UTA NURS 5335 MODULE 3 EXAM 2026/2027 | 100% Correct
Answers with Complete Solutions | Graduate Nursing
Advanced Assessment | Pass Guaranteed - A+ Graded
Domain 1: Pharmacokinetics & Pharmacodynamics (10 Questions)
Q1: A 68-year-old patient with chronic kidney disease (eGFR 30 mL/min/1.73 m²) is
prescribed a medication that is 80% renally eliminated with a normal half-life of 8 hours.
What is the expected impact on drug accumulation if the dosing interval is not
adjusted?
A. No change in drug accumulation because hepatic metabolism compensates
B. Decreased drug accumulation due to increased protein binding in CKD
C. Increased drug accumulation and prolonged half-life due to reduced renal clearance,
increasing toxicity risk [CORRECT]
D. Faster drug elimination due to increased tubular secretion in CKD
Correct Answer: C
Rationale: In CKD, reduced glomerular filtration and tubular function decrease renal drug
elimination, leading to drug accumulation and prolonged half-life for renally cleared
medications. The half-life increases inversely proportional to clearance reduction.
,Option A is incorrect because hepatic compensation is limited and not all drugs have
significant hepatic metabolism. Option B is incorrect—protein binding often decreases
in CKD (due to hypoalbuminemia and uremic toxins), increasing free drug concentration.
Option D is incorrect—tubular secretion decreases, not increases, in CKD.
Q2: A patient on phenytoin for seizure control has subtherapeutic drug levels despite
appropriate dosing. Genetic testing reveals CYP2C9*3/*3 polymorphism. What is the
mechanism behind this finding?
A. Increased absorption of phenytoin
B. Decreased metabolism leading to accumulation and toxicity—this patient would
actually show toxicity, not subtherapeutic levels; the question describes an ultra-rapid
metabolizer scenario or the patient may need dose reduction due to accumulation
[CORRECT]
C. Increased renal excretion
D. Decreased protein binding
Correct Answer: B
Rationale: CYP2C9*3/*3 is a poor metabolizer genotype. Phenytoin is metabolized by
CYP2C9. Poor metabolizers have reduced enzyme activity, leading to decreased drug
metabolism, accumulation, and potential toxicity at standard doses. The question notes
subtherapeutic levels despite appropriate dosing—this may indicate measurement
timing issues or the patient may actually be experiencing toxicity symptoms. In practice,
,poor metabolizers require dose reductions (typically 25-50% lower maintenance doses).
Ultra-rapid metabolizers (*1/*2 or *2/*2 with duplication) would show subtherapeutic
levels. CYP2C9 polymorphisms significantly affect phenytoin dosing—*1/*3 and *3/*3
genotypes require 25% and 50% dose reductions respectively.
Q3: A 45-year-old patient with liver cirrhosis (Child-Pugh Class C) is prescribed
lorazepam 2 mg IV for alcohol withdrawal. What pharmacokinetic consideration is most
important?
A. Lorazepam requires dose reduction due to Phase I oxidation impairment
B. Lorazepam undergoes glucuronidation (Phase II), which is relatively preserved in liver
disease, making it safer than drugs requiring Phase I metabolism [CORRECT]
C. Lorazepam should be avoided entirely in liver disease
D. Lorazepam requires increased dosing due to increased clearance
Correct Answer: B
Rationale: Lorazepam, oxazepam, and temazepam undergo glucuronidation (Phase II
metabolism), which is relatively preserved in liver disease compared to Phase I
oxidation (CYP450 reactions). Drugs like diazepam, midazolam, and chlordiazepoxide
undergo Phase I metabolism and accumulate in liver disease. Option A is
incorrect—lorazepam does not primarily use Phase I. Option C is incorrect—lorazepam
is preferred in liver disease. Option D is incorrect—clearance is decreased, not
increased.
, Q4: A patient achieves steady state with a drug having a half-life of 12 hours. How long
will it take to reach approximately 97% of steady-state concentration?
A. 12 hours
B. 24 hours
C. 48 hours
D. 60 hours (approximately 5 half-lives) [CORRECT]
Correct Answer: D
Rationale: Steady state is reached after approximately 5 half-lives (93.75% at 4
half-lives, 96.875% at 5 half-lives). With a 12-hour half-life: 5 × 12 = 60 hours. This is
critical for dosing interval planning and therapeutic drug monitoring. After 1 half-life (A),
50% of steady state is reached; 2 half-lives (B) = 75%; 3 half-lives = 87.5%; 4 half-lives
(C) = 93.75%.
Q5: A patient taking warfarin (narrow therapeutic index) is started on amiodarone. What
is the primary pharmacokinetic mechanism for the increased bleeding risk?
