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Pharmacology II > Exam 1 shuffled > Flashcards

Exam 1 shuffled Flashcards

1
Q

Aminocaproic acid

A

Bleeding treatment, inhibits plasminogen activation to encourage clotting. Oral

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2
Q

What anticoagulant is very good in combination?

A

Dipyridamole

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3
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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4
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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5
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++

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6
Q

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

A

Ca channel blockers (-Pine –zem -mil)

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7
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)

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8
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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9
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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10
Q

Carvedilol

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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11
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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12
Q

Pentoxifylline

A

Sickle cell anemia treatment. Improves erythrocyte flexibility and reduces viscosity

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13
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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14
Q

What is the most common diuretic used in HTN?

A

Thiazide Diuretics ( Chlor Inda- -Zone)

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15
Q

What can cause decreased libido?

A

Beta blockers

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16
Q

What drugs do you want to avoid in kidney failure?

A

Thiazide diuretics, Gemfibrozil and Fenofibrate (fibrates)

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17
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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18
Q

How do Diuretics help in HF?

A

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

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19
Q

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

A

Heparin

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20
Q

What drugs are good for atrial flutter?

A

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

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21
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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22
Q

What angina treatment does NOT produce much orthostatic htn?

A

Calcium channel blockers

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23
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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24
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.

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25
Q

What treats mountain sickness?

A

CAI diuretics.

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26
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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27
Q

Alteplase

A

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

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28
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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29
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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30
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)

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31
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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32
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

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33
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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34
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.

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35
Q

Which anticoagulant can be reversed with vit K?

A

Warfarin

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36
Q

What hormone can induce cardiac hypertrophy?

A

Angiotensin II

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37
Q

What are the most commonly used HF diuretics?

A

Loop diuretics

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38
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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39
Q

What can cause ototoxicity?

A

Loop diuretics

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40
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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41
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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42
Q

What are the 2 basic mechanisms for arrhythmias?

A

Disturbances in impulse formation or conduction

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43
Q

Potassium

A

Other Antiarrhythmic Drugs. proper dose balances K gradients

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44
Q

What do Chylomicrons do?

A

They transport dietary lipids from gut to adipose tissue and liver

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45
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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46
Q

Tirofiban

A

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

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47
Q

Eptifibatide

A

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

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48
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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49
Q

What drugs are good for atrial fibrillation?

A

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

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50
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.

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51
Q

Which meds do NOT produce peripheral edema?

A

Diuretics, Beta blockers, ACE inhibitors, ARBs, Aliskiren (renin inhibitor)

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52
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

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53
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

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54
Q

What are the steps 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)

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55
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.

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56
Q

What can cause arrhythmia?

A

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

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57
Q

What drug is contraindicated in pts with glaucoma?

A

Fenoldopam (Vasodilator for HTN).

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58
Q

Class IV antiarrhythmics are what?

A

Ca blockers

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59
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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60
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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61
Q

What do LDLs do?

A

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

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62
Q

What are the 4 endogenous inhibitors of coagulation?

A

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

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63
Q

Argatroban

A

Direct thrombin inhibitor (anticoagulant). Parenteral, liver metabolized

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64
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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65
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 sites.

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66
Q

What drugs are good for AV Nodal reentry

(supraventricular tachycardia)?

A

Metoprolol, Verapamil, Digoxin

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67
Q

What drug can cause metabolic acidosis?

A

CAI diuretics.

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68
Q

What can cause cardiac depression?

A

Calcium channel blockers (in the case of angina treatment)

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69
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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70
Q

What drugs are good for ventricular fibrillation?

A

Amiodarone, epinephrine, lidocaine

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71
Q

Darbepoetin

A

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

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72
Q

What drugs work on the ascending loop of Henle?

A

Loop diuretics

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73
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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74
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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75
Q

What drugs work in the distal convoluted tubule?

A

Thiazide diuretics

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76
Q

Eicosapentaenoic acid

A

Omega-3 Fatty Acids for hyperlipidemia

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77
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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78
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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79
Q

What is reserved for advanced HF?

A

Spironolactone (although Eplerenone has fewer side effects)

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80
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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81
Q

What are the most common causes of resistant HTN?

A

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

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82
Q

What drugs do you give in a hypertensive emergency?

A

Nitroprusside, Fenoldopam or Nicardipine (Ca channel blocker).

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83
Q

What drug class should be avoided in HF?

A

Calcium channel blockers because they decrease heart contraction.

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84
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.

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85
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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86
Q

Rivaroxaban (Xarelto)

A

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

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87
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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88
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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89
Q

Reteplase

A

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

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90
Q

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

A

160

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5
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91
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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92
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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93
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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94
Q

Which drug can develop tolerance?

A

Alpha 1 blockers (-sin)

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95
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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96
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.

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97
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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98
Q

What is the least appropriate drug for acute HF?

A

Beta blockers

99
Q

What can cause gynecomastia and menstrual irregularities?

A

Potassium-sparing diuretics

100
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!

101
Q

What do VLDLs do?

A

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

102
Q

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

A

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

103
Q

What is the first line therapy for increased LDL?

A

HMG CoA reductase inhibitors (statins)

104
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

105
Q

Docosahexaenoic acid

A

Omega-3 Fatty Acids for hyperlipidemia

106
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

107
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.

108
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

109
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

110
Q

What can be used to prevent migraines and cluster HA?

A

Beta blockers

111
Q

Erythropoietin

A

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

112
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

113
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

114
Q

What is the most effective treatments for elevated triglycerides?

A

Diet and exercise, niacin and fibric acid derivatives.

115
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.

116
Q

What drug is poisonous if given orally?

