MOA Flashcards

(46 cards)

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

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

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
Amplodine
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
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)
Amlodipine
27
Verapamil
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
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
Verapamil
29
Diltiazem
Inhibit Ca2+ influx through L type calcium channels (LTCC) during membrane depol of cardiac and vascular smooth muscle
30
Inhibit Ca2+ influx through L type calcium channels (LTCC) during membrane depol of cardiac and vascular smooth muscle
Diltiazem
31
Nitrates and nitrodilators
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
Metabolised to NO (potent vasodilator) which increases guanylate cyclase activity and formation of cGMP, causing activation of protein kinases that promote smooth muscle relaxation
Nitrates and nitrodilators
33
Osmotic diuretics
Freely filtered through glomerulus and not reabsorbed in PT. Osmotic force limits water reabsorption in PT (mostly), tAL & CD
34
Freely filtered through glomerulus and not reabsorbed in PT. Osmotic force limits water reabsorption in PT (mostly), tAL & CD
Osmotic diuretic
35
Loop diuretic
Inhibits Na+/K+/Cl- (NKCC2) cotransporter on TAL by competing with Cl- for binding. NKCC2 prevented from reabsorbing 25% of filtered Na+ load
36
Inhibits Na+/K+/Cl- (NKCC2) cotransporter on TAL by competing with Cl- for binding. NKCC2 prevented from reabsorbing 25% of filtered Na+ load
Loop diuretic
37
Thiazide diuretic
Secreted in PT. Inhibits Na+/Cl- (NCC1) co transporter and reabsorption in cortical diluting segment of DT. NCC1 prevent from 5% Na+ reabsorption
38
Secreted in PT. Inhibits Na+/Cl- (NCC1) co transporter and reabsorption in cortical diluting segment of DT. NCC1 prevent from 5% Na+ reabsorption
Thiazide diuretic
39
Potassium sparing diuretic
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
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
Potassium sparing diuretic
41
Sodium channel antagonist
Blocks fast Na+ channels responsible for the rapid depol (phase 0) of cardiomyocytes
42
Blocks fast Na+ channels responsible for the rapid depol (phase 0) of cardiomyocytes
Sodium channel antagonist
43
Potassium channel antagonist
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
Blocks K+ channels involved in repol. Can also affect Na+ flux (decrease nodal rate of firing) and Ca2+ channels (affects SA and AV node)
Potassium channel antagonist
45
Cardiac glycoside
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
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
Cardiac glycoside