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Pharmacology II > Exam 1 > Flashcards

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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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12
Q

Methyldopa

A

Centrally acting alpha-2 agonist (for HTN). MOA: Lowers CO. UNIQUE: can be used in pregnancy, AE: Drowsiness, peripheral edema

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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

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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

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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

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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!

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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

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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!

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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!

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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

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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!

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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!

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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!

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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!

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25
Q

Labetalol

A

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!

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26
Q

Amlodipine (Norvasc)

A

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

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27
Q

Clevidipine

A

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

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28
Q

Diltiazem

A

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

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29
Q

Felodipine

A

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

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30
Q

Isradipine

A

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.

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31
Q

Nicardipine

A

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.

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32
Q

Nifedipine (Procardia)

A

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.

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33
Q

Nisoldipine

A

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.

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34
Q

Verapamil

A

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

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35
Q

Hydralazine

A

Vasodilator (for HTN and heart failure). MOA: Increases NO. can cause reflex heart stim, causing problems. pregnant ok!

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36
Q

Minoxidil

A

Vasodilator (for HTN). MOA: opens K channels that hypopolarize smooth muscle. can cause reflex heart stim, causing problems. Used topically to treat baldness

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37
Q

Fenoldopam

A

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

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38
Q

Nitroprusside (Nitropress)

A

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)

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39
Q

Benazepril (Lotensin)

A

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

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40
Q

Captopril

A

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

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41
Q

Cilazapril

A

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

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42
Q

Enalapril

A

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

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43
Q

Fosinopril

A

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

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44
Q

Lisinopril

A

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

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45
Q

Moexipril

A

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

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46
Q

Perindopril

A

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

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47
Q

Quinapril (Accupril)

A

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

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48
Q

Ramipril

A

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

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49
Q

Trandolapril

A

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

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50
Q

Azilsartan

A

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

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51
Q

Candesartan

A

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

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52
Q

Eprosartan

A

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

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53
Q

Irbesartan

A

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

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54
Q

Losartan

A

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

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55
Q

Olmesartan

A

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

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56
Q

Telmisartan

A

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

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57
Q

Valsartan

A

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

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58
Q

Aliskiren

A

Renin inhibitor (for HTN), MOA: decreases blood volume. metabolized by p450 system. AE: Cough (not like ace inhibitors, though), hyperkalemia. NOT for pregnancy

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59
Q

Acetazolamide (Diamox)

A

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)

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60
Q

Methazolamide

A

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.

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61
Q

Mannitol (Osmitrol)

A

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.

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62
Q

Ranolazine (Ranexa)

A

Sodium channel blocker (for angina). MOA: Inhibits late phase of Na current to improve diastolic function. used for chroinic angina

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63
Q

Isosorbide dinitrate (Dilatrate-SR, Isordil)

A

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”

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64
Q

Isosorbide mononitrate (Imdur, Ismo)

A

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”

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65
Q

Nitroglycerin

A

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

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66
Q

Digoxin

A

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

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67
Q

Inamrinone

A

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

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68
Q

Milrinone

A

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

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69
Q

Dobutamine

A

Beta agonist (for heart failure). MOA: Increases contraction of heart increased protein kinase increases Ca influx. AE: risk of angina or arrhythmias

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70
Q

Dopamine

A

Beta agonist (for heart failure). MOA: Increases contraction of heart increased protein kinase increases Ca influx. AE: risk of angina or arrhythmias

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71
Q

Disopyramide

A

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

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72
Q

Procainamide

A

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

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73
Q

Quinidine

A

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.

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74
Q

Lidocaine

A

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

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75
Q

Mexiletine

A

Class 1B Antiarrhythmic (Na channel blocker) Shortens phase 3 repolarization in ventricular muscle fibers. UNIQUE: often used after MI.

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76
Q

Flecainide

A

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.

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77
Q

Propafenone

A

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

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78
Q

Amiodarone

A

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

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79
Q

Dofetilide

A

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

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80
Q

Dronedarone

A

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.

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81
Q

Ibutilide

A

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.

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82
Q

Sotalol

A

Class III Antiarrhythmic (actually non-selective beta-blocker) Prolongs phase 3 repolarization in ventricular muscle fibers. Lowest rate of AE

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83
Q

Adenosine

A

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.

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84
Q

Magnesium

A

Other Antiarrhythmic Drugs. MOA unknown

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85
Q

Potassium

A

Other Antiarrhythmic Drugs. proper dose balances K gradients

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86
Q

Abciximab

A

Platelet aggregation inhibitor. MOA: blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. Expensive

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87
Q

Aspirin

A

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.

