Cardiovascular Drugs Actions

Question 1

Fibrates

Answer 1

decrease circulating VLDL and triglyceride. Only small effect on LDL but increase protective HDL. Increase hepatic LDL uptake.

Question 2

Statins

Answer 2

HMG-CoA reductase (rate determining step) inhibitors, increase LDL receptor expression, increase clearance of LDL from circulation, improve endothelial function, inhibit inflammation, stabilise plaques, inhibit thrombus formation

Question 3

Nitrates

Answer 3

Metabolised to NO. Activates guanylyl cyclase = increased cGMP = relaxation of smooth muscle. Dilate veins so decrease venous return. Reduce PVR and after load on arterioles. Improve supply to coronary arteries.

Question 4

B-adrenoreceptor antagonists

Answer 4

cardiac receptors = reduce heart rate and therefore O2 demand. Renal = reduce blood volume by reducing renin and RAAS activation, preload reduced, decrease O2 demand. Initial vasoconstriction, final vasodilation.

Question 5

Calcium channel blockers

Answer 5

blocks Ca2+ entry into myocyte, reduce availability to contractile apparatus. Reduce force of contraction = reduce O2 demand. Vasodilation. Decrease conduction through SAN and AVN.

Question 6

COX inhibitors

Answer 6

Inhibits cOX, prevents TxA2 formation and therefore platelet activation inhibited

Question 7

P2Y12 inhibitors

Answer 7

blocks effect of ADP and prevents platelet activation

Question 8

Thrombin-receptor antagonsist

Answer 8

prevent activation of PAR-1 receptors on platelets

Question 9

IV Heparin

Answer 9

promotes formation of endogenous antithrombin 3, inhibits factor Xa and thrombin = no formation of fibrin to stabilise platelet plug

Question 10

Warfarin

Answer 10

inhibits VitK reductase so Vit K cannot be reduced. No Vit K = no gamma-carboxyglutamic acid (AA) which is a component of factors II, VII, IX and X

Question 11

Fibrinolytic

Answer 11

accelerate conversion of plasminogen to plasmin = degrading fibrin in thrombus

Question 12

Cardiac glycosides

Answer 12

inhibit NA+/K+ pump in cardiac myocytes by binding to NA +/K+ ATPase. This means more Ca2+ remains in sarcoplasmic reticulum = increase force of heart contraction, positive inotrope, block/slow AV conduction, increase ectopic pacemaker activity

Question 13

Loop Diuretic

Answer 13

block Na+/K+/Cl- in ascending loop of Henlé so water is lost. Reduces blood volume. Reduced pre-load

Question 14

Aldosterone Receptor Antagonist

Answer 14

blocks effects of aldosterone on Na/K reabsorption, reduce fibrosis of heart muscle

Question 15

ACE inhibitors

Answer 15

angiotensin 1 not converted to angiotensin 2, increase bradykinin, dilate arteries

Question 16

Angiotensin 2 receptor blockers (ARBs)

Answer 16

effects of angiotensin 2 not felt

Question 17

Vasodilators

Answer 17

IM: Metabolised to NO. Activates guanylyl cyclase = increased cGMP = relaxation of smooth muscle.
Dilate veins so decrease venous return. Reduce PVR and after load

Question 18

Thiazide diuretics

Answer 18

act on DCT of nephron, loss of sodium and chloride ions, water follows, reduced blood volume. Reduce Ca2+ excretion (good for older patients at risk of osteoporosis). Dilation of veins and arteries.

Question 19

Purine nucleoside

Answer 19

acts on alpha-1 receptors in AV node (K+ channels), hyperpolarises conduction tissue, transient blockage of AV node conduction, temp blocking of re-entry through AV nod

Question 20

Membrane-stabilising anti-arrhythmic

Answer 20

blocks Na+ channels in excitable tissues so decreased excitability and cardiac conduction. -ve inotropic effect = decrease contractibility. Must be IV for VT.

Question 21

Class 3 anti-arrhythmic

Answer 21

large volume of distribution. IV infusion in emergencies. Prolongs cardiac action potential. Blocks potassium channels.

Question 22

Muscarinic antagonist

Answer 22

inhibits parasympathetic tone, CNS stimulant. Usually induces tachycardia