Exam 1 Flashcards
1
Q
Chlorthalidone
A
Thiazide diuretic, antiHTN, and heart failure med. MOA: inhibits Na/Cl cotransporter in the distal convoluted tubule, causing Na,Cl, K, and water excretion (retains Ca). lowers peripheral resistance
2
Q
Hydrochlorothiazide (HCTZ)
A
Thiazide diuretic, antiHTN, and heart failure med. MOA: inhibits Na/Cl cotransporter in the distal convoluted tubule, causing Na,Cl, K, and water excretion (retains Ca). lowers peripheral resistance
3
Q
Indapamide
A
Thiazide diuretic, antiHTN, and heart failure med. MOA: inhibits Na/Cl cotransporter in the distal convoluted tubule, causing Na,Cl, K, and water excretion (retains Ca). lowers peripheral resistance
4
Q
Metolazone
A
Thiazide diuretic, antiHTN, and heart failure med. MOA: inhibits Na/Cl cotransporter in the distal convoluted tubule, causing Na,Cl, K, and water excretion (retains Ca). lowers peripheral resistance
5
Q
Bumetanide
A
Loop Diuretic, antiHTN, and heart failure med.MOA: Inhibits Na/K/2Cl cotransporter in ascending loop of Henle, causing Na, K, Ca, and water excretion. lowers peripheral resistance. Treats acute pulmonary edema of heart failure, hypercalcemia and hyperkalemia. AE: Ototoxicity, Hyperuricemia (causes gout), acute hypovolemia, hypomagnesemia. NET CHANGE: excrete Na+, K+, Ca++, urine
6
Q
Ethacrynic acid
A
Loop Diuretic, antiHTN, and heart failure med.MOA: Inhibits Na/K/2Cl cotransporter in ascending loop of Henle, causing Na, K, Ca, and water excretion. lowers peripheral resistance. Treats acute pulmonary edema of heart failure, hypercalcemia and hyperkalemia. AE: Ototoxicity, Hyperuricemia (causes gout), acute hypovolemia, hypomagnesemia. NET CHANGE: excrete Na+, K+, Ca++, urine
7
Q
Furosemide (Lasix)
A
Loop Diuretic, antiHTN, and heart failure med.MOA: Inhibits Na/K/2Cl cotransporter in ascending loop of Henle, causing Na, K, Ca, and water excretion. lowers peripheral resistance. Treats acute pulmonary edema of heart failure, hypercalcemia and hyperkalemia. AE: Ototoxicity, Hyperuricemia (causes gout), acute hypovolemia, hypomagnesemia. NET CHANGE: excrete Na+, K+, Ca++, urine
8
Q
Torsemide
A
Loop Diuretic, antiHTN, and heart failure med.MOA: Inhibits Na/K/2Cl cotransporter in ascending loop of Henle, causing Na, K, Ca, and water excretion. lowers peripheral resistance. Treats acute pulmonary edema of heart failure, hypercalcemia and hyperkalemia. AE: Ototoxicity, Hyperuricemia (causes gout), acute hypovolemia, hypomagnesemia. NET CHANGE: excrete Na+, K+, Ca++, urine
9
Q
Eplerenone (Inspra)
A
“Potassium-Sparing” Diuretic, antiHTN, (also for heart failure). MOA: inhibits aldosterone receptors in collecting tubule, causing Na/water excretion (retains K/H). lowers peripheral resistance; relieves edema and cardiac workload. PHARMACOKINETICS: Metabolized by P450 system into active metabolite, Highly bound to plasma proteins. AE: gynecomastia (in men), menstrual irregularities. NET CHANGE: excrete Na, urine. Retain K
10
Q
Spironolactone (Aldactone)
A
“Potassium-Sparing” Diuretic, antiHTN, (also for heart failure). MOA: inhibits aldosterone receptors in collecting tubule, causing Na/water excretion (retains K/H). lowers peripheral resistance; relieves edema and cardiac workload. PHARMACOKINETICS: Metabolized by P450 system into active metabolite, Highly bound to plasma proteins. AE: gynecomastia (in men), menstrual irregularities. NET CHANGE: excrete Na, urine. Retain K. UNIQUE: used for advanced HF
11
Q
Clonidine
A
Centrally acting alpha-2 agonist (for HTN). MOA: Lowers CO. UNIQUE Used when 2 or more HTN drugs have failed. Food for renal disease. AE: all mild: sedation, dry mouth, constipation, rebound hypertension, peripheral edema
12
Q
Methyldopa
A
Centrally acting alpha-2 agonist (for HTN). MOA: Lowers CO. UNIQUE: can be used in pregnancy, AE: Drowsiness, peripheral edema
13
Q
Doxazosin
A
Alpha blocker (for HTN). MOA: Relaxes arterial and venous smooth muscle. Rarely used by itself because of tolerance. can cause peripheral edema
14
Q
Prazosin (Minipress)
A
Alpha blocker (for HTN). MOA: Relaxes arterial and venous smooth muscle. Rarely used by itself because of tolerance. can cause peripheral edema
15
Q
Terazosin (Hytrin)
A
Alpha blocker (for HTN). MOA: Relaxes arterial and venous smooth muscle. Rarely used by itself because of tolerance. can cause peripheral edema
16
Q
Acebutolol
A
Beta 1 blocker (for HTN and angina). MOA: Decreases CO and renin and increases NO production causing vasodilation. AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
