How to use these pharmacology practice questions
These questions cover core pharmacology rather than a named national examination. They are written in single-best-answer style and test the decisions that commonly distinguish recall from applied understanding: mechanism, pharmacokinetics, adverse effects, interactions and safe prescribing.
Choose an answer in each question, then read the explanation immediately afterwards. For every error, identify the type of mistake:
- Mechanism error: you selected the wrong target or pathway.
- Application error: you knew the fact but did not apply it to the case.
- Safety error: you missed toxicity, contraindication or monitoring.
- Kinetics error: you confused absorption, distribution, metabolism, elimination or receptor behaviour.
The explanations use standard pharmacology principles. Always check local product information and prescribing guidance for doses, contraindications and monitoring requirements.
Pharmacology practice questions
Question 1 — drug metabolism and interactions
This tests whether you can connect an enzyme interaction with a clinically important change in drug exposure. Answer the question before reading the explanation.
A patient taking warfarin is prescribed trimethoprim–sulfamethoxazole for a urinary tract infection. Five days later, the INR is substantially higher than the patient's previous result. Which explanation is most likely?
A patient taking warfarin is prescribed trimethoprim–sulfamethoxazole for a urinary tract infection. Five days later, the INR is substantially higher than the patient's previous result. Which explanation is most likely?
The correct answer is inhibition of warfarin metabolism, with a possible reduction in vitamin K production by the intestinal flora. The result is increased anticoagulant effect and a higher INR. The strongest distractor is enzyme induction: induction generally lowers exposure over time, whereas inhibition raises exposure.
The important reasoning is not simply that the INR rose after a new medicine. Sulfamethoxazole can inhibit CYP2C9-mediated warfarin metabolism, while antibiotic effects on gut bacteria may further reduce vitamin K availability. In practice, the patient needs prompt review and INR monitoring rather than an assumption that the interaction is harmless.
Question 2 — receptor pharmacology
This tests the effect of a competitive antagonist on a full agonist dose–response curve.
A reversible competitive antagonist is added to a tissue preparation containing a full agonist. What change is expected?
A reversible competitive antagonist is added to a tissue preparation containing a full agonist. What change is expected?
A reversible competitive antagonist causes a parallel rightward shift: more agonist is needed to produce the same response, but a sufficiently high agonist concentration can still reach the original maximum response. The strongest distractor is a reduced maximum response, which is typical of a non-competitive or insurmountable antagonism rather than simple reversible competition.
This distinction is frequently examined because it separates potency from efficacy. The agonist's apparent potency falls, but its efficacy is unchanged. A fall in the maximum response points instead towards an insurmountable antagonist, irreversible binding, or loss of functional receptors.
Question 3 — adverse drug effects
This tests recognition of a characteristic adverse effect and its mechanism.
A patient develops a persistent dry cough several weeks after starting an antihypertensive. Which drug is the most likely cause?
A patient develops a persistent dry cough several weeks after starting an antihypertensive. Which drug is the most likely cause?
Ramipril is an ACE inhibitor. ACE inhibition reduces breakdown of bradykinin and related peptides, which can produce a persistent dry cough. The strongest distractor is losartan: an angiotensin receptor blocker acts downstream of ACE and is much less associated with this bradykinin-mediated cough.
Do not explain this adverse effect as a direct increase in angiotensin II. ACE inhibitors reduce angiotensin II formation and also reduce bradykinin breakdown. If an ACE inhibitor is stopped because of cough, the choice of an alternative depends on the patient's clinical circumstances and local guidance.
Question 4 — pharmacokinetics
This tests the meaning of zero-order elimination.
Which statement best describes a drug eliminated by zero-order kinetics over the relevant concentration range?
Which statement best describes a drug eliminated by zero-order kinetics over the relevant concentration range?
In zero-order elimination, elimination pathways are saturated and a constant amount is removed per unit time. The strongest distractor is first-order elimination, in which a constant fraction is removed per unit time and the half-life is usually concentration-independent. In zero-order elimination, small dose increases can cause disproportionately large concentration increases.
Phenytoin is a classic example of capacity-limited elimination over part of its therapeutic range. This is why concentration changes should not be assumed to follow a simple proportional relationship with dose. Always interpret drug concentrations with the dose, timing of sampling, adherence, formulation and clinical response.
Question 5 — antimicrobial pharmacology
This tests a major toxicity associated with an antibiotic class.
Which adverse-effect combination is most characteristic of gentamicin?
Which adverse-effect combination is most characteristic of gentamicin?
Gentamicin, an aminoglycoside, is associated with nephrotoxicity and ototoxicity. The strongest distractor is tendon rupture, which is associated with fluoroquinolones rather than aminoglycosides. Renal function and, when indicated, drug concentrations are important parts of safe use.
The class clue is useful: aminoglycosides bind the bacterial 30S ribosomal subunit and have concentration-dependent antibacterial activity, but their toxicity limits use. Risk is affected by renal function, treatment duration and exposure to other nephrotoxic or ototoxic medicines.
Question 6 — antidotes
This tests whether you can match an anticoagulant with its reversal agent.
A patient has serious bleeding while receiving unfractionated heparin. Which medicine directly neutralises the anticoagulant effect?
A patient has serious bleeding while receiving unfractionated heparin. Which medicine directly neutralises the anticoagulant effect?
