Midterm 1 Drugs Flashcards
(142 cards)
1
Q
Magnesium
A
Other Anti-Arrhythmic Drugs MOA: unknown
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
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
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)
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)
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
7
Q
Fondaparinux
A
Factor Xa Inhibitors MOA: Selectively inhibit Factor Xa in the clotting cascade
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
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
10
Q
Nitroprusside
A
Parenteral Agents MOA: Causes release of NO with result of increased intracellular cGMP and dilates arterioles and veins
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
12
Q
Lidocaine
A
Class 1 - Sodium Channel Blockers (Type IB) MOA: Shortens phase 3 repolarization in ventricular muscle
13
Q
Methyldopa
A
Centrally-acting Alpha-2 Agonists MOA: Decrease sympathetic output and reduces NE release
14
Q
Pentoxifylline
A
Treatment of Sickle Cell Anemia MOA: Improves RBC flexibility and reduced blood viscosity
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)
16
Q
Chlorthalidone
A
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
17
Q
Erythropoietin
A
Treatment of Anemia MOA: a protein that regulates RBC proliferation and differentiation in the kidney
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)
19
Q
Nicardipine
A
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
20
Q
Streptokinase
A
Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot
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)
22
Q
Isradipine
A
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
23
Q
Propranolol
A
Class II - Beta-adrenoreceptor Blockers MOA: Diminish phase 4 depolarization in the SA and AV node
24
Q
Esmolol
A
Class II - Beta-adrenoreceptor Blockers MOA: Diminish phase 4 depolarization in the SA and AV node
25
Acebutolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
26
Methazolamide
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
27
Vitamin K
Treatment of Bleeding MOA: Antagonizes agents that interfere with Vitamin K (like Warfain!)
28
Acetazolamide
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
29
Candesartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
30
Dobutamine
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
31
Adenosine
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
32
Digoxin
Inotropes (Cardiac glycosides) MOA: Inhibits the ability of the monocyte to actively pump Na from the cell
33
Epleronone
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
34
Flecainide
Class 1 - Sodium Channel Blockers (Type IC) MOA: Markedly shows Phase 0 depolarization in ventricular muscle (same as IA but NO class III activity)
35
Fosinopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
36
Milrinone
Inotropes (Phosphodiesterase inhibitors) MOA: Prevent hydrolysis of cAMP, Increase activity of calcium channel causing greater influx of Ca and also cause vasodilation
37
Ethacrynic acid
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
38
Supplements
Treatment of Anemia Iron (ferrous suldate), folic acid, Vitamin B12
39
Rivaroxaban
Factor Xa Inhibitors MOA: Selectively inhibit Factor Xa in the clotting cascade
40
Ticagrelor
Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)
41
Dipyridamole
Anti-platelet Inhibitors MOA: coronary vasodilator that increases intracellular levels of cAMP to result in decreased thromboxane A2 levels and decreased platelet adhesion
42
Disopyramide
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)
43
Desirudin
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)
44
Hydroxyurea
Treatment of Sickle Cell Anemia MOA: Increases fetal HB levels, diluting the normal Hb-S
45
Cholestyramine
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)
46
Propranolol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
47
Quinapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
48
Amlodipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
49
Alteplase
Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot
50
Tocainide
Class 1 - Sodium Channel Blockers (Type IB) MOA: Shortens phase 3 repolarization in ventricular muscle
51
Furosemide
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
52
Perindopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
53
Diltiazem
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
54
Captopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
55
Lepirudin
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)
56
Felodipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
57
Sotalol
Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers
58
Ezetimibe
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
Ranolazine
Sodium (NA) Channel MOA: Inhibits the late phase of the Na current, and reduces intracellular sodium and calcium overload Improves diastolic function
60
Verapamil
Class IV - Calcium Channel Blockers MOA: Inhibits action potential in the SA and AV nodes
61
Moexipril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
62
Hydrochlorothiazide (HCTZ)
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
63
Eptifibatide
Anti-platelet Inhibitors MOA: Binds to and blocks the GP receptor
64
Hydralazine
Vasodilators MOA: Releases NO
65
Trandolapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
66
Atenolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
67
Inamrione
Inotropes (Phosphodiesterase inhibitors) MOA: Prevent hydrolysis of cAMP, Increase activity of calcium channel causing greater influx of Ca and also cause vasodilation
68
Colesevelam
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
Isosorbide mononitrate
Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP
70
Lovastatin
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
Cilazapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
72
Lisinopril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
73
Nifedipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
74
Dofetilide
Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers
75
Eprosartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
76
Urokinase
Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot
77
Bivalirudin
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
Metolazone
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
79
Clonidine
Centrally-acting Alpha-2 Agonists MOA: Decrease sympathetic output and reduces NE release
80
Bisoprolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
81
Tirofiban
Anti-platelet Inhibitors MOA: Binds to and blocks the GP receptor
82
Warfarin
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
Labetalol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
84
Aminodarone
Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers
85
Protamine
Treatment of Bleeding MOA: Antagonizes heparin and forms a complex
86
Dopamine
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
Nisoldopine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
88
Carvedilol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
89
Aliskiren
Renin Inhibitor MOA: Directly inhibits renin
90
Simvastatin
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
Pitavastatin
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
Ramipril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
93
Procainamide
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
Clopidogrel
Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)
95
Propafenone
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
Darbepoetin
Treatment of Anemia MOA: Long-acting version of darbopoetin
97
Telmisartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
98
Aminocaproic Acid
Treatment of Bleeding MOA: Inhibits plasminogen activation
99
Metroprolol
Class II - Beta-adrenoreceptor Blockers MOA: Diminish phase 4 depolarization in the SA and AV node
100
Diltiazem
Class IV - Calcium Channel Blockers MOA: Inhibits action potential in the SA and AV nodes
101
Reteplase
Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot
102
Eicosapentaenioc acid
Omega 3 Fatty Acids
103
Fluvastatin
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
Indapamide
Thiazide Diuretics MOA: Act on the distal convoluted tubule; Inhibits the Na/Cl co-transporter
105
Ibutilide
Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers
106
Heparin (high molecular weight protein)
Anticoagulants MOA: Binds to antithrombin III, leads to rapid inactivation of Thrombin and Factor Xa (antithrombin III activity is normally very slow)
107
Isosorbide dinitrate
Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP
108
Nadolol
Beta Non-Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
109
Digoxin
Other Anti-Arrhythmic Drugs MOA: Shortens refractory period in myocardial cells and prolongs refractory period in the AV node
110
Benazepril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
111
Mexiletine
Class 1 - Sodium Channel Blockers (Type IB) MOA: Shortens phase 3 repolarization in ventricular muscle
112
Cilostazol
Anti-platelet Inhibitors MOA: Inhibits PDE III which ultimately increases cAMP levels (to result in decreased thromboxane A2 levels and decreased platelet adhesion)
113
Olmesartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
114
Valsartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
115
Quinidine
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
Rosuvastatin
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
Abciximab
Anti-platelet Inhibitors MOA: Binds to GP receptor and blocks the binding of fibrinogen
118
Bumetanide
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
119
Potassium
Other Anti-Arrhythmic Drugs MOA: Either too much or too little potassium can cause arrhythmia
120
Aspirin (ASA)
Anti-platelet Inhibitors MOA: Inhibits COX-1 (which shifts the balance of chemical mediators to favor prostacyclin and impedes platelet aggregation
121
Nitroglycerin
Organic Nitrates MOA: Enzyme activation of drug causes release of NO and NO combines with guanylyl cyclase causing an increase in cGMP
122
Irbesartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
123
Ticlopidine
Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)
124
Minoxidil
Vasodilators MOA: Hyperpolarizes smooth muscle by opening potassium channels
125
Apixaban
Factor Xa Inhibitors MOA: Selectively inhibit Factor Xa in the clotting cascade
126
Atorvastatin
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
Mannitol
Osmotic Diuretics MOA: Filtered through the glomerulus and carries water with them
128
Prasugrel
Anti-platelet Inhibitors MOA: Block ADP P2Y receptors and inhibit expression of GP receptors for fibrinogen (Prevents ADP-induced platelet aggregation)
129
Docosahexaenoic acid
Omega 3 Fatty Acids
130
Losartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
131
Verapamil
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
132
Enalapril
ACE Inhibitors MOA: Prevent the conversion of angiotension I to angiotension II and Increase levels of bradykinin (vasodilator)
133
Dronedarone
Class III - Potassium Channel Blockers MOA: Prolongs phase 3 repolarization in ventricular muscle fibers
134
Clevidipine
Calcium Channel Blockers MOA: Prevent inward movement of Ca and causes muscle to relax
135
Dalteparin
Anticoagulants (Low Molecular Weight Forms of Heparin/ LMWHs) MOA: LMWHs binds to antithrombin III complex which ONLY inactivates Factor Xa
136
Tenecteplase
Thrombolytic Agents MOA: Activate conversion of plasminogen to plasmin - hydrolyzes fibrin and dissolves clot
137
Enoxaparin
Anticoagulants (Low Molecular Weight Forms of Heparin/ LMWHs) MOA: LMWHs binds to antithrombin III complex which ONLY inactivates Factor Xa
138
Azilsartan
Angiotension-Receptor Blockers MOA: Blocks Angiotension II from binding to its receptor and thus blocking its action, BUT DOES NOT increase bradykinin levels
139
Metoprolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
140
Torsemide
Loop Diuretics MOA: Act on the ascending loop of henle; Inhibit cotransport of Na/K/2Cl
141
Terazosin
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
Esmolol
Beta 1 Selective Blockers MOA: Lower BP mainly by decreasing cardiac output, also decrease sympathetic outflow from CNS and inhibit release of renin