A. Amiodarone induces CYP2C9, increasing warfarin metabolism
B. Amiodarone inhibits CYP2C9 and CYP1A2, decreasing warfarin metabolism and
increasing INR [CORRECT]
Answers with Complete Solutions | Graduate Nursing
Advanced Assessment | Pass Guaranteed - A+ Graded
Domain 1: Pharmacokinetics & Pharmacodynamics (10 Questions)
Q1: A 68-year-old patient with chronic kidney disease (eGFR 30 mL/min/1.73 m²) is
prescribed a medication that is 80% renally eliminated with a normal half-life of 8 hours.
What is the expected impact on drug accumulation if the dosing interval is not
adjusted?
A. No change in drug accumulation because hepatic metabolism compensates
B. Decreased drug accumulation due to increased protein binding in CKD
C. Increased drug accumulation and prolonged half-life due to reduced renal clearance,
increasing toxicity risk [CORRECT]
D. Faster drug elimination due to increased tubular secretion in CKD
Correct Answer: C
Rationale: In CKD, reduced glomerular filtration and tubular function decrease renal drug
elimination, leading to drug accumulation and prolonged half-life for renally cleared
medications. The half-life increases inversely proportional to clearance reduction.
,Option A is incorrect because hepatic compensation is limited and not all drugs have
significant hepatic metabolism. Option B is incorrect—protein binding often decreases
in CKD (due to hypoalbuminemia and uremic toxins), increasing free drug concentration.
Option D is incorrect—tubular secretion decreases, not increases, in CKD.
Q2: A patient on phenytoin for seizure control has subtherapeutic drug levels despite
appropriate dosing. Genetic testing reveals CYP2C9*3/*3 polymorphism. What is the
mechanism behind this finding?
A. Increased absorption of phenytoin
B. Decreased metabolism leading to accumulation and toxicity—this patient would
actually show toxicity, not subtherapeutic levels; the question describes an ultra-rapid
metabolizer scenario or the patient may need dose reduction due to accumulation
[CORRECT]
C. Increased renal excretion
D. Decreased protein binding
Correct Answer: B
Rationale: CYP2C9*3/*3 is a poor metabolizer genotype. Phenytoin is metabolized by
CYP2C9. Poor metabolizers have reduced enzyme activity, leading to decreased drug
metabolism, accumulation, and potential toxicity at standard doses. The question notes
subtherapeutic levels despite appropriate dosing—this may indicate measurement
timing issues or the patient may actually be experiencing toxicity symptoms. In practice,
,poor metabolizers require dose reductions (typically 25-50% lower maintenance doses).
Ultra-rapid metabolizers (*1/*2 or *2/*2 with duplication) would show subtherapeutic
levels. CYP2C9 polymorphisms significantly affect phenytoin dosing—*1/*3 and *3/*3
genotypes require 25% and 50% dose reductions respectively.
Q3: A 45-year-old patient with liver cirrhosis (Child-Pugh Class C) is prescribed
lorazepam 2 mg IV for alcohol withdrawal. What pharmacokinetic consideration is most
important?
A. Lorazepam requires dose reduction due to Phase I oxidation impairment
B. Lorazepam undergoes glucuronidation (Phase II), which is relatively preserved in liver
disease, making it safer than drugs requiring Phase I metabolism [CORRECT]
C. Lorazepam should be avoided entirely in liver disease
D. Lorazepam requires increased dosing due to increased clearance
Correct Answer: B
Rationale: Lorazepam, oxazepam, and temazepam undergo glucuronidation (Phase II
metabolism), which is relatively preserved in liver disease compared to Phase I
oxidation (CYP450 reactions). Drugs like diazepam, midazolam, and chlordiazepoxide
undergo Phase I metabolism and accumulate in liver disease. Option A is
incorrect—lorazepam does not primarily use Phase I. Option C is incorrect—lorazepam
is preferred in liver disease. Option D is incorrect—clearance is decreased, not
increased.
, Q4: A patient achieves steady state with a drug having a half-life of 12 hours. How long
will it take to reach approximately 97% of steady-state concentration?
A. 12 hours
B. 24 hours
C. 48 hours
D. 60 hours (approximately 5 half-lives) [CORRECT]
Correct Answer: D
Rationale: Steady state is reached after approximately 5 half-lives (93.75% at 4
half-lives, 96.875% at 5 half-lives). With a 12-hour half-life: 5 × 12 = 60 hours. This is
critical for dosing interval planning and therapeutic drug monitoring. After 1 half-life (A),
50% of steady state is reached; 2 half-lives (B) = 75%; 3 half-lives = 87.5%; 4 half-lives
(C) = 93.75%.
Q5: A patient taking warfarin (narrow therapeutic index) is started on amiodarone. What
is the primary pharmacokinetic mechanism for the increased bleeding risk?
A. Amiodarone induces CYP2C9, increasing warfarin metabolism
B. Amiodarone inhibits CYP2C9 and CYP1A2, decreasing warfarin metabolism and
increasing INR [CORRECT]
