NURS 6521 ADVANCED PHARMACOLOGY MIDTERM EXAM
2026/2027 | Questions and Answers | Scored 99/100 | Pass
Guaranteed - A+ Graded
Unit 1: Pharmacokinetics & Pharmacodynamics (15 Questions)
Q1: A 68-year-old male with hepatic cirrhosis (Child-Pugh Class B) and chronic kidney
disease (eGFR 45 mL/min/1.73m²) is prescribed morphine 10 mg orally every 4 hours
as needed for post-operative pain. His serum albumin is 2.8 g/dL. On day 3, he becomes
increasingly somnolent with respiratory rate of 8 breaths/min. Which pharmacokinetic
principle best explains this adverse event?
A. Decreased first-pass metabolism leading to increased bioavailability of active
metabolites
B. Increased volume of distribution due to hypoalbuminemia requiring higher loading
doses
C. Decreased renal clearance of morphine-6-glucuronide (M6G) causing accumulation
D. Upregulation of opioid receptors in hepatic failure increasing sensitivity
Correct Answer: C
Rationale: Morphine undergoes hepatic glucuronidation to form morphine-6-glucuronide
(M6G), a potent active metabolite that is primarily renally eliminated. In this patient with
CKD (eGFR 45), M6G accumulates, causing delayed-onset respiratory depression
despite "normal" morphine dosing. The somnolence on day 3 represents accumulation
of M6G, not the parent drug.
Why others are incorrect:
, ● A: While hepatic cirrhosis reduces first-pass metabolism, morphine's
bioavailability actually increases only modestly (to ~40%); this doesn't explain the
delayed respiratory depression.
● B: Hypoalbuminemia affects highly protein-bound drugs (morphine is 35%
bound); increased Vd would actually lower initial concentrations, not cause
toxicity.
● D: Opioid receptors do not upregulate in hepatic failure; this demonstrates a
misunderstanding of receptor dynamics in organ dysfunction.
Q2: A 45-year-old female with treatment-resistant depression is started on phenelzine
15 mg TID. Two weeks later, she presents to the emergency department with severe
headache, blood pressure 220/110 mmHg, and diaphoresis after eating aged cheese.
Which pharmacodynamic mechanism explains this hypertensive crisis?
A. Irreversible inhibition of MAO-A leading to accumulation of tyramine and
norepinephrine
B. Competitive antagonism at α₁-adrenergic receptors causing reflex tachycardia
C. Increased serotonin synthesis triggering serotonin syndrome with hypertension
D. Inhibition of CYP2D6 causing accumulation of sympathomimetic amines
Correct Answer: A
Rationale: Phenelzine is an irreversible non-selective MAO inhibitor. MAO-A metabolizes
dietary tyramine in the gut wall and liver. When inhibited, tyramine enters systemic
circulation, displacing norepinephrine from storage vesicles (indirect sympathomimetic
effect), causing precipitous hypertension. This is the classic "cheese reaction" requiring
dietary restrictions.
Why others are incorrect:
● B: α₁-antagonism causes hypotension, not hypertension; this reverses the
mechanism.
● C: While MAOIs can cause serotonin syndrome, the presentation (tyramine-rich
meal, severe hypertension) is pathognomonic for tyramine-induced hypertensive
, crisis, not serotonin syndrome (which would show hyperthermia, clonus, mental
status changes).
● D: MAOIs do not significantly inhibit CYP2D6; this confuses metabolic inhibition
with enzyme inhibition.
Q3: A 28-year-old male requires loading dose calculation for vancomycin to treat MRSA
bacteremia. He weighs 80 kg with ideal body weight of 70 kg. Actual body weight is
130% of ideal body weight. Current creatinine clearance is 90 mL/min. Using
pharmacokinetic principles, which loading dose strategy is most appropriate?
A. 25 mg/kg based on actual body weight (2000 mg) due to hydrophilic drug distribution
B. 20 mg/kg based on adjusted body weight (1540 mg) to prevent nephrotoxicity
C. 25 mg/kg based on ideal body weight (1750 mg) as vancomycin distributes poorly in
adipose tissue
D. 30 mg/kg based on total body weight (2400 mg) for severe infection regardless of
distribution
Correct Answer: A
Rationale: Vancomycin is hydrophilic with poor adipose tissue penetration, distributing
primarily in extracellular fluid. However, for loading doses in severe infections
(bacteremia), actual body weight is used because the increased total body water in
obesity accommodates larger absolute volumes. The goal is rapid achievement of
therapeutic concentrations (AUC/MIC ≥400). A 25 mg/kg loading dose (2000 mg)
achieves this faster than weight-adjusted dosing.