17
Q
Atenolol
A
Beta 1 blocker (for HTN and angina). MOA: Decreases CO and renin and increases NO production causing vasodilation. AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death! UNIQUE: preferred in angina treatment
18
Q
Bisoprolol
A
Beta 1 blocker (for HTN and angina). MOA: Decreases CO and renin and increases NO production causing vasodilation. AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
19
Q
Esmolol
A
Beta 1 blocker (for HTN and angina) and Class II antiarrhythmic. MOA: Decreases CO and renin and increases NO production causing vasodilation. MOA 2:Inhibits phase 4 depolarization in SA and AV nodes. IV emergency arrhythmias AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
20
Q
Metoprolol
A
Beta 1 blocker, Class II Antiarrhythmic (for HTN, angina AND heart failure). Decreases CO and renin and increases NO production causing vasodilation. This reduces negative effects of heart remodeling. AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death! MOA 2: Inhibits phase 4 depolarization in SA and AV nodes. most common beta blocker for arrhythmias. UNIQUE: preferred in angina treatment…. good for atrial flutter, atrial fibrillation
21
Q
Nebivolol*
A
Beta 1 blocker (for HTN, angina AND heart failure). Decreases CO and renin and increases NO production causing vasodilation. This reduces negative effects of heart remodeling. AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
22
Q
Carvedilol
A
AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!non-selective beta blocker (for HTN, angina, AND heart failure). MOA: Decreases CO and renin. This reduces negative effects of heart remodeling. Not for asthmatics!
23
Q
Nadolol
A
non-selective beta blocker (for HTN, angina, AND heart failure). MOA: Decreases CO and renin. This reduces negative effects of heart remodeling. Not for asthmatics! AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
24
Q
Propranolol
A
non-selective beta blocker (for HTN, angina) and Class II antiarrhythmic. MOA: Decreases CO and renin. Not for asthmatics! MOA 2: Inhibits phase 4 depolarization in SA and AV nodes. Reduces sudden arrhythmic death after MI. AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
25
Labetalol
non-selective beta blocker (for HTN, angina). MOA: Decreases CO and renin. Not for asthmatics! AE: Bradycardia, fatigue, decreased libido, sudden cessation can cause angina, MI, or death!
26
Amlodipine (Norvasc)
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. can cause peripheral edema. UNIQUE: has a long half life
27
Clevidipine
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. can cause peripheral edema. Short half life
28
Diltiazem
Calcium channel blocker (vasodilator for HTN and Angina). and Class IV Antiarrhythmic. MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. Short half life. can cause peripheral edema. UNIQUE: favorable side effect profile. MOA 2: Inhibits AP in SA and AV nodes in phase 4 to prevent spontaneous depolarization, prolongs refractory period. UNIQUE: contraindicated depressed cardiac function. good for atrial fibrillation and acute supraventricular tachycardia
29
Felodipine
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. Short half life. can cause peripheral edema
30
Isradipine
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. Short half life. can cause peripheral edema.
31
Nicardipine
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. can cause peripheral edema. UNIQUE: long half life, tx hypertensive emergency.
32
Nifedipine (Procardia)
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. Short half life. can cause peripheral edema.
33
Nisoldipine
Calcium channel blocker (vasodilator for HTN and Angina). MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. Short half life. can cause peripheral edema.
34
Verapamil
Calcium channel blocker (vasodilator for HTN and Angina). And Class IV Antiarrhythmic. MOA: Dilates arteries by blocking inward Ca to prevent muscle contraction. Has natural diuretic effect. Short half life. can cause peripheral edema. UNIQUE: Least selective calcium channel blocker..... MOA 2: Inhibits AP in SA and AV nodes in phase 4 to prevent spontaneous depolarization, prolongs refractory period. UNIQUE: contraindicated depressed cardiac function. Good for atrial flutter and AV Nodal reentry
35
Hydralazine
Vasodilator (for HTN and heart failure). MOA: Increases NO. can cause reflex heart stim, causing problems. pregnant ok!
