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Cardiac Drugs > MOA > Flashcards

MOA Flashcards

1
Q

Beta blocker

A

Inhibits binding of NA and adrenaline to B receptors. Decreases sympathetic activity causing decreased HR (-C) and force of contraction (-I) so decreases CO and BP and reduced juxtaglomerular renin secretion

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2
Q

Alpha 1 blockers

A

Inhibits binding of NA and adrenaline to alpha 1 receptor located in vascular. Prevents vasoconstriction of vessels and decreases total peripheral resistance

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3
Q

Inhibits binding of NA and adrenaline to relevant receptor located in vascular. Prevents vasoconstriction of vessels and decreases total peripheral resistance

A

Alpha 1 blockers

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4
Q

Alpha 2 blockers

A

Binding to a2 receptor reduces presynaptic Ca2+ levels in medulla and stops NA from being released

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5
Q

Binding to relevant receptor reduces presynaptic Ca2+ levels in medulla and stops NA from being released

A

Alpha 2

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6
Q

Inhibits binding of NA and adrenaline to relevant receptors. Decreases sympathetic activity causing decreased HR (-C) and force of contraction (-I) so decreases CO and BP and reduced juxtaglomerular renin secretion

A

Beta blockers

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7
Q

Ace inhibitors

A

Inhibits angiotensin converting enzyme (ACE) —> decreasing ANG2 (vasoconstrictor) levels, also prevents ACE-induced breakdown of bradykinin (vasodilator)

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8
Q

Inhibits relevant enzyme —> decreasing ANG2 (vasoconstrictor) levels, also prevents enzyme-induced breakdown of bradykinin (vasodilator)

A

ACE inhibitor

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9
Q

Angiotensin receptor blockers

A

Selectively blocks ANG2 from binding to the At1 receptor

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10
Q

Selectively blocks ANG2 from binding to the At1 receptor

A

Angiotensin receptor blocker

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11
Q

Statins: explain what HMG-CoA reductase inhibitor normally does

A

HMG-CoA reductase inhibitor (reversible and competitive) which normally converts HMG-CoA to mevalonate which can be further converted to cholesterol.

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12
Q

Statin

A

Pleiotropic effects by inhibiting cell signalling proteins: increased angiotensin and fibrinolysis, decreased platelet aggregation, anti-inflammatory, decreased cellular proliferation and growth

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13
Q

Fibrates

A

Binds to PPAR alpha located in hepatocytes, skeletal muscle, macrophages and the heart. Increases fatty acid oxidation in muscle and liver and increases lipogenesis in the liver. Lover LDL modestly by shifting hepatocyte metabolism to fatty acid oxidation

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14
Q

Binds to PPAR alpha located in hepatocytes, skeletal muscle, macrophages and the heart. Increases fatty acid oxidation in muscle and liver and increases lipogenesis in the liver. Lover LDL modestly by shifting hepatocyte metabolism to fatty acid oxidation

A

Fibrates

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15
Q

Low dose aspirin

A

Irreversibly acetylates platelet COX-1, reducing TXA2 production by the platelet

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16
Q

Irreversibly acetylates platelet COX-1, reducing TXA2 production by the platelet

A

Low dose aspirin

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17
Q

Clopidogrel

A

Non-competitively irreversibly blocks ADP receptors, preventing activation of GPIIb/IIIa (fibrinogen receptor), reducing platelet activation

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18
Q

Non-competitively irreversibly blocks ADP receptors, preventing activation of GPIIb/IIIa (fibrinogen receptor), reducing platelet activation

A

Clopidrogrel

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19
Q

Enoxaparin

A

Binds to antithrombin III and prevents factor 10a from converting prothrombin to thrombin

20
Q

Binds to antithrombin III and prevents factor 10a from converting prothrombin to thrombin

A

Enoxaparin

21
Q

Warfarin

A

Competitively inhibits vit k epoxied reductase, depleting functional reduced vit k required for gamma carboxylation of factor II, VII, IX & X, prothrombin, protein C and S

22
Q

Competitively inhibits vit k epoxied reductase, depleting functional reduced vit k required for gamma carboxylation of factor II, VII, IX & X, prothrombin, protein C and S

A

Warfarin

23
Q

Fibrinolytics

A

Catalyses the conversion of plasminogen to plasmin (serine protease) which degrades fibrin and dissolves the thrombus

24
Q

Catalyses the conversion of plasminogen to plasmin (serine protease) which degrades fibrin and dissolves the thrombus

