PHARMACOLOGY PRACTICE
TEST – REAL EXAM QUESTIONS
(2026 CURRICULUM)|| Questions
And Answers With Rationales/Graded
A+/2026 Update/100% Correct
/Instant Download
Total Questions: 85
Format: Multiple Choice
Instructions: Select the best answer. Correct answers are bolded & highlighted.
Rationales explain key concepts.
SECTION A: PHARMACOKINETICS & PHARMACODYNAMICS (Q1–15)
1. A drug with a half-life of 4 hours is administered intravenously.
Approximately how long will it take to reach 94% of steady-state
concentration?
• A) 8 hours
• B) 16 hours
• C) 20 hours
• D) 24 hours
Rationale: Steady state reaches ~94% after 4 half-lives (4 × 4h = 16h). Each half-
life increases drug accumulation by 50% of remaining difference.
2. Which phase of drug metabolism involves conjugation reactions (e.g.,
glucuronidation)?
, • A) Phase I
• B) Phase II
• C) Absorption
• D) Distribution
Rationale: Phase II metabolism adds polar groups (glucuronide, sulfate) to increase
renal excretion. Phase I includes oxidation (CYP450).
3. A patient has a genetic variation in CYP2D6 (poor metabolizer). Which
drug would most likely cause toxicity at standard doses?
• A) Lisinopril
• B) Codeine
• C) Metformin
• D) Aspirin
Rationale: Codeine requires CYP2D6 conversion to morphine for analgesia. Poor
metabolizers get no pain relief; but the question tests toxicity—actually, poor
metabolizers have no effect, not toxicity. Correct answer for toxicity: **Codeine is
prodrug; but if asking toxicity: Ultrarapid metabolizers get toxicity. Poor
metabolizers have reduced effect. However, standard exam trick: They
expect Codeine as example of genetic impact. For true toxicity,
consider warfarin but not listed. Let’s correct: The better answer for toxicity risk
is Warfarin (VKORC1). But among options, codeine is classic exam example of
genetic variation → poor metabolizer = inefficacy, not toxicity. I will adjust:
Corrected Q3: Genetic variation in CYP2D6 leading to toxicity at standard doses
occurs in:
• A) Lisinopril
• B) Nortriptyline (but not in options – I will change option B
to Fluoxetine – no. Let me redo Q3 properly.)
Revised Q3 (valid): A patient is a CYP2D6 poor metabolizer. Which drug may
cause serotonin toxicity at normal doses if also taking another serotonergic agent?
Options unchanged – poor. I’ll replace Q3:
, Q3 (corrected). A patient with a CYP2C9*2/*3 genotype is started on
warfarin. What is the most appropriate initial action?
• A) Increase warfarin dose
• B) Decrease warfarin dose
• C) Give vitamin K
• D) No change needed
Rationale: CYP2C9 poor metabolizers have reduced warfarin clearance, requiring
30–50% lower starting dose to prevent bleeding.
4. Bioavailability of an oral drug is 0.5 (50%). IV dose of 10 mg produces AUC
of 100 mg·h/L. What oral dose gives same AUC?
• A) 10 mg
• B) 20 mg
• C) 5 mg
• D) 40 mg
Rationale: Oral dose = IV dose / F = .5 = 20 mg.
5. Which transporter is responsible for hepatic uptake of statins and is
associated with myopathy risk if inhibited?
• A) P-gp
• B) OATP1B1
• C) BCRP
• D) MATE1
Rationale: OATP1B1 transports statins into hepatocytes. Inhibition (e.g.,
cyclosporine) increases plasma statin levels → myopathy. Genetic SLCO1B1
variant increases simvastatin myopathy risk.
6. A drug follows zero-order kinetics. Which statement is true?
• A) Half-life is constant
• B) A constant amount is eliminated per unit time
TEST – REAL EXAM QUESTIONS
(2026 CURRICULUM)|| Questions
And Answers With Rationales/Graded
A+/2026 Update/100% Correct
/Instant Download
Total Questions: 85
Format: Multiple Choice
Instructions: Select the best answer. Correct answers are bolded & highlighted.
Rationales explain key concepts.
SECTION A: PHARMACOKINETICS & PHARMACODYNAMICS (Q1–15)
1. A drug with a half-life of 4 hours is administered intravenously.
Approximately how long will it take to reach 94% of steady-state
concentration?
• A) 8 hours
• B) 16 hours
• C) 20 hours
• D) 24 hours
Rationale: Steady state reaches ~94% after 4 half-lives (4 × 4h = 16h). Each half-
life increases drug accumulation by 50% of remaining difference.
2. Which phase of drug metabolism involves conjugation reactions (e.g.,
glucuronidation)?
, • A) Phase I
• B) Phase II
• C) Absorption
• D) Distribution
Rationale: Phase II metabolism adds polar groups (glucuronide, sulfate) to increase
renal excretion. Phase I includes oxidation (CYP450).
3. A patient has a genetic variation in CYP2D6 (poor metabolizer). Which
drug would most likely cause toxicity at standard doses?
• A) Lisinopril
• B) Codeine
• C) Metformin
• D) Aspirin
Rationale: Codeine requires CYP2D6 conversion to morphine for analgesia. Poor
metabolizers get no pain relief; but the question tests toxicity—actually, poor
metabolizers have no effect, not toxicity. Correct answer for toxicity: **Codeine is
prodrug; but if asking toxicity: Ultrarapid metabolizers get toxicity. Poor
metabolizers have reduced effect. However, standard exam trick: They
expect Codeine as example of genetic impact. For true toxicity,
consider warfarin but not listed. Let’s correct: The better answer for toxicity risk
is Warfarin (VKORC1). But among options, codeine is classic exam example of
genetic variation → poor metabolizer = inefficacy, not toxicity. I will adjust:
Corrected Q3: Genetic variation in CYP2D6 leading to toxicity at standard doses
occurs in:
• A) Lisinopril
• B) Nortriptyline (but not in options – I will change option B
to Fluoxetine – no. Let me redo Q3 properly.)
Revised Q3 (valid): A patient is a CYP2D6 poor metabolizer. Which drug may
cause serotonin toxicity at normal doses if also taking another serotonergic agent?
Options unchanged – poor. I’ll replace Q3:
, Q3 (corrected). A patient with a CYP2C9*2/*3 genotype is started on
warfarin. What is the most appropriate initial action?
• A) Increase warfarin dose
• B) Decrease warfarin dose
• C) Give vitamin K
• D) No change needed
Rationale: CYP2C9 poor metabolizers have reduced warfarin clearance, requiring
30–50% lower starting dose to prevent bleeding.
4. Bioavailability of an oral drug is 0.5 (50%). IV dose of 10 mg produces AUC
of 100 mg·h/L. What oral dose gives same AUC?
• A) 10 mg
• B) 20 mg
• C) 5 mg
• D) 40 mg
Rationale: Oral dose = IV dose / F = .5 = 20 mg.
5. Which transporter is responsible for hepatic uptake of statins and is
associated with myopathy risk if inhibited?
• A) P-gp
• B) OATP1B1
• C) BCRP
• D) MATE1
Rationale: OATP1B1 transports statins into hepatocytes. Inhibition (e.g.,
cyclosporine) increases plasma statin levels → myopathy. Genetic SLCO1B1
variant increases simvastatin myopathy risk.
6. A drug follows zero-order kinetics. Which statement is true?
• A) Half-life is constant
• B) A constant amount is eliminated per unit time
