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Systemic Pharmacology II > Midterm 1 Drugs > Flashcards

Midterm 1 Drugs Flashcards

1
Q

Magnesium

A

Other Anti-Arrhythmic Drugs MOA: unknown

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2
Q

Nebivolol

A

Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

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3
Q

Spironolactone

A

Potassium-Sparing Diuretics MOA: Act on the collecting tubule/duct; Blocks aldosterone receptors and prevents production of proteins that stimulate Na/K exchange sites of the collecting tubules

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4
Q

Dabigatran (Pradaxa)

A

Anticoagulants MOA: Direct thrombin inhibitor that are competitive and reversible. (Thrombin, when present, causes the conversion of fibrinogen to fibrin to form a stable clot)

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5
Q

Gemfibrozil

A

Fibrates

MOA: Increase the expression of GENES coding for proteins responsible for lipoprotein structure and function, which causes a decrease in triglyceride concentrations and increased HDL level (used to treat increased triglyceride levels)

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6
Q

Prazosin

A

Alpha Blockers MOA: Competitive block of alpha 1 receptors to result in a relaxation of arterial and venous smooth muscle. Vasodilation decreases peripheral vascular resistance and decreases BP

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7
Q

Fondaparinux

A

Factor Xa Inhibitors MOA: Selectively inhibit Factor Xa in the clotting cascade

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8
Q

Doxazosin

A

Alpha Blockers MOA: Competitive block of alpha 1 receptors to result in a relaxation of arterial and venous smooth muscle. Vasodilation decreases peripheral vascular resistance and decreases BP

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9
Q

Niacin

A

Other Hyperlipidemia Drugs

MOA: Strongly inhibits lipolysis in adipose tissue, increases secretion of tissue plasminogen activator and lowers level of plasma fibrinogen (reverses some endothelial cell dysfunction), may prevent liver from removing HDL from the blood

Most effective agent for increasing HDL levels

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10
Q

Nitroprusside

A

Parenteral Agents MOA: Causes release of NO with result of increased intracellular cGMP and dilates arterioles and veins

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11
Q

Fenoldopam

A

Parenteral Agents MOA: Peripheral dopamine-1 receptor agonist Relaxes mainly the renal and mesenteric arterial vessels and increases renal blood flow

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12
Q

Lidocaine

A

Class 1 - Sodium Channel Blockers (Type IB) MOA: Shortens phase 3 repolarization in ventricular muscle

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13
Q

Methyldopa

A

Centrally-acting Alpha-2 Agonists MOA: Decrease sympathetic output and reduces NE release

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14
Q

Pentoxifylline

A

Treatment of Sickle Cell Anemia MOA: Improves RBC flexibility and reduced blood viscosity

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15
Q

Colestipol

A

Bile Acid Sequestrants

MOA: BInd to bile acids and bile salts in the small intestine, so the liver must then increase the conversion of cholesterol to bile acids (so increase cell surface LDL receptors, thus used to treat high LDL level)

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16
Q

Chlorthalidone

A

Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter

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17
Q

Erythropoietin

A

Treatment of Anemia MOA: a protein that regulates RBC proliferation and differentiation in the kidney

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18
Q

Argatroban

A

Anticoagulants MOA: Direct thrombin inhibitor that are competitive and reversible. (Thrombin, when present, causes the conversion of fibrinogen to fibrin to form a stable clot)

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19
Q

Nicardipine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

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20
Q

Streptokinase

A

Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot

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21
Q

Fenofibrate

A

Fibrates

MOA: Increase the expression of GENES coding for proteins responsible for lipoprotein structure and function, which causes a decrease in triglyceride concentrations and increased HDL level (used to treat increased triglyceride levels)

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22
Q

Isradipine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

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23
Q

Propranolol

A

Class II - Beta-adrenoreceptor Blockers MOA: Diminish phase 4 depolarization in the SA and AV node

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24
Q

Esmolol

A

Class II - Beta-adrenoreceptor Blockers MOA: Diminish phase 4 depolarization in the SA and AV node

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25
Q

Acebutolol

A

Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

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26
Q

Methazolamide

A

Carbonic Anhydrase Inhibitor MOA: Prevent carbonic anhydrase from catalyzing the reaction that form bicarbonate and decrease the kidney’s ability to exchange Na for H

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27
Q

Vitamin K

A

Treatment of Bleeding MOA: Antagonizes agents that interfere with Vitamin K (like Warfain!)

