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Systemic Pharmacology II > Drugs to Know > Flashcards

Drugs to Know Flashcards

1
Q

Benazepril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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2
Q

Captopril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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3
Q

Enalapril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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4
Q

Fosinopril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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5
Q

Lisinopril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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6
Q

Moexipril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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7
Q

Perindopril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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8
Q

Quinapril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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9
Q

Ramipril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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10
Q

Trandolapril

A

ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II

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11
Q

Azilsartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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12
Q

Candesartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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13
Q

Eprosartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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14
Q

Irbesartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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15
Q

Losartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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16
Q

Olmesartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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17
Q

Telmisartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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18
Q

Valsartan

A

Angiotensin-Receptor Blocker- antagonist at angiotensin receptor

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19
Q

Aliskiren

A

Renin Inhibitor- directly inhibits renin

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20
Q

Atenolol

A

Beta Blocker- lower BP mainly by decreasing cardiac output

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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21
Q

Bisoprolol

A

Beta Blocker- lower BP mainly by decreasing cardiac output

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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22
Q

Carvedilol

A

Beta Blocker- lower BP mainly by decreasing cardiac output

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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23
Q

Labetalol

A

Beta Blocker- lower BP mainly by decreasing cardiac output

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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24
Q

Metoprolol

A

Beta Blocker- lower BP mainly by decreasing cardiac output;

Class II antiarrhythmic- depresses conductivity of the SA node; prolongs AV conduction; inhibits phase 4 depolarization in node; decrease heart rate and contractility

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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25
Q

Nadolol

A

Beta Blocker- lower BP mainly by decreasing cardiac output

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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26
Q

Nebivolol

A

Beta Blocker- lower BP mainly by decreasing cardiac output

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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27
Q

Propranolol

A

Beta Blocker- lower BP mainly by decreasing cardiac output;

Class II antiarrhythmic- depresses conductivity of the SA node; prolongs AV conduction; inhibits phase 4 depolarization in node; decrease heart rate and contractility

for angina: lower rate and force of heart contraction; suppress activation of the heart by blocking beta-1 receptors; reduce work of the heart by decreasing HR, contractility, cardiac output, and blood pressure

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28
Q

Chlorthalidone

A

Thiazide Diuretic- inhibits Na/Cl transporter in distal convoluted tubule; increases concentration of Na and Cl in the tubular fluid, increased excretion of Na and Cl, loss of K, loss of Mg, decreased urinary calcium excretion, reduced peripheral vascular resistance

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29
Q

Hydrochlorothiazide

A

Thiazide Diuretic- inhibits Na/Cl transporter in distal convoluted tubule; increases concentration of Na and Cl in the tubular fluid, increased excretion of Na and Cl, loss of K, loss of Mg, decreased urinary calcium excretion, reduced peripheral vascular resistance

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30
Q

Metolazone

A

Thiazide Diuretic- inhibits Na/Cl transporter in distal convoluted tubule; increases concentration of Na and Cl in the tubular fluid, increased excretion of Na and Cl, loss of K, loss of Mg, decreased urinary calcium excretion, reduced peripheral vascular resistance

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31
Q

Bumetanide

A

Loop Diuretic- major action on ascending limb of loop of Henle; inhibit co-transport of Na/K/2Cl; reabsorption is decreased, increased Na and K excretion, increased Ca excretion, decrease renal vascular resistance and increased renal blood flow, increased prostaglandin synthesis

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32
Q

Furosemide

A

Loop Diuretic- major action on ascending limb of loop of Henle; inhibit co-transport of Na/K/2Cl; reabsorption is decreased, increased Na and K excretion, increased Ca excretion, decrease renal vascular resistance and increased renal blood flow, increased prostaglandin synthesis

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33
Q

Torsemide

A

Loop Diuretic- major action on ascending limb of loop of Henle; inhibit co-transport of Na/K/2Cl; reabsorption is decreased, increased Na and K excretion, increased Ca excretion, decrease renal vascular resistance and increased renal blood flow, increased prostaglandin synthesis

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34
Q

Amiloride

A

Potassium Sparing Diuretic, Sodium channel blocker-
acts in the collecting tubule, inhibits Na reabsorption and K excretion; blocks sodium transport channels, resulting in decreased sodium/potassium exchange

