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Pharmacology medical question bank

Practise every pharmacology topic with explained SBAs.

Recall Engine has 650+ pharmacology questions across 30+ topics in 10+ body systems. Every question explains each option.

questions
650+
topics
30+
topic notes
30+
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Pharmacology by body system

Pharmacology has 30+ topics in 10+ body systems. Each section shows how many questions it has and every topic it covers.

Cardiovascular

40+ questions across 2 topics. It also has 2 topic notes.

  • Antiarrhythmics
  • Antihypertensive drugs: targets and adverse effects

Respiratory

8 questions across 1 topic. It also has 1 topic note.

  • Respiratory pharmacology

Gastrointestinal and liver

20+ questions across 1 topic. It also has 1 topic note.

  • Gastrointestinal drugs: acid, emesis, and bowel

Kidney and urinary

10+ questions across 1 topic. It also has 1 topic note.

  • Diuretics: nephron sites and electrolytes

Endocrine and metabolic

80+ questions across 5 topics. It also has 5 topic notes.

  • Adrenal and autonomic drugs
  • Diabetes drugs: choice and special situations
  • Glucose-lowering drugs and insulin profiles
  • Pituitary and growth hormone drugs
  • Thyroid drugs

Nervous system

40+ questions across 1 topic. It also has 1 topic note.

  • Movement disorder, myasthenia, and MS drugs

Mental health and behaviour

70+ questions across 3 topics. It also has 3 topic notes.

  • Overdose and withdrawal: drug treatment
  • Psychotropic drugs: uses and adverse effects
  • Rapid tranquillisation

Blood and cancer

100+ questions across 7 topics. It also has 7 topic notes.

  • Anticancer drug toxicities
  • Antimetabolites
  • Cancer drug resistance
  • DNA-directed cytotoxic drugs
  • Microtubule-targeting drugs
  • Systemic anticancer therapy: intent and regimens
  • Targeted cancer drugs

Infection and immunity

100+ questions across 8 topics. It also has 8 topic notes.

  • Antibacterial drugs
  • Antibiotic stewardship
  • Antibiotics: classes and choice
  • Antibiotics: classes, targets, and resistance
  • Antimicrobial resistance
  • Antimicrobial resistance and stewardship
  • Antiviral drugs: targets and selectivity
  • Dental abscess, aspiration pneumonia, and antibiotic prescribing

General principles

80+ questions across 4 topics. It also has 4 topic notes.

  • Drug-receptor interactions: agonists and antagonists
  • Fundamentals of pharmacology
  • GI tract absorption and renal excretion of drugs
  • Safer prescribing: prescription writing and information sources

Multisystem and acute care

30+ questions across 3 topics. It also has 3 topic notes.

  • Analgesics: NSAIDs, paracetamol, and opioids
  • Prescription writing: legal elements and errors
  • Safe prescribing

Pharmacology sample questions

These 3 are published pharmacology questions shown exactly as students see them. Open an answer to see why it is right and why every other option is wrong.

Question 1 · Pharmacology, Preclinical

A patient has an infection with Pseudomonas aeruginosa. Which of these drugs has no activity against it?

  1. A. Ciprofloxacin
  2. B. Levofloxacin
  3. C. Moxifloxacin
  4. D. Gentamicin
  5. E. Meropenem
Show the answer and explanation

Answer: C. Moxifloxacin

Quinolones are good against resistant Gram negatives, but moxifloxacin has no activity against Pseudomonas. Aminoglycosides cover pseudomonas and meropenem is among the broadest-spectrum beta-lactams.

Why the other options are wrong

  • A. Ciprofloxacin: Quinolones are good against resistant Gram negatives, though resistance may be a problem.
  • B. Levofloxacin: Quinolones are good against resistant Gram negatives, though resistance may be a problem.
  • D. Gentamicin: Aminoglycosides have good Gram-negative and pseudomonas activity.
  • E. Meropenem: Meropenem is among the broadest-spectrum beta-lactams, good for resistant Gram negatives.

