NURS 6521 ADVANCED PHARMACOLOGY MIDTERM |
NGN-STYLE QUESTIONS AND EXPLAINED ANSWERS
LATEST UPDATED 2026/2027
1. [CALC] A provider orders a drug with a half-life of 10 hours.
Approximately how many hours will it take for the drug to reach
steady-state concentration? ANSWER : 50 hours Rationale: Steady
state is achieved in approximately 4 to 5 half-lives. (5 x 10 hours = 50
hours). At steady state, the amount of drug administered equals the
amount eliminated.
2. [SATA] Which of the following routes of administration bypass the
first-pass effect? (Select all that apply) A. Oral B. Intravenous (IV) C.
Sublingual (SL) D. Intramuscular (IM) E. Transdermal ANSWER : B, C, E
Rationale: The first-pass effect occurs when drugs are absorbed from
the GI tract and go directly to the liver via the portal vein before
entering systemic circulation. IV, SL, and transdermal routes enter
systemic circulation directly, bypassing the liver initially. Oral
undergoes first-pass; IM is absorbed into capillaries but largely
bypasses extensive first-pass metabolism compared to the GI tract.
3. [EXHIBIT] A 75-year-old patient with hypoalbuminia is taking a highly
protein-bound drug (99%). The patient exhibits signs of toxicity. What is
the pharmacokinetic rationale? ANSWER : Decreased plasma proteins
lead to increased free (unbound) drug, increasing pharmacologic effect
and toxicity. Rationale: Highly protein-bound drugs rely on albumin to
stay inactive in the blood. In hypoalbuminia, fewer binding sites exist,
leaving more "free" drug available to act on receptors and cross the
blood-brain barrier, causing toxicity even if the total serum drug level
appears normal.
4. [ORDER] Place the phases of pharmacokinetics in the correct
chronological order from drug administration to elimination.
1. Metabolism
, 2. Absorption
3. Excretion
4. Distribution ANSWER : 2, 4, 1, 3 Rationale: Pharmacokinetics
follows the acronym ADME: Absorption (entering blood),
Distribution (spreading to tissues), Metabolism (liver breakdown),
Excretion (renal/bowel removal).
5. [SATA] A patient is taking a drug that is a CYP450 enzyme inducer.
Which of the following are clinical implications? (Select all that apply) A.
Increased metabolism of the CYP450 drug B. Decreased effectiveness
of concurrently taken substrates C. Increased risk of toxicity from
concurrently taken substrates D. Need for a higher dose of the CYP450
inducer over time E. Potential therapeutic failure of the concurrent
medication ANSWER : A, B, D, E Rationale: Inducers speed up enzyme
activity, causing the inducer drug itself to be metabolized faster
(requiring a higher dose over time—autoinduction) and causing other
drugs (substrates) to be broken down faster, leading to decreased
effectiveness and therapeutic failure. Option C describes an inhibitor,
not an inducer.
6. [MATRIX] Match the receptor type to its mechanism of action.
• Agonist -> B. Binds to a receptor and stimulates the response
• Antagonist -> C. Binds to a receptor and blocks the response
• Partial Agonist -> A. Binds to a receptor and produces a weaker
response than a full agonist Rationale: Agonists mimic
endogenous ligands. Antagonists occupy the receptor to prevent
other ligands from binding. Partial agonists have intrinsic activity
but cannot produce a maximal response even at full receptor
occupancy.
7. [EXHIBIT] A patient with a history of Raynaud's disease is prescribed
a drug. The provider explains that the drug's therapeutic effect is
secondary to its side effect. Which drug is this, and what is the
mechanism? ANSWER : Prazosin (Alpha-1 blocker); Therapeutic effect =
vasodilation of peripheral vessels. Side effect = orthostatic hypotension.
Rationale: Alpha-1 blockers block vasoconstriction. In Raynaud's, this
relieves vasospasm (therapeutic). However, blocking alpha-1 receptors
systemically prevents the sympathetic nervous system from
,constricting blood vessels when standing, causing orthostatic
hypotension (side effect).
Section 2: Autonomic Nervous System
8. [SATA] A patient is experiencing a cholinergic crisis
(organophosphate poisoning). Which of the following manifestations
should the nurse anticipate? (Select all that apply) A. Dry mouth B.