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88
Q

Dipyridamole

A

Platelet aggregation inhibitor. MOA increases cAMP, which decreases Thromboxane A2 and clot formation. Very good in combination, poor alone

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89
Q

Eptifibatide

A

Platelet aggregation inhibitor. MOA blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. UNIQUE: IV only

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90
Q

Tirofiban

A

Platelet aggregation inhibitor. MOA blocks ADP receptors, prevents fibrinogen binding to glycoprotein receptor. UNIQUE: IV only

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91
Q

Clopidogrel (Plavix)

A

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

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92
Q

Prasugrel

A

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

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93
Q

Ticagrelor

A

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

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94
Q

Ticlopidine

A

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

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95
Q

Argatroban

A

Direct thrombin inhibitor (anticoagulant). Parenteral, liver metabolized

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96
Q

Bivalirudin

A

Direct thrombin inhibitor (anticoagulant)

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97
Q

Dabigatran (Pradaxa)

A

Direct thrombin inhibitor (anticoagulant). Prodrug. Tx prevent stroke in pts with atrial fibrillation. First oral anticoagulat since warfain. AE: bleeding

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98
Q

Desirudin

A

Direct thrombin inhibitor (anticoagulant)

99
Q

Lepirudin

A

Direct thrombin inhibitor (anticoagulant). IV administered. AE: patient can develop antibodies that will slow renal elimination.

100
Q

Fondaparinux

A

Factor Xa Inhibitor (anticoagulant), Subcutaneous. does not have variable activity. tx hip/knee surgery, renal eliminated.

101
Q

Rivaroxaban (Xarelto)

A

Factor Xa Inhibitor (anticoagulant), oral. does not have variable activity. tx hip/knee surgery, renal eliminated.

102
Q

Apixaban (Eliquis)

A

Factor Xa Inhibitor (anticoagulant)

103
Q

Dalteparin

A

Low Molecular Weight Heparins (LMWH) (anticoagulant)

104
Q

Enoxaparin

A

Low Molecular Weight Heparins (LMWH) (anticoagulant)

105
Q

Heparin

A

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
Q

Warfarin (Coumadin)

A

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
Q

Alteplase

A

Thrombolytic Agent. MOA: converts plasminogen > plasmin cleaves fibrin. AE: bleeding. UNIQUE: “fibrin selective”, administer within 3 hours of ischemic stroke.

108
Q

Reteplase

A

Thrombolytic Agent. MOA: converts plasminogen > plasmin cleaves fibrin. AE: bleeding. UNIQUE: “fibrin selective”, administer within 3 hours of ischemic stroke.

109
Q

Streptokinase

A

Thrombolytic Agent. MOA: activates plasminogen > plasmin cleaves fibrin. AE: bleeding, immune response. UNIQUE: use within 4 hours of MI

110
Q

Tenecteplase

A

Thrombolytic Agent. MOA: binds to fibrin, plasminogen > plasmin cleaves fibrin.

111
Q

Urokinase

A

Thrombolytic Agent. MOA: directly cleaves plasminogen into plasmin cleaves fibrin. Tx pulmonary emboli

112
Q

Aminocaproic acid

A

Bleeding treatment, inhibits plasminogen activation to encourage clotting. Oral

113
Q

Protamine

A

Bleeding treatment, FISH SPERM! antagonizes heparin.

114
Q

Darbepoetin

A

Anemia treatment during renal disease, HIV, or cancer. Not for acute anemia. HTN may result

115
Q

Erythropoietin

A

Anemia treatment during renal disease, HIV, or cancer. Not for acute anemia. HTN may result

116
Q

Hydroxyurea

A

Sickle cell anemia treatment. Increase fetal Hb. Prevents painful crises. AE bone marrow suppression can result

117
Q

Pentoxifylline

A

Sickle cell anemia treatment. Improves erythrocyte flexibility and reduces viscosity

118
Q

Atorvastatin (Lipitor)

A

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
Q

Fluvastatin

A

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
Q

Lovastatin

A

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
Q

Pitavastatin

A

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
Q

Pravastatin

A

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
Q

Rosuvastatin (Crestor)

A

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
Q

Simvastatin (Zocor)

A

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
Q

Gemfibrozil

A

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
Q

Fenofibrate (Tricor)

A

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
Q

Cholestyramine

A

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
Q

Colesevelam

A

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
Q

Colestipol

A

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
Q

Ezetimibe

A

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
Q

Niacin

A

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
Q

Docosahexaenoic acid

A

Omega-3 Fatty Acids for hyperlipidemia

133
Q

Eicosapentaenoic acid

A

Omega-3 Fatty Acids for hyperlipidemia

134
Q

What is the most effective treatments for elevated triglycerides?

