Cardiology Flashcards

1
Q

What is the MOA of aspirin?

A

Antiplatelet - inhibits COX-1 (cyclo-oxygenase), which prevents production of thromboxane A2 and inhibits platelet aggregation.
(Also has NSAID properties and can be used to reduce pain and inflammation).

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2
Q

What is aspirin prescribed for?

A

Secondary prevention following MI, TIA and stroke and for patients with angina or peripheral vascular disease.

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3
Q

What is the MOA of clopidogrel, prasugrel and ticagrelor?

A

Antiplatelet drug - ADP receptor antagonists that inhibit the binding of ADP to the P2Y12 receptor on platelets, which inhibits the activation of the GPIIb/IIIa complex and inhibits platelet aggregation.

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4
Q

What is the MOA of warfarin?

A

Inhibits the Vitamin K-dependent synthesis of clotting factors II, VII, IX and X, as well as protein C, protein S and protein Z

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5
Q

What is warfarin mainly prescribed for?

A

Treatment of AF and in people who have had blood clots.

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6
Q

What is the MOA of apixaban?

A

DOAC - inhibits Xa, leading to reduced clotting

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7
Q

Why are DOACs increasingly used over warfarin?

A

Don’t require monitoring in the way that warfarin does (weekly INR checks).

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8
Q

What is the MOA of beta blockers?

A

Block B-adrenoceptors, blocking B1 causes decrease in inotropy and chronotropy, blocking B2 causes peripheral vasoconstriction and bronchoconstriction

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9
Q

What is the MOA of bisoprolol vs propranolol?

A

Bisoprolol - B1 selective beta blocker

Propranolol - non-selective beta blocker

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10
Q

What are the uses of beta-blockers?

A

Angina, hypertension, post MI, heart failure

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11
Q

Name some contraindications for beta blockers

A

Severe asthma/COPD

Heart block

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12
Q

Name some side effects of beta blockers

A

Lethargy
Erectile dysfunction
Headaches
Nightmares

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13
Q

What are the uses of ACEi?

A

Hypertension
Heart failure
Post-MI

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14
Q

What is the MOA of ACEi such as ramipril?

A

Inhibit ACE enzyme, which inhibits conversion of angiotensin I to angiotensin II. Absence of potent vasoconstrictor angiotensin II and aldosterone leads to peripheral vasodilation and a decrease in BP

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15
Q

What is the most common side effect of ACEi and why does this occur?

A

Dry cough

ACEi bind to substrate instead of bradykinin, leads to excess bradykinin.

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16
Q

What type of diuretic is furosemide and how does it work?

A

Loop diuretic
Inhibits co-transporter Na/2Cl/K in loop of henle, leads to reduced ion reabsorption and therefore reduced water reabsorption, causing a diuretic

17
Q

What is the MOA of adenosine?

A

Blocks AVN conduction, it is commonly used to treat certain forms of supraventricular tachycardia.

18
Q

What is the MOA of ivabradine?

A

Inhibits the funny current in cardiac pacemaker cells leading to a slower pulse,it is used to treat heart failure.

19
Q

What is the MOA of digoxin?

A

Increases the force of contraction of cardiac muscle by blocking the Na+/K+ pump, is used to treat heart failure or AF as it helps make the heart beat stronger and more regular.

20
Q

What is the MOA of the anticoagulant dabigatran?

A

Direct thrombin inhibitor

21
Q

What is the MOA of the anticoagulant fondaparinux?

A

Xa inhibitor, reduces clotting.

22
Q

What is the meaning of inotropy and chronotropy?

A

Inotropy - force of contractility

Chronotropy - rate of contraction

23
Q

What is the main use of furosemide?

A

Heart failure

24
Q

What is the MOA of thiazide-like diuretics such as bendroflumethiazide and indapamide?

A

Inhibits NaCl transporter in DCT, leads to a natiuresis and diuresis.

25
Q

What is the MOA of K+ sparing diuretics e.g. Spironolactone, amiloride? What is the difference between the actions of these 2 examples?

A

Spironolactone is an aldosterone antagonist that directly blocks aldosterone receptors.
Amiloride inhibits ENaC.
Both lead to a natiuresis and diuresis.

26
Q

What is the MOA of GTN spray?

A

It’s a nitrate that cause vasodilation of veins and large arteries, reducing pulmonary vascular resistance and decreasing the preload.

27
Q

What is the MOA of calcium channel blockers?

A

Decrease cell entry of Ca2+ via L-type voltage-gated Ca2+ channels in smooth muscle, promoting coronary and peripheral artery vasodilation. There are 3 classes: dihydropyridines, phenylalkylamines and benzothiazepines.

28
Q

What is the difference in dihydropyridine and non-dihydropyridine calcium channel blockers? Give examples of drugs.

A

Dihydropyridines e.g. Amlodipine - mainly peripheral and coronary vasodilators that cause a reflex tachycardia so are often given with beta blockers.
Non-dihydropyridines e.g. Verapamil, diltiazem - have vasodilation effects as well as slowing conduction at the SAN and AVN, never give with beta blockers.

29
Q

What is digoxin toxicity?

A

Digoxin toxicity/poisoning occurs when someone takes too much digoxin. It can lead to electrolyte imbalances and arrhythmias.

30
Q

What is the MOA of class I antiarrhythmic drugs (Vaughn Williams classification) e.g. Lidocaine, flecanide?

A

Block sodium channels, reducing fast depolarisation of cardiac myocytes.

31
Q

What is the MOA of class III antiarrhythmics e.g. Amiodarone?

A

Prolongs the action potential, reducing the possibility of tachyarrhythmias.