Is pharmacokinetics high yield on the PEBC exam?

Yes, and more than it looks, because the same concepts drive therapeutic drug monitoring and renal dosing across many other topics. Half-life, steady state, drug monitoring, and interactions show up both directly and woven into clinical questions.

What pharmacokinetics topics should I focus on for the PEBC?

Focus on half-life and steady state, loading versus maintenance dosing, therapeutic drug monitoring for the narrow-therapeutic-index drugs, and enzyme induction versus inhibition. Being comfortable with these makes both the dedicated questions and the dosing questions elsewhere easier.

Do I need to do calculations for pharmacokinetics on the PEBC?

Some, yes. Expect to apply the core relationships, such as estimating a level at steady state or adjusting a dose, so practice the math and always carry your units. The concepts matter as much as the arithmetic, since many questions are about interpreting a level rather than computing one.

How should I study pharmacokinetics for the PEBC?

Master the core relationships between half-life, volume of distribution, and clearance, learn the therapeutic drug monitoring rules, and practice the calculations.

PEBC Pharmacokinetics Practice Questions

Pharmacokinetics is high yield on the PEBC exam, and it pays off twice, because the same concepts drive therapeutic drug monitoring and renal dosing throughout the rest of the exam. Half-life, steady state, clearance, drug monitoring, and interactions all show up.

Below is a sample drawn from those areas. Each explanation argues every option, right and wrong, down to the relationship that tips the answer.

Written and reviewed against current Canadian guidelines and references.

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All 4

options explained

full clinical case

How to approach a PEBC pharmacokinetics question

1Know the core relationships cold: half-life, volume of distribution, and clearance, and how they connect, since a loading dose depends on volume of distribution and a maintenance dose depends on clearance.
2For steady state, remember it takes about four to five half-lives to reach it, and about the same to wash a drug out.
3For therapeutic drug monitoring (vancomycin, aminoglycosides, digoxin, lithium, phenytoin), know which level to draw, when to draw it, and how to adjust.
4For drug interactions, separate enzyme inducers from inhibitors and know what each does to a substrate's drug level.
5Carry your units through every calculation, the same discipline that the calculation questions reward.

Practice questions

Tap an answer to see why each option is right or wrong.

Question 1ADME & Compartment Models

KM is a 58 year old male with chronic heart failure and atrial fibrillation. He is taking digoxin 0.125 mg po daily. After reviewing his plasma concentration-time profile on a semi-logarithmic plot, the pharmacist observes a biphasic decline with two distinct slopes. Which of the following best explains this observation?

Incorrect · Answer: D

PEBC Yield: Highmonitoring

Zero-order kinetics describes a constant rate of elimination independent of concentration, which does not produce the characteristic biphasic decline seen on a semi-log plot. Digoxin elimination follows first-order kinetics.

A three-compartment model produces a triphasic curve with three distinct slopes on a semi-log plot. The observation of two slopes specifically indicates two compartments, not three.

A one-compartment model produces a single straight line on a semi-log plot, not two distinct slopes. Digoxin distributes slowly into cardiac and skeletal muscle, which is inconsistent with the instantaneous distribution assumed in one-compartment models.

D) (Correct)

Correct -- digoxin follows a two-compartment model. The initial steep slope (alpha phase) represents distribution from the central compartment into peripheral tissues, while the second shallower slope (beta phase) represents elimination after distribution equilibrium is reached.

Question 2Therapeutic Drug Monitoring

KR is a 72 year old female with atrial fibrillation and heart failure (LVEF 30%). She was started on digoxin 0.125 mg po daily one week ago. Her serum creatinine is 142 umol/L (eGFR 34 mL/min/1.73m^2). A digoxin level is drawn 4 hours after her morning dose and returns at 2.1 nmol/L. Which of the following is the most appropriate next step?

Incorrect · Answer: D

PEBC Yield: Highmonitoringdose-adjustment

Tempting because 2.1 nmol/L exceeds the therapeutic range (0.6-1.2 nmol/L). However, the sample was drawn only 4 hours post-dose, during the distribution phase, which yields falsely elevated levels. Dose adjustment should not be made based on this timing.

Tempting because steady state takes 7-14 days for digoxin. However, the immediate issue is incorrect sampling time, not insufficient time to steady state. The level was drawn during the distribution phase and should be repeated at proper post-dose timing first.

