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Pharmacology > Exam 3- Anti-Thrombotics > Flashcards

Exam 3- Anti-Thrombotics Flashcards

1
Q

Primary hemostatic (4):

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

What does endothelial injury expose?

A

Collagen and Von Willebrande’s factor

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3
Q

What happens in the stage of adhesion?

A

Circulating platelets bind to vWF and collagen

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4
Q

What 4 things occur during activation of primary hemostasis:

A
  1. Shape change
  2. Thromboxane A2 (TXA2) release
  3. Granule release ADP and coagulation factors
  4. GP IIb/IIIa conformation change
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5
Q

What does anti-thrombotic therapy do?

A

Prevent thombosis

Promote bleeding

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6
Q

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

A
  • Hb
  • bloody stools
  • melena
  • hematuria
  • bruising
  • oozing from arterial or venous puncture sites
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7
Q

MOA of aspirin:

A

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

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8
Q

Clinical uses for aspirin 3:

A

Acute coronary syndrome
MI
Percutaneous coronary intervention

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9
Q

What kind of secondary prevention does aspirin have?

A

Stroke
TIA
PAD
CAD

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10
Q

What 2 additional things does aspirin have?

A

Antipyretic

Analgesic

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11
Q

4 adverse effects of aspirin:

A

Bleeding
GI upset
Anaphylaxis
Children develop Reye’s syndrome

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12
Q

4 P2Y12 receptor antagonists:

A

Clopidogrel
Prasurgrel
Ticagrelor
Cangrelor

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13
Q

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

A

Cangrelor

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14
Q

MOA of clopidogrel and prasugrel:

A

Inhibits ADP-induced platelet activation and aggregation

-irreversibly inhibit ADP P2Y12 receptor

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15
Q

Compare clopidogrel and prasugrel:

A

Prasugrel is more potent and faster onset

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16
Q

MOA of ticagrelor and cangrelor:

A

Inhibits ADP-induced platelet activation and aggregation

-reversible inhibit ADP P2Y12 receptor

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17
Q

Compare ticagrelor and cangrelor:

A

Ticagrelor: twice daily administration
Cangrelor: continuous IV infusion

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18
Q

Clinical uses for P2Y12 preceptor antagonists (3):

A

Acute coronary syndrome
MI
Percutaneous coronary intervention

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19
Q

What secondary prevention does P2Y12 receptor antagonists have?

A

Stroke
TIA
PAD
CAD

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20
Q

Adverse effects of ticagrelor:

A

Dyspnea

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21
Q

When is prasugrel contraindicated?

A

In patients with history of stroke/TIA

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22
Q

MOA of GP IIb/IIIa inhibitors:

A

Prevent platelet aggregation

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

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23
Q

Clinical uses for GP IIb/IIIa inhibitors:

A

Prevent ischemic compilations of percutaneous coronary intervention (PCI)

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24
Q

Adverse effects of GP IIa/IIIb inhibitors:

A

Hemorrhage

Thrombocytopenia

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25
Q

MOA of vorapaxar:

A

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

26
Q

Clinical uses for vorapaxar:

A

Secondary prevention of ischemic heart disease after MI or PAD

27
Q

Adverse effects of vorapaxar:

A

Increased risk of bleeding (life-threatening and fatal)

28
Q

What are the 4 parenteral anticoagulants:

A

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

29
Q

MOA of unfractionated heparin:

A

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

30
Q

5 clinical uses for unfractionated heparin:

A
  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
31
Q

Adverse effects of unfractionated heparin:

A

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

32
Q

MOA of low molecular weight heparins:

A

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

33
Q

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

A

FXa

34
Q

What do large heparin molecules are needed to inhibit:

A

Thrombin

35
Q

Clinical uses for low molecular weight heparins:

A 
Venous thrombosis (PE and DVT) 
Acute coronary syndrome or MI
36
Q

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

A

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

37
Q

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

A

Low-molecular weight heparins

38
Q

MOA of fondaparinux:

A

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

39
Q

Clinical uses of fondaparinux: (3)

A

Venous thromboembolism
Post-op venous thromboembolism
Anticoagulation with HIT

40
Q

Adverse effects of fondaparinux: (3)

A

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

41
Q

MOA of direct thrombin inhibitors:

A

Directly bind and inhibit unbound and fibrin-bound thrombin

42
Q

Clinical uses for direct thrombin inhibitors: (2)

A

Argatroban (treat pts with HIT)

Bivalirudin (treat pts undergoing coronary angioplasty)

43
Q

Adverse effect of direct thrombin inhibitors:

A

Hemorrhage

44
Q

3 oral anticoagulants:

A

Warfarin
Dabigatran
Direct factor X inhibitors

45
Q

MOA of warfarin:

A

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

46
Q

Clinical uses for warfarin (2)

A

Venous thromboembolism

Thromboembolic complications with atrial fibrillation and/or cardiac valve replacement

47
Q

Adverse effects of warfarin (3)

A

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

48
Q

MOA of dabigatron:

A

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

49
Q

Clinical uses for dabigatran (2)

A

Venous thromboembolism

Thromboembolic complications associated with atrial fibrillation

50
Q

Adverse effects of dabigatran (2)

A

Fatal or non-fatal bleeding

Dyspepsia

51
Q

3 drugs that are direct factor X inhibitors:

A

Apixaban
Edoxaban
Rivaroxaban

52
Q

MOA of direct factor X inhibitors:

A

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

53
Q

Clinical uses for direct factor X inhibitors (3)

A
  1. Venous thromboembolic events (VTE) with replacements
  2. Prevent stroke and systemic embolism with no valvular atrial fibrillation
  3. Treat DVT and PE
54
Q

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

A

Rivaroxaban

55
Q

Adverse effects of direct factor X inhibitors:

A

Fatal or non-fatal bleeding

56
Q

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

A

All blood goes through portal quickly within 15 minutes

57
Q

What is problem with ibuprofen and aspirin?

A

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

58
Q

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

A

Reduce cause this coverts into active form (metabolite)

59
Q

Why does P2Y12 inhibitors cause sensation of dyspnea?

A

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

60
Q

5 indications for thrombocytes:

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

Pharmacology (14 decks)

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