A

Diet and exercise, niacin and fibric acid derivatives.

135
Q

all hyperlipidemic drugs require what?

A

diets low in saturated and trans fat

136
Q

What are some examples of combination therapy? What toxicities can occur?

A

niacin with cholestyramine (for type II hyperlipidemia). Statin with bile acid-binding agent (lowers LDL). liver and muscle toxicity.

137
Q

Where is the nephron impermeable?

A

In the ascending loop of Henle and distal convoluted tubule

138
Q

What drugs work on the proximal convoluted tubule?

A

CAIs

139
Q

What drugs work on the descending loop of Henle?

A

Osmotic diuretics

140
Q

What drugs work on the ascending loop of Henle?

A

Loop diuretics

141
Q

What drugs work in the distal convoluted tubule?

A

Thiazide diuretics

142
Q

What drugs work in the collecting tubule and duct?

A

Potassium-sparing diuretics (aldosterone inhibitors)

143
Q

What can diuretics treat?

A

Hypertension, Hypercalcemia (loop diuretics), Diabetes insipidus (Thiazide diuretics reduce glomerular filtration rate)

144
Q

How can Diabetes Insipidus be treated with diuretics?

A

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
Q

What is the only diuretic that causes hyperosmolar (concentrated) urine

A

Thiazide diuretics (Chlor Inda- -zone)

146
Q

Thiazide Diuretics. MoA, Therapeutic uses, pharmacokinetics, AE, net change in absorption/secretion:

A

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
Q

With which diuretics must you monitor the heart?

A

Thiazide diuretics because loss of K

148
Q

What drug can reduce effect of loop diuretics?

A

NSAIDs

149
Q

What is the drug of choice for reducing acute pulmonary edema of heart failure?

A

Loop Diuretics (Bu Eth Fur Tor)

150
Q

Loop Diuretics. MoA, Therapeutic uses, AE, net change in absorption/secretion:

A

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
Q

What can cause ototoxicity?

A

Loop diuretics

152
Q

Potassium-sparing Diuretics. MoA, Therapeutic uses, pharmacokinetics AE, net change in absorption/secretion:

A

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
Q

What can cause gynecomastia and menstrual irregularities?

A

Potassium-sparing diuretics

154
Q

CAI Diuretics. MoA, Therapeutic uses, AE, net change in absorption/secretion:

A

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
Q

What treats mountain sickness?

A

CAI diuretics.

156
Q

What drug can cause metabolic acidosis?

A

CAI diuretics.

157
Q

What drug do you want to avoid with cirrhosis?

A

CAI diuretics.

158
Q

What is definition of HTN?

A

Higher than 120/80 in either systolic/diastolic

159
Q

What are the 2 systems that control BP? Which is more long-term?

A

Baroreceptors and sympathetic system and Renin-Angiotensin-aldosterone system. RAA is long-term

160
Q

What are the stems of the Renin-Angiotensin-Aldosterone System?

A

Angiotensinogen (renin>) Angiotensin 1 (ACE>) angiotensin 2, which stimulates vasoconstriction and aldosterone secretion (Na retention increases blood volume)

161
Q

What is the most common diuretic used in HTN?

A

Thiazide Diuretics ( Chlor Inda- -Zone)

162
Q

What drugs do you want to avoid in kidney failure?

A

Thiazide diuretics

163
Q

Which drugs can be used during pregnancy?

A

Methyldopa (alpha 2 agonist), Hydralazine (vasodilator for HTN and HF), Labetalol for severe HTN

164
Q

Which drug can develop tolerance?

A

Alpha 1 blockers (-sin)

165
Q

What can be used to prevent migraines and cluster HA?

A

Beta blockers

166
Q

What can cause decreased libido?

A

Beta blockers

167
Q

What HTN drug is good for severe/malignant HTN that doesn’t respond to other drugs?

A

Minoxidil

168
Q

What can treat male pattern baldness?

A

Minoxidil

169
Q

What is effective treating HTN in patients with angina or diabetes?

A

Ca channel blockers (-Pine –zem -mil)

170
Q 
What drug class AE?:
 Flushing, Constipation, Dizziness, Headache, Fatigue, Hypotension, Peripheral edema (not from water retention but from vessels leaking), cardiac depression
A

Ca channel blocker (vasodilator for HTN and Angina)

171
Q

What hormone can induce cardiac hypertrophy?

A

Angiotensin II

172
Q

What HTN treatment is good for Diabetes and asthma patients because beta blockers are bad for them?