Why others are incorrect:
● B: Adjusted body weight is used for maintenance dosing in obesity, not loading
doses; underdosing risks treatment failure.
● C: Ideal body weight significantly underdoses obese patients; vancomycin
penetration into infected tissues requires adequate absolute concentrations.
● D: While 30 mg/kg is used for severe infections, using total body weight in
obesity (130% IBW) risks acute kidney injury without pharmacokinetic benefit.
, Q4: A 55-year-old male with atrial fibrillation on warfarin (INR 2.5 therapeutic) is started
on amiodarone for rhythm control. Two weeks later, his INR is 4.8 without bleeding.
Which pharmacokinetic interaction mechanism is primarily responsible?
A. Amiodarone inhibits CYP2C9, reducing S-warfarin clearance
B. Amiodarone displaces warfarin from albumin binding sites
C. Amiodarone induces CYP1A2, increasing R-warfarin metabolism
D. Amiodarone inhibits P-glycoprotein, increasing warfarin absorption
Correct Answer: A
Rationale: S-warfarin (3-5x more potent than R-warfarin) is metabolized primarily by
CYP2C9. Amiodarone is a potent inhibitor of CYP2C9 (and CYP1A2, CYP3A4), reducing
S-warfarin clearance by 30-50%. This predictable interaction requires preemptive
warfarin dose reduction (typically 30-50%) when initiating amiodarone.
Why others are incorrect:
● B: Displacement interactions are transient (hours) and clinically insignificant for
warfarin due to its large volume of distribution; the INR elevation here (2 weeks)
indicates metabolic inhibition.
● C: CYP1A2 induction would decrease warfarin effect; amiodarone inhibits, not
induces, CYP enzymes.
● D: Warfarin bioavailability is already near 100%; P-gp inhibition does not
significantly increase absorption.
Q5: A 72-year-old female with heart failure is prescribed digoxin 0.25 mg daily. Her
pharmacokinetic parameters include: bioavailability 0.7, clearance 7 L/h, volume of
distribution 500 L. What is her estimated half-life, and how many days to reach 97%
steady state?
A. t½ = 50 hours; steady state in ~2 days
B. t½ = 50 hours; steady state in ~8-9 days
2026/2027 | Questions and Answers | Scored 99/100 | Pass
Guaranteed - A+ Graded
Unit 1: Pharmacokinetics & Pharmacodynamics (15 Questions)
Q1: A 68-year-old male with hepatic cirrhosis (Child-Pugh Class B) and chronic kidney
disease (eGFR 45 mL/min/1.73m²) is prescribed morphine 10 mg orally every 4 hours
as needed for post-operative pain. His serum albumin is 2.8 g/dL. On day 3, he becomes
increasingly somnolent with respiratory rate of 8 breaths/min. Which pharmacokinetic
principle best explains this adverse event?
A. Decreased first-pass metabolism leading to increased bioavailability of active
metabolites
B. Increased volume of distribution due to hypoalbuminemia requiring higher loading
doses
C. Decreased renal clearance of morphine-6-glucuronide (M6G) causing accumulation
D. Upregulation of opioid receptors in hepatic failure increasing sensitivity
Correct Answer: C
Rationale: Morphine undergoes hepatic glucuronidation to form morphine-6-glucuronide
(M6G), a potent active metabolite that is primarily renally eliminated. In this patient with
CKD (eGFR 45), M6G accumulates, causing delayed-onset respiratory depression
despite "normal" morphine dosing. The somnolence on day 3 represents accumulation
of M6G, not the parent drug.
Why others are incorrect:
, ● A: While hepatic cirrhosis reduces first-pass metabolism, morphine's
bioavailability actually increases only modestly (to ~40%); this doesn't explain the
delayed respiratory depression.
● B: Hypoalbuminemia affects highly protein-bound drugs (morphine is 35%
bound); increased Vd would actually lower initial concentrations, not cause
toxicity.
● D: Opioid receptors do not upregulate in hepatic failure; this demonstrates a
misunderstanding of receptor dynamics in organ dysfunction.
Q2: A 45-year-old female with treatment-resistant depression is started on phenelzine
15 mg TID. Two weeks later, she presents to the emergency department with severe
headache, blood pressure 220/110 mmHg, and diaphoresis after eating aged cheese.
Which pharmacodynamic mechanism explains this hypertensive crisis?