Urinary incontinence C. Pinpoint pupils (miosis) D. Tachycardia E.
Excessive salivation F. Muscle fasciculations ANSWER : B, C, E, F
Rationale: Use the mnemonic SLUDGE (Salivation, Lacrimation,
Urination, Defecation, GI distress, Emesis) plus miosis and muscle
fasciculations. Dry mouth and tachycardia are anticholinergic
(parasympatholytic) effects.
9. [ORDER] A patient arrives in the ED with suspected organophosphate
poisoning. Place the following interventions in the correct order.
1. Administer Pralidoxime (2-PAM)
2. Assess ABCs and secure airway
3. Decontaminate the patient (remove clothing/wash skin)
4. Administer Atropine ANSWER : 2, 3, 4, 1 Rationale: ABCs always
come first. Decontamination is crucial to prevent further
absorption. Atropine is given to dry up secretions and treat life-
threatening bronchoconstriction/bradycardia. Pralidoxime is given
secondarily to regenerate the cholinesterase enzyme.
10. [EXHIBIT] A patient with myasthenia gravis is taking Pyridostigmine.
They present with new-onset severe muscle weakness, dyspnea, and
excessive drooling. What is the nurse’s priority action? ANSWER : Hold
the Pyridostigmine and prepare to administer Atropine. Rationale:
These are signs of a cholinergic crisis (too much medication), which
must be differentiated from a myasthenic crisis (too little medication).
Giving more Pyridostigmine to a patient in cholinergic crisis can be
fatal. Atropine is the antidote.
11. [SATA] A nurse is educating a patient starting on Atropine. Which
statements by the patient indicate understanding of the side effects?
(Select all that apply) A. "I may need to use artificial tears." B. "I should
increase my fiber and water intake." C. "I might feel my heart racing." D.
, "I will sweat more in the summer." E. "I may have trouble emptying my
bladder." ANSWER : A, B, C, E Rationale: Atropine is an anticholinergic.
It causes dry eyes (need tears), decreased GI motility (constipation—
need fiber), tachycardia, anhidrosis (decreased sweating, not
increased), and urinary retention (trouble emptying bladder).
12. [SATA] Which of the following patients should NOT receive a non-
selective beta-blocker (e.g., Propranolol) safely without extreme
caution? (Select all that apply) A. A patient with bradycardia B. A patient
with severe asthma C. A patient with essential hypertension D. A patient
with acute heart failure E. A patient with a history of migraine ANSWER
: A, B, D Rationale: Beta-blockers lower heart rate (contraindicated in
bradycardia), block Beta-2 receptors causing bronchospasm
(contraindicated in asthma), and decrease contractility (contraindicated
in acute decompensated heart failure, though they are used in chronic
stable HF). Hypertension and migraines are approved indications.
13. [EXHIBIT] A patient is prescribed Clonidine for hypertension. They
suddenly stop taking it. What immediate pharmacologic phenomenon
occurs, and what is the clinical result? ANSWER : phenomenon = Up-
regulation of alpha-1 receptors; result = Rebound severe hypertensive
crisis. Rationale: Clonidine is a central-acting alpha-2 agonist. It
suppresses sympathetic outflow. When stopped abruptly, the body has
up-regulated (created more) alpha-1 receptors due to the perceived
lack of norepinephrine. A massive catecholamine surge binds to these
receptors, causing dangerous hypertension.
Section 3: Cardiovascular System
14. [SATA] A patient is started on Lisinopril. Which of the following are
potential adverse effects the nurse should monitor for? (Select all that
apply) A. Angioedema B. Persistent dry cough C. Hyperkalemia D.
Reflex tachycardia E. Elevated blood urea nitrogen (BUN) ANSWER : A,
B, C, E Rationale: Use the mnemonic ABCD for ACE inhibitors:
Angioedema, Bradycardia (or hyperkalemia), Cough, Dizziness. They
also dilate the efferent arteriole in the kidney, which can decrease GFR
and elevate BUN/creatinine, especially in renal artery stenosis. Reflex
tachycardia is associated with vasodilators like hydralazine, not ACEi.
15. [MATRIX] Match the antihypertensive class to its primary mechanism
of action.
