Which autonomic receptor activation is primarily responsible for the
bronchodilation effect of epinephrine in this emergency?
A. Alpha-1 adrenergic receptor activation causing vasoconstriction
B. Beta-1 adrenergic receptor activation increasing cardiac output
C. Beta-2 adrenergic receptor activation causing smooth muscle relaxation
[CORRECT]
D. Muscarinic-2 receptor activation inhibiting acetylcholine release
Correct Answer: C
Rationale: Correct because beta-2 adrenergic receptor activation in bronchial smooth
muscle leads to relaxation and bronchodilation, which is the primary mechanism
epinephrine uses to reverse bronchospasm in anaphylaxis.

Q2: A nurse practitioner administers atropine to a patient with symptomatic
bradycardia. Which neurotransmitter receptor does atropine competitively
antagonize to produce the desired chronotropic effect?
A. Nicotinic receptors at the neuromuscular junction
B. Muscarinic acetylcholine receptors on cardiac pacemaker cells [CORRECT]
C. Alpha-1 adrenergic receptors on vascular smooth muscle
D. Beta-2 adrenergic receptors on bronchial smooth muscle
Correct Answer: B
Rationale: Correct because atropine is a competitive muscarinic antagonist that
blocks acetylcholine at M2 receptors on sinoatrial node cells, thereby removing
parasympathetic tone and increasing heart rate.

,Q3: A patient receiving a nonselective beta-blocker for hypertension reports
wheezing and dyspnea. Which underlying mechanism explains this adverse effect?
A. Unopposed alpha-1 stimulation causing bronchoconstriction
B. Blockade of beta-2 receptors preventing bronchodilation [CORRECT]
C. Increased acetylcholine release at muscarinic receptors
D. Direct histamine release from pulmonary mast cells
Correct Answer: B
Rationale: Correct because nonselective beta-blockers antagonize both beta-1 and
beta-2 receptors; blockade of beta-2 receptors on bronchial smooth muscle prevents
catecholamine-mediated bronchodilation and can precipitate bronchospasm in
susceptible patients.

Q4: Clonidine is prescribed for a patient with hypertension. Which mechanism best
describes its antihypertensive action?
A. Direct vasodilation via nitric oxide release
B. Selective alpha-1 receptor antagonism causing arterial dilation
C. Central alpha-2 agonism reducing sympathetic outflow [CORRECT]
D. Ganglionic blockade at nicotinic receptors
Correct Answer: C
Rationale: Correct because clonidine is a centrally acting alpha-2 adrenergic agonist
that stimulates presynaptic alpha-2 receptors in the medulla, thereby decreasing
sympathetic nervous system outflow and reducing peripheral vascular resistance.

Q5: A patient with myasthenia gravis is prescribed pyridostigmine. Which
pharmacologic action explains the therapeutic benefit of this agent?
A. Inhibition of acetylcholinesterase at the neuromuscular junction [CORRECT]
B. Direct stimulation of nicotinic receptors on skeletal muscle
C. Blockade of muscarinic receptors in the autonomic ganglia
D. Enhancement of norepinephrine release from sympathetic terminals
Correct Answer: A
Rationale: Correct because pyridostigmine is a reversible acetylcholinesterase
inhibitor that increases acetylcholine concentration at the neuromuscular junction,
thereby improving neuromuscular transmission in myasthenia gravis.

Q6: A patient receives phenylephrine nasal spray for severe nasal congestion. Which
receptor-mediated effect is primarily responsible for the decongestant action?
A. Beta-2 receptor agonism causing vasodilation
B. Alpha-1 receptor agonism causing vasoconstriction [CORRECT]

,C. Muscarinic receptor antagonism reducing glandular secretions
D. Histamine H1 receptor blockade preventing vascular permeability
Correct Answer: B
Rationale: Correct because phenylephrine is a selective alpha-1 adrenergic agonist
that causes vasoconstriction of nasal mucosal blood vessels, thereby reducing nasal
congestion and edema.

Q7: A patient with benign prostatic hyperplasia and hypertension is prescribed
doxazosin. Which autonomic receptor does this medication block to achieve both
therapeutic goals?
A. Alpha-1 adrenergic receptors [CORRECT]
B. Beta-1 adrenergic receptors
C. Muscarinic-3 receptors
D. Dopamine-2 receptors
Correct Answer: A
Rationale: Correct because doxazosin is a selective alpha-1 adrenergic antagonist
that relaxes vascular smooth muscle to lower blood pressure and relaxes prostatic
smooth muscle and bladder neck tone to improve urinary outflow.

Q8: A patient with asthma is prescribed albuterol for rescue therapy. Which
statement accurately describes the selectivity and mechanism of this agent?
A. Nonselective beta-blocker causing bronchoconstriction
B. Selective beta-2 agonist causing bronchodilation [CORRECT]
C. Muscarinic antagonist reducing airway secretions
D. Alpha-1 agonist causing pulmonary vasoconstriction
Correct Answer: B
Rationale: Correct because albuterol is a short-acting selective beta-2 adrenergic
agonist that stimulates beta-2 receptors on bronchial smooth muscle, producing
rapid bronchodilation for acute asthma relief.

Q9: A patient receiving a cholinesterase inhibitor for Alzheimer disease develops
bradycardia and increased salivation. These effects result from enhanced activity at
which receptor type?
A. Alpha-1 adrenergic receptors
B. Beta-2 adrenergic receptors
C. Muscarinic acetylcholine receptors [CORRECT]
D. Nicotinic acetylcholine receptors at the neuromuscular junction
Correct Answer: C

, Rationale: Correct because cholinesterase inhibitors increase acetylcholine levels,
which stimulate muscarinic receptors throughout the body, producing
parasympathomimetic effects including bradycardia and increased secretions.

Q10: A patient with pheochromocytoma is scheduled for surgery. Which preoperative
medication is indicated to block catecholamine-induced hypertension during tumor
manipulation?
A. Propranolol alone
B. Phenoxybenzamine, a nonselective alpha-blocker [CORRECT]
C. Atropine, a muscarinic antagonist
D. Bethanechol, a muscarinic agonist
Correct Answer: B
Rationale: Correct because phenoxybenzamine is a nonselective, irreversible
alpha-adrenergic antagonist that blocks alpha-1 and alpha-2 receptors, thereby
preventing catecholamine-mediated vasoconstriction and hypertensive crises during
pheochromocytoma surgery.

Q11: A patient with orthostatic hypotension is prescribed midodrine. Which
mechanism explains the therapeutic effect of this agent?
A. Central alpha-2 agonism reducing sympathetic tone
B. Direct alpha-1 adrenergic agonism causing vasoconstriction [CORRECT]
C. Beta-1 receptor stimulation increasing cardiac contractility
D. Dopamine receptor agonism in the renal vasculature
Correct Answer: B
Rationale: Correct because midodrine is a prodrug converted to desglymidodrine, a
selective alpha-1 adrenergic agonist that causes arterial and venous
vasoconstriction, thereby increasing blood pressure in orthostatic hypotension.

Q12: A patient with chronic obstructive pulmonary disease is prescribed ipratropium
bromide. Which pharmacologic classification best describes this medication?
A. Selective beta-2 adrenergic agonist
B. Muscarinic acetylcholine receptor antagonist [CORRECT]
C. Nonselective beta-adrenergic antagonist
D. Alpha-1 adrenergic receptor agonist
Correct Answer: B
Rationale: Correct because ipratropium bromide is a quaternary ammonium
compound that acts as a competitive antagonist at muscarinic acetylcholine
receptors in the airway, reducing vagally mediated bronchoconstriction.

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