Protamine sulfate binds and neutralises unfractionated heparin. The strongest distractor is vitamin K: it supports synthesis of vitamin K-dependent clotting factors and is used for vitamin K antagonists, not as the direct reversal agent for unfractionated heparin. Reversal decisions also depend on bleeding severity and local protocols.
An answer that merely says “give an antidote” misses the pharmacological matching step. Keep the pairs separate in revision: unfractionated heparin–protamine, vitamin K antagonists–vitamin K-based reversal strategies, dabigatran–idarucizumab, and factor Xa inhibitor reversal according to the medicine, indication and local guidance.
Question 7 — toxicity and electrolytes
This tests a clinically important factor that increases digoxin toxicity.
Which abnormality increases the risk of digoxin toxicity at a given digoxin concentration?
Which abnormality increases the risk of digoxin toxicity at a given digoxin concentration?
Hypokalaemia increases digoxin binding to the sodium–potassium ATPase and increases toxicity risk. The strongest distractor is hyperkalaemia: it may occur in acute severe digoxin poisoning because of pump inhibition, but it does not increase digoxin binding in the same way as hypokalaemia in chronic exposure. Clinical assessment and ECG findings remain essential.
This is a good example of why a serum concentration is not interpreted in isolation. Renal impairment, interacting medicines and electrolyte abnormalities can change risk even when the measured concentration does not look extreme. Look for gastrointestinal, visual and cardiac features as well as the laboratory result.
Question 8 — glucocorticoids
This tests the mechanism behind a common long-term glucocorticoid safety issue.
Why should long-term systemic prednisolone generally be reduced gradually rather than stopped suddenly?
Why should long-term systemic prednisolone generally be reduced gradually rather than stopped suddenly?
Exogenous glucocorticoid suppresses hypothalamic CRH and pituitary ACTH, which can reduce adrenal cortisol production. Sudden withdrawal after prolonged treatment may therefore precipitate adrenal insufficiency. The strongest distractor is permanent receptor blockade: that is not the mechanism of steroid withdrawal.
The need for tapering depends on factors such as dose, duration, treatment pattern and the patient's condition. Do not turn this principle into an automatic schedule: the prescribing clinician should follow the indication and current local guidance, particularly if the patient is acutely unwell.
Question 9 — diabetes medicines
This tests the immediate adverse effect most directly linked to insulin excess.
Which adverse effect is most directly caused by an excessive dose of insulin?
Which adverse effect is most directly caused by an excessive dose of insulin?
Excess insulin increases glucose uptake and suppresses hepatic glucose output, causing hypoglycaemia. The strongest distractor is hypercalcaemia, which is not a characteristic direct effect of insulin excess. The response to suspected hypoglycaemia depends on consciousness, ability to swallow and the clinical setting.
A complete answer links the drug to the physiological change: insulin lowers circulating glucose by increasing uptake and reducing hepatic glucose production. When revising, separate predictable dose-related effects from immunological reactions and from complications of the underlying disease.
Question 10 — folate rescue
This tests the purpose of folinic acid in methotrexate treatment.
What is the main pharmacological rationale for giving folinic acid after methotrexate in situations where rescue is required?
What is the main pharmacological rationale for giving folinic acid after methotrexate in situations where rescue is required?
Folinic acid is a reduced folate. It can replenish usable folate pools and bypass the inhibited dihydrofolate reductase step, helping rescue normal cells after methotrexate exposure. The strongest distractor is blocking renal secretion: delayed methotrexate clearance is managed with urgent specialist treatment and supportive measures, not by folinic acid through that mechanism.
The key distinction is between folic acid supplementation used in some treatment regimens and folinic acid rescue after significant methotrexate exposure or high-dose therapy. Timing, dose and route are clinically important, so follow the relevant protocol rather than applying a memorised generic schedule.
What to do with your errors
Ten questions are enough to expose patterns, but not enough to prove mastery. After marking, group errors by mechanism rather than simply counting the total score. A learner who scores eight out of ten but misses both pharmacokinetics questions needs a different next session from one who misses two antidote questions.
A useful review sequence is:
- State the drug or class involved.
- Name the molecular target or physiological process.
- Predict the main clinical effect.
- Add the important toxicity, interaction or monitoring point.
- Re-answer the question without looking at the options.
A question set on this topic can be organised into a board so that mechanisms, adverse effects, kinetics and antidotes are kept separate. A board on this topic ends up looking like this:
The percentage here should be read as performance on the platform's practice work, not as a result from any external examination. The most useful next step is to convert the lowest section into short retrieval questions with one answer each.
When the same mark is lost twice, reduce the error to one precise prompt rather than rereading an entire chapter. For example, do not write “revise anticoagulants”. Write the question that would have prevented the error:
You lost this mark twice: which reversal agent directly neutralises unfractionated heparin?
Answer the remediation prompt aloud, then explain why the nearest distractor is wrong. That second step checks whether you understand the distinction or have only memorised a pair of words.
How MySummaries helps
MySummaries can turn your own pharmacology notes, lecture slides and photographed revision pages into a focused board, then generate question drills, spaced-repetition cards and written practice marked against that material. For this task, use the weak areas to decide which section to revise next, and keep missed questions in the remediation tray rather than restarting the whole topic. Start at MySummaries.