36
Minoxidil
Vasodilator (for HTN). MOA: opens K channels that hypopolarize smooth muscle. can cause reflex heart stim, causing problems. Used topically to treat baldness
37
Fenoldopam
Parenteral agent (Vasodilator for HTN). MOA: Peripheral dopamine-1 receptor agonist to increase renal blood flow. increases IOP--avoid in glaucoma, send note to ER
38
Nitroprusside (Nitropress)
Parenteral agent (Vasodilator for HTN and heart failure). UNIQUE: MoA: increases cGMP, > NO increases to cause rapid vasodilation. very short half life. Poisonous if taken orally (converts to cyanide)
39
Benazepril (Lotensin)
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
40
Captopril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
41
Cilazapril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
42
Enalapril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
43
Fosinopril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
44
Lisinopril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
45
Moexipril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
46
Perindopril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
47
Quinapril (Accupril)
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
48
Ramipril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
49
Trandolapril
ACE inhibitor (for HTN and heart failure). MOA: Decreases angiotensin II and increases bradykinin, reducing water retention. AE: dry cough. hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
50
Azilsartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
51
Candesartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
52
Eprosartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
53
Irbesartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
54
Losartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
55
Olmesartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
56
Telmisartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
57
Valsartan
Angiotensin-2-receptor blockers (for HTN and heart failure) MOA: Reduces water retention; decreased preload and afterload for increased CO. AE: hyperkalemia when used with K-sparing diuretics, rash, fever, **Fetotoxic**
58
Aliskiren
Renin inhibitor (for HTN), MOA: decreases blood volume. metabolized by p450 system. AE: Cough (not like ace inhibitors, though), hyperkalemia. NOT for pregnancy
59
Acetazolamide (Diamox)
Carbonic Anhydrase Inhibitors (diuretic). MOA: CAI affects proximal convoluted tubule, TREATS glaucoma, mountain sickness. AE: metabolic acidosis, renal stones, drowsiness, paresthesia. NET CHANGE: excrete Na, K, HCO3- (bicarb), urine. UNIQUE systemic dose is good for angle closure (and glaucoma)
60
Methazolamide
Carbonic Anhydrase Inhibitors (diuretic). MOA: CAI affects proximal convoluted tubule, TREATS glaucoma, mountain sickness. AE: metabolic acidosis, renal stones, drowsiness, paresthesia. NET CHANGE: excrete Na, K, HCO3- (bicarb), urine.
61
Mannitol (Osmitrol)
Osmotic diuretic. MOA Carries water with it as it filters through glomerulus. used to prevent acute renal failure and in treatment of increased intracranial pressure.
62
Ranolazine (Ranexa)
Sodium channel blocker (for angina). MOA: Inhibits late phase of Na current to improve diastolic function. used for chroinic angina
63
Isosorbide dinitrate (Dilatrate-SR, Isordil)
Organic Nitrate (for angina and heart failure). MOA: Increases NO and cGMP (both for dilation). rapid onset, liver inactivates drug so it's given sublingual or patch. AE: tachycardia, orthostatic hypertension, HA from brain vasodilation, tollerance requires "nitrate-free interval"
64
Isosorbide mononitrate (Imdur, Ismo)
Organic Nitrate (for angina) MOA: Increases NO and cGMP (both for dilation). rapid onset, liver inactivates drug so it's given sublingual or patch. AE: tachycardia, orthostatic hypertension, HA from brain vasodilation, tollerance requires "nitrate-free interval"
65
Nitroglycerin
Organic Nitrate (for angina) MOA: Increases NO and cGMP (both for dilation). rapid onset, liver inactivates drug so it's given sublingual or patch. AE: tachycardia, orthostatic hypertension, HA from brain vasodilation, tollerance requires "nitrate-free interval" UNIQUE: Tx classic angina
66
Digoxin
Inotrope (for heart failure) and antiarrhythmic. MOA: increases Ca by inhibiting Na/K pump, increase CO reduces heart rate. PHARMACOKINETICS: long half-life,narrow therapeutic index, never used alone, accumulates in muscle. Use ACE inhibitors/diuretics before Digoxin. AE: arrhythmia, toxicity especially with from decreased K levels. HA, fatigue, blurred vision, altered color, halos. MOA 2: shortens refractory period in myocardial cells and prolongs refractory period in AV node. good for atrial flutter, atrial fibrillation, and AV nodal rentry
67
Inamrinone
Inotrope (for heart failure). MOA: this phosphodiesterase inhibitor causes increase of cAMP, increases Ca. Long-term use increases mortality, so it's short term via IV
68
Milrinone
Inotrope (for heart failure). MOA: this phosphodiesterase inhibitor causes increase of cAMP, increases Ca. Long-term use increases mortality, so it's short term via IV
69
Dobutamine
Beta agonist (for heart failure). MOA: Increases contraction of heart increased protein kinase increases Ca influx. AE: risk of angina or arrhythmias
70
Dopamine
Beta agonist (for heart failure). MOA: Increases contraction of heart increased protein kinase increases Ca influx. AE: risk of angina or arrhythmias
71
Disopyramide
Class 1A Antiarrhythmic (Na channel blocker) Slows phase 0 depolarization in ventricular muscle fibers. Similar AE as cholinergic blocker: Dry mouth, urine retention, blurred vision, constipation
72
Procainamide
Class 1A Antiarrhythmic (Na channel blocker) Slows phase 0 depolarization in ventricular muscle fibers. UNIQUE: AE: lupus-like rash in 20-30% pts, some GI disturbances, CNS problems
73
Quinidine
Class 1A Antiarrhythmic (Na channel blocker) Slows phase 0 depolarization in ventricular muscle fibers. UNIQUE: Absorbs quickly orally, CP450 metabolized. AE: arrhythmia, GI disturbances, blurred vision. Other: increases digoxin, displaces from tissue-binding.
74
Lidocaine
Class 1B Antiarrhythmic (Na channel blocker) Shortens phase 3 repolarization in ventricular muscle fibers. UNIQUE: Also local anesthetic, large therapeutic index. Good for acute ventricular tachycardia and ventricular fibrillation
75
Mexiletine
Class 1B Antiarrhythmic (Na channel blocker) Shortens phase 3 repolarization in ventricular muscle fibers. UNIQUE: often used after MI.