Key point: Moxifloxacin has no activity against Pseudomonas.

References

Question 2 · Pharmacology, Preclinical

A synchronised tumour culture is exposed briefly to a nucleotide analogue. Cells incorporating labelled thymidine show the greatest loss of viability, whereas quiescent cells are less affected. Which property best explains this pattern?

  1. A. Intracellular methotrexate polyglutamation
  2. B. Competition from endogenous dCTP
  3. C. Dihydrofolate reductase inhibition
  4. D. Dependence on S-phase DNA synthesis
  5. E. Asparagine depletion outside tumour cells
Show the answer and explanation

Answer: D. Dependence on S-phase DNA synthesis

Thymidine incorporation identifies DNA replication rather than spindle formation. Antimetabolites preferentially affect cells engaged in DNA synthesis during S phase. The observations should be interpreted at this specific mechanistic level; the alternative processes require their own distinguishing findings.

Why the other options are wrong

  • A. Intracellular methotrexate polyglutamation: Addition of glutamate residues promotes intracellular retention and activity of methotrexate derivatives. This does not explain the decisive finding here: thymidine incorporation identifies DNA replication rather than spindle formation.
  • B. Competition from endogenous dCTP: An increased endogenous nucleotide pool can oppose incorporation or action of a competing cytidine analogue. This does not explain the decisive finding here: thymidine incorporation identifies DNA replication rather than spindle formation.
  • C. Dihydrofolate reductase inhibition: Methotrexate reduces regeneration of tetrahydrofolate, impairing folate-dependent nucleotide synthesis. This does not explain the decisive finding here: thymidine incorporation identifies DNA replication rather than spindle formation.
  • E. Asparagine depletion outside tumour cells: Asparaginase lowers extracellular asparagine, exploiting limited synthesis by susceptible lymphoblasts. This does not explain the decisive finding here: thymidine incorporation identifies DNA replication rather than spindle formation.

Key point: Antimetabolites preferentially affect cells engaged in DNA synthesis during S phase.

References

Question 3 · Pharmacology, Preclinical

A tumour culture initially arrests after platinum exposure, then activates caspases and fragments its DNA. Which downstream response accounts for the transition from growth arrest to cell loss?

  1. A. Platinum-DNA adduct formation
  2. B. DNA intercalation
  3. C. Topoisomerase II cleavage-complex trapping
  4. D. Apoptotic response to irreparable DNA damage
  5. E. Covalent DNA cross-link formation
Show the answer and explanation

Answer: D. Apoptotic response to irreparable DNA damage

Caspase activation and fragmentation indicate apoptosis after unresolved injury. Cytotoxic DNA damage can engage programmed cell death when damage exceeds cellular repair capacity. The observations should be interpreted at this specific mechanistic level; the alternative processes require their own distinguishing findings.

Why the other options are wrong

  • A. Platinum-DNA adduct formation: Cisplatin forms platinum-DNA adducts, commonly intrastrand links, that distort DNA and inhibit replication. This does not explain the decisive finding here: caspase activation and fragmentation indicate apoptosis after unresolved injury.
  • B. DNA intercalation: Dactinomycin intercalates into DNA and interferes particularly with RNA synthesis. This does not explain the decisive finding here: caspase activation and fragmentation indicate apoptosis after unresolved injury.
  • C. Topoisomerase II cleavage-complex trapping: Etoposide interferes with topoisomerase II-mediated DNA break repair, promoting persistent strand breaks. This does not explain the decisive finding here: caspase activation and fragmentation indicate apoptosis after unresolved injury.
  • E. Covalent DNA cross-link formation: Alkylating agents can form covalent DNA links that interfere with replication and transcription. This does not explain the decisive finding here: caspase activation and fragmentation indicate apoptosis after unresolved injury.

Key point: Cytotoxic DNA damage can engage programmed cell death when damage exceeds cellular repair capacity.

References

More preclinical disciplines

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