NGN-STYLE QUESTIONS AND EXPLAINED ANSWERS
LATEST UPDATED 2026/2027
1. [CALC] A provider orders a drug with a half-life of 10 hours.
Approximately how many hours will it take for the drug to reach
steady-state concentration? ANSWER : 50 hours Rationale: Steady
state is achieved in approximately 4 to 5 half-lives. (5 x 10 hours = 50
hours). At steady state, the amount of drug administered equals the
amount eliminated.
2. [SATA] Which of the following routes of administration bypass the
first-pass effect? (Select all that apply) A. Oral B. Intravenous (IV) C.
Sublingual (SL) D. Intramuscular (IM) E. Transdermal ANSWER : B, C, E
Rationale: The first-pass effect occurs when drugs are absorbed from
the GI tract and go directly to the liver via the portal vein before
entering systemic circulation. IV, SL, and transdermal routes enter
systemic circulation directly, bypassing the liver initially. Oral
undergoes first-pass; IM is absorbed into capillaries but largely
bypasses extensive first-pass metabolism compared to the GI tract.
3. [EXHIBIT] A 75-year-old patient with hypoalbuminia is taking a highly
protein-bound drug (99%). The patient exhibits signs of toxicity. What is
the pharmacokinetic rationale? ANSWER : Decreased plasma proteins
lead to increased free (unbound) drug, increasing pharmacologic effect
and toxicity. Rationale: Highly protein-bound drugs rely on albumin to
stay inactive in the blood. In hypoalbuminia, fewer binding sites exist,
leaving more "free" drug available to act on receptors and cross the
blood-brain barrier, causing toxicity even if the total serum drug level
appears normal.
4. [ORDER] Place the phases of pharmacokinetics in the correct
chronological order from drug administration to elimination.
1. Metabolism
, 2. Absorption
3. Excretion
4. Distribution ANSWER : 2, 4, 1, 3 Rationale: Pharmacokinetics
follows the acronym ADME: Absorption (entering blood),
Distribution (spreading to tissues), Metabolism (liver breakdown),
Excretion (renal/bowel removal).
5. [SATA] A patient is taking a drug that is a CYP450 enzyme inducer.
Which of the following are clinical implications? (Select all that apply) A.
Increased metabolism of the CYP450 drug B. Decreased effectiveness
of concurrently taken substrates C. Increased risk of toxicity from
concurrently taken substrates D. Need for a higher dose of the CYP450
inducer over time E. Potential therapeutic failure of the concurrent
medication ANSWER : A, B, D, E Rationale: Inducers speed up enzyme
activity, causing the inducer drug itself to be metabolized faster
(requiring a higher dose over time—autoinduction) and causing other
drugs (substrates) to be broken down faster, leading to decreased
effectiveness and therapeutic failure. Option C describes an inhibitor,
not an inducer.
6. [MATRIX] Match the receptor type to its mechanism of action.
• Agonist -> B. Binds to a receptor and stimulates the response
• Antagonist -> C. Binds to a receptor and blocks the response
• Partial Agonist -> A. Binds to a receptor and produces a weaker
response than a full agonist Rationale: Agonists mimic
endogenous ligands. Antagonists occupy the receptor to prevent
other ligands from binding. Partial agonists have intrinsic activity
but cannot produce a maximal response even at full receptor
occupancy.
7. [EXHIBIT] A patient with a history of Raynaud's disease is prescribed
a drug. The provider explains that the drug's therapeutic effect is
secondary to its side effect. Which drug is this, and what is the
mechanism? ANSWER : Prazosin (Alpha-1 blocker); Therapeutic effect =
vasodilation of peripheral vessels. Side effect = orthostatic hypotension.
Rationale: Alpha-1 blockers block vasoconstriction. In Raynaud's, this
relieves vasospasm (therapeutic). However, blocking alpha-1 receptors
systemically prevents the sympathetic nervous system from
,constricting blood vessels when standing, causing orthostatic
hypotension (side effect).
Section 2: Autonomic Nervous System
8. [SATA] A patient is experiencing a cholinergic crisis
(organophosphate poisoning). Which of the following manifestations
should the nurse anticipate? (Select all that apply) A. Dry mouth B.