A

Fibrinolytics

25
Q

Amplodine

A

Selectively inhibits Ca2+ influx through vascular L type Ca2+ channels (LTCC) by only binding the stabilising LTCC in their inactive forms (more often in the vasculature)

26
Q

Selectively inhibits Ca2+ influx through vascular L type Ca2+ channels (LTCC) by only binding the stabilising LTCC in their inactive forms (more often in the vasculature)

A

Amlodipine

27
Q

Verapamil

A

Selectively inhibits Ca2+ influx through cardiac L type Ca2+ channels (LTCC) by only binding to open LTCC (more often in heart) and increasing their refractory period

28
Q

Selectively inhibits Ca2+ influx through cardiac L type Ca2+ channels (LTCC) by only binding to open LTCC (more often in heart) and increasing their refractory period

A

Verapamil

29
Q

Diltiazem

A

Inhibit Ca2+ influx through L type calcium channels (LTCC) during membrane depol of cardiac and vascular smooth muscle

30
Q

Inhibit Ca2+ influx through L type calcium channels (LTCC) during membrane depol of cardiac and vascular smooth muscle

A

Diltiazem

31
Q

Nitrates and nitrodilators

A

Metabolised to NO (potent vasodilator) which increases guanylate cyclase activity and formation of cGMP, causing activation of protein kinases that promote smooth muscle relaxation

32
Q

Metabolised to NO (potent vasodilator) which increases guanylate cyclase activity and formation of cGMP, causing activation of protein kinases that promote smooth muscle relaxation

A

Nitrates and nitrodilators

33
Q

Osmotic diuretics

A

Freely filtered through glomerulus and not reabsorbed in PT. Osmotic force limits water reabsorption in PT (mostly), tAL & CD

34
Q

Freely filtered through glomerulus and not reabsorbed in PT. Osmotic force limits water reabsorption in PT (mostly), tAL & CD

A

Osmotic diuretic

35
Q

Loop diuretic

A

Inhibits Na+/K+/Cl- (NKCC2) cotransporter on TAL by competing with Cl- for binding. NKCC2 prevented from reabsorbing 25% of filtered Na+ load

36
Q

Inhibits Na+/K+/Cl- (NKCC2) cotransporter on TAL by competing with Cl- for binding. NKCC2 prevented from reabsorbing 25% of filtered Na+ load

A

Loop diuretic

37
Q

Thiazide diuretic

A

Secreted in PT. Inhibits Na+/Cl- (NCC1) co transporter and reabsorption in cortical diluting segment of DT. NCC1 prevent from 5% Na+ reabsorption

38
Q

Secreted in PT. Inhibits Na+/Cl- (NCC1) co transporter and reabsorption in cortical diluting segment of DT. NCC1 prevent from 5% Na+ reabsorption

A

Thiazide diuretic

39
Q

Potassium sparing diuretic

A

Inhibits aldosterone by competitively binding to and prevent translocation of MR in DT & CD. Binds to surface receptors on basolateral side, no access to lumen required

40
Q

Inhibits aldosterone by competitively binding to and prevent translocation of MR in DT & CD. Binds to surface receptors on basolateral side, no access to lumen required

A

Potassium sparing diuretic

41
Q

Sodium channel antagonist

A

Blocks fast Na+ channels responsible for the rapid depol (phase 0) of cardiomyocytes

42
Q

Blocks fast Na+ channels responsible for the rapid depol (phase 0) of cardiomyocytes

A

Sodium channel antagonist

43
Q

Potassium channel antagonist

A

Blocks K+ channels involved in repol. Can also affect Na+ flux (decrease nodal rate of firing) and Ca2+ channels (affects SA and AV node)

44
Q

Blocks K+ channels involved in repol. Can also affect Na+ flux (decrease nodal rate of firing) and Ca2+ channels (affects SA and AV node)

A

Potassium channel antagonist

45
Q

Cardiac glycoside

A
  1. Inhibits Na+/K+ ATPase and allows Ca2+ accumulation via NCX (Na+/Ca2+ exchanger)
  2. Increases vagal activity to heart, which reduces SA node firing and AV node conduction
46
Q
  1. Inhibits Na+/K+ ATPase and allows Ca2+ accumulation via NCX (Na+/Ca2+ exchanger)
  2. Increases vagal activity to heart, which reduces SA node firing and AV node conduction
A

Cardiac glycoside

Cardiac Drugs (6 decks)

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