#114 Heart And Blood Drugs

Front 1

What is the DOC for stroke prevention in those with CAD?

Back 1

ASPIRIN

Front 2

MOA of Aspirin?

Back 2

IRREVERSIBLE COX (-)
platelet aggregation inhibitor

Front 3

Agent that inhibits degranulation, minimizing ACP and TXA release and is also a uricosuric agent?

Back 3

Sulfinpyrazone

Front 4

What is a uricosuric agent?

Back 4

blocks proximal tubule resorption of uric acid
(so, much uric acid goes out with the urine --> uric-os-uric)

Front 5

MOA of Dipyridamole (Persantine) ?

Back 5

phosphodiesterase (-); therefore increases cAMP and this inhibits TXA2

Front 6

In combination with warfarin what is Dipyridamole used for?

Back 6

to prevent thromboembolic events of cardiac valve replacement

Front 7

In combination with aspirin what is Dipyridamole used for?

Back 7

chronic platelet aggregation inhibition

Front 8

What drug is used in conjunction with radioactively tagged thallium or sestamibi, to facilitate max delivery of these agents to HEALTHY bv's of the heart?

Back 8

Dipyridamole (persantine)

Front 9

MOA of Clopidogrel?

Back 9

Inhibits the ADP-mediated platelet aggregation process; thus powerful platelet aggregation (-)

Front 10

All patients who receive stents, as a standard of practice, are prescribed what?

Back 10

Clopidogrel

Front 11

What is used for prophylaxis of MI in those with CAD?

Back 11

Clopidogrel

Front 12

What is used for prophylaxis of CVA for those with carotid artery disease?

Back 12

Clopidogrel

Front 13

List the 2 other pharmaceuticals with similar MOA as Clopidogrel?

Back 13

Ticlopidine
prasugrel

Front 14

How are Glycoprotein IIbIIIa antagonists administered?

Back 14

by IV drip

Front 15

What are the 3 Glycoprotein IIbIIa antagonists?

Back 15

eptifibatide
abciximab
tirofiban

Front 16

MOA of eptifibatide, abciximab, and tirofiban?

Back 16

glycoprotein IIbIIIa antagonists; platelet aggregation is powerfully (-)

Front 17

What agents are used to minimize the risk for recurrent MI, recurrent unstable angina, and to decrease the risk of stent re-occlusion following coronary artery angioplasty?

Back 17

Glycoprotein IIbIIIa antagonists
eptifibatide, abciximab, and tirofiban

Front 18

MOA of heparin?

Back 18

binds antithrombin III and enhances its activity of (-) clotting factors IX, X, XI, XII and factors II and XIII

Front 19

What clotting factors does Antithrombin III normally bind and inhibit?

Back 19

IX, X, XI and XII
also affects factor II and XIII

Front 20

What is the major drug for pulmonary embolus, DVT, acute phase of MI, and in dialysis machines?

Back 20

HEPARIN

Front 21

In case of Heparin overdose what may be used as the antidote?

Back 21

protamine sulfate

Front 22

Low molecular weight heparin (LMWH) includes what 3 agents?

Back 22

dalteparin, enoxaparin, tinzaparin

Front 23

MOA of LMWH?

Back 23

inhibits primarily factor X

Front 24

How is LMWH advantageous?

Back 24

serum anticoaguglation studies do not need to be monitored

Front 25

Do serum anticoagulation studies need to be monitored in LMWH therapy or in heparin use?

Back 25

Regular heparin use

Front 26

What agents antagonize vit K-dependent activation of factors X, IX, VII, II?

Back 26

Warfarin (coumadin) and dicumarol

Front 27

How long does it take for therapeutic effect of Warfarin to take place?

Back 27

3-5 days

Front 28

What is the major ADR of Warfarin?

Back 28

hemorrhage

Front 29

This anticoagulant is CI in pregnancy?

Back 29

Warfarin

Front 30

Overdose of Warfarin (coumadin) may be counteracted by what?

Back 30

vitaminK

Front 31

What is the DOC for stroke prevention in those with CAD?

Back 31

ASPIRIN

Front 32

MOA of Aspirin?

Back 32

IRREVERSIBLE COX (-)
platelet aggregation inhibitor

Front 33

Agent that inhibits degranulation, minimizing ACP and TXA release and is also a uricosuric agent?

Back 33

Sulfinpyrazone

Front 34

What is a uricosuric agent?

Back 34

blocks proximal tubule resorption of uric acid
(so, much uric acid goes out with the urine --> uric-os-uric)

Front 35

MOA of Dipyridamole (Persantine) ?

