Antithrombins, Antiplatlet, Thrombolytic

Front 1

what are three low mw heparins

Back 1

• Enoxaparin (Lovenox), Dalteparin (Fragmin), Tinzaparin (Innohep)

Front 2

what is this drug a synthetic analog of heparin, inhibits factor Xa; injected SQ, indicated for the prevention of DVT and treatment of pulmonary embolism.

Back 2

Fondaparinux ,

Front 3

what is this drug: Inhibits formation of TXA2 by platelets and inhibits aggregation Prophylaxis and treatment of MI and stroke, peripheral arterial disease (PAD)

Back 3

aspirin

Front 4

Blocks platelet aggregation by blocking P2Y12 ADP receptor Prophylaxis of stroke, MI, PAD, and acute coronary syndromes (ACS)

Back 4

clopidogrel

Front 5

New drug; prodrug that binds to P2Y12 ADP receptor, irreversibly inhibits platelet aggregation Prophylaxis of thrombotic CV events in patients with ACS being managed with PCI

Back 5

prasugrel

Front 6

Blocks platelet aggregation by blocking P2Y12 ADP receptor Prophylaxis of recurrent stroke, prophylaxis of thrombosis during stent placement
Adverse side effects limit use! Clopidogrel preferred.

Back 6

ticlopidine

Front 7

Blocks platelet aggregation, causes vasodilation Intermittent claudication, peripheral arterial disease

Back 7

cilostazol

Front 8

Blocks platelet aggregation, inhibits adenosine uptake and is a cAMP phosphodiesterase inhibitor Prophylaxis of arterial thromboembolism

Back 8

dipyridamole

Front 9

Monoclonal antibody vs glycoprotein IIb/IIIa complex Acute coronary syndromes; during percutaneous coronary intervention (PCI)/angioplasty

Back 9

abciximab

Front 10

Blocks fibrinogen binding to IIb/IIIa complex.Acute coronary syndromes; during percutaneous coronary intervention (PCI)/angioplasty

Back 10

Eptifibatide (Integrilin)
Tirofiban (Aggrastat)

Front 11

Direct binding to thrombin Tx of heparin-induced thrombocytopenia (HIT);

Back 11

Lepirudin (Refludan)

Front 12

Direct binding to thrombin, inhibition of platelet activation Percutaneous coronary angioplasty

Back 12

Bivalirudin (Angiomax)

Front 13

Direct binding to thrombin HIT; coronary angioplasty in patients with HIT

Back 13

Argatroban (Acova)

Front 14

Activator of plasminogen Acute MI, pulmonary embolism,
arterial thrombosis, non-hemorrhagic ischemic stroke, DVT* (*not FDA approved)

Back 14

Alteplase (rt-PA) (Activase)

Front 15

Activator of plasminogen Acute MI, coronary artery thrombosis

Back 15

reteplase

Front 16

Activator of plasminogen Acute MI

Back 16

tenecteplase

Front 17

Nonenzymatic activator of plasminogen; stimulates dissolution of fibrin clots. Acute myocardial infarction
Pulmonary embolism
Deep venous thrombosis
Arterial thrombosis

Back 17

Streptokinase (Streptase)

Front 18

what is the purpose of anticoagulants

Back 18

sow clotting time and suppress coagulation

Front 19

what are the three types of anticoagulants

Back 19

heparin, warfarin, direct thrombin inhibitors

Front 20

what is uiques ab warfarin

Back 20

slow prolonged oral anticoag

Front 21

what is unique about the heparins

Back 21

rapid, sq parenteral anticoag

Front 22

what is unique about these
• Abciximab, eptifibatide, tirofiban

Back 22

blockers of glycoproetin iib/iia complex

Front 23

what antiplatlet drug is this: cAMP PDE inhibitor, blocks platelet aggregation and stimulates vasodilation

Back 23

cilostazol

Front 24

what three antiplatelt drugs do this: inhibit platelet ADP receptor and platelet aggregation

Back 24

• Clopidogrel, Ticlopidine, and Prasugrel

Front 25

____is a protein synthesized by the liver and which circulates in the plasma. It rapidly inhibits thrombin but only in the presence of heparin or naturally occurring heparin-like molecules.

Back 25

antithrombin III

Front 26

____inhibits activated coagulation factors of the intrinsic and common pathways, including thrombin, Xa, IXa, XIa, XIIa, and kallikrein.

Back 26

heparin

Front 27

Inhibition of ___ and __ are most important in the anticoagulant effect.

Back 27

thrombin and factor Xa

Front 28

Heparin __both the aPTT and the thrombin time; the PT is less effected, but at high plasma concentrations will also __ the PT.