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28
Q

Acetazolamide

A

Carbonic Anhydrase Inhibitor MOA: Prevent carbonic anhydrase from catalyzing the reaction that form bicarbonate and decrease the kidney’s ability to exchange Na for H

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29
Q

Candesartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

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30
Q

Dobutamine

A

Inotropes (Beta-adrenergic agonists) MOA: Cause positive inotropic effects and vasodilation; increase cAMP which activates protein kinase, and protein kinase increases calcium influx into cells

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31
Q

Adenosine

A

Other Anti-Arrhythmic Drugs MOA: Activates an inward rectifier K current and inhibits Ca current; Marked hyperpolarization and suppression of Ca-dependent action potentials; also directly inhibits AV nodal conduction and increases the AV nodal refractory period when given as a bolus dose

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32
Q

Digoxin

A

Inotropes (Cardiac glycosides) MOA: Inhibits the ability of the monocyte to actively pump Na from the cell

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33
Q

Epleronone

A

Potassium-Sparing Diuretics MOA: Act on the collecting tubule/duct; Blocks aldosterone receptors and prevents production of proteins that stimulate Na/K exchange sites of the collecting tubules

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34
Q

Flecainide

A

Class 1 - Sodium Channel Blockers (Type IC) MOA: Markedly shows Phase 0 depolarization in ventricular muscle (same as IA but NO class III activity)

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35
Q

Fosinopril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

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36
Q

Milrinone

A

Inotropes (Phosphodiesterase inhibitors) MOA: Prevent hydrolysis of cAMP, Increase activity of calcium channel causing greater influx of Ca and also cause vasodilation

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37
Q

Ethacrynic acid

A

Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl

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38
Q

Supplements

A

Treatment of Anemia Iron (ferrous suldate), folic acid, Vitamin B12

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39
Q

Rivaroxaban

A

Factor Xa Inhibitors MOA: Selectively inhibit Factor Xa in the clotting cascade

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40
Q

Ticagrelor

A

Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)

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41
Q

Dipyridamole

A

Anti-platelet Inhibitors MOA: coronary vasodilator that increases intracellular levels of cAMP to result in decreased thromboxane A2 levels and decreased platelet adhesion

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42
Q

Disopyramide

A

Class 1 - Sodium Channel Blockers (Type IA) MOA: Slows phase 0 depolarization in ventricular muscle fibers (Metabolites show class III activity which slows Phase 3 of the AP)

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43
Q

Desirudin

A

Anticoagulants MOA: Direct thrombin inhibitor that are competitive and reversible. (Thrombin, when present, causes the conversion of fibrinogen to fibrin to form a stable clot)

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44
Q

Hydroxyurea

A

Treatment of Sickle Cell Anemia MOA: Increases fetal HB levels, diluting the normal Hb-S

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45
Q

Cholestyramine

A

Bile Acid Sequestrants

MOA: BInd to bile acids and bile salts in the small intestine, so the liver must then increase the conversion of cholesterol to bile acids (so increase cell surface LDL receptors, thus used to treat high LDL level)

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46
Q

Propranolol

A

Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

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47
Q

Quinapril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

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48
Q

Amlodipine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

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49
Q

Alteplase

A

Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot

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50
Q

Tocainide

A

Class 1 - Sodium Channel Blockers (Type IB) MOA: Shortens phase 3 repolarization in ventricular muscle

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51
Q

Furosemide

A

Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl

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52
Q

Perindopril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

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53
Q

Diltiazem

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

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54
Q

Captopril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

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55
Q

Lepirudin

A

Anticoagulants MOA: Direct thrombin inhibitor that are competitive and reversible. (Thrombin, when present, causes the conversion of fibrinogen to fibrin to form a stable clot)

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56
Q

Felodipine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

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57
Q

Sotalol

A

Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers

58
Q

Ezetimibe

A

Cholesterol Absorption Inhibitor

MOA: Inhibits the absorption of dietary and biliary cholesterol in the small intestine, which decrease the delivery of intestinal cholesterol to the liver and reduces hepatic cholesterol stores and increase clearance of cholesterol from blood

59
Q

Ranolazine

A

Sodium (NA) Channel MOA: Inhibits the late phase of the Na current, and reduces intracellular sodium and calcium overload Improves diastolic function

60
Q

Verapamil

A

Class IV - Calcium Channel Blockers MOA: Inhibits action potential in the SA and AV nodes