76
Flecainide
Class 1C Antiarrhythmic (Na channel blocker) Markedly slows phase 0 depolarization in ventricular muscle fibers. AE can/does interfere with normal heart beat, Dizziness, blurred vision, HA, nausea...... slows down rise in action potential. Absorbed orally, long half-life.
77
Propafenone
Class 1C Antiarrhythmic (Na channel blocker) Markedly slows phase 0 depolarization in ventricular muscle fibers. AE can/does interfere with normal heart beat, Dizziness, blurred vision, HA, nausea...... slows down rise in action potential. Absorbed orally, long half-life. UNIQUE: good for atrial fibrillation
78
Amiodarone
Class III Antiarrhythmic (K Channel blocker) Prolongs phase 3 repolarization in ventricular muscle fibers. They prolong the AP and refractory period. AE: ventricular tachyarrhythmias. UNIQUE: shows ALL classes of actions, therapy of choice for atrial fibrillation. PHARMACOKINETICS: half life of several weeks. AE: interstitial pulmonary fibrosis, GI problems, blue skin, NAION and whorl keratopathy. good for atrial fibrillation and acute ventricular tachycardia and ventricular fibrillation
79
Dofetilide
Class III Antiarrhythmic (K Channel blocker) Prolongs phase 3 repolarization in ventricular muscle fibers. They prolong the AP and refractory period. AE: ventricular tachyarrhythmias. UNIQUE: risk of proarrhythmia, 6-10 hr half life, adjust dose if there is renal insufficiency. good for atrial fibrillation
80
Dronedarone
Class III Antiarrhythmic (K Channel blocker) Prolongs phase 3 repolarization in ventricular muscle fibers. They prolong the AP and refractory period. AE: ventricular tachyarrhythmias. UNIQUE: shorter half life, fewer side effects.
81
Ibutilide
Class III Antiarrhythmic (K Channel blocker) Prolongs phase 3 repolarization in ventricular muscle fibers. They prolong the AP and refractory period. AE: ventricular tachyarrhythmias. UNIQUE: risk of proarrhythmia, 6-10 hr half life, adjust dose if there is renal insufficiency.
82
Sotalol
Class III Antiarrhythmic (actually non-selective beta-blocker) Prolongs phase 3 repolarization in ventricular muscle fibers. Lowest rate of AE
83
Adenosine
Other Antiarrhythmic Drugs. MOA: activates inward K current and inhibits Ca current. This causes hyperpolarization. also inhibits AV conduction. less effective w/ caffeine. AE: flushing, SOB, chest burning. Good for acute supraventricular tachycardia.
84
Magnesium
Other Antiarrhythmic Drugs. MOA unknown
85
Potassium
Other Antiarrhythmic Drugs. proper dose balances K gradients
86
Abciximab
Platelet aggregation inhibitor. MOA: blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. Expensive
87
Aspirin
Platelet aggregation inhibitor. MOA: inhibits Cox-1. (platelet activation > arachidonic acid [Cox-1>] Prostaglandic H2 > Thromboxane A2 > clot formation). rapid effect that lasts platelet life. Tx prophylactic stroke or MI. AE: hemorrhagic stroke, GI bleeding.
88
Dipyridamole
Platelet aggregation inhibitor. MOA increases cAMP, which decreases Thromboxane A2 and clot formation. Very good in combination, poor alone
89
Eptifibatide
Platelet aggregation inhibitor. MOA blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. UNIQUE: IV only
90
Tirofiban
Platelet aggregation inhibitor. MOA blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. UNIQUE: IV only
91
Clopidogrel (Plavix)
Platelet aggregation inhibitor. MOA irreversibly blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. plasma protein bound, P450 metabolism, renal/fecal elimination. AE: prolonged bleeding, life-threatening Thrombotic thrombocytopenic purpura. UNIQUE: prodrug, can inhibit P450
92
Prasugrel
Platelet aggregation inhibitor. MOA irreversibly blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. plasma protein bound, P450 metabolism, renal/fecal elimination. AE: prolonged bleeding, life-threatening Thrombotic thrombocytopenic purpura. UNIQUE: prodrug, can inhibit P450
93
Ticagrelor
Platelet aggregation inhibitor. MOA blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. plasma protein bound, P450 metabolism, renal/fecal elimination. AE: prolonged bleeding, life-threatening Thrombotic thrombocytopenic purpura. UNIQUE: is not irreversible so it's good for surgery
94
Ticlopidine
Platelet aggregation inhibitor. MOA irreversibly blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. plasma protein bound, P450 metabolism, renal/fecal elimination. AE: prolonged bleeding, life-threatening Thrombotic thrombocytopenic purpura. UNIQUE: prodrug, can inhibit P450
95
Argatroban
Direct thrombin inhibitor (anticoagulant). Parenteral, liver metabolized
96
Bivalirudin
Direct thrombin inhibitor (anticoagulant)
97
Dabigatran (Pradaxa)
Direct thrombin inhibitor (anticoagulant). Prodrug. Tx prevent stroke in pts with atrial fibrillation. First oral anticoagulat since warfain. AE: bleeding
98
Desirudin
Direct thrombin inhibitor (anticoagulant)
99
Lepirudin
Direct thrombin inhibitor (anticoagulant). IV administered. AE: patient can develop antibodies that will slow renal elimination.
