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Pharmacology - Winter > 2 - Antithrombotics & Anticoagulants > Flashcards

2 - Antithrombotics & Anticoagulants Flashcards

1
Q

What is aspirin?

A

COX 1 and 2 inhibitor (irreversible)

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2
Q

What is clopidogril?

A

ADP receptor antagonist

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3
Q

What is abciximab?

A

GPIIb/IIIa antagonist

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4
Q

What is heparin?

A

Antithrombin III activator

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5
Q

What is protamine sulfate?

A

Binds heparin and LMW heparin, so heparin inhibitor

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6
Q

What is warfarin?

A

Vitamin K antagonist

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7
Q

What is vitamin K needed for?

A

To activate coagulation factors

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8
Q

What is dabigatran?

A

Direct thrombin inhibitor

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9
Q

What is idarucizumab?

A

Binds direct thrombin inhibitors, so dabigatran inhibitor

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10
Q

What is rivaroxaban?

A

Direct factor Xa inhibitor

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11
Q

What is andexanet alfa?

A

Binds direct factor Xa inhibitors, so rivaroxaban inhibitor

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12
Q

What do tissue plasminogen activator (tPa) and streptokinase do?

A

Activate plasminogen

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13
Q

What is hemostasis?

A

Process of arresting the loss of blood from injured vessels (good thing)

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14
Q

How is a hemostatic plug formed and stabilized?

A
  • Formed by aggregated platelets

- Stabilized by cross-linked fibrin fibers

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15
Q

What is another name for a hemostatic plug?

A

Blood clot

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16
Q

What is a thrombosis?

A

Unwanted formation of a hemostatic plug or clot inside a blood vessel or heart chamber

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17
Q

What is an emboli?

A
  • Portion of thrombus that breaks away and floats in blood

- If mobilized, will get stuck in capillaries; damage depends on where it lodges

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18
Q

What is the difference between venous and arterial clots?

A
  • Arterial are platelet rich, so can be prevented or controlled w/ anti-platelet agents
  • Venous are red blood cell rich, so can be prevented or controlled w/ agents that chew up fibrin
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19
Q

What stimulates thrombus formation in arteries?

A

Damaged endothelial layer, which can be caused by atherosclerosis or physical damage (ex: balloon angioplasty, stenting)

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20
Q

What happens if an emboli lodges in a cerebral capillary?

A

Acute ischemic stroke

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21
Q

What happens if an emboli lodges in coronary artery?

A

Acute myocardial infarction

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22
Q

When are venous thrombotic disorders a concern?

A
  • Post surgery
  • Long term bed rest
  • Sitting for long periods (plane ride)
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23
Q

What happens if an emboli lodges in capillaries in the lungs?

A

Pulmonary embolism

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24
Q

What are the 2 major sites where venous clots form?

A
  • Lower leg veins => deep vein thrombosis

- Right atria

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25
Q

Describe the process of formation of a platelet plug

A
  • Damaged endothelium causes exposed collagen
  • Platelets stick to exposed collagen
  • Platelets activate, releasing mediators (TxA2, ADP, serotonin) to excite other platelets
  • Released mediators activate resting platelets and recruit them to platelet plug
  • Activation of GPIIb/IIIa receptors binds fibrinogen linking platelets
  • Avalanche of platelet aggregation, which activates more platelets
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26
Q

Which drugs are platelet inhibitors?

A
  • Aspirin
  • Clopidogrel
  • Abciximab
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27
Q

Which drugs are anti-coagulants?

A
  • Heparin
  • Warfarin
  • Dabigatran
  • Rivaroxaban
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28
Q

Which drugs are thrombolytic agents?

A
  • tPa
  • Streptokinase
  • Urokinase
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29
Q

What is coagulation?

A
  • Clot formation

- Stabilizes platelet plug and thrombin increases fibrin formation to re-enforce platelet plug

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30
Q

What is fibrinolysis?

A

Clot dissolving

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31
Q

How can you prevent plug formation?

A
  • Selective change in prostaglandin levels (increase/maintain endothelial prostacyclin, decrease TxA2 levels in platelets)
  • Block effects of released mediators (block ADP receptor)
  • Prevent GPIIb/IIIa receptor coupling (block GPIIb/IIIa receptor)
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32
Q

What is the function of the COX enzyme?

A
  • Formation of prostaglandins
  • In platelets, produce TxA2, which promotes aggregation
  • In vascular endothelium, produces PGI2, which acts on platelets to increase stability
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33
Q

What determines how “sticky” platelets will be?

A

The balance between TxA2 and PGI2

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34
Q

What happens to platelets when aspirin blocks COX?

