2026/2027 | Family Care Comprehensive Review |
Chamberlain | Pass Guaranteed - A+ Graded
SECTION 1: PHARMACOKINETICS, PHARMACODYNAMICS &
PHARMACOGENOMICS (25 Questions)
Q1: A 68-year-old male with liver cirrhosis is prescribed a medication metabolized by
CYP3A4. Which pharmacokinetic change should the nurse practitioner anticipate?
A. Increased drug metabolism and decreased half-life
B. Decreased first-pass metabolism and increased bioavailability of oral drugs
[CORRECT]
C. Enhanced renal clearance of the medication
D. Increased plasma protein binding
Correct Answer: B
Rationale: Liver cirrhosis reduces hepatic blood flow and CYP450 enzyme activity,
decreasing first-pass metabolism and increasing bioavailability of oral drugs; dosage
reductions are often required. Renal clearance is not directly enhanced. Plasma protein
binding typically decreases due to hypoalbuminemia.
Q2: A patient who is a CYP2D6 poor metabolizer takes codeine for postoperative pain.
Which response is expected?
A. Enhanced analgesic effect due to rapid conversion to morphine
B. Reduced or absent analgesia due to inability to convert codeine to morphine
[CORRECT]
C. Increased risk of serotonin syndrome
D. Faster elimination of the parent drug
Correct Answer: B
Rationale: Codeine is a prodrug requiring CYP2D6-mediated conversion to morphine for
analgesic effect; poor metabolizers cannot efficiently perform this conversion, resulting
,in subtherapeutic pain relief. Ultra-rapid metabolizers experience exaggerated effects.
Serotonin syndrome is unrelated to CYP2D6 phenotype for codeine.
Q3: A patient on warfarin with the VKORC1 -1639 G>A variant is prescribed standard
dosing. Which risk is increased?
A. Warfarin resistance requiring higher doses
B. Increased bleeding risk due to enhanced warfarin sensitivity [CORRECT]
C. Thrombosis due to reduced anticoagulant effect
D. No change in warfarin response
Correct Answer: B
Rationale: The VKORC1 -1639 G>A variant reduces VKORC1 expression, increasing
sensitivity to warfarin and requiring lower doses to achieve therapeutic INR; standard
dosing increases bleeding risk. This variant is a key component of pharmacogenomic
warfarin dosing algorithms.
Q4: A highly protein-bound drug (95%) is prescribed to a patient with low albumin (2.1
g/dL). Which effect is anticipated?
A. Decreased free drug concentration and reduced pharmacological effect
B. Increased free drug concentration and potential toxicity [CORRECT]
C. No change in drug distribution
D. Decreased volume of distribution
Correct Answer: B
Rationale: Low albumin reduces binding sites for highly protein-bound drugs, increasing
the free (unbound) fraction that is pharmacologically active; this increases risk of
toxicity, especially for drugs with narrow therapeutic indices like phenytoin or warfarin.
Volume of distribution may increase, not decrease.
Q5: A patient takes levothyroxine and calcium carbonate concurrently. Which interaction
occurs?
A. Enhanced levothyroxine absorption
B. Reduced levothyroxine absorption due to chelation; separate by at least 4 hours
[CORRECT]
C. Increased risk of hypercalcemia
D. Decreased calcium absorption only
Correct Answer: B
,Rationale: Calcium carbonate, iron, aluminum, and magnesium-containing products
chelate levothyroxine in the GI tract, reducing its absorption by up to 50%; these
medications should be separated by at least 4 hours. This interaction does not
significantly increase hypercalcemia risk.
Q6: A patient with renal impairment (CrCl 28 mL/min) is prescribed a drug eliminated
renally unchanged. Which adjustment is necessary?
A. Increase the dose to compensate for reduced clearance
B. Reduce the dose or extend the dosing interval to prevent accumulation and toxicity
[CORRECT]
C. Switch to the intravenous route to bypass renal elimination
D. No adjustment needed if hepatic function is normal
Correct Answer: B
Rationale: Drugs eliminated primarily by the kidneys (e.g., aminoglycosides,
vancomycin, digoxin, metformin) accumulate in renal impairment, necessitating dose
reduction or interval extension based on creatinine clearance. IV administration does
not bypass renal elimination. Hepatic function does not compensate for renal clearance
deficits.
Q7: A patient taking phenytoin develops toxic levels after starting fluconazole. Which
mechanism explains this interaction?
A. Fluconazole induces CYP2C9, increasing phenytoin metabolism
B. Fluconazole inhibits CYP2C9 and CYP2C19, reducing phenytoin metabolism
[CORRECT]
C. Fluconazole increases phenytoin renal excretion
D. Fluconazole displaces phenytoin from albumin, increasing its metabolism
Correct Answer: B
Rationale: Fluconazole is a potent inhibitor of CYP2C9 and CYP2C19, the primary
enzymes metabolizing phenytoin; concurrent use reduces phenytoin clearance,
increasing plasma levels and risk of neurotoxicity. Phenytoin is not primarily renally
excreted. Displacement increases free fraction but does not increase metabolism.
Q8: A patient with TPMT deficiency is prescribed azathioprine. Which adverse effect is
of greatest concern?
, A. Enhanced therapeutic immunosuppression
B. Life-threatening myelosuppression (leukopenia, thrombocytopenia, pancytopenia)
[CORRECT]
C. Increased risk of hepatotoxicity only
D. Reduced risk of infection
Correct Answer: B
Rationale: Thiopurine S-methyltransferase (TPMT) metabolizes azathioprine and 6-MP;
deficiency causes accumulation of toxic thiopurine nucleotides, resulting in severe,
potentially fatal myelosuppression. TPMT genotyping or phenotyping guides dose
reduction (to 30-50% of standard) or alternative therapy.
Q9: A patient on a narrow therapeutic index drug requires therapeutic drug monitoring
(TDM). Which drug is LEAST likely to require TDM?
A. Lithium
B. Digoxin
C. Metformin [CORRECT]
D. Phenytoin
Correct Answer: C
Rationale: Metformin has a wide therapeutic index and does not require routine TDM;
efficacy is monitored by glucose and HbA1c, and toxicity by renal function and clinical
signs. Lithium, digoxin, and phenytoin have narrow therapeutic indices with significant
toxicity risk, necessitating routine blood level monitoring.
Q10: A patient taking a medication with a half-life of 8 hours is started on a twice-daily
regimen. How long will it take to reach steady state?
A. 8 hours
B. 24 hours
C. Approximately 40 hours (5 half-lives) [CORRECT]
D. 16 hours
Correct Answer: C
Rationale: Steady state is achieved after approximately 5 half-lives (5 × 8 hours = 40
hours), regardless of dosing interval; this represents 97% of the theoretical steady-state
concentration. Loading doses may be used for drugs with long half-lives when
immediate effect is needed.