Urinary incontinence C. Pinpoint pupils (miosis) D. Tachycardia E.
Excessive salivation F. Muscle fasciculations ANSWER : B, C, E, F
Rationale: Use the mnemonic SLUDGE (Salivation, Lacrimation,
Urination, Defecation, GI distress, Emesis) plus miosis and muscle
fasciculations. Dry mouth and tachycardia are anticholinergic
(parasympatholytic) effects.
9. [ORDER] A patient arrives in the ED with suspected organophosphate
poisoning. Place the following interventions in the correct order.
1. Administer Pralidoxime (2-PAM)
2. Assess ABCs and secure airway
3. Decontaminate the patient (remove clothing/wash skin)
4. Administer Atropine ANSWER : 2, 3, 4, 1 Rationale: ABCs always
come first. Decontamination is crucial to prevent further
absorption. Atropine is given to dry up secretions and treat life-
threatening bronchoconstriction/bradycardia. Pralidoxime is given
secondarily to regenerate the cholinesterase enzyme.
10. [EXHIBIT] A patient with myasthenia gravis is taking Pyridostigmine.
They present with new-onset severe muscle weakness, dyspnea, and
excessive drooling. What is the nurse’s priority action? ANSWER : Hold
the Pyridostigmine and prepare to administer Atropine. Rationale:
These are signs of a cholinergic crisis (too much medication), which
must be differentiated from a myasthenic crisis (too little medication).
Giving more Pyridostigmine to a patient in cholinergic crisis can be
fatal. Atropine is the antidote.
11. [SATA] A nurse is educating a patient starting on Atropine. Which
statements by the patient indicate understanding of the side effects?
(Select all that apply) A. "I may need to use artificial tears." B. "I should
increase my fiber and water intake." C. "I might feel my heart racing." D.
, "I will sweat more in the summer." E. "I may have trouble emptying my
bladder." ANSWER : A, B, C, E Rationale: Atropine is an anticholinergic.
It causes dry eyes (need tears), decreased GI motility (constipation—
need fiber), tachycardia, anhidrosis (decreased sweating, not
increased), and urinary retention (trouble emptying bladder).
12. [SATA] Which of the following patients should NOT receive a non-
selective beta-blocker (e.g., Propranolol) safely without extreme
caution? (Select all that apply) A. A patient with bradycardia B. A patient
with severe asthma C. A patient with essential hypertension D. A patient
with acute heart failure E. A patient with a history of migraine ANSWER
: A, B, D Rationale: Beta-blockers lower heart rate (contraindicated in
bradycardia), block Beta-2 receptors causing bronchospasm
(contraindicated in asthma), and decrease contractility (contraindicated
in acute decompensated heart failure, though they are used in chronic
stable HF). Hypertension and migraines are approved indications.
13. [EXHIBIT] A patient is prescribed Clonidine for hypertension. They
suddenly stop taking it. What immediate pharmacologic phenomenon
occurs, and what is the clinical result? ANSWER : phenomenon = Up-
regulation of alpha-1 receptors; result = Rebound severe hypertensive
crisis. Rationale: Clonidine is a central-acting alpha-2 agonist. It
suppresses sympathetic outflow. When stopped abruptly, the body has
up-regulated (created more) alpha-1 receptors due to the perceived
lack of norepinephrine. A massive catecholamine surge binds to these
receptors, causing dangerous hypertension.
Section 3: Cardiovascular System
14. [SATA] A patient is started on Lisinopril. Which of the following are
potential adverse effects the nurse should monitor for? (Select all that
apply) A. Angioedema B. Persistent dry cough C. Hyperkalemia D.
Reflex tachycardia E. Elevated blood urea nitrogen (BUN) ANSWER : A,
B, C, E Rationale: Use the mnemonic ABCD for ACE inhibitors:
Angioedema, Bradycardia (or hyperkalemia), Cough, Dizziness. They
also dilate the efferent arteriole in the kidney, which can decrease GFR
and elevate BUN/creatinine, especially in renal artery stenosis. Reflex
tachycardia is associated with vasodilators like hydralazine, not ACEi.
15. [MATRIX] Match the antihypertensive class to its primary mechanism
of action.