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35
Q

Eplerenone

A

Potassium Sparing Diuretic, Aldosterone Antagonist-
acts in the collecting tubule, inhibits Na reabsorption and K excretion; blocks aldosterone receptors, preventing production of proteins that stimulate Na/K exchange sites of the collecting tubules, prevents Na reabsorption and K/H secretion (Na remains to be eliminated, K is reabsorbed into blood)

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36
Q

Spironolactone

A

Potassium Sparing Diuretic, Aldosterone Antagonist-
acts in the collecting tubule, inhibits Na reabsorption and K excretion; blocks aldosterone receptors, preventing production of proteins that stimulate Na/K exchange sites of the collecting tubules, prevents Na reabsorption and K/H secretion (Na remains to be eliminated, K is reabsorbed into blood)

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37
Q

Triamterene

A

Potassium Sparing Diuretic, Sodium channel blocker-
acts in the collecting tubule, inhibits Na reabsorption and K excretion; blocks sodium transport channels, resulting in decreased sodium/potassium exchange

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38
Q

Acetazolamide

A

Carbonic Anhydrase Inhibitor- inhibits carbonic anhydrase in proximal tubule; decreases the kidney’s ability to exchange Na for H, so Na is excreted at a higher rate

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39
Q

Methazolamide

A

Carbonic Anhydrase Inhibitor- inhibits carbonic anhydrase in proximal tubule; decreases the kidney’s ability to exchange Na for H, so Na is excreted at a higher rate

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40
Q

Mannitol

A

Osmotic Diuretic- filtered through glomerulus and carry water with them; increase water excretion but not Na

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41
Q

Amlodipine

A

Vasodilator: Calcium Channel Blocker, Dihydropyridine-

blocks inward movement of calcium

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42
Q

Diltiazem

A

Vasodilator: Calcium Channel Blocker, Non- Dihydropyridine-
blocks inward movement of calcium

Class IV Antiarrhythmic: inhibit action potential in nodes (highly calcium dependent); AV node conduction prolonged, SA node slowed; refractory period prolonged

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43
Q

Felodipine

A

Vasodilator: Calcium Channel Blocker, Dihydropyridine-

blocks inward movement of calcium

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44
Q

Isradipine

A

Vasodilator: Calcium Channel Blocker, Dihydropyridine-

blocks inward movement of calcium

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45
Q

Nifedipine

A

Vasodilator: Calcium Channel Blocker, Dihydropyridine-

blocks inward movement of calcium

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46
Q

Verapamil

A

Vasodilator: Calcium Channel Blocker, Non- Dihydropyridine-
blocks inward movement of calcium

Class IV Antiarrhythmic: inhibit action potential in nodes (highly calcium dependent); AV node conduction prolonged, SA node slowed; refractory period prolonged

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47
Q

Hydralazine

A

Direct Vasodilator- produce relaxation of vascular smooth muscle by releasing nitric oxide

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48
Q

Minoxidil

A

Direct Vasodilator- produce relaxation of vascular smooth muscle; hyperpolarizes smooth muscle by opening potassium channels

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49
Q

Fenoldopam

A

Parenteral Agent- peripheral dopamine-1 receptor and alpha-2 receptor agonist; relaxes mainly the renal and mesenteric arterial vessels and increases renal blood flow

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50
Q

Nitroprusside

A

Parenteral Agent- causes release of NO with result of increased intracellular cGMP; dilates both arterioles and veins

51
Q

Clonidine

A

Centrally Acting Alpha-2 Agonist- acts in the vasomotor center within the medulla; decreases sympathetic outflow which decreases vascular tone and cardiac output

52
Q

Methyldopa

A

Centrally Acting Alpha-2 Agonist- acts in the vasomotor center within the medulla; decreases sympathetic outflow which decreases vascular tone and cardiac output

53
Q

Doxazosin

A

Alpha Blocker- produces competitive block of alpha 1 receptors; causes vasodilation in both arteries and veins, decreasing peripheral vascular resistance

54
Q

Prazosin

A

Alpha Blocker- produces competitive block of alpha 1 receptors; causes vasodilation in both arteries and veins, decreasing peripheral vascular resistance

55
Q

Terazosin

A

Alpha Blocker- produces competitive block of alpha 1 receptors; causes vasodilation in both arteries and veins, decreasing peripheral vascular resistance

