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NR 565 ADVANCED PHARMACOLOGY FUNDAMENTALS MIDTERM EXAM*** 150 QUESTIONS AND VERIFIED ANSWERS | 2026/2027 UPDATE

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NR 565 ADVANCED PHARMACOLOGY FUNDAMENTALS MIDTERM EXAM*** 150 QUESTIONS AND VERIFIED ANSWERS | 2026/2027 UPDATE

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NR 565 ADVANCED PHARMACOLOGY
FUNDAMENTALS MIDTERM EXAM*** 150
QUESTIONS AND VERIFIED ANSWERS |
2026/2027 UPDATE



Chamberlain University College of Nursing
Course: NR 565 Advanced Pharmacology Fundamentals
Subject: Pharmacotherapeutics for Advanced Practice Nurses
Exam: Midterm Examination


Section 1: Questions 1-50
1. An APRN is prescribing a new medication for a patient and
wants to ensure it will produce the maximum possible effect.
Which pharmacodynamic property is the APRN evaluating?
A. Potency
B. Efficacy
C. Selectivity
D. Therapeutic index
❖ Rationale: Efficacy refers to the maximum effect a drug can
produce, regardless of the dose. Potency (A) refers to the
amount of drug needed to produce a given effect.

,Page 2 of 79


Selectivity (C) refers to a drug's ability to bind to its
intended receptor. The therapeutic index (D) is a safety
ratio.
2. A patient is prescribed a drug that is a known substrate of
CYP3A4. Which concomitant medication would the APRN
expect to significantly increase the risk of toxicity for this
drug?
A. Phenytoin
B. Rifampin
C. Ketoconazole
D. Carbamazepine
❖ Rationale: Ketoconazole is a potent CYP3A4 inhibitor, which
would decrease the metabolism of the substrate, leading
to higher serum concentrations and increased risk of
toxicity. Phenytoin (A), Rifampin (B), and Carbamazepine
(D) are potent CYP450 inducers, which would increase the
metabolism of the substrate, potentially reducing its
efficacy.
3. A 75-year-old patient with an eGFR of 35 mL/min is
prescribed a medication that is primarily renally excreted. The
APRN should anticipate which dosing adjustment to prevent
drug accumulation and toxicity?
A. Increase the dose to achieve therapeutic levels.
B. Administer the drug more frequently.

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C. Decrease the dose and/or increase the dosing interval.
D. No adjustment is needed as excretion is not significantly
affected by age.
❖ Rationale: In older adults with reduced renal function,
drugs that are renally excreted will have decreased
clearance. The standard approach is to reduce the dose
and/or extend the dosing interval to prevent accumulation.
Increasing the dose (A) or frequency (B) would exacerbate
the problem. The APRN must adjust the dose (D) as renal
function is a primary determinant of drug excretion.
4. A patient on warfarin therapy is started on a new
medication. The APRN is most concerned about a drug
interaction that involves which mechanism?
A. Displacement from plasma protein binding sites.
B. Inhibition of CYP2C9 enzyme metabolism.
C. Induction of P-glycoprotein transporters.
D. Increased renal excretion of warfarin.
❖ Rationale: Warfarin is primarily metabolized by the CYP2C9
enzyme. Inhibition of CYP2C9 (e.g., by amiodarone or
trimethoprim-sulfamethoxazole) will increase warfarin
levels and significantly raise the risk of bleeding. While
displacement from protein binding (A) can occur, it is often
a transient effect; the CYP inhibition is a more clinically
significant and persistent concern.

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5. A drug has a half-life of 4 hours. How long will it take for the
drug to reach steady-state plasma concentration with a
consistent dosing regimen?
A. 4 hours
B. 8 hours
C. 16 hours
D. 20 hours
❖ Rationale: It takes approximately 5 half-lives for a drug to
reach steady state. Therefore, 5 x 4 hours = 20 hours. This
is a fundamental principle of pharmacokinetics.
6. Which statement correctly describes the difference between
an agonist and an antagonist?
A. An agonist binds to a receptor to produce a response, while
an antagonist binds without producing a response.
B. An agonist binds to a receptor and blocks its action, while an
antagonist produces a response.
C. An agonist requires a higher dose to be effective compared to
an antagonist.
D. An agonist is a type of drug that is always selective, while an
antagonist is not.
❖ Rationale: By definition, an agonist activates a receptor to
produce a biological response, while an antagonist binds to
a receptor and blocks the action of an agonist without
producing its own response.

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