100
Fondaparinux
Factor Xa Inhibitor (anticoagulant), Subcutaneous. does not have variable activity. tx hip/knee surgery, renal eliminated.
101
Rivaroxaban (Xarelto)
Factor Xa Inhibitor (anticoagulant), oral. does not have variable activity. tx hip/knee surgery, renal eliminated.
102
Apixaban (Eliquis)
Factor Xa Inhibitor (anticoagulant)
103
Dalteparin
Low Molecular Weight Heparins (LMWH) (anticoagulant)
104
Enoxaparin
Low Molecular Weight Heparins (LMWH) (anticoagulant)
105
Heparin
Other anticoagulant. MOA binds to antithrombin III to quickly (within minutes) inactivate thrombin and factor Xa. High molecular weight protein. Tx deep vein thrombosis and pulmonary embolism. Good for surgery. Does not cross the placenta. parenterally. Excreted in urine. AE:Bleeding, hypersensitivity, thrombocytopenia. contraindicated in recent surgery of brain, eye, or spinal cord.
106
Warfarin (Coumadin)
Other anticoagulant. MOA: inhibits vitamin K epoxide reductase, preventing vit K regeneration. PHARMACOKINETICS: 99% albumin bound. Other protein-binding drugs can displace Warfarin, increasing its concentration. AE: bleeding. not for pregnancy!
107
Alteplase
Thrombolytic Agent. MOA: converts plasminogen > plasmin cleaves fibrin. AE: bleeding. UNIQUE: "fibrin selective", administer within 3 hours of ischemic stroke.
108
Reteplase
Thrombolytic Agent. MOA: converts plasminogen > plasmin cleaves fibrin. AE: bleeding. UNIQUE: "fibrin selective", administer within 3 hours of ischemic stroke.
109
Streptokinase
Thrombolytic Agent. MOA: activates plasminogen > plasmin cleaves fibrin. AE: bleeding, immune response. UNIQUE: use within 4 hours of MI
110
Tenecteplase
Thrombolytic Agent. MOA: binds to fibrin, plasminogen > plasmin cleaves fibrin.
111
Urokinase
Thrombolytic Agent. MOA: directly cleaves plasminogen into plasmin cleaves fibrin. Tx pulmonary emboli
112
Aminocaproic acid
Bleeding treatment, inhibits plasminogen activation to encourage clotting. Oral
113
Protamine
Bleeding treatment, FISH SPERM! antagonizes heparin.
114
Darbepoetin
Anemia treatment during renal disease, HIV, or cancer. Not for acute anemia. HTN may result
115
Erythropoietin
Anemia treatment during renal disease, HIV, or cancer. Not for acute anemia. HTN may result
116
Hydroxyurea
Sickle cell anemia treatment. Increase fetal Hb. Prevents painful crises. AE bone marrow suppression can result
117
Pentoxifylline
Sickle cell anemia treatment. Improves erythrocyte flexibility and reduces viscosity
118
Atorvastatin (Lipitor)
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
119
Fluvastatin
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
120
Lovastatin
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
121
Pitavastatin
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
122
Pravastatin
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
123
Rosuvastatin (Crestor)
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
124
Simvastatin (Zocor)
HMG COA Reductase inhibitor. MOA: analogs of HMG (cholesterol precursor). Stabilizes plaque, causes LDL to go into cells and prevents VLDL secretion. Less effective in familial hypercholesterolemia because they lack LDL receptors. Excretion through bile and feces. AE: elevated liver enzymes, disintegration of muscle (rare), increased warfarin levels. not for pregnant or nursing or children.
125
Gemfibrozil
Fibrate. MOA: prevents bile acids/salts from going to liver so liver makes bile a/s from cholesterol instead. causes genes to make proteins responsible for lipoprotein structure/function, resulting in decreased triglyceride and increased HDL. Also lowers LDL PHARMICOKINETICS: oral, albumin bound, excreted in urine. AE: Gallstones, voluntary muscle inflammation, warfarin increase. bad for liver/kidney/gallbaldder disease
126
Fenofibrate (Tricor)
Fibrate. MOA: prevents bile acids/salts from going to liver so liver makes bile a/s from cholesterol instead. causes genes to make proteins responsible for lipoprotein structure/function, resulting in decreased triglyceride and increased HDL. Also lowers LDL PHARMICOKINETICS: oral, albumin bound, excreted in urine. AE: Gallstones, voluntary muscle inflammation, warfarin increase. bad for liver/kidney/gallbaldder disease
127
Cholestyramine
Bile acid sequestrant. Binds biles a/s in small intestine, causing liver to use cholesterol to make bile acids. increases LDL receptors. excreted in feces. AE: GI disturbances, impair absorption of vit ADEK, and other drugs. UNIQUE: relieves pruritis caused by accumulation of bile acids in patients with biliary obstruction.
128
Colesevelam
Bile acid sequestrant. Binds biles a/s in small intestine, causing liver to use cholesterol to make bile acids. increases LDL receptors. excreted in feces. AE: GI disturbances, impair absorption of vit ADEK, and other drugs.
