Drugs to Know Flashcards
1
Q
Benazepril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
2
Q
Captopril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
3
Q
Enalapril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
4
Q
Fosinopril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
5
Q
Lisinopril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
6
Q
Moexipril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
7
Q
Perindopril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
8
Q
Quinapril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
9
Q
Ramipril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
10
Q
Trandolapril
A
ACE Inhibitor- prevents conversion of angiotensin I to angiotensin II
11
Q
Azilsartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
12
Q
Candesartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
13
Q
Eprosartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
14
Q
Irbesartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
15
Q
Losartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
16
Q
Olmesartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
17
Q
Telmisartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
18
Q
Valsartan
A
Angiotensin-Receptor Blocker- antagonist at angiotensin receptor
19
Q
Aliskiren
A
Renin Inhibitor- directly inhibits renin
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
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
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
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
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
25
Nadolol
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
26
Nebivolol
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
27
Propranolol
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
28
Chlorthalidone
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
29
Hydrochlorothiazide
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
30
Metolazone
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
31
Bumetanide
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
32
Furosemide
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
33
Torsemide
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
34
Amiloride
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
35
Eplerenone
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)
36
Spironolactone
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)
37
Triamterene
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
38
Acetazolamide
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
39
Methazolamide
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
40
Mannitol
Osmotic Diuretic- filtered through glomerulus and carry water with them; increase water excretion but not Na
41
Amlodipine
Vasodilator: Calcium Channel Blocker, Dihydropyridine-
| blocks inward movement of calcium
42
Diltiazem
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
43
Felodipine
Vasodilator: Calcium Channel Blocker, Dihydropyridine-
| blocks inward movement of calcium
44
Isradipine
Vasodilator: Calcium Channel Blocker, Dihydropyridine-
| blocks inward movement of calcium
45
Nifedipine
Vasodilator: Calcium Channel Blocker, Dihydropyridine-
| blocks inward movement of calcium
46
Verapamil
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
47
Hydralazine
Direct Vasodilator- produce relaxation of vascular smooth muscle by releasing nitric oxide
48
Minoxidil
Direct Vasodilator- produce relaxation of vascular smooth muscle; hyperpolarizes smooth muscle by opening potassium channels
49
Fenoldopam
Parenteral Agent- peripheral dopamine-1 receptor and alpha-2 receptor agonist; relaxes mainly the renal and mesenteric arterial vessels and increases renal blood flow
50
Nitroprusside
Parenteral Agent- causes release of NO with result of increased intracellular cGMP; dilates both arterioles and veins
51
Clonidine
Centrally Acting Alpha-2 Agonist- acts in the vasomotor center within the medulla; decreases sympathetic outflow which decreases vascular tone and cardiac output
52
Methyldopa
Centrally Acting Alpha-2 Agonist- acts in the vasomotor center within the medulla; decreases sympathetic outflow which decreases vascular tone and cardiac output
53
Doxazosin
Alpha Blocker- produces competitive block of alpha 1 receptors; causes vasodilation in both arteries and veins, decreasing peripheral vascular resistance
54
Prazosin
Alpha Blocker- produces competitive block of alpha 1 receptors; causes vasodilation in both arteries and veins, decreasing peripheral vascular resistance
55
Terazosin
Alpha Blocker- produces competitive block of alpha 1 receptors; causes vasodilation in both arteries and veins, decreasing peripheral vascular resistance
56
Digoxin
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
Milrinone
Inotrope, Phosphodiester Inhibitor- increases intracellular concentration of cAMP; increases intracellular calcium and cardiac contractility is increased
58
Isosorbide Dinitrate
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
Disopyramide
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
Procainamide
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
Quinidine
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
Lidocaine
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
Mexiletine
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
Flecainide
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
Propafenone
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
Esmolol
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
Amiodarone
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
Dofetilide
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
Dronedarone
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
Ibutilide
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
Sotalol
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
Adenosine
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
Magnesium
antiarrhythmic
exact MOA unknown
74
Potassium
antiarrhythmic
either too much or too little potassium can cause arrhythmia; supplementation is aimed at balancing potassium gradients
75
Isosorbide mononitrate
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
Nitroglycerin
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
Ranolazine
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
Sildenafil
vasodilator: potentiate the vasodilative effect of acetylcholine
inhibits the breakdown of cGMP by type 5 phosphodiesterase
79
Tadalafil
vasodilator: potentiate the vasodilative effect of acetylcholine
inhibits the breakdown of cGMP by type 5 phosphodiesterase
80
Vardenafil
vasodilator: potentiate the vasodilative effect of acetylcholine
inhibits the breakdown of cGMP by type 5 phosphodiesterase
81
Aspirin
platelet inhibitor;
inhibits COX-1, preventing the synthesis of TXA2, impeding platelet aggregation
82
Clopidogrel
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
Prasugrel
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
Ticagrelor
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
Ticlopidine
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
Abciximab
Platelet Inhibitor, GP Receptor Blocker
directly inhibit receptor to prevent binding of fibrinogen; platelet aggregation does not occur
87
Eptifibatide
Platelet Inhibitor, GP Receptor Blocker
directly inhibit receptor to prevent binding of fibrinogen; platelet aggregation does not occur
88
Tirofiban
Platelet Inhibitor, GP Receptor Blocker
directly inhibit receptor to prevent binding of fibrinogen; platelet aggregation does not occur
89
Argatroban
Anticoagulant, Direct Thrombin Inhibitor
competitive, reversible inhibitor of thrombin
90
Bivalirudin
Anticoagulant, Direct Thrombin Inhibitor
competitive, reversible inhibitor of thrombin
91
Dabigatran
Anticoagulant, Direct Thrombin Inhibitor
competitive, reversible inhibitor of thrombin
92
Desirudin
Anticoagulant, Direct Thrombin Inhibitor
competitive, reversible inhibitor of thrombin
93
Lepirudin
Anticoagulant, Direct Thrombin Inhibitor
competitive, reversible inhibitor of thrombin
94
Apixaban
Anticoagulant, Factor Xa Inhibitor
selectively inhibits only Factor Xa; does not have variable activity
95
Fondaparinux
Anticoagulant, Factor Xa Inhibitor
selectively inhibits only Factor Xa; does not have variable activity
96
Rivaroxaban
Anticoagulant, Factor Xa Inhibitor
selectively inhibits only Factor Xa; does not have variable activity
97
Dalteparin
Anticoagulant, Low Molecular Weight Heparin
binds to antithrombin III and inactivates Factor Xa only
98
Enoxaparin
Anticoagulant, Low Molecular Weight Heparin
binds to antithrombin III and inactivates Factor Xa only
99
Heparin
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
Warfarin
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
Alteplase
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
Reteplase
Thrombolytic Agent- activates the conversion of plasminogen to plasmin; hydrolyzes fibrin and dissolves clots
103
Streptokinase
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
Tenecteplase
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
Urokinase
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
Aminocaproic Acid
Treatment of bleeding- inhibits plasminogen activation
107
Protamine
Treatment of bleeding- antagonizes heparin, forms a complex
108
Atorvastatin
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
Fluvastatin
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
Lovastatin
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
Pitavastatin
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
Pravastatin
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
Rosuvastatin
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
Simvastatin
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
Gemfibrozil
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
Fenofibrate
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
Cholestyramine
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
Colesevelam
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
Colestipol
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
Ezetimibe
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
Niacin
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
Docoshexaenoic Acid
Omega-3 Fatty Acid- hyperlipidemia drug
123
Eicosapentaenoic Acid
Omega-3 Fatty Acid- hyperlipidemia drug