A. Irreversible inhibition of MAO-A leading to accumulation of tyramine and
norepinephrine
B. Competitive antagonism at α₁-adrenergic receptors causing reflex tachycardia
C. Increased serotonin synthesis triggering serotonin syndrome with hypertension
D. Inhibition of CYP2D6 causing accumulation of sympathomimetic amines
Correct Answer: A
Rationale: Phenelzine is an irreversible non-selective MAO inhibitor. MAO-A metabolizes
dietary tyramine in the gut wall and liver. When inhibited, tyramine enters systemic
circulation, displacing norepinephrine from storage vesicles (indirect sympathomimetic
effect), causing precipitous hypertension. This is the classic "cheese reaction" requiring
dietary restrictions.
Why others are incorrect:
● B: α₁-antagonism causes hypotension, not hypertension; this reverses the
mechanism.
● C: While MAOIs can cause serotonin syndrome, the presentation (tyramine-rich
meal, severe hypertension) is pathognomonic for tyramine-induced hypertensive
, crisis, not serotonin syndrome (which would show hyperthermia, clonus, mental
status changes).
● D: MAOIs do not significantly inhibit CYP2D6; this confuses metabolic inhibition
with enzyme inhibition.
Q3: A 28-year-old male requires loading dose calculation for vancomycin to treat MRSA
bacteremia. He weighs 80 kg with ideal body weight of 70 kg. Actual body weight is
130% of ideal body weight. Current creatinine clearance is 90 mL/min. Using
pharmacokinetic principles, which loading dose strategy is most appropriate?
A. 25 mg/kg based on actual body weight (2000 mg) due to hydrophilic drug distribution
B. 20 mg/kg based on adjusted body weight (1540 mg) to prevent nephrotoxicity
C. 25 mg/kg based on ideal body weight (1750 mg) as vancomycin distributes poorly in
adipose tissue
D. 30 mg/kg based on total body weight (2400 mg) for severe infection regardless of
distribution
Correct Answer: A
Rationale: Vancomycin is hydrophilic with poor adipose tissue penetration, distributing
primarily in extracellular fluid. However, for loading doses in severe infections
(bacteremia), actual body weight is used because the increased total body water in
obesity accommodates larger absolute volumes. The goal is rapid achievement of
therapeutic concentrations (AUC/MIC ≥400). A 25 mg/kg loading dose (2000 mg)
achieves this faster than weight-adjusted dosing.
Why others are incorrect:
● B: Adjusted body weight is used for maintenance dosing in obesity, not loading
doses; underdosing risks treatment failure.
● C: Ideal body weight significantly underdoses obese patients; vancomycin
penetration into infected tissues requires adequate absolute concentrations.
● D: While 30 mg/kg is used for severe infections, using total body weight in
obesity (130% IBW) risks acute kidney injury without pharmacokinetic benefit.
, Q4: A 55-year-old male with atrial fibrillation on warfarin (INR 2.5 therapeutic) is started
on amiodarone for rhythm control. Two weeks later, his INR is 4.8 without bleeding.
Which pharmacokinetic interaction mechanism is primarily responsible?
A. Amiodarone inhibits CYP2C9, reducing S-warfarin clearance
B. Amiodarone displaces warfarin from albumin binding sites
C. Amiodarone induces CYP1A2, increasing R-warfarin metabolism
D. Amiodarone inhibits P-glycoprotein, increasing warfarin absorption
Correct Answer: A
Rationale: S-warfarin (3-5x more potent than R-warfarin) is metabolized primarily by
CYP2C9. Amiodarone is a potent inhibitor of CYP2C9 (and CYP1A2, CYP3A4), reducing
S-warfarin clearance by 30-50%. This predictable interaction requires preemptive
warfarin dose reduction (typically 30-50%) when initiating amiodarone.
Why others are incorrect:
● B: Displacement interactions are transient (hours) and clinically insignificant for
warfarin due to its large volume of distribution; the INR elevation here (2 weeks)
indicates metabolic inhibition.
● C: CYP1A2 induction would decrease warfarin effect; amiodarone inhibits, not
induces, CYP enzymes.
● D: Warfarin bioavailability is already near 100%; P-gp inhibition does not
significantly increase absorption.
Q5: A 72-year-old female with heart failure is prescribed digoxin 0.25 mg daily. Her
pharmacokinetic parameters include: bioavailability 0.7, clearance 7 L/h, volume of
distribution 500 L. What is her estimated half-life, and how many days to reach 97%
steady state?
A. t½ = 50 hours; steady state in ~2 days
B. t½ = 50 hours; steady state in ~8-9 days