56
Q

Digoxin

A

Inotrope, Cardiac Glycoside- inhibits the ability of the muscle cell to actively pump Na from the cell

antiarrhythmic- shortens refractory period in myocardial cells and prolongs refractory period in the AV node

57
Q

Milrinone

A

Inotrope, Phosphodiester Inhibitor- increases intracellular concentration of cAMP; increases intracellular calcium and cardiac contractility is increased

58
Q

Isosorbide Dinitrate

A

Vasodilator, organic nitrate

enzyme activation of drug causes release of nitric oxide; cause a rapid reduction in myocardial oxygen demand; relaxation of smooth muscle in arteries and veins; decreases venous return to heart; dilate coronary vasculature, increases blood supply to the heart; relieves coronary artery spasm

59
Q

Disopyramide

A

Antiarrhythmic: Class IA Na Channel Blocker

binds to sodium channels and potassium channels; inhibition of K efflux; slow the rate of rise of action potential; slows conduction (phase 0), slows repolarization (phase 3); increases duration of action potential and refractory period

60
Q

Procainamide

A

Antiarrhythmic: Class IA Na Channel Blocker

binds to sodium channels and potassium channels; inhibition of K efflux; slow the rate of rise of action potential; slows conduction (phase 0), slows repolarization (phase 3); increases duration of action potential and refractory period

61
Q

Quinidine

A

Antiarrhythmic: Class IA Na Channel Blocker

binds to sodium channels and potassium channels; inhibition of K efflux; slow the rate of rise of action potential; slows conduction (phase 0), slows repolarization (phase 3); increases duration of action potential and refractory period

62
Q

Lidocaine

A

Antiarrhythmic: Class IB Na Channel Blocker

specific for sodium channels; actually increases K efflux (increase in K leaving the cell); slow phase 0; accelerates repolarization (phase 3); decreases duration of action potential

63
Q

Mexiletine

A

Antiarrhythmic: Class IB Na Channel Blocker

specific for sodium channels; actually increases K efflux (increase in K leaving the cell); slow phase 0; accelerates repolarization (phase 3); decreases duration of action potential

64
Q

Flecainide

A

Antiarrhythmic: Class IC Na Channel Blocker

bind to sodium and potassium channels (effect on K channels is minimal); markedly depresses the rate of rise of action potential (phase 0); marked slowing of conduction with little effect on duration of action potential or refractory period

65
Q

Propafenone

A

Antiarrhythmic: Class IC Na Channel Blocker

bind to sodium and potassium channels (effect on K channels is minimal); markedly depresses the rate of rise of action potential (phase 0); marked slowing of conduction with little effect on duration of action potential or refractory period

66
Q

Esmolol

A

Class II Antiarrhythmic- depresses conductivity of the SA node; prolongs AV conduction; inhibits phase 4 depolarization in node; decrease heart rate and contractility

(Beta blocker)

67
Q

Amiodarone

A

Class III Antiarryhthmic: K channel blocker

diminish the outward potassium current during repolarization of cardiac cells; prolong the duration of the action potential (phase 3); do not alter phase 0 of depolarization or the resting membrane potential; prolong the effective refractory period

68
Q

Dofetilide

A

Class III Antiarryhthmic: K channel blocker

diminish the outward potassium current during repolarization of cardiac cells; prolong the duration of the action potential (phase 3); do not alter phase 0 of depolarization or the resting membrane potential; prolong the effective refractory period

69
Q

Dronedarone

A

Class III Antiarryhthmic: K channel blocker

diminish the outward potassium current during repolarization of cardiac cells; prolong the duration of the action potential (phase 3); do not alter phase 0 of depolarization or the resting membrane potential; prolong the effective refractory period

70
Q

Ibutilide

A

Class III Antiarryhthmic: K channel blocker

diminish the outward potassium current during repolarization of cardiac cells; prolong the duration of the action potential (phase 3); do not alter phase 0 of depolarization or the resting membrane potential; prolong the effective refractory period

71
Q

Sotalol

A

Class III Antiarryhthmic: K channel blocker

diminish the outward potassium current during repolarization of cardiac cells; prolong the duration of the action potential (phase 3); do not alter phase 0 of depolarization or the resting membrane potential; prolong the effective refractory period;

also has potent beta-blocker activity

72
Q

Adenosine

A

antiarrhythmic

activates an inward rectifier K current and inhibits calcium current; marked hyperpolarization and suppression of calcium-dependent action potentials; also directly inhibits AV nodal conduction and increases the AV nodal refractory period