Tempting given the apparently high level, but discontinuation is premature. The level is unreliable because it was drawn during the distribution phase. Digoxin requires a 2-compartment model with at least 6 hours (ideally 12 hours) for tissue distribution.

D) (Correct)

Correct. Digoxin follows a 2-compartment model and requires at least 6 hours (ideally 12 hours) post-dose for distribution equilibrium. A sample drawn at 4 hours reflects distribution-phase concentrations, not steady-state tissue levels. The level should be redrawn at the appropriate timing.

Question 3Drug Interactions

TH is a 62 year old female with hypertension, depression, and chronic pain. She takes amlodipine 10 mg po daily, duloxetine 60 mg po daily, and codeine 30 mg po q4h prn. She reports that codeine provides no pain relief despite taking it regularly. What is the most likely explanation for the lack of analgesic effect?

Incorrect · Answer: A

PEBC Yield: Highdrug-interactionADR-recognition

A) (Correct)

Correct -- codeine is a prodrug that requires CYP2D6 to convert it to its active metabolite morphine. Duloxetine is a potent CYP2D6 inhibitor, blocking this bioactivation and rendering codeine ineffective for pain control.

While CYP3A4 does metabolize codeine to norcodeine, amlodipine is a CYP3A4 substrate, not an inhibitor. Additionally, the norcodeine pathway is not the analgesic pathway for codeine.

Duloxetine is a CYP2D6 inhibitor, not a CYP1A2 inducer. Duloxetine is itself a CYP1A2 substrate. Increased clearance of codeine would not explain complete loss of analgesic effect.

Protein binding displacement is not a clinically significant mechanism for the codeine-duloxetine interaction. Codeine is not highly protein-bound, and amlodipine does not cause meaningful displacement.

Question 4Drug Interactions

BP is a 70 year old male with hypothyroidism and osteoporosis. He takes levothyroxine 100 mcg po daily and calcium carbonate 500 mg po bid. His recent TSH is elevated at 8.2 mIU/L (previously well-controlled at 2.1 mIU/L). No dose changes have been made. What is the most appropriate recommendation?

Incorrect · Answer: D

PEBC Yield: Highdrug-interactioncounselling

Switching to calcium citrate does not eliminate the chelation interaction with levothyroxine. All calcium salts can bind levothyroxine. Separation by time is the standard management regardless of calcium formulation.

Discontinuing calcium is unnecessary and harmful for a patient with osteoporosis. The interaction is manageable through appropriate timing of administration without sacrificing either therapy.

Increasing the levothyroxine dose does not address the root cause. The elevated TSH is likely due to decreased absorption from chelation with calcium, not an insufficient dose. Addressing the interaction first is more appropriate.

D) (Correct)

Correct -- calcium binds to levothyroxine in the GI tract through chelation, reducing its absorption. Separating the two medications by at least 4 hours allows adequate levothyroxine absorption and should restore TSH to target.

Question 5Drug Interactions

NP is a 48 year old female with depression and a fungal nail infection. She takes paroxetine 20 mg po daily and was recently started on terbinafine 250 mg po daily. She also takes tamoxifen 20 mg po daily for breast cancer prevention. Which interaction poses the greatest clinical risk?

Incorrect · Answer: C

PEBC Yield: Highdrug-interactioncontraindication-check

Paroxetine inhibits CYP2D6, not CYP1A2. Terbinafine metabolism does not depend primarily on CYP1A2. This option misidentifies the enzyme pathway for both drugs involved in the proposed interaction.

Terbinafine is a CYP2D6 inhibitor, not a CYP3A4 inhibitor. Paroxetine is metabolized primarily by CYP2D6, not CYP3A4. This option misidentifies both the inhibiting enzyme and the metabolic pathway.

C) (Correct)

Correct -- paroxetine is one of the strongest CYP2D6 inhibitors. Tamoxifen is a prodrug requiring CYP2D6 to form its active metabolite endoxifen. This interaction reduces tamoxifen efficacy and is associated with increased breast cancer recurrence.

Terbinafine is a CYP2D6 inhibitor and could reduce tamoxifen activation, but paroxetine is a more potent CYP2D6 inhibitor with stronger clinical evidence of reducing endoxifen levels and compromising tamoxifen efficacy.

Question 6ADME & Compartment Models

A pharmacist is reviewing the bioavailability of a new oral formulation. The fraction absorbed across the intestinal membrane (Fa) is 0.9, the fraction escaping gut wall metabolism (Fg) is 0.8, and the fraction escaping hepatic first-pass metabolism (Fh) is 0.5. What is the overall oral bioavailability (F)?