129
Colestipol
Bile acid sequestrant. Binds biles a/s in small intestine, causing liver to use cholesterol to make bile acids. increases LDL receptors. excreted in feces. AE: GI disturbances, impair absorption of vit ADEK, and other drugs.
130
Ezetimibe
Cholesterol Absorption Inhibitor (in the small intestine), reduces hepatic cholesterol stores and increases clearance of cholesterol from blood. Very long half life (22 hours). Bad for hepatic insufficiency. biliary and renal excretion.
131
Niacin
increases HDL by inhibiting lipolysis in adipose tissue, lowering blood triglycerides. Helps reverse endothelial cell dysfunction. Great for familial hyperlipidemias. Excreted in urine. AE: intense cutaneous flush and feeling of warmth (helped via aspirin), nausea, inhibits secretion of uric acid which can cause gout.
132
Docosahexaenoic acid
Omega-3 Fatty Acids for hyperlipidemia
133
Eicosapentaenoic acid
Omega-3 Fatty Acids for hyperlipidemia
134
What is the most effective treatments for elevated triglycerides?
Diet and exercise, niacin and fibric acid derivatives.
135
all hyperlipidemic drugs require what?
diets low in saturated and trans fat
136
What are some examples of combination therapy? What toxicities can occur?
niacin with cholestyramine (for type II hyperlipidemia). Statin with bile acid-binding agent (lowers LDL). liver and muscle toxicity.
137
Where is the nephron impermeable?
In the ascending loop of Henle and distal convoluted tubule
138
What drugs work on the proximal convoluted tubule?
CAIs
139
What drugs work on the descending loop of Henle?
Osmotic diuretics
140
What drugs work on the ascending loop of Henle?
Loop diuretics
141
What drugs work in the distal convoluted tubule?
Thiazide diuretics
142
What drugs work in the collecting tubule and duct?
Potassium-sparing diuretics (aldosterone inhibitors)
143
What can diuretics treat?
Hypertension, Hypercalcemia (loop diuretics), Diabetes insipidus (Thiazide diuretics reduce glomerular filtration rate)
144
How can Diabetes Insipidus be treated with diuretics?
Polyuria (peeing) and polydipsia (thirst) treated with diuretics (huh?!). Thiazide diuretic reduces plasma volume causing a drop in glomerular filtration rate. Promoting reabsorption of Na and water
145
What is the only diuretic that causes hyperosmolar (concentrated) urine
Thiazide diuretics (Chlor Inda- -zone)
146
Thiazide Diuretics. MoA, Therapeutic uses, pharmacokinetics, AE, net change in absorption/secretion:
antiHTN, and heart failure med. MOA: inhibits Na/Cl cotransporter in the distal convoluted tubule, causing Na,Cl, K, and water excretion (retains Ca). lowers peripheral resistance. THERAPEUTIC USES: htn, heart failure, hypercalciuria (excess Ca in urine), kidney stone prevention. PHARMACOKINETICS: oral, effects in 1-3 weeks, kidney! excreted. AE: K depletion (can cause arrhythmias), hyponatremia, hyperuricemia (causes gout), orthostatic hypotension, Hypercalcemia (excess Ca can mess with glucose uptake), Hyperlipidemia, rare sulfa hypersensitivity. NET CHANGE: excretion of Na, K, urine; retention of Ca++
147
With which diuretics must you monitor the heart?
Thiazide diuretics because loss of K
148
What drug can reduce effect of loop diuretics?
NSAIDs
149
What is the drug of choice for reducing acute pulmonary edema of heart failure?
Loop Diuretics (Bu Eth Fur Tor)
150
Loop Diuretics. MoA, Therapeutic uses, AE, net change in absorption/secretion:
MOA: Inhibits Na/K/2Cl cotransporter in ascending loop of Henle, causing Na, K, Ca, and water excretion. lowers peripheral resistance. Treats acute pulmonary edema of heart failure, hypercalcemia and hyperkalemia. AE: Ototoxicity, Hyperuricemia (causes gout), acute hypovolemia, hypomagnesemia. NET CHANGE: excrete Na+, K+, Ca++, urine
151
What can cause ototoxicity?
Loop diuretics
152
Potassium-sparing Diuretics. MoA, Therapeutic uses, pharmacokinetics AE, net change in absorption/secretion:
MOA: inhibits aldosterone receptors in collecting tubule, causing Na/water excretion (retains K/H). lowers peripheral resistance; relieves edema and cardiac workload. PHARMACOKINETICS: Metabolized by P450 system into active metabolite, Highly bound to plasma proteins. AE: gynecomastia (in men), menstrual irregularities. Gluten intolerance. NET CHANGE: excrete Na, urine. Retain K
153
What can cause gynecomastia and menstrual irregularities?
Potassium-sparing diuretics
154
CAI Diuretics. MoA, Therapeutic uses, AE, net change in absorption/secretion:
MOA: CAI affects proximal convoluted tubule, reduces Na/Cl/bicarb reabsorption, excretes water/K/some Na. TREATS glaucoma, mountain sickness. AE: metabolic acidosis, renal stones, drowsiness, paresthesia. NET CHANGE: excrete Na, K, HCO3- (bicarb), urine
155
What treats mountain sickness?
CAI diuretics.
156
What drug can cause metabolic acidosis?
CAI diuretics.