Back 35

phosphodiesterase (-); therefore increases cAMP and this inhibits TXA2

Front 36

In combination with warfarin what is Dipyridamole used for?

Back 36

to prevent thromboembolic events of cardiac valve replacement

Front 37

In combination with aspirin what is Dipyridamole used for?

Back 37

chronic platelet aggregation inhibition

Front 38

What drug is used in conjunction with radioactively tagged thallium or sestamibi, to facilitate max delivery of these agents to HEALTHY bv's of the heart?

Back 38

Dipyridamole (persantine)

Front 39

MOA of Clopidogrel?

Back 39

Inhibits the ADP-mediated platelet aggregation process; thus powerful platelet aggregation (-)

Front 40

All patients who receive stents, as a standard of practice, are prescribed what?

Back 40

Clopidogrel

Front 41

This agent binds to antithrombin and activates it to selectively inhibit only factor X?

Back 41

Fondaparinux

Front 42

What is Fondaparinux used for?

Back 42

DVT and patients with a heparin hypersensitivity

Front 43

What is the MOA of Argatroban, bivalirudin, and lepirudin?

Back 43

Direct thrombin (-); bind to a block the active site on thrombin (factor II)

Front 44

How are Argatroban, bivalirudin, and lepirudin administered?

Back 44

IV

Front 45

What direct thrombin (-) is hepatotoxic?

Back 45

Argatroban

Front 46

What direct thrombin inhibitor has been associated with fatal anaphylactic rxns?

Back 46

Lepirudin

Front 47

What agents prevent coagulation?

Back 47

anticoagulants;
heparin, LMWH, warfarin/dicumarol, fondaparinux, and the direct thrombin inhibitors

Front 48

What agents lyse or break preformed clots?

Back 48

throbolytics;
streptokinase, urokinase, and tPA

Front 49

Some uses of what agents include PE, DVT, acute MI, arterial thrombosis, and occluded access shunts?

Back 49

Thrombolytics

Front 50

MOA of streptokinase?

Back 50

ACTIVATES PLASMINOGEN; and also catalyzes degadation of fibrinogen and factors V and VII

Front 51

MOA of Urokinase?

Back 51

activating plasminogen

Front 52

What is Urokinase derived from?

Back 52

fetal renal cells

Front 53

What is streptokinase derived from?

Back 53

bacteria

Front 54

Which agent is less antigenic; streptokinase or urokinase?

Back 54

Urokinase because it is derived from fetal renal cells and not bacteria

Front 55

What agents will ONLY activate plasmin that is already bound to fibrin?

Back 55

tPA; also known as alteplase

Front 56

This agent is unlike the other thrombolytics in that is targets just the areas that have already begun to form clots, what is the agent?

Back 56

tPA; also known as alteplase

Front 57

What 2 agents have the same MOA as tPA?

Back 57

Tenecteplase and reteplase

Front 58

tPA is very effective for what 3 things?

Back 58

MI, PE, and acute ischemic stroke

Front 59

Which agent is a recombinant non-glycosylated form with a longer half-life than alteplase? Tenecteplase OR reteplase?

Back 59

Reteplase

Front 60

What are the 4 classes of antiarrhythmics?

Back 60

silly bunnies punch cats
Sodium Channel Blocker
Beta Blocker
Potassium Channel Blockers
Calcium Channel Blockers

Front 61

Class 1 antiarrhythmics are what?

Back 61

sodium channel blockers

Front 62

What effect do sodium channel blockers have?

Back 62

decrease the upstoke during depol and overall, decrease the cardiac AP amplitude

Front 63

What are the class 1A antiarrythmics?

Back 63

quinidine
procainamide

Front 64

What are the Class 1B antiarrhythimcs?

Back 64

lidocaine and phenytoin

Front 65

what is the class 1C antiarrhythmic?

Back 65

flecainide

Front 66

Class 1A antiarrhythmics serve to slow what phase of depolarization?

Back 66

phase 0

Front 67

Quinidine is effective for what?

Back 67

both atrial and ventricular tachycardias

Front 68

Procainamide is used for what?

Back 68

ventricular and supraventricular tachycardias

Front 69

What adverse effects may the Class1A antiarrhymics have?

Back 69

may cause hypotension as well as QT prolongation

Front 70

What class of antiarrhythmics are particularly suited to minimizing and controlling abnormal arrhythmias that are generated from abnormal automaticity?