Incorrect · Answer: D

PEBC Yield: Highcalculation

This value would result from multiplying 0.9 x 0.5 x 0.6, which incorrectly uses 0.6 for Fg instead of the stated 0.8. Each component must be used exactly as provided.

This value would result from multiplying only Fa x Fh (0.9 x 0.5 = 0.45), omitting the gut wall metabolism component. All three sequential barriers must be included in the bioavailability calculation.

This value would result from multiplying 0.9 x 0.8 x 0.75, which overestimates hepatic bioavailability. The stated Fh of 0.5 indicates 50% extraction by the liver during first pass.

D) (Correct)

Correct -- F = Fa x Fg x Fh = 0.9 x 0.8 x 0.5 = 0.36. Only 36% of the administered oral dose reaches systemic circulation, with the largest reduction occurring during hepatic first-pass metabolism.

Question 7ADME & Compartment Models

Which of the following statements about drug absorption transporters is NOT correct?

Incorrect · Answer: B

PEBC Yield: Highdrug-interaction

This statement is correct. Efflux transporters including P-gp, MRP, BCRP, BSEP, and MATE all require ATP to actively pump drugs out of cells against concentration gradients.

B) (Correct)

Correct -- this statement is NOT correct. P-gp inhibition actually increases plasma levels of substrates such as digoxin, dabigatran, and fexofenadine. P-gp normally pumps drug back into the intestinal lumen or bile; inhibiting this pump allows more drug to reach systemic circulation.

This statement is correct. BCRP (Breast Cancer Resistance Protein) is an efflux transporter located on the bile duct-facing (canalicular) side of hepatocytes, along with P-gp, MRP, BSEP, and MATE.

This statement is correct. Influx transporters including OATP, OAT, OCT, and PEPT mediate bidirectional facilitated diffusion without ATP, moving drugs into cells down or along their concentration gradient.

Question 8Therapeutic Drug Monitoring

PL is a 45 year old male with a seizure disorder controlled on phenytoin 300 mg po daily. He is admitted to hospital with nephrotic syndrome. His labs show: Albumin: 22 g/L (normal 35-50 g/L) Total phenytoin: 8 mg/L SCr: 95 umol/L Using the Sheiner-Tozer equation, what is the corrected phenytoin concentration?

Incorrect · Answer: B

PEBC Yield: Highcalculationmonitoring

This result would be obtained by using the wrong equation form or by calculating the denominator incorrectly as 0.44 without adding the 0.1 constant.

B) (Correct)

Correct. Sheiner-Tozer: Ccorrected = Cmeasured / ((0.2 x Albumin) + 0.1). Convert albumin: 22 g/L = 2.2 g/dL. Ccorrected = 8 / ((0.2 x 2.2) + 0.1) = 8 / (0.44 + 0.1) = 8 / 0.54 = 14.8 mg/L, approximately 14.5 mg/L. This falls within the therapeutic range (10-20 mg/L).

This result would be obtained if the albumin value is incorrectly entered as 32 g/L or if a conversion error is made. The correct calculation uses albumin of 2.2 g/dL in the Sheiner-Tozer equation.

This result arises from using albumin of 22 directly in g/L without converting to g/dL, or from miscalculating the denominator as 0.49 instead of 0.54.

Question 9Therapeutic Drug Monitoring

RT is a 55 year old male with a seizure disorder maintained on phenytoin 400 mg po daily. He has cirrhosis and CKD stage 3b (eGFR 38 mL/min/1.73m^2). His labs show: Albumin: 28 g/L (normal 35-50 g/L) Total phenytoin: 12 mg/L Which of the following factors does NOT increase the free (unbound) fraction of phenytoin in this patient?

Incorrect · Answer: C

PEBC Yield: Highmonitoringdrug-interaction

Valproic acid competes with phenytoin for albumin binding sites and also inhibits phenytoin metabolism. This drug-drug interaction increases the free fraction of phenytoin.

Uremia from renal failure displaces phenytoin from albumin binding sites through accumulation of uremic toxins. This increases the free fraction even when total levels appear therapeutic.

C) (Correct)

Correct. Induction of CYP2C9 increases the rate of phenytoin metabolism, which would lower total and free phenytoin concentrations proportionally. It does not alter protein binding or increase the free fraction. Factors that increase the free fraction are those affecting protein binding: hypoalbuminemia, uremia, and displacing drug interactions.