A

Nitroprusside (Vasodilator for HTN and heart failure).

117
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

118
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

119
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

120
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.

121
Q

What can diuretics treat?

A

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

122
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

123
Q

Where is the nephron impermeable?

A

In the ascending loop of Henle and distal convoluted tubule

124
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

125
Q

What are atheromas?

A

Accumulation of macrophages, collagen, fibrin, and calcium.

126
Q

Deficiency of folic acid can lead to what?

A

Megaloblastic anemia

127
Q

Tenecteplase

A

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

128
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.

129
Q

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

A

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

130
Q

Nadolol

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!

131
Q

How is anemia treated?

A

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

132
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

133
Q

Which drugs can be used during pregnancy?

A

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

134
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

135
Q

Class Ia antiarrhythmics are what?

A

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

136
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

137
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

138
Q

Mexiletine

A

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

139
Q

Desirudin

A

Direct thrombin inhibitor (anticoagulant)

140
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

141
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)

142
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.

143
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)

144
Q

What is the only NSAID that irreversibly exhibits antithrombotic efficacy?

A

Aspirin

145
Q

What drug can reduce effect of loop diuretics?

A

NSAIDs

146
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

147
Q

What do LMWH/antithrombin III complex inactivate what?

A

Factor Xa, (does not include thrombin)

148
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

149
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

150
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

151
Q

Protamine

A

Bleeding treatment, FISH SPERM! antagonizes heparin.

152
Q

What do HDLs do?

A

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

153
Q

Urokinase

A

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

154
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.

155
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

156
Q

What drugs are good for Acute ventricular tachycardia?

A

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

157
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

158
Q

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

A

Minoxidil

159
Q

How do platelet inhibitors work?

A

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

160
Q

Class Ib antiarrhythmics are what?

A

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

161
Q

Methyldopa

A

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

162
Q

What is definition of HTN?

A

Higher than 120/80 in either systolic/diastolic

163
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)

164
Q

Dalteparin

A

Low Molecular Weight Heparins (LMWH) (anticoagulant)

165
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

166
Q

What drugs work on the proximal convoluted tubule?

A

CAIs

167
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

168
Q

Bivalirudin

A

Direct thrombin inhibitor (anticoagulant)

169
Q

Hydroxyurea

A

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

170
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.

171
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.

172
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

173
Q

What drugs can increase Digoxin toxicity? 5

A

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

174
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.

175
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.

176
Q

What drugs work in the collecting tubule and duct?

A

Potassium-sparing diuretics (aldosterone inhibitors)

177
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.

178
Q

Enoxaparin

A

Low Molecular Weight Heparins (LMWH) (anticoagulant)

179
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

180
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)

181
Q

With which diuretics must you monitor the heart?

A

Thiazide diuretics because loss of K

182
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”

183
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

184
Q

Apixaban (Eliquis)

A

Factor Xa Inhibitor (anticoagulant)

185
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

186
Q

What drugs are good for Acute Supraventricular tachycardia?

A

Adenosine, Diltiazem.

187
Q

Abciximab

A

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

188
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.

189
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

190
Q

Lepirudin

A

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

191
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

192
Q

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

A

Loop Diuretics (Bu Eth Fur Tor)

193
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

194
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”

195
Q

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

A

IB Antiarrhythmics

196
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

197
Q

Which antiarrhythmics are useful for emergency treatment

A

Class IB antiarrhythmics

198
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

199
Q

Hydralazine

A

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

200
Q

What is the order of therapy for HF?

A

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

201
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

202
Q

all hyperlipidemic drugs require what?

A

diets low in saturated and trans fat

203
Q

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

A

ACE inhibitors

204
Q

Sotalol

A

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

205
Q

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

A

Clopidogrel, prasugrel, and ticlopidine. NOT Ticagrelor

206
Q

What drugs work on the descending loop of Henle?

A

Osmotic diuretics

207
Q

What can treat male pattern baldness?

A

Minoxidil

208
Q

What should you avoid in HF?

A

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

209
Q

Fondaparinux

A

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

210
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

211
Q

Class III antiarrhythmics are what?

A

K blockers

212
Q

Which vasodilators are used in HF?

A

Hydralazine, isosorbide dinitrate, isosorbide mononitrate, nitroprusside

213
Q

Long-term use of what drugs increase mortality?

A

The phosphodiesterase inhibitor c and c

214
Q

Describe abnormal impulse conduction:

A

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

215
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

216
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

217
Q

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

A

Thiazide diuretics (Chlor Inda- -zone)

218
Q

Streptokinase

A

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

219
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

220
Q

What drug do you want to avoid with cirrhosis?

A

CAI diuretics.

221
Q

What is used to treat sickle cell?

A

Hydroxyurea (increases fetal hb levels),

222
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

223
Q

What drug can cause NAION and whorl keratopathy?

A

Amiodarone (class III but is complex)

224
Q

Magnesium

A

Other Antiarrhythmic Drugs. MOA unknown

225
Q

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

A

Amiodarone (class III but is complex)

226
Q

NO and prostacyclin inhibit what?

A

Platelet aggregation

227
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.

228
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

229
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.

230
Q

What is treatment for rest angina?

A

Vasodilators and ca channel blockers

231
Q

What is used in severe HTN during pregnancy?

A

Labetalol or hydralazine

232
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.

233
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.

234
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

235
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.

236
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)

237
Q

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

A

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

238
Q

What are the 2 goals of HF treatment?

A

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

239
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

240
Q

Ranolazine (Ranexa)

A

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

241
Q

What is becoming more widely used than medications for arrhythmias?

A

Implantable defibrillators (basically pacemaker 2.0)

242
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!

243
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!

Pharmacology II (7 decks)

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