Back 70

Class 1B

Front 71

Which class 1B antiarrhythmic is rarely used as as an antiarrhythmic?

Back 71

Phenytoin

Front 72

What is lidocaine used for?

Back 72

ventricular tachycardia or ventricular fivrillation

Front 73

What class of drugs mildly sow phase 0 while significantly shortening phase 3 repolarization?

Back 73

Class 1B

Front 74

This agent is effective in minimizing the chance of ectopic beats in the ventricle but is rarely used because of the risk of causing death?

Back 74

Flecainide

Front 75

What are the Class II antiarrhythmic agents?

Back 75

Propranolol and Metoprolol

Front 76

Which Class II antiarrhythmic agent is preferred? and why?

Back 76

Metoprolol; because it's beta-one specific

Front 77

What class of antiarrhythimc agents are particularly suited to reateing sympathetically-driven tachyarrhythmias, as well as atrial fibrillation, atrial flutter, and AV nodal re-entrant tachycardia?

Back 77

Class II antiarrhythmic agents

Front 78

Class II antiarrhythimcs supress what phase?

Back 78

Phase 4

Front 79

This agent can be used post-MI prophylactically b/c the #1 cause of death post-MI is arrhythmia?

Back 79

Metoprolol

Front 80

This class of antiarrhythmics increase action potentioal duration as phase 3 depolarization is prolonged?

Back 80

class III

Front 81

What agents are Class III antiarrhythmics?

Back 81

Bretylium and Amiodarone

Front 82

What is the first line aent for many ventricular and supraventricular arrhythmias?

Back 82

Amiodarone

Front 83

What are the side effects of Amiodarone? (2)

Back 83

pulmonary fibrosis as well as thyroid function derangements

Front 84

What agent potentiates digitoxin toxicity ?

Back 84

quinidine

Front 85

What agent causes reversible drug-induced lupu in 1/4th to 1/3rd of patients who take it on a chronic basis?

Back 85

Procainamide

Front 86

Verapaiml and diltiazem are useful in controlling what?

Back 86

ventricular rates in atrial fibrillation

Front 87

What agents are Class IV antiarrhythmics?

Back 87

calcium channel blockers;
diltiazem and verapamil

Front 88

This class of antiarrhythmics slow calcium conduction in tissues dependent on it (such as the AV node) and they slow phase 4, yielding a prolonged AP?

Back 88

Class IV antiarrhythmics

Front 89

MOA of glycosides?

Back 89

combine with Na/K ATPase of the cardiac cell membrane, inhibiting the Na-K pump

Front 90

What happens as a result of glycosides inhibiting the Na-K pump?

Back 90

prevents Na from being pumped out, Na levels rise and this (-) the Na/Ca exchanger (The Na-Ca exchanger normally pumps Na in and Ca out) As a result no Ca is pumped out and levels rise and excess Ca is pumped into the SR and this aids in overall contractility and therefore CO is increased

Front 91

What effect do glycosides have on overall cardiac muscle contractility and CO?

Back 91

They aid in overall cardiac muscle contractility and as a result CO is increased

Front 92

What agents are used for severe LV systolic dysfunction such as in CHF?

Back 92

glycosides

Front 93

change in vision can be one of the first indication of toxicity of what?

Back 93

glycosides

Front 94

Cardiac side effects of AV block and arrhythmias d/t glycosides is due primarily to what?

Back 94

decrease in intracellular K

Front 95

What agent cannot be used in those with liver problems as it relies on the liver for its metabolism?

Back 95

Digitoxin

Front 96

What agent is used instead of Digitoxin?

Back 96

Digoxin - excreted unchanged in the urine

Front 97

MOA of Dobutamine and dopamine?

Back 97

beta agonists for the beta-1 receptor - activating adenyl cyclase which converts AMP to cAMP; cAMP activates protein kinase which phosphorylates Ca channels = increase Ca in cells and increased force of contraction

Front 98

What agents are PDE inhibitors? (2)

Back 98

inamrinone ( new name for amrinone) and milrinone

Front 99

What normally converts cAMP to AMP?

Back 99

PDE - phosphodiesterase

Front 100

What is the MOA of PDE (-) ?

Back 100

(-) PDE which normally converts cAMP to AMP therefore incresing cAMP and causing a prolonged action of protein kinase resulting in an increase in Ca = + inotropy

Front 101

What may enhance glycoside toxicity?

Back 101

hypokalemia

Front 102

What is a common mode for such hypokalemia that may enhance toxicity of glycosides?

Back 102

concomitant use of thiazides or loop diuretics