Wattle Pharmacy Prep

Cardiovascular pharmacology
Practice questions with explanations

Cardiovascular pharmacology belongs to Pharmacology and toxicology, which makes up about 15% of the Overseas Pharmacist Readiness Assessment (OPRA®). Answer each question yourself before opening the explanation.

1. Which property of aspirin explains the once-daily dosing for antiplatelet effect despite a short half-life?

  1. It has a long half-life
  2. Irreversible COX-1 acetylation lasts the platelet's lifespan, so daily dosing simply covers newly formed platelets
  3. It is a modified-release formulation
  4. It accumulates in platelets
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B. Irreversible COX-1 acetylation lasts the platelet's lifespan, so daily dosing simply covers newly formed platelets

About ten per cent of platelets are replaced daily, so a small daily dose maintains near-complete inhibition of the population. This also explains why aspirin's effect persists for days after stopping and why enteric coating changes absorption without altering the duration of platelet inhibition.

2. What is the mechanism by which ACE inhibitors lower blood pressure?

  1. They block calcium entry into vascular smooth muscle
  2. They inhibit renin release from the kidney
  3. They block conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone release, and they raise bradykinin
  4. They block angiotensin II receptors directly
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C. They block conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone release, and they raise bradykinin

Angiotensin-converting enzyme also degrades bradykinin, so inhibiting it both reduces angiotensin II and allows bradykinin to accumulate, which contributes to vasodilation and to the cough and angioedema. Sartans block the AT1 receptor without affecting bradykinin, aliskiren inhibits renin directly, and calcium channel blockers act on vascular smooth muscle.

3. What is the mechanism of spironolactone, and what limits its use?

  1. Carbonic anhydrase inhibition limited by acidosis
  2. Mineralocorticoid receptor antagonism, limited by hyperkalaemia and by antiandrogenic effects such as gynaecomastia
  3. Loop diuretic action limited by ototoxicity
  4. Thiazide-like action limited by hyperglycaemia
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B. Mineralocorticoid receptor antagonism, limited by hyperkalaemia and by antiandrogenic effects such as gynaecomastia

Blocking aldosterone reduces sodium retention and potassium loss, reduces cardiac fibrosis, and improves survival in heart failure with reduced ejection fraction. The dose-limiting problems are hyperkalaemia, especially with an ACE inhibitor or renal impairment, and cross-reactivity at androgen and progesterone receptors causing gynaecomastia. Eplerenone is more selective and avoids the latter.

These are 3 of the 40 questions on cardiovascular pharmacology in the app.

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More topics in Pharmacology and toxicology

Adverse drug reactions · Analgesics and anti-inflammatories · Antimicrobial pharmacology · Autonomic pharmacology · Chemotherapy and immunomodulators · CNS pharmacology · Endocrine pharmacology · Respiratory and gastrointestinal pharmacology · Toxicology and antidotes