73
Q

Magnesium

A

antiarrhythmic

exact MOA unknown

74
Q

Potassium

A

antiarrhythmic

either too much or too little potassium can cause arrhythmia; supplementation is aimed at balancing potassium gradients

75
Q

Isosorbide mononitrate

A

Vasodilator, organic nitrate

enzyme activation of drug causes release of nitric oxide; cause a rapid reduction in myocardial oxygen demand; relaxation of smooth muscle in arteries and veins; decreases venous return to heart; dilate coronary vasculature, increases blood supply to the heart; relieves coronary artery spasm

76
Q

Nitroglycerin

A

Vasodilator, organic nitrate

enzyme activation of drug causes release of nitric oxide; cause a rapid reduction in myocardial oxygen demand; relaxation of smooth muscle in arteries and veins; decreases venous return to heart; dilate coronary vasculature, increases blood supply to the heart; relieves coronary artery spasm

77
Q

Ranolazine

A

for angina: sodium channel blocker

inhibits the late phase of the sodium current; reduces intracellular sodium and calcium overload; improves diastolic function and improves oxygen supply

78
Q

Sildenafil

A

vasodilator: potentiate the vasodilative effect of acetylcholine

inhibits the breakdown of cGMP by type 5 phosphodiesterase

79
Q

Tadalafil

A

vasodilator: potentiate the vasodilative effect of acetylcholine

inhibits the breakdown of cGMP by type 5 phosphodiesterase

80
Q

Vardenafil

A

vasodilator: potentiate the vasodilative effect of acetylcholine

inhibits the breakdown of cGMP by type 5 phosphodiesterase

81
Q

Aspirin

A

platelet inhibitor;

inhibits COX-1, preventing the synthesis of TXA2, impeding platelet aggregation

82
Q

Clopidogrel

A

Platelet Inhibitor, ADP Receptor Blocker

when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP

83
Q

Prasugrel

A

Platelet Inhibitor, ADP Receptor Blocker

when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP

84
Q

Ticagrelor

A

Platelet Inhibitor, ADP Receptor Blocker

when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP

85
Q

Ticlopidine

A

Platelet Inhibitor, ADP Receptor Blocker

when ADP binds to platelet, GP receptors are expressed; ADP receptor blockers inhibit expression of GP receptors for fibrinogen by binding to ADP

86
Q

Abciximab

A

Platelet Inhibitor, GP Receptor Blocker

directly inhibit receptor to prevent binding of fibrinogen; platelet aggregation does not occur

87
Q

Eptifibatide

A

Platelet Inhibitor, GP Receptor Blocker

directly inhibit receptor to prevent binding of fibrinogen; platelet aggregation does not occur

88
Q

Tirofiban

A

Platelet Inhibitor, GP Receptor Blocker

directly inhibit receptor to prevent binding of fibrinogen; platelet aggregation does not occur

89
Q

Argatroban

A

Anticoagulant, Direct Thrombin Inhibitor

competitive, reversible inhibitor of thrombin

90
Q

Bivalirudin

A

Anticoagulant, Direct Thrombin Inhibitor

competitive, reversible inhibitor of thrombin

91
Q

Dabigatran

A

Anticoagulant, Direct Thrombin Inhibitor

competitive, reversible inhibitor of thrombin

92
Q

Desirudin

A

Anticoagulant, Direct Thrombin Inhibitor

competitive, reversible inhibitor of thrombin

93
Q

Lepirudin

A

Anticoagulant, Direct Thrombin Inhibitor

competitive, reversible inhibitor of thrombin

94
Q

Apixaban

A

Anticoagulant, Factor Xa Inhibitor

selectively inhibits only Factor Xa; does not have variable activity

95
Q

Fondaparinux

A

Anticoagulant, Factor Xa Inhibitor

selectively inhibits only Factor Xa; does not have variable activity

96
Q

Rivaroxaban

A

Anticoagulant, Factor Xa Inhibitor

selectively inhibits only Factor Xa; does not have variable activity

97
Q

Dalteparin

A

Anticoagulant, Low Molecular Weight Heparin

binds to antithrombin III and inactivates Factor Xa only

98
Q

Enoxaparin

A

Anticoagulant, Low Molecular Weight Heparin

binds to antithrombin III and inactivates Factor Xa only

99
Q

Heparin

A

Anticoagulant

binds to antithrombin III and increases activity; leads to rapid inactivation of thrombin and Factor Xa; antithrombin III activity is usually very slow