Back 28

increase
increase

Front 29

where is hepain destroyed in the body

Back 29

GIT

Front 30

why cant heparin be given IM

Back 30

bc liklihood of hematoma

Front 31

what is teh diff bewtween how heparin is administered in emergent and non emergent situations

Back 31

Thus, when rapid anticoagulation is required, therapy is initiated with a bolus IV injection followed by a continuous IV infusion. When a slower onset is sufficient, i.e., prophylaxis prior to surgery, a subcutaneous injection of heparin or LMWH is typically used.

Front 32

after the start of infusion of heparin how long do you wait to do a PTT

Back 32

4 hrs

Front 33

how and where should SQ heparin be administered

Back 33

The drug should be injected in the smallest volume possible at different sites around the iliac crest, over the lower abdomen, or thigh. A small needle should be used to prevent massive hematoma.

Front 34

what is the dosing of heparin for surgical uses

Back 34

5,000 units two hours before surgery and every 8 or 12 hours thereafter

Front 35

what is the aPTT for heparin monitoring therapy

Back 35

aPTT = 1.5 to 2.5 times control.

Front 36

what are the three main side effects of heparin

Back 36

hemorrhage for overdsose, HIT ( due to formatio of antibodies direct against herpain platelet complexes

Front 37

what are contraindications for heparin

Back 37

HTN, vascular aneurysm, hemophilia, thrombocytopenia, intracranial hemorrhage, active tuberculosis, ulcerative lesions of the GI tract, threatened abortion, or visceral carcinoma, during or after eye and brain surgery, lumbar punction

Front 38

what are indication for heparin use

Back 38

DVT< pulm embolism. extra corpeal circulation, prophylaxis in post op. MI and unstable angina. DIC

Front 39

what do you use for OD of heparin

Back 39

proamin sulfate

Front 40

how do low mw heparins differe from unfractionated heparin

Back 40

having a greater ratio of anti-factor Xa to antithrombin (IIa) activity and less effect on platelet activity.

Front 41

what was the goal in devel of low mw heparins

Back 41

decreasing bleeding episodes while still retaining anticoagulant activity, especially for the prevention of deep venous thrombosis (DVT) in surgical patients.

Front 42

what are the more favorable characteristics of L MW heparins over reg heparin

Back 42

greater bioavailability after subcutaneous administration, a longer duration of anti-factor Xa activity that allows for less frequent dosing intervals, linear pharmacokinetics, possibly fewer side effects, i.e., less incidence of HIT syndrome, and lack of required laboratory monitoring

Front 43

when is Enozaparin ( L MWH) indicated for use:

Back 43

• In patients undergoing abdominal surgery who are at risk for thromboembolic complications.
• In patients undergoing hip replacement surgery, during and following hospitalization.
• In patients undergoing knee replacement surgery.
• In medical patients who are at risk for thromboembolic complications due to severely restricted mobility during acute illness.

Front 44

when is enoxaparin sodium injection indicated for use

Back 44

prophylaxis of ischemic complications of unstable angina and non-Q-wave myocardial infarction, when concurrently administered with aspirin.

Front 45

when is LMWH contraindicated

Back 45

during spinal / epidural anesthesia or spinal puncture because of the increased risk of spinal hematomas.

Front 46

administered in conjunction with warfarin sodium in the treatment of acute DVT or acute pulmonary embolism (PE) when initial therapy is administered in the hospital.

Back 46

Fondaparinux

Front 47

approved for use in patients with thrombosis related to heparin-induced thrombocytopenia (HIT). bind to active site of thrombin

Back 47

Lepirudin

Front 48

short-acting, synthetic direct thrombin binding inhibitor approved for patients with unstable angina undergoing coronary angioplasty

Back 48

bivalirudin

Front 49

short-acting, direct thrombin inhibitor that reversibly binds to the thrombin active site. does not require antithrombin III for antithrombotic activity and is highly selective for thrombin. capable of inhibiting the action of both free and clot-associated thrombin.

Back 49

Agatroban

Front 50

Warfarin prevent the reduction of vitamin K once it is oxidized by inhibiting

Back 50

the enzyme vitamin K epoxide reductase.

Front 51

is the onset and half of of warfarin long or shor

Back 51

long half life and delayed onset bc of it

Front 52

warfarin is 99 percent bound to __

Back 52

Albumin

Front 53

what are the main SEs of warfarin

Back 53

Hemorrhagem anorexia, vomiting. cutaneous lesions.

Front 54

what are contraindications for warfain

Back 54

preg, recent eye brain surgerry, severe htn, aneurysm

Front 55

how is long term anticoagulant therpay started

Back 55

with heparin and followed with warfarin

Front 56

what are the indications for warfarin

Back 56

DVTs and pulmonary embAtrial fibrillation (valvular heart disease, CHF, mitral stenosis, cardiomyopathy) MI (prevent mural thrombosis and systemic embolism). Rheumatic heart disease (emboli frequently associated with this disorder). Mechanical prosthetic valves, bioprosthetic mitral valves.