A

Ca channel blockers (vasodilator for HTN and angina)

173
Q

What is the 1st line therapy for treating HF, HTN patients with chronic renal disease, and patients with increased risk for coronary artery disease

A

ACE inhibitors (for HTN and HF)

174
Q

What drugs should NOT be used in pregnancy?

A

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
Q

What is the criteria for a hypertensive emergency? What symptoms are there?

A

210/150 or 210/130 if they have pre-existing conditions. Severe HA, confusion, apprehension, blurred vision

176
Q

What drugs do you give in a hypertensive emergency?

A

Nitroprusside, Fenoldopam or Nicardipine (Ca channel blocker).

177
Q

What drug is poisonous if given orally?

A

Nitroprusside (Vasodilator for HTN and heart failure).

178
Q

What drug is contraindicated in pts with glaucoma?

A

Fenoldopam (Vasodilator for HTN).

179
Q

What are the most common causes of resistant HTN?

A

Poor compliance, alcoholism, NSAIDS/antidepressants, insufficient dose, similar MOA.

180
Q

What is used in severe HTN during pregnancy?

A

Labetalol or hydralazine

181
Q

What 3 drug types are used to treat HTN in combination?

A

Thiazide diuretic, beta blocker, and ACE inhibitor or Angiotensin-2-receptor blocker

182
Q

Which meds do NOT produce peripheral edema?

A

Diuretics, Beta blockers, ACE inhibitors, ARBs, Aliskiren

183
Q

What are the two strategies of treating angina?

A

Decrease oxygen demand of the HEART by decreasing cardiac work, or increase oxygen delivery to heart.

184
Q

What is treatment for classic angina?

A

Effort-induced angina is treated with rest or nitroglycerin and also beta blockers (especially metoprolol and atenolol)

185
Q

What is treatment for rest angina?

A

Vasodilators and ca channel blockers

186
Q

What angina treatment does NOT produce much orthostatic htn?

A

Calcium channel blockers

187
Q

What can cause cardiac depression?

A

Calcium channel blockers (in the case of angina treatment)

188
Q

What are the 3 compensatory responses in HF?

A

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
Q

What are the 2 goals of HF treatment?

A

Reducing symptoms and slowing progression, managing acute episodes of decompensated failure

190
Q

What should you avoid in HF?

A

NSAIDs, alcohol, calcium-channel blockers, high dose beta-blockers and some antiarrhythmic drugs

191
Q

What drugs can increase Digoxin toxicity? 5

A

VQuATE verapamil, quinidine, amiodarone, tetracycline erythromycin, tetracycline. These all increase Digoxin concentration

192
Q

Long-term use of what drugs increase mortality?

A

The phosphodiesterase inhibitor c and c

193
Q

How do Diuretics help in HF?

A

They relieve pulmonary congestion and peripheral edema. Decreased venous return reduces cardiac workload and oxygen demand.

194
Q

What are the most commonly used HF diuretics?

A

Loop diuretics

195
Q

What is reserved for advanced HF?

A

Spironolactone (although C has fewer side effects)

196
Q

Which drug class is indicated in pts with all stages of left ventricular failure?

A

ACE inhibitors

197
Q

What drug class should be avoided in HF?

A

Calcium channel blockers because they decrease heart contraction.

198
Q

Which vasodilators are used in HF?

A

Hydralazine, isosorbide dinitrate, isosorbide mononitrate, nitroprusside

199
Q

Why are beta blockers helpful in HF?

A

They decrease sympathetic activity, reduce water retention, vasoconstriction, high bp, high workload, and cardiac remodeling. NOT good for acute HF.

200
Q

What is the least appropriate drug for acute HF?

A

Beta blockers

201
Q

What is the order of therapy for HF?

A

ACE inhibitors or ARBs, then Beta blocker, then diuretics and digoxin

202
Q

What are the 2 basic mechanisms for arrhythmias?

A

Disturbances in impulse formation or conduction

203
Q

What can cause arrhythmia?

A

Ischemia/hypoxia, pH imbalances, autonomics, electrolyte imbalance, stretching/scarring of cardiac tissue drug toxicity

204
Q

What is the treatment for damaged myocardial cells or non-SA node automaticity?

A

Since they depolarize the heart sooner, blocking Na or Ca channels is good

205
Q

Describe abnormal impulse conduction:

A

Instead of branching symmetrically, a block on one side can cause a delay because of retrograde impulses

206
Q

What is becoming more widely used than medications for arrhythmias?

A

Implantable defibrillators (basically pacemaker 2.0)

207
Q

Class Ia antiarrhythmics are what?