157
What drug do you want to avoid with cirrhosis?
CAI diuretics.
158
What is definition of HTN?
Higher than 120/80 in either systolic/diastolic
159
What are the 2 systems that control BP? Which is more long-term?
Baroreceptors and sympathetic system and Renin-Angiotensin-aldosterone system. RAA is long-term
160
What are the stems of the Renin-Angiotensin-Aldosterone System?
Angiotensinogen (renin>) Angiotensin 1 (ACE>) angiotensin 2, which stimulates vasoconstriction and aldosterone secretion (Na retention increases blood volume)
161
What is the most common diuretic used in HTN?
Thiazide Diuretics ( Chlor Inda- -Zone)
162
What drugs do you want to avoid in kidney failure?
Thiazide diuretics
163
Which drugs can be used during pregnancy?
Methyldopa (alpha 2 agonist), Hydralazine (vasodilator for HTN and HF), Labetalol for severe HTN
164
Which drug can develop tolerance?
Alpha 1 blockers (-sin)
165
What can be used to prevent migraines and cluster HA?
Beta blockers
166
What can cause decreased libido?
Beta blockers
167
What HTN drug is good for severe/malignant HTN that doesn't respond to other drugs?
Minoxidil
168
What can treat male pattern baldness?
Minoxidil
169
What is effective treating HTN in patients with angina or diabetes?
Ca channel blockers (-Pine –zem -mil)
170
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What drug class AE?:
Flushing, Constipation, Dizziness, Headache, Fatigue, Hypotension, Peripheral edema (not from water retention but from vessels leaking), cardiac depression
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Ca channel blocker (vasodilator for HTN and Angina)
171
What hormone can induce cardiac hypertrophy?
Angiotensin II
172
What HTN treatment is good for Diabetes and asthma patients because beta blockers are bad for them?
Ca channel blockers (vasodilator for HTN and angina)
173
What is the 1st line therapy for treating HF, HTN patients with chronic renal disease, and patients with increased risk for coronary artery disease
ACE inhibitors (for HTN and HF)
174
What drugs should NOT be used in pregnancy?
Aliskiren (renin inhibitor for HTN), ACE inhibitors (for HTN and HF), Angiotensin II receptor blockers (for HTN and HF), Warfarin (anticoagulant), -statins (HMG COA reductase inhibitor)
175
What is the criteria for a hypertensive emergency? What symptoms are there?
210/150 or 210/130 if they have pre-existing conditions. Severe HA, confusion, apprehension, blurred vision
176
What drugs do you give in a hypertensive emergency?
Nitroprusside, Fenoldopam or Nicardipine (Ca channel blocker).
177
What drug is poisonous if given orally?
Nitroprusside (Vasodilator for HTN and heart failure).
178
What drug is contraindicated in pts with glaucoma?
Fenoldopam (Vasodilator for HTN).
179
What are the most common causes of resistant HTN?
Poor compliance, alcoholism, NSAIDS/antidepressants, insufficient dose, similar MOA.
180
What is used in severe HTN during pregnancy?
Labetalol or hydralazine
181
What 3 drug types are used to treat HTN in combination?
Thiazide diuretic, beta blocker, and ACE inhibitor or Angiotensin-2-receptor blocker
182
Which meds do NOT produce peripheral edema?
Diuretics, Beta blockers, ACE inhibitors, ARBs, Aliskiren
183
What are the two strategies of treating angina?
Decrease oxygen demand of the HEART by decreasing cardiac work, or increase oxygen delivery to heart.
184
What is treatment for classic angina?
Effort-induced angina is treated with rest or nitroglycerin and also beta blockers (especially metoprolol and atenolol)
185
What is treatment for rest angina?
Vasodilators and ca channel blockers
186
What angina treatment does NOT produce much orthostatic htn?
Calcium channel blockers
187
What can cause cardiac depression?
Calcium channel blockers (in the case of angina treatment)
188
What are the 3 compensatory responses in HF?
Increased sympathetic activity (increased CO, increased venous return), renin-angiotensin system activation (increase BP), and myocardial hypertrophy (bad compensation). Note that higher BP can lead to pulmonary edema.
189
What are the 2 goals of HF treatment?
Reducing symptoms and slowing progression, managing acute episodes of decompensated failure
190
What should you avoid in HF?
NSAIDs, alcohol, calcium-channel blockers, high dose beta-blockers and some antiarrhythmic drugs
191
What drugs can increase Digoxin toxicity? 5
VQuATE verapamil, quinidine, amiodarone, tetracycline erythromycin, tetracycline. These all increase Digoxin concentration
192
Long-term use of what drugs increase mortality?
The phosphodiesterase inhibitor c and c
193
How do Diuretics help in HF?
They relieve pulmonary congestion and peripheral edema. Decreased venous return reduces cardiac workload and oxygen demand.
194
What are the most commonly used HF diuretics?
Loop diuretics
195
What is reserved for advanced HF?
Spironolactone (although C has fewer side effects)
196
Which drug class is indicated in pts with all stages of left ventricular failure?
ACE inhibitors
197
What drug class should be avoided in HF?
Calcium channel blockers because they decrease heart contraction.
198
Which vasodilators are used in HF?