61
Q

Moexipril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

62
Q

Hydrochlorothiazide (HCTZ)

A

Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter

63
Q

Eptifibatide

A

Anti-platelet Inhibitors MOA: Binds to and blocks the GP receptor

64
Q

Hydralazine

A

Vasodilators MOA: Releases NO

65
Q

Trandolapril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

66
Q

Atenolol

A

Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

67
Q

Inamrione

A

Inotropes (Phosphodiesterase inhibitors) MOA: Prevent hydrolysis of cAMP, Increase activity of calcium channel causing greater influx of Ca and also cause vasodilation

68
Q

Colesevelam

A

Bile Acid Sequestrants

MOA: BInd to bile acids and bile salts in the small intestine, so the liver must then increase the conversion of cholesterol to bile acids (so increase cell surface LDL receptors, thus used to treat high LDL level)

69
Q

Isosorbide mononitrate

A

Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP

70
Q

Lovastatin

A

HMG CoA Reductase Inhibitors

MOA: Inhibits the first comitted enzymatic step of cholesterol synthesis,

Analogs of HMG and competes with HMG for the HMG CoA reductase enzyme, causing a lowering of circulating LDL level

71
Q

Cilazapril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

72
Q

Lisinopril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

73
Q

Nifedipine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

74
Q

Dofetilide

A

Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers

75
Q

Eprosartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

76
Q

Urokinase

A

Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot

77
Q

Bivalirudin

A

Anticoagulants MOA: Direct thrombin inhibitor that are competitive and reversible. (Thrombin, when present, causes the conversion of fibrinogen to fibrin to form a stable clot)

78
Q

Metolazone

A

Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter

79
Q

Clonidine

A

Centrally-acting Alpha-2 Agonists MOA: Decrease sympathetic output and reduces NE release

80
Q

Bisoprolol

A

Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

81
Q

Tirofiban

A

Anti-platelet Inhibitors MOA: Binds to and blocks the GP receptor

82
Q

Warfarin

A

Anticoagulants MOA: Vitamin K antagonist; Inhibits vitamin K epoxide reductase, which prevents the regeneration of Vit K and results in the production of clotting factors with diminished activity

83
Q

Labetalol

A

Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

84
Q

Aminodarone

A

Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers

85
Q

Protamine

A

Treatment of Bleeding MOA: Antagonizes heparin and forms a complex

86
Q

Dopamine

A

Inotropes (Beta-adrenergic agonists) MOA: Cause positive inotropic effects and vasodilation; increase cAMP which activates protein kinase, and protein kinase increases calcium influx into cells

87
Q

Nisoldopine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

88
Q

Carvedilol

A

Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

89
Q

Aliskiren

A

Renin Inhibitor MOA: Directly inhibits renin

90
Q

Simvastatin

A

HMG CoA Reductase Inhibitors

MOA: Inhibits the first comitted enzymatic step of cholesterol synthesis,

Analogs of HMG and competes with HMG for the HMG CoA reductase enzyme, causing a lowering of circulating LDL level

91
Q

Pitavastatin

A

HMG CoA Reductase Inhibitors

MOA: Inhibits the first comitted enzymatic step of cholesterol synthesis,

Analogs of HMG and competes with HMG for the HMG CoA reductase enzyme, causing a lowering of circulating LDL leve

92
Q

Ramipril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

93
Q

Procainamide

A

Class 1 - Sodium Channel Blockers (Type IA) MOA: Slows phase 0 depolarization in ventricular muscle fibers (Metabolites show class III activity which slows Phase 3 of the AP)

94
Q

Clopidogrel

A

Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)

95
Q

Propafenone

A

Class 1 - Sodium Channel Blockers (Type IC) MOA: Markedly shows Phase 0 depolarization in ventricular muscle (same as IA but NO class III activity)

96
Q

Darbepoetin

A

Treatment of Anemia MOA: Long-acting version of darbopoetin

97
Q

Telmisartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

98
Q

Aminocaproic Acid

A

Treatment of Bleeding MOA: Inhibits plasminogen activation

99
Q

Metroprolol

A

Class II - Beta-adrenoreceptor Blockers MOA: Diminish phase 4 depolarization in the SA and AV node

100
Q

Diltiazem

A

Class IV - Calcium Channel Blockers MOA: Inhibits action potential in the SA and AV nodes

