UNIVERSITY NURS 629 Advanced
Pharmacology – Exam 4
SECTION 1: Pharmacokinetics & Pharmacodynamics (Questions 1–5)
Q1: A patient with hepatic cirrhosis (Child-Pugh Class B) is prescribed a medication that
undergoes extensive first-pass metabolism. Which pharmacokinetic change would the
prescriber anticipate?
A. Decreased bioavailability requiring higher doses
B. Increased bioavailability requiring lower doses. [CORRECT]
C. No change in bioavailability due to enterohepatic recirculation
D. Increased renal excretion requiring higher doses
Correct Answer: B
Rationale: First-pass metabolism occurs in the liver. Cirrhosis impairs hepatic function, reducing
first-pass extraction and increasing oral bioavailability. This requires LOWER doses to avoid
toxicity. Common error: assuming liver disease always requires higher doses. Clinical pearl:
Drugs with high first-pass metabolism (propranolol, morphine, lidocaine) are most affected.
Always start low and titrate slowly in hepatic impairment.
Q2: A 35-year-old patient with normal renal function is prescribed phenytoin for seizure
control. After 4 weeks, the patient develops toxic symptoms despite a "therapeutic" serum
level. Which pharmacokinetic principle explains this finding?
A. Zero-order kinetics at therapeutic concentrations
B. First-order kinetics transitioning to zero-order kinetics at higher concentrations. [CORRECT]
C. Increased protein binding due to hypoalbuminemia
D. Decreased volume of distribution with chronic use
Correct Answer: B
Rationale: Phenytoin exhibits Michaelis-Menten (saturable) kinetics. At low concentrations,
elimination follows first-order kinetics; as concentrations rise, the metabolic enzymes become
,saturated, shifting to zero-order kinetics. Small dose increases can cause dramatic toxicity.
Common error: assuming linear pharmacokinetics for all drugs. Clinical pearl: Monitor free
phenytoin levels in hypoalbuminemia or renal failure, as total levels may be misleading.
Q3: A patient taking warfarin is started on a new medication that is a potent CYP3A4 inhibitor.
The prescriber should anticipate which change in warfarin pharmacokinetics?
A. Increased hepatic metabolism of warfarin → decreased INR
B. Decreased hepatic metabolism of warfarin → increased INR. [CORRECT]
C. Increased protein binding → decreased free warfarin
D. Increased renal clearance → decreased half-life
Correct Answer: B
Rationale: CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin, grapefruit juice) reduce
warfarin metabolism, increasing its plasma concentration and INR. This raises bleeding risk.
Common error: confusing induction with inhibition. Clinical pearl: Always check for CYP
interactions before prescribing new medications to patients on warfarin. Key CYP3A4 inducers
include rifampin, carbamazepine, and St. John's wort.
Q4: A 68-year-old patient with heart failure has a drug with high protein binding (99%) and
low volume of distribution (0.1 L/kg). Which statement is MOST accurate regarding this drug's
distribution?
A. The drug will rapidly cross the blood-brain barrier
B. The drug will have a long half-life due to extensive tissue distribution
C. The drug will be highly affected by changes in albumin levels. [CORRECT]
D. The drug will have minimal drug-drug interactions via displacement
Correct Answer: C
Rationale: Drugs with high protein binding (e.g., warfarin, phenytoin) are highly affected by
hypoalbuminemia (common in elderly, malnutrition, liver disease). Reduced albumin increases
free drug fraction, potentially causing toxicity at "normal" total levels. Common error: assuming
high protein binding means low clinical significance. Clinical pearl: In patients with low albumin,
monitor free drug levels when available (e.g., free phenytoin, free valproic acid) to guide dosing.
, Q5: A patient asks why their extended-release morphine tablet must be swallowed whole and
not crushed. The BEST explanation relates to which pharmacokinetic principle?
A. Crushing increases first-pass metabolism
B. Crushing eliminates the controlled-release mechanism, causing dose dumping. [CORRECT]
C. Crushing reduces absorption in the stomach
D. Crushing increases renal excretion
Correct Answer: B
Rationale: Extended-release formulations use matrix or osmotic systems to slowly release drug
over time. Crushing destroys this mechanism, causing rapid release of the entire dose ("dose
dumping"), which can cause fatal respiratory depression. Common error: assuming crushing
only affects absorption rate slightly. Clinical pearl: Never crush extended-release opioids (MS
Contin, OxyContin, fentanyl patches). If a patient cannot swallow pills, use liquid formulations or
transdermal alternatives.
SECTION 2: Cardiovascular Pharmacology (Questions 6–13)
Q6: A 58-year-old Black male with hypertension (BP 152/92) and no other comorbidities is
started on monotherapy. According to the 2024 ACC/AHA guidelines, which agent would be
LEAST effective as first-line therapy for this patient?
A. Amlodipine (CCB)
B. Chlorthalidone (Thiazide diuretic)
C. Lisinopril (ACE inhibitor). [CORRECT]
D. Telmisartan (ARB)
Correct Answer: C
Rationale: ACE inhibitors (and ARBs) are less effective as monotherapy in Black patients due to
lower renin activity. CCBs and thiazides are preferred first-line in this population. This is a board-
style question testing guideline awareness and population-specific pharmacology. Clinical pearl:
Combination therapy (CCB + thiazide or ACEi + CCB) is often needed regardless of race. Always
individualize based on comorbidities (e.g., CKD, diabetes may still warrant ACEi/ARB).