A
  • Aspirin blocks COX irreversibly, so the cell must produce new COX to be able to synthesize prostaglandins
  • Platelets don’t have a nucleus, so cannot generate new COX
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35
Q

What is the difference between platelets and vascular endothelial cells?

A

Endothelial cells have a nucleus, so they can produce COX, while platelets don’t

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36
Q

When is aspirin used w/ respect to thrombosis?

A
  • As prophylactic therapy, 81 mg daily
  • After MI, start w/ higher dose
  • To prevent cerebral ischemia and myocardial infarction
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37
Q

What are disadvantages to aspirin?

A

May produce problems associated w/ increased bleeding (ex: hemorrhagic stroke, GI bleeding, easy bruising)

38
Q

What happens when ADP binds to platelets?

A

Activates GPIIb/IIIa receptors

39
Q

When is clopidogrel used?

A
  • Effective in preventing ischemic stroke and MI

- Used during stent insertion during an MI

40
Q

What are disadvantages to clopidogrel?

A
  • Prolonged bleeding
  • Bleeding hard to stop
  • Easy bruising
41
Q

What happens when GPIIb/IIIa receptor on platelets is activated?

A

Fibrinogen can link platelets, causing aggregation

42
Q

Which platelet inhibitor is a pro-drug?

A

Clopidogrel

43
Q

What are some adverse effects of clopidogrel?

A
  • Neutropenia
  • Thrombotic thrombocytopenic purpura
  • Hemorrhage (increased w/ co-administration of ASA)
44
Q

How is abciximab administered?

A

IV

45
Q

What is the function of abciximab?

A
  • Monoclonal Ab against the GPIIb/IIIa receptor

- Prevents fibrinogen from binding and linking platelets, so prevents plug formation

46
Q

What is coagulation?

A
  • Consolidation/stabilization of the platelet clot

- Formation of fibrin strands

47
Q

What are the 2 pathways that result in thrombin and fibrin formation?

A
  • Intrinsic pathway – factors released from site of damage

- Extrinsic pathway – tissue factors released from elsewhere

48
Q

What happens to the platelet plug if there is no fibrin?

A

Platelet plug will dissolve

49
Q

What is the function of vitamin K?

A

Important cofactor in the synthesis of many coagulation factors

50
Q

Low vitamin K is associated w/ ______

A

Bleeding disorders

51
Q

What is the function of antithrombin III?

A

Inactivates thrombin and factor Xa => decreased fibrin formation

52
Q

____ activates the intrinsic pathway

A

Platelet-derived polyphosphates

53
Q

What is needed for factor X and II activation?

A

The pro-coagulant that is presented on the surface of activated platelets

54
Q

What is the function of thrombin?

A
  • Platelet agonist

- Converts fibrinogen to fibrin, which stabilizes the clot

55
Q

Where is heparin normally found?

A

In mast cells

56
Q

Which portion of heparin binds antithrombin?

A
  • Pentasaccharide sequence

- SO3 groups are critical for high affinity binding

57
Q

When is heparin used?

A
  • Prevention of arterial and venous thrombosis

- Tx of pulmonary embolism and acute MI

58
Q

_____ are anticoagulant of choice for use in pregnancy

A

Heparin and LWMH

59
Q

What is the antidote for heparin?

A

Protamine sulfate given IV

60
Q

How is heparin administered?

A

Parenterally (IV or deep subcutaneously)

61
Q

How is LMW heparin administered?

A

Parenterally (IV or subcutaneously)

62
Q

What is an advantage of LMWH over heparin?

A

LMWH has predictable effects

63
Q

What is LMWH used for?

A
  • Prevent post-op deep vein thrombosis/pulmonary embolism
  • Maintain extracorporeal circulation
  • Unstable angina
  • Ischemic stroke
64
Q

Warfarin is a _____

A

Coumarin

65
Q

What is an advantage to warfarin over heparin?

A

Warfarin is orally active

66
Q

Why is warfarin losing popularity?

A
  • Requires constant monitoring (INR)

- LMWH is given easily subcutaneously and has predictable effect

67
Q

What is the antidote to warfarin?

A

Administration of vitamin K

68
Q

What is enoxaparin?

A

LMWH

69
Q

What are some adverse effects of warfarin?

A
  • Dietary vitamin K may alter bleeding
  • Bleeding disorders
  • Many drug interactions that increase/decrease metabolism
70
Q

Is warfarin safe during pregnancy?

A

No

71
Q

What is the international normalized ratio (INR)?

A

Ratio of the patient’s prothrombin time to that