A

Na blockers. They slow conduction, prolong AP, and increase refractory period. Phase 0

208
Q

Class Ib antiarrhythmics are what?

A

Na blockers. They shorten repolarization to increase the duration of AP

209
Q

Class II antiarrhythmics are what? What do they do? Which drugs?

A

Beta blockers. Diminish automaticity in phase 4. Propranolol, metoprolol, Esmolol.

210
Q

Class III antiarrhythmics are what?

A

K blockers

211
Q

Class IV antiarrhythmics are what?

A

Ca blockers

212
Q

What drug class has a greater affinity for open sodium channels?

A

IA and IC antiarrhythmics. Weird note: can cause blurred vision

213
Q

What drug class has a greater affinity for inactivated sodium channels?

A

IB Antiarrhythmics

214
Q

Which antiarrhythmics are useful for emergency treatment

A

Class IB antiarrhythmics

215
Q

What is the antiarrhythmic of choice for atrial fibrillation and is more widely prescribed?

A

Amiodarone (class III but is complex)

216
Q

What drug can cause NAION and whorl keratopathy?

A

Amiodarone (class III but is complex)

217
Q

Digoxin Shortens refractory period in ____ and prolongs refractory period in ____

A

Digoxin Shortens refractory period In MYOCARDIAL CELLS and prolongs refractory period in THE AV NODE

218
Q

What drugs are good for atrial flutter?

A

Verapamil. (also for atrial fibrillation): Metoprolol, Digoxin

219
Q

What drugs are good for atrial fibrillation?

A

Propafenone, Amiodarone, Dofetilide, Diltiazem. (also for Atrial flutter): Metoprolol, Digoxin

220
Q

What drugs are good for AV Nodal reentry

(supraventricular tachycardia)?

A

Metoprolol, Verapamil, Digoxin

221
Q

What drugs are good for Acute Supraventricular tachycardia?

A

Adenosine, Diltiazem.

222
Q

What drugs are good for Acute ventricular tachycardia?

A

Acute ventricular tachycardia is common death cause after MI. Lidocaine, amiodarone

223
Q

What drugs are good for ventricular fibrillation?

A

Amiodarone, epinephrine, lidocaine

224
Q

NO and prostacyclin inhibit what?

A

Platelet aggregation

225
Q

How do platelet inhibitors work?

A

They either (3):1. inhibit cyclooxygenase-1 2. block glycoprotein or 3. block ADP receptors

226
Q

What is the only NSAID that irreversibly exhibits antithrombotic efficacy?

A

Aspirin

227
Q

Which platelet aggregation inhibitors are prodrugs that can inhibit the P450 system?

A

Clopidogrel, prasugrel, and ticlopidine. NOT Ticagrelor

228
Q

What anticoagulant is very good in combination?

A

Dipyridamole

229
Q

What are the 4 endogenous inhibitors of coagulation?

A

Protein C, protein S, antithrombin III, tissue factor pathway inhibitor

230
Q

What do LMWH/antithrombin III complex inactivate what?

A

Factor Xa, (does not include thrombin)

231
Q

What should you not give to people that have had brain, eye, or spinal surgery?

A

Heparin

232
Q

Which anticoagulant can be reversed with vit K?

A

Warfarin

233
Q

How is anemia treated?

A

Iron, folic acid, Vitamin B12, Erythropoietin and Darbepoetin (these two treat anemia involved in renal disease, HIV, cancer)

234
Q

Deficiency of folic acid can lead to what?

A

Megaloblastic anemia

235
Q

What is used to treat sickle cell?

A

Hydroxyurea (increases fetal hb levels),

236
Q

What do Chylomicrons do?

A

They transport dietary lipids from gut to adipose tissue and liver

237
Q

What do VLDLs do?

A

Deliver triglycerides to peripheral tissue and are transformed into LDLs as triglycerides are removed

238
Q

What do LDLs do?

A

Transport cholesterol to peripheral tissues for incorporation into cell membranes and steroids. also deliver cholesterol to artery wall.

239
Q

What are atheromas?

A

Accumulation of macrophages, collagen, fibrin, and calcium.

240
Q

What do HDLs do?

A

Secreted by liver and intestine. They return idle cholesterol, even from atheroma, back to liver

241
Q

What is cholesterol goals (total, LDL, HDL)?

A

Less than 200 total. 130 or less for LDL, 60+ for HDL

242
Q

An LDL higher than ____ plus additional risk factor prompts drug therapy

A

160

243
Q

What is the first line therapy for increased LDL?

A

HMG CoA reductase inhibitors (statins)

Pharmacology II (7 decks)

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