Exam 3- Anti-Thrombotics

Question 1

Primary hemostatic (4):

Answer 1

1. Endothelial injury
2. Adhesion
3. Activation
4. Aggregation

Question 2

What does endothelial injury expose?

Answer 2

Collagen and Von Willebrande’s factor

Question 3

What happens in the stage of adhesion?

Answer 3

Circulating platelets bind to vWF and collagen

Question 4

What 4 things occur during activation of primary hemostasis:

Answer 4

1. Shape change
2. Thromboxane A2 (TXA2) release
3. Granule release ADP and coagulation factors
4. GP IIb/IIIa conformation change

Question 5

What does anti-thrombotic therapy do?

Answer 5

Prevent thombosis

Promote bleeding

Question 6

What should you monitor on patients who are bleeding? (6)

Answer 6

• Hb
• bloody stools
• melena
• hematuria
• bruising
• oozing from arterial or venous puncture sites

Question 7

MOA of aspirin:

Answer 7

Inhibits platelet activation and aggregation but irreversibly inhibiting COX-1 which prevents conversion of arachidonic acid into thromboxane (platelet agonist and vasoconstrictor)

Question 8

Clinical uses for aspirin 3:

Answer 8

Acute coronary syndrome
MI
Percutaneous coronary intervention

Question 9

What kind of secondary prevention does aspirin have?

Answer 9

Stroke
TIA
PAD
CAD

Question 10

What 2 additional things does aspirin have?

Answer 10

Antipyretic

Analgesic

Question 11

4 adverse effects of aspirin:

Answer 11

Bleeding
GI upset
Anaphylaxis
Children develop Reye’s syndrome

Question 12

4 P2Y12 receptor antagonists:

Answer 12

Clopidogrel
Prasurgrel
Ticagrelor
Cangrelor

Question 13

Of the P2Y12 receptor antagonists, which one is IV only:

Answer 13

Cangrelor

Question 14

MOA of clopidogrel and prasugrel:

Answer 14

Inhibits ADP-induced platelet activation and aggregation

-irreversibly inhibit ADP P2Y12 receptor

Question 15

Compare clopidogrel and prasugrel:

Answer 15

Prasugrel is more potent and faster onset

Question 16

MOA of ticagrelor and cangrelor:

Answer 16

Inhibits ADP-induced platelet activation and aggregation

-reversible inhibit ADP P2Y12 receptor

Question 17

Compare ticagrelor and cangrelor:

Answer 17

Ticagrelor: twice daily administration
Cangrelor: continuous IV infusion

Question 18

Clinical uses for P2Y12 preceptor antagonists (3):

Answer 18

Acute coronary syndrome
MI
Percutaneous coronary intervention

Question 19

What secondary prevention does P2Y12 receptor antagonists have?

Answer 19

Stroke
TIA
PAD
CAD

Question 20

Adverse effects of ticagrelor:

Answer 20

Dyspnea

Question 21

When is prasugrel contraindicated?

Answer 21

In patients with history of stroke/TIA

Question 22

MOA of GP IIb/IIIa inhibitors:

Answer 22

Prevent platelet aggregation

-bind to GP IIb/IIIa receptors and prevent formation of fibrinogen platelet to platelet cross links

Question 23

Clinical uses for GP IIb/IIIa inhibitors:

Answer 23

Prevent ischemic compilations of percutaneous coronary intervention (PCI)

Question 24

Adverse effects of GP IIa/IIIb inhibitors:

Answer 24

Hemorrhage

Thrombocytopenia

Question 25

MOA of vorapaxar:

Answer 25

Inhibits thrombin-mediated platelet activation and aggregation by binding to the platelet protease-activated receptor-1 (PAR-1)

Question 26

Clinical uses for vorapaxar:

Answer 26

Secondary prevention of ischemic heart disease after MI or PAD

Question 27

Adverse effects of vorapaxar:

Answer 27

Increased risk of bleeding (life-threatening and fatal)

Question 28

What are the 4 parenteral anticoagulants:

Answer 28

Unfractionated heparin Low-molecular weight heparins (LMWH) Fondaparinux Direct Thrombin Inhibitors

Question 29

MOA of unfractionated heparin:

Answer 29

Heparin interacts with antithrombin to change its conformation and enhance its ability to inactivate clotting factor protease, especially thrombin (IIa), IXa, and Xa

Question 30

5 clinical uses for unfractionated heparin:

Answer 30

1. Venous thrombosis (PE and DVT) 2. Prevention of clotting in arterial and cardiac surgery 3. Arterial fibrillation with embolization 4. Prevent post-op DVT and PE after major abdominal-thoracic surgery 5. Acute coronary syndrome or MI

Question 31

Adverse effects of unfractionated heparin:

Answer 31

Hemorrhage Heparin-induced thrombocytopenia (HIT) -HIT is pro-thrombotic

Question 32

MOA of low molecular weight heparins:

Answer 32

Interacts with antithrombin to inactivate clotting factors IIa (thrombin) and Xa

Question 33

What do small size of heparin particles included in LMWH focus inhibition toward?