Hydralazine, isosorbide dinitrate, isosorbide mononitrate, nitroprusside
199
Why are beta blockers helpful in HF?
They decrease sympathetic activity, reduce water retention, vasoconstriction, high bp, high workload, and cardiac remodeling. NOT good for acute HF.
200
What is the least appropriate drug for acute HF?
Beta blockers
201
What is the order of therapy for HF?
ACE inhibitors or ARBs, then Beta blocker, then diuretics and digoxin
202
What are the 2 basic mechanisms for arrhythmias?
Disturbances in impulse formation or conduction
203
What can cause arrhythmia?
Ischemia/hypoxia, pH imbalances, autonomics, electrolyte imbalance, stretching/scarring of cardiac tissue drug toxicity
204
What is the treatment for damaged myocardial cells or non-SA node automaticity?
Since they depolarize the heart sooner, blocking Na or Ca channels is good
205
Describe abnormal impulse conduction:
Instead of branching symmetrically, a block on one side can cause a delay because of retrograde impulses
206
What is becoming more widely used than medications for arrhythmias?
Implantable defibrillators (basically pacemaker 2.0)
207
Class Ia antiarrhythmics are what?
Na blockers. They slow conduction, prolong AP, and increase refractory period. Phase 0
208
Class Ib antiarrhythmics are what?
Na blockers. They shorten repolarization to increase the duration of AP
209
Class II antiarrhythmics are what? What do they do? Which drugs?
Beta blockers. Diminish automaticity in phase 4. Propranolol, metoprolol, Esmolol.
210
Class III antiarrhythmics are what?
K blockers
211
Class IV antiarrhythmics are what?
Ca blockers
212
What drug class has a greater affinity for open sodium channels?
IA and IC antiarrhythmics. Weird note: can cause blurred vision
213
What drug class has a greater affinity for inactivated sodium channels?
IB Antiarrhythmics
214
Which antiarrhythmics are useful for emergency treatment
Class IB antiarrhythmics
215
What is the antiarrhythmic of choice for atrial fibrillation and is more widely prescribed?
Amiodarone (class III but is complex)
216
What drug can cause NAION and whorl keratopathy?
Amiodarone (class III but is complex)
217
Digoxin Shortens refractory period in ____ and prolongs refractory period in ____
Digoxin Shortens refractory period In MYOCARDIAL CELLS and prolongs refractory period in THE AV NODE
218
What drugs are good for atrial flutter?
Verapamil. (also for atrial fibrillation): Metoprolol, Digoxin
219
What drugs are good for atrial fibrillation?
Propafenone, Amiodarone, Dofetilide, Diltiazem. (also for Atrial flutter): Metoprolol, Digoxin
220
What drugs are good for AV Nodal reentry
| (supraventricular tachycardia)?
Metoprolol, Verapamil, Digoxin
221
What drugs are good for Acute Supraventricular tachycardia?
Adenosine, Diltiazem.
222
What drugs are good for Acute ventricular tachycardia?
Acute ventricular tachycardia is common death cause after MI. Lidocaine, amiodarone
223
What drugs are good for ventricular fibrillation?
Amiodarone, epinephrine, lidocaine
224
NO and prostacyclin inhibit what?
Platelet aggregation
225
How do platelet inhibitors work?
They either (3):1. inhibit cyclooxygenase-1 2. block glycoprotein or 3. block ADP receptors
226
What is the only NSAID that irreversibly exhibits antithrombotic efficacy?
Aspirin
227
Which platelet aggregation inhibitors are prodrugs that can inhibit the P450 system?
Clopidogrel, prasugrel, and ticlopidine. NOT Ticagrelor
228
What anticoagulant is very good in combination?
Dipyridamole
229
What are the 4 endogenous inhibitors of coagulation?
Protein C, protein S, antithrombin III, tissue factor pathway inhibitor
230
What do LMWH/antithrombin III complex inactivate what?
Factor Xa, (does not include thrombin)
231
What should you not give to people that have had brain, eye, or spinal surgery?
Heparin
232
Which anticoagulant can be reversed with vit K?
Warfarin
233
How is anemia treated?
Iron, folic acid, Vitamin B12, Erythropoietin and Darbepoetin (these two treat anemia involved in renal disease, HIV, cancer)
234
Deficiency of folic acid can lead to what?
Megaloblastic anemia
235
What is used to treat sickle cell?
Hydroxyurea (increases fetal hb levels),
236
What do Chylomicrons do?
They transport dietary lipids from gut to adipose tissue and liver
237
What do VLDLs do?
Deliver triglycerides to peripheral tissue and are transformed into LDLs as triglycerides are removed
238
What do LDLs do?
Transport cholesterol to peripheral tissues for incorporation into cell membranes and steroids. also deliver cholesterol to artery wall.
239
What are atheromas?
Accumulation of macrophages, collagen, fibrin, and calcium.
240
What do HDLs do?
Secreted by liver and intestine. They return idle cholesterol, even from atheroma, back to liver
241
What is cholesterol goals (total, LDL, HDL)?
Less than 200 total. 130 or less for LDL, 60+ for HDL
242
An LDL higher than ____ plus additional risk factor prompts drug therapy
160
243
What is the first line therapy for increased LDL?
HMG CoA reductase inhibitors (statins)
