Cardiovascular pharmacology flashcards
20 high-yield MRCP Part 1 cards from the Intellect Medicos Cardiology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Why should adenosine be avoided in a patient with severe asthma?
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It can cause bronchospasm.
Why? Adenosine acts on adenosine receptors in the airways as well as the AV node and can trigger bronchoconstriction.
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How does adenosine terminate AV-node-dependent SVT, and which drug potentiates it?
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It stimulates A1 receptors, causing transient complete AV nodal block. Dipyridamole potentiates it (theophylline/aminophylline reduces its effect).
Why? AVNRT and AVRT use the AV node as part of the re-entry circuit, so a few seconds of block breaks the loop. Its very short half-life makes side effects brief.
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What is the mechanism of action of sacubitril in sacubitril–valsartan?
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Neprilysin inhibition, raising levels of natriuretic peptides.
Why? Neprilysin breaks down natriuretic peptides; blocking it boosts natriuresis and vasodilation. Valsartan is added to block angiotensin II, which neprilysin also degrades.
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What are the two mechanisms by which digoxin acts in AF with heart failure?
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It inhibits Na⁺/K⁺-ATPase (raising intracellular calcium → positive inotropy) and increases vagal tone (slowing AV node conduction → rate control).
Why? Because digoxin binds at the potassium site of the pump, hypokalaemia increases its effect and toxicity.
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What is the Vaughan Williams class of amiodarone and its main channel action?
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Class III — potassium channel blockade, prolonging repolarisation (and the QT interval).
Why? Amiodarone also has class I, II and IV actions, which is why it works for both atrial and ventricular arrhythmias and is the preferred antiarrhythmic in structural heart disease.
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How do P2Y12 inhibitors work, and which one is reversible?
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They block the platelet P2Y12 ADP receptor, preventing ADP-induced platelet activation. Ticagrelor is reversible; clopidogrel and prasugrel bind irreversibly.
Why? Clopidogrel and prasugrel are prodrugs that need hepatic activation; ticagrelor acts directly.
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How does fondaparinux work, and when does NICE avoid it in NSTEMI?
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It binds antithrombin to selectively inhibit factor Xa. NICE: offer it unless there is high bleeding risk or immediate angiography is planned.
Why? Unfractionated heparin is preferred if creatinine is above 265 micromol/L, because fondaparinux is renally cleared.
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What is the mechanism of action of nicorandil, and its distinctive adverse effect?
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It opens ATP-sensitive potassium channels and has a nitrate component (vasodilation). It can cause ulceration of the mouth, GI tract, anus and skin.
Why? Potassium channel opening hyperpolarises vascular smooth muscle, dilating arteries; the nitrate part dilates veins. Because of ulcer complications, MHRA (2016) made nicorandil a second-line drug for stable angina.
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How do SGLT2 inhibitors (dapagliflozin, empagliflozin) work, and name one serious adverse effect.
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They block sodium–glucose co-transporter 2 in the proximal tubule, causing glycosuria and natriuresis. Adverse effect: euglycaemic diabetic ketoacidosis (also genital infections, Fournier's gangrene).
Why? They benefit HFrEF even in people without diabetes, which is why they are part of quadruple therapy.
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Why is verapamil dangerous when combined with a beta-blocker?
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Both slow AV nodal conduction and reduce contractility, so together they can cause severe bradycardia, heart block, hypotension and asystole.
Why? Verapamil is a non-dihydropyridine L-type calcium channel blocker that acts strongly on the heart (unlike amlodipine).
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Name the classic adverse effect for each: thiazide, dihydropyridine CCB, ACE inhibitor, spironolactone.
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Thiazide — gout (also low sodium/potassium). Amlodipine — ankle swelling. ACE inhibitor — dry cough. Spironolactone — gynaecomastia (and hyperkalaemia).
Why? ACE inhibitor cough is caused by bradykinin accumulation, as ACE also breaks down bradykinin; ARBs rarely cause it.
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How do nitrates relieve angina, and which drug class must not be taken with them?
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They release nitric oxide → guanylate cyclase → cGMP → smooth muscle relaxation, mainly venodilation (reduced preload). Do not combine with PDE-5 inhibitors (for example sildenafil).
Why? Both raise cGMP, so together they can cause profound hypotension.
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Which blood tests are needed before starting amiodarone and every 6 months during treatment?
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Thyroid function tests and liver function tests.
Why? Amiodarone contains iodine and can cause hypo- or hyperthyroidism, and it can cause hepatotoxicity. A baseline chest X-ray and potassium are also checked.
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A patient on digoxin and warfarin is started on amiodarone. What interactions must be managed?
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Amiodarone raises digoxin levels (halve the digoxin dose) and potentiates warfarin (reduce the dose and monitor INR closely).
Why? Amiodarone inhibits P-glycoprotein and CYP enzymes. It has a very long half-life, so interactions can persist for weeks after stopping.
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What is the specific treatment for atropine-resistant bradycardia and hypotension from beta-blocker overdose?
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IV glucagon.
Why? Glucagon raises cardiac cAMP through its own receptor, bypassing the blocked beta-receptor. The RCUK bradyarrhythmia algorithm lists it for beta-blocker or calcium channel blocker overdose.
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What is the specific antidote for life-threatening digoxin toxicity?
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Digoxin-specific antibody fragments (Fab).
Why? They are used for life-threatening arrhythmias or severe hyperkalaemia. Toxicity features include nausea, confusion, yellow-green vision (xanthopsia), AV block and bidirectional VT.
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Name two factors that precipitate digoxin toxicity.
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Any two of: hypokalaemia, hypomagnesaemia, hypercalcaemia, renal impairment, or interacting drugs such as amiodarone or verapamil.
Why? Low potassium increases digoxin binding to Na⁺/K⁺-ATPase. Digoxin is renally cleared, and amiodarone and verapamil raise its plasma level.
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Where and how do thiazide and thiazide-like diuretics (e.g. indapamide) act?
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They inhibit the Na⁺–Cl⁻ co-transporter in the distal convoluted tubule.
Why? Side effects include hyponatraemia, hypokalaemia, hyperuricaemia (gout), hyperglycaemia and hypercalcaemia, because they reduce urinary calcium loss.
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Where and how do loop diuretics such as furosemide act?
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They inhibit the Na⁺–K⁺–2Cl⁻ co-transporter (NKCC2) in the thick ascending limb of the loop of Henle.
Why? Key side effects: hypokalaemia, hyponatraemia, hypocalcaemia, gout, and ototoxicity with high doses or rapid IV infusion, especially alongside aminoglycosides.
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Which visual side effect is characteristic of ivabradine?
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Phosphenes — transient areas of increased brightness in the visual field.
Why? Ivabradine also blocks a similar current (Ih) in retinal cells. The effect is usually mild and fades on treatment.
More Cardiology topics
- Physiology & haemodynamics
- Heart sounds, pulses & murmurs
- Valvular heart disease
- ECG & arrhythmias
- Inherited & sudden cardiac death syndromes
- Ischaemic heart disease
- Heart failure & cardiomyopathies
- Pericardial disease
- Endocarditis & rheumatic fever
- Congenital heart disease
- Hypertension, aorta & emboli
- Lipids & statins