101
Q

Reteplase

A

Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot

102
Q

Eicosapentaenioc acid

A

Omega 3 Fatty Acids

103
Q

Fluvastatin

A

HMG CoA Reductase Inhibitors

MOA: Inhibits the first comitted enzymatic step of cholesterol synthesis,

Analogs of HMG and competes with HMG for the HMG CoA reductase enzyme, causing a lowering of circulating LDL level

104
Q

Indapamide

A

Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter

105
Q

Ibutilide

A

Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers

106
Q

Heparin (high molecular weight protein)

A

Anticoagulants MOA: Binds to antithrombin III, leads to rapid inactivation of Thrombin and Factor Xa (antithrombin III activity is normally very slow)

107
Q

Isosorbide dinitrate

A

Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP

108
Q

Nadolol

A

Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

109
Q

Digoxin

A

Other Anti-Arrhythmic Drugs MOA: Shortens refractory period in myocardial cells and prolongs refractory period in the AV node

110
Q

Benazepril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

111
Q

Mexiletine

A

Class 1 - Sodium Channel Blockers (Type IB) MOA: Shortens phase 3 repolarization in ventricular muscle

112
Q

Cilostazol

A

Anti-platelet Inhibitors MOA: Inhibits PDE III which ultimately increases cAMP levels (to result in decreased thromboxane A2 levels and decreased platelet adhesion)

113
Q

Olmesartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

114
Q

Valsartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

115
Q

Quinidine

A

Class 1 - Sodium Channel Blockers (Type IA) MOA: Slows phase 0 depolarization in ventricular muscle fibers (Metabolites show class III activity which slows Phase 3 of the AP)

116
Q

Rosuvastatin

A

HMG CoA Reductase Inhibitors

MOA: Inhibits the first comitted enzymatic step of cholesterol synthesis,

Analogs of HMG and competes with HMG for the HMG CoA reductase enzyme, causing a lowering of circulating LDL level

117
Q

Abciximab

A

Anti-platelet Inhibitors MOA: Binds to GP receptor and blocks the binding of fibrinogen

118
Q

Bumetanide

A

Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl

119
Q

Potassium

A

Other Anti-Arrhythmic Drugs MOA: Either too much or too little potassium can cause arrhythmia

120
Q

Aspirin (ASA)

A

Anti-platelet Inhibitors MOA: Inhibits COX-1 (which shifts the balance of chemical mediators to favor prostacyclin and impedes platelet aggregation

121
Q

Nitroglycerin

A

Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP

122
Q

Irbesartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

123
Q

Ticlopidine

A

Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)

124
Q

Minoxidil

A

Vasodilators MOA: Hyperpolarizes smooth muscle by opening potassium channels

125
Q

Apixaban

A

Factor Xa Inhibitors MOA: Selectively inhibit Factor Xa in the clotting cascade

126
Q

Atorvastatin

A

HMG CoA Reductase Inhibitors

MOA: Inhibits the first comitted enzymatic step of cholesterol synthesis,

Analogs of HMG and competes with HMG for the HMG CoA reductase enzyme, causing a lowering of circulating LDL level

127
Q

Mannitol

A

Osmotic Diuretics MOA: Filtered through the glomerulus and carries water with them

128
Q

Prasugrel

A

Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)

129
Q

Docosahexaenoic acid

A

Omega 3 Fatty Acids

130
Q

Losartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

131
Q

Verapamil

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

132
Q

Enalapril

A

ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)

133
Q

Dronedarone

A

Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers

134
Q

Clevidipine

A

Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax

135
Q

Dalteparin

A

Anticoagulants (Low Molecular Weight Forms of Heparin/ LMWHs) MOA: LMWHs binds to antithrombin III complex which ONLY inactivates Factor Xa

136
Q

Tenecteplase

A

Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot

137
Q

Enoxaparin

A

Anticoagulants (Low Molecular Weight Forms of Heparin/ LMWHs) MOA: LMWHs binds to antithrombin III complex which ONLY inactivates Factor Xa

138
Q

Azilsartan

A

Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels

139
Q

Metoprolol

A

Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

140
Q

Torsemide

A

Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl

141
Q

Terazosin

A

Alpha Blockers MOA: Competitive block of alpha 1 receptors to result in a relaxation of arterial and venous smooth muscle. Vasodilation decreases peripheral vascular resistance and decreases BP

142
Q

Esmolol

A

Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin

Systemic Pharmacology II (5 decks)

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