100
Q

Warfarin

A

Anticoagulant

Vitamin K antagonist; several protein coagulation factors require Vitamin K as a cofactor for synthesis; warfarin inhibits vitamin K epoxide reductase (enzyme that is responsible for regenerating vitamin K after reaction); results in the production of clotting factors with diminished activity

101
Q

Alteplase

A

Thrombolytic Agent- activates the conversion of plasminogen to plasmin; hydrolyzes fibrin and dissolves clots

rapidly activates plasminogen that is bound to fibrin in a thromus; no degradation of other proteins

102
Q

Reteplase

A

Thrombolytic Agent- activates the conversion of plasminogen to plasmin; hydrolyzes fibrin and dissolves clots

103
Q

Streptokinase

A

Thrombolytic Agent- activates the conversion of plasminogen to plasmin; hydrolyzes fibrin and dissolves clots

forms active complex with plasminogen; also catalyzes the degradation of fibrinogen and other clotting factors

104
Q

Tenecteplase

A

Thrombolytic Agent- activates the conversion of plasminogen to plasmin; hydrolyzes fibrin and dissolves clots

binds to fibrin and converts tissue plasminogen to plasmin; promotes fibrinolysis

105
Q

Urokinase

A

Thrombolytic Agent- activates the conversion of plasminogen to plasmin; hydrolyzes fibrin and dissolves clots

directly cleaves the bond of plasminogen to yield active plasmin

106
Q

Aminocaproic Acid

A

Treatment of bleeding- inhibits plasminogen activation

107
Q

Protamine

A

Treatment of bleeding- antagonizes heparin, forms a complex

108
Q

Atorvastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

109
Q

Fluvastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

110
Q

Lovastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

111
Q

Pitavastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

112
Q

Pravastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

113
Q

Rosuvastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

114
Q

Simvastatin

A

HMG CoA Reductase Inhibitor

inhibits the first committed enzymatic step of cholesterol synthesis; analog of HMG (precursor of cholesterol), competes with HMG for the HMG CoA reductase enzyme; end result- lowers intracellular supply of cholesterol in liver; lowered intracellular cholesterol causes hepatocyte to increase LDL receptors on the surface, internalize circulating LDL and prevent release of VLDL

115
Q

Gemfibrozil

A

Fibrate

increases expression of genes coding for lipoprotein lipase; increases oxidation of fatty acids (esp. triglycerides) in liver and muscle; VLDL decreases, slight reduction in LDL, moderate increase in HDL

116
Q

Fenofibrate

A

Fibrate

increases expression of genes coding for lipoprotein lipase; increases oxidation of fatty acids (esp. triglycerides) in liver and muscle; VLDL decreases, slight reduction in LDL, moderate increase in HDL

117
Q

Cholestyramine

A

Bile Acid Sequestrant

bind bile acids and bile salts in the small intestine (prevents reabsorption into liver); liver must then increase conversion of cholesterol to bile acids; cell surface LDL receptors increase

118
Q

Colesevelam

A

Bile Acid Sequestrant

bind bile acids and bile salts in the small intestine (prevents reabsorption into liver); liver must then increase conversion of cholesterol to bile acids; cell surface LDL receptors increase

119
Q

Colestipol

A

Bile Acid Sequestrant

bind bile acids and bile salts in the small intestine (prevents reabsorption into liver); liver must then increase conversion of cholesterol to bile acids; cell surface LDL receptors increase

120
Q

Ezetimibe

A

Cholesterol Absorption Inhibitor

inhibits absorption of cholesterol from the small intestine; decreases delivery of intestinal cholesterol to the liver; reduces hepatic cholesterol stores and increases clearance of cholesterol from blood

121
Q

Niacin

A

inhibits VLDL secretion; decreases production of LDL; increases HDL levels (decreases breakdown); increases secretion of tissue plasminogen activator and lowers level of plasma fibrinogen; reverse some endothelial cell dysfunction

122
Q

Docoshexaenoic Acid

A

Omega-3 Fatty Acid- hyperlipidemia drug

123
Q

Eicosapentaenoic Acid

A

Omega-3 Fatty Acid- hyperlipidemia drug

Systemic Pharmacology II (4 decks)

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