Answer 33

FXa

Question 34

What do large heparin molecules are needed to inhibit:

Answer 34

Thrombin

Question 35

Clinical uses for low molecular weight heparins:

Answer 35

``` Venous thrombosis (PE and DVT) Acute coronary syndrome or MI ```

Question 36

Adverse effects of low-molecular weight heparins: (3)

Answer 36

Hemorrhage Heparin-induced thrombocytopenia (HIT) Epidural or spinal hematoma

Question 37

Does unfractionated heparin or low molecular weight heparins have a lower risk of HIT?

Answer 37

Low-molecular weight heparins

Question 38

MOA of fondaparinux:

Answer 38

Avidly binds antithrombin with high specificity, resulting in inactivation of factor Xa

Question 39

Clinical uses of fondaparinux: (3)

Answer 39

Venous thromboembolism Post-op venous thromboembolism Anticoagulation with HIT

Question 40

Adverse effects of fondaparinux: (3)

Answer 40

Hemorrhage Does not cross react with HIT antibodies Epidural or spinal hematoma

Question 41

MOA of direct thrombin inhibitors:

Answer 41

Directly bind and inhibit unbound and fibrin-bound thrombin

Question 42

Clinical uses for direct thrombin inhibitors: (2)

Answer 42

Argatroban (treat pts with HIT) | Bivalirudin (treat pts undergoing coronary angioplasty)

Question 43

Adverse effect of direct thrombin inhibitors:

Answer 43

Hemorrhage

Question 44

3 oral anticoagulants:

Answer 44

Warfarin Dabigatran Direct factor X inhibitors

Question 45

MOA of warfarin:

Answer 45

Prevent reductive metabolism of inactive form of Vit K to its active form by Vit K reductase -Active Vit K is needed for production of function clotting factors 2, 7, 9, 10 as well as endogenous anticoagulant protein C and S

Question 46

Clinical uses for warfarin (2)

Answer 46

Venous thromboembolism | Thromboembolic complications with atrial fibrillation and/or cardiac valve replacement

Question 47

Adverse effects of warfarin (3)

Answer 47

Fatal or non-fatal bleeding Necrosis of skin DO NOT use with pregnancy

Question 48

MOA of dabigatron:

Answer 48

Active prodrug that inhibits thrombin that prevents development of thrombus -serine protease that enables the conversion of fibrinogen to fibrin during the coagulation cascade

Question 49

Clinical uses for dabigatran (2)

Answer 49

Venous thromboembolism | Thromboembolic complications associated with atrial fibrillation

Question 50

Adverse effects of dabigatran (2)

Answer 50

Fatal or non-fatal bleeding | Dyspepsia

Question 51

3 drugs that are direct factor X inhibitors:

Answer 51

Apixaban Edoxaban Rivaroxaban

Question 52

MOA of direct factor X inhibitors:

Answer 52

Competitively inhibits free and clot bound factor Xa (needed to activated thrombin)

Question 53

Clinical uses for direct factor X inhibitors (3)

Answer 53

1. Venous thromboembolic events (VTE) with replacements 2. Prevent stroke and systemic embolism with no valvular atrial fibrillation 3. Treat DVT and PE

Question 54

Combo of what with aspirin is used to reduce risk of major CV event in pts with chronic CAD or PAD

Answer 54

Rivaroxaban

Question 55

Adverse effects of direct factor X inhibitors:

Answer 55

Fatal or non-fatal bleeding

Question 56

How is oral aspirin effective if it has a high first pass metabolism?

Answer 56

All blood goes through portal quickly within 15 minutes

Question 57

What is problem with ibuprofen and aspirin?

Answer 57

Ibuprofen can block aspirin from doing its job since aspirin is irreversible and ibuprofen is

Question 58

Would a drug that inhibits CYP 2C19 amplify or reduce clopidogrel antiplatelet effect?

Answer 58

Reduce cause this coverts into active form (metabolite)

Question 59

Why does P2Y12 inhibitors cause sensation of dyspnea?

Answer 59

Increase neuronal signaling and increases conductivity of pulmonary vagal C-fibers

Question 60

5 indications for thrombocytes:

Answer 60

1. STEMI 2. DVT 3. Pulmonary embolism 4. Acute ischemic stroke 5. Acute peripheral arterial occlusion