Front 57

warfarin is involved in many __ __ interactions

Back 57

drug drug

Front 58

how do you monitor warfarin therapy

Back 58

INR
INR should be 2-3 for less intense therapy

Front 59

how can treatment w warfarin be reversed

Back 59

withdraw therpay, admin vitamin K1, infusion of fresh frozen plasma

Front 60

what is the MOA of aspirin

Back 60

blocks production of TXA2 by covalently modifying and irreversibly inhibiting cyclooxygenase (COX-1), the enzyme that produces the precursor for TXA2. Thus, aspirin inhibits platelet aggregation and platelet mediator release.

Front 61

do higher doses of aspirin improve efficacy

Back 61

no but they do increase toxicty and interfere with PGI2 which would increase platlet aggregation and stim vasoconstriction

Front 62

what drug should given to almost all pts with evolvng MI

Back 62

Aspirin-Continue aspirin at a dose of 160 -162.5 mg daily for at least 30 days.

Front 63

what dosing can achieve the antiplatlet effects of aspirin

Back 63

1/2 of one 160 mg tablet

Front 64

when should aspirin use be avoided

Back 64

severe anemia, history of blood coagulation defects, gastrointestinal ulcers, or take anticoagulants.

Front 65

clopidogrel acts by irreversibly odifying the platlet ___ receptor

Back 65

ADP

Front 66

an cause life-threatening hematological adverse reactions, including neutropenia/agranulocytosis, thrombotic thrombocytopenic purpura (TTP) and aplastic anemia.

Back 66

ticlopidine

Front 67

indicated for the reduction of symptoms of intermittent claudication, as indicated by an increased walking distance. The use of this drug is contraindicated in patients with CHF of any severity.

Back 67

cilostazol

Front 68

Two additional drugs, ___ and __ are small peptide analogs of critical domains of fibrinogen that inhibit platelet aggregation by blocking ligand binding to the IIb/IIIa receptor. These two drugs are also used to percutaneous transluminal coronary angioplasty.

Back 68

eptifibatide and tirofiban,

Front 69

monoclonal antibody that prevents clot formation by binding the glycoprotein IIb/IIIa receptor, thus inhibiting platelet aggregation. The drug has greater antithrombotic activity than aspirin or heparin.

Back 69

abciximab

Front 70

a dimethylxanthine derivative and its metabolites improve blood flow by decreasing blood viscosity and improving erythrocyte flexibility

Back 70

Pentoxifylline

Front 71

what are some uses of pentoxifylline

Back 71

Intermittent claudication on the basis of chronic occlusive arterial disease of the limbs. Unlabelled uses: cerebrovascular insufficiency, TIAs, diabetic angiopathies, high-altitude sickness, Raynaud’s phenomenon, and others.

Front 72

when is it good to use thrombolytic therapy

Back 72

Acute myocardial infarction
b. Pulmonary embolism
c. Deep venous thrombosis
d. Ischemic stroke (special circumstances only).

Front 73

who should not get thrombolytic therapy

Back 73

pt with signif risk of hemorrhage

Front 74

to achieve a therapeutic effect, levels of rt-PA are much -- than normal in vivo levels.

Back 74

HIGHER

Front 75

Reteplase has a __plasma clearance and __ half-life than alteplase.

Back 75

FASTER AND SHORTER

Front 76

What thrombolytic is approved for use in acute ischmic stroke- if given within three house of onset

Back 76

alteplase

Front 77

Streptokinase has been shown to be effective when given IV for dissolution of __ __ in myocardial infarction.

Back 77

intracoronary thrombi

Front 78

how soon after start of sx should stroptokinase be admin

Back 78

within 90 mins

Front 79

what are normal values for a platlet count

Back 79

Normal Values = 130,000-400,000 per microliter)

Front 80

what is aPTT used for

Back 80

monitor anticoag therapy with unfractionated heparin

Front 81

what does warfarin therapy do to clotting tme int the PT test

Back 81

prlong it bc of inactivation of several clotting factors

Front 82

the __ is used to normalize PT test and monitor warfarin therapy

Back 82

INR

Front 83

how soon after addtion of ca ion and thromboplasin will plasma clot

Back 83

in 12-14 seconds

Front 84

is a format for reporting prothrombin times of patients on warfarin.

Back 84

INR

Front 85

what is the equation for PT ratio

Back 85

PT (Patient) /PT (Control)

Front 86

what is the equation for INR

Back 86

[PT (Patient) /PT (Control)] ISI

Front 87

what could a long thrombin time be caused by

Back 87

ncreased antithrombin activity, for example when plasma contains heparin.

Front 88

what is thrombin time and how is it measured

Back 88

Dilute thrombin is added to the patient’s plasma and control plasma and the clotting time are compared. Since no Ca++ is added to the plasma, clotting time is independent of reactions involved in the generation of thrombin and depends only upon the reactions initiated by adding the weak exogenous thrombin.