Hypoalbuminemia directly reduces protein binding sites for phenytoin (92% albumin-bound). With fewer binding sites, the free fraction increases, which is why the Sheiner-Tozer correction is needed.

Question 10Steady-State & Non-Linear Kinetics

A drug has a half-life of 8 hours. A patient begins taking the drug on a fixed-dose schedule. Approximately how long will it take to reach steady-state plasma concentrations?

Incorrect · Answer: B

PEBC Yield: Highcalculationmonitoring

This range corresponds to 6 to 7 half-lives, by which time steady state has already been established. While the drug is at steady state during this period, it is reached earlier at 4 to 5 half-lives.

B) (Correct)

Correct -- steady state is reached in approximately 4 to 5 half-lives. With a half-life of 8 hours, this equals 32 to 40 hours (4 x 8 = 32 hours; 5 x 8 = 40 hours). At this point, the rate of drug input equals the rate of elimination.

This range corresponds to 8 to 9 half-lives. Steady state was already achieved approximately 30 hours earlier, making this an overestimate of the time required.

This range corresponds to 2 to 3 half-lives, at which point the drug has only accumulated to 75-87.5% of steady state. Clinically meaningful steady state requires 4 to 5 half-lives.

Want the full bank?

These are a sample. The full bank adds full-length cases and timed mock exams.

Sample full case

One patient with several linked questions, the format the real exam uses for case clusters.

HM is a 58-year-old man admitted to your infectious-disease service with MRSA bacteremia from a port-catheter infection. He weighs 72 kg, has a serum creatinine of 85 µmol/L (CrCl ≈ 95 mL/min — normal renal function, with some augmented clearance expected given his young age and active infection), and has been started on vancomycin 1 g IV q8h, infused over 1 hour. After his first dose on hospital day 1, the clinical pharmacist draws the following therapeutic drug monitoring levels (no additional vancomycin given between the two levels):

Time	Setting	Concentration
11:00	2 hours after the end of the 1-hour infusion (≈ post-distribution)	30 mg/L
18:00	9 hours after the end of the 1-hour infusion	7 mg/L

Required PK equations:

Equation	Variable
k = ln(C₁ / C₂) / (t₂ − t₁)	elimination rate constant
t½ = 0.693 / k	half-life
t = ln(C₀ / C) / k	time to reach target concentration

The pharmacist needs to calculate HM's vancomycin elimination half-life before adjusting the regimen.

Question 1ADME & Compartment Models

Using the two levels above, what is HM's vancomycin elimination half-life (t½), rounded to the nearest 0.5 hour?

Incorrect · Answer: A

PEBC Yield: Highelimination-rate-constanthalf-life-calculationaugmented-renal-clearancevancomycin-tdm

A) (Correct)

Correct. Δt = 18:00 − 11:00 = 7 hours. Elimination rate constant k = ln(30/7) / 7 = ln(4.29) / 7 = 1.455 / 7 ≈ 0.208 hr⁻¹. Half-life t½ = 0.693 / k = 0.693 / 0.208 ≈ 3.33 hours, which rounds to 3.5 hours. This short half-life is consistent with augmented renal clearance (ARC) frequently seen in young adults with severe infection or sepsis — a clinically important scenario where standard q8–12h dosing may under-dose.

5.0 hours overstates the half-life — it would imply k ≈ 0.139 hr⁻¹, which would produce a trough much higher than 7 mg/L at 9 hours post-infusion. The arithmetic does not support this answer.

7.0 hours overstates the half-life — k would be ≈ 0.099 hr⁻¹ and the 9-hour level would predict a concentration of ~12 mg/L, not 7. The observed 7 mg/L excludes this option.

12.0 hours corresponds to moderately impaired renal clearance and is incompatible with HM's normal CrCl and the observed rate of fall (30 → 7 mg/L over 7 hours).

Question 2ADME & Compartment Models

Three days later, HM's follow-up trough returns at 32 mg/L. The team holds the next scheduled vancomycin dose and asks when a repeat level should be drawn before restarting therapy. Using HM's calculated k ≈ 0.208 hr^-1 and the same first-order elimination assumption, approximately how long will it take for the concentration to fall to 20 mg/L?

Incorrect · Answer: B

PEBC Yield: Moderatetarget-concentration-timingfirst-order-eliminationredraw-planningvancomycin-tdm

1 hour is too short for the observed k and the 32 → 20 mg/L drop. ln(32/20)/k would only equal 1 hr if k ≈ 0.47 hr⁻¹ — more than double HM's actual rate.

B) (Correct)

Correct. Using the first-order elimination equation t = ln(C₀ / C) / k: t = ln(32 / 20) / 0.208 = ln(1.6) / 0.208 = 0.470 / 0.208 ≈ 2.26 hours, which rounds to 2.3 hours. This is the correct time to plan a redraw if the clinician wants to confirm entry into the <20 mg/L range before the next dose. Note: one half-life (3.5 h) would drop the level to 16 mg/L, which is below the threshold — so the level crosses the 20 mg/L threshold noticeably earlier than one half-life.

4.5 hours overstates the drop time. At t = 4.5 h the predicted concentration is C = 32 × e^(−0.208 × 4.5) = 32 × 0.393 ≈ 12.6 mg/L — the level has already fallen well past 20 mg/L by then. Drawing at 4.5 h provides late confirmation, not threshold detection.

7 hours (~2 half-lives) would predict C ≈ 32 × 0.25 = 8 mg/L — far below the 20 mg/L threshold. The 'two-t½-rule' is used for re-assessing steady-state after interval changes, not for projecting threshold-crossing timing.

Question 3ADME & Compartment Models

HM's MRSA bacteremia is being managed with intermittent vancomycin dosing. The team is choosing among practical intervals before the next dose is entered, and no new drug level is available yet. Using HM's calculated elimination rate constant (k ≈ 0.208 hr^-1) and a predicted post-distribution peak of 30 mg/L after a 1 g dose, approximately what is the maximum dosing interval that keeps the concentration at or above 10 mg/L before the next dose?

Incorrect · Answer: B

PEBC Yield: Moderatedosing-interval-calculationtarget-trough-maintenanceaugmented-renal-clearanceinterval-adjustment

Continuous infusion is one option for vancomycin but is not required for a patient with a 3.5-hour half-life — 5-hour intermittent dosing is clinically manageable. The distractor exaggerates the PK consequence of ARC.

B) (Correct)

Correct. Maximum interval to reach exactly the 10 mg/L trough starting from a 30 mg/L peak: t = ln(30 / 10) / k = ln(3) / 0.208 = 1.099 / 0.208 ≈ 5.28 hours, rounded to q5h for clinical planning. In practice this patient with ARC will require an approximately q6h dosing interval or a continuous infusion to maintain trough concentrations of 10–20 mg/L. This calculation is what flags standard q8–12h regimens as under-dosing in ARC.

q8h is the conventional starting interval for normal renal function but overshoots the trough target in ARC. At 8 hours post-peak, C = 30 × e^(−0.208 × 8) = 30 × 0.190 ≈ 5.7 mg/L — below the 10 mg/L threshold. Using q8h in this patient would leave him sub-therapeutic for 2–3 hours of every dosing cycle.

q12h dosing produces concentrations far below target in ARC. At 12 hours post-peak, C = 30 × e^(−0.208 × 12) ≈ 2.5 mg/L — essentially zero coverage for the last third of the interval. Using q12h here would be clinically inappropriate.

Full-length cases like this, across every PEBC domain, live in the question bank.

Frequently asked questions

Is pharmacokinetics high yield on the PEBC exam?: Yes, and more than it looks, because the same concepts drive therapeutic drug monitoring and renal dosing across many other topics. Half-life, steady state, drug monitoring, and interactions show up both directly and woven into clinical questions.
What pharmacokinetics topics should I focus on for the PEBC?: Focus on half-life and steady state, loading versus maintenance dosing, therapeutic drug monitoring for the narrow-therapeutic-index drugs, and enzyme induction versus inhibition. Being comfortable with these makes both the dedicated questions and the dosing questions elsewhere easier.
Do I need to do calculations for pharmacokinetics on the PEBC?: Some, yes. Expect to apply the core relationships, such as estimating a level at steady state or adjusting a dose, so practice the math and always carry your units. The concepts matter as much as the arithmetic, since many questions are about interpreting a level rather than computing one.
How should I study pharmacokinetics for the PEBC?: Master the core relationships between half-life, volume of distribution, and clearance, learn the therapeutic drug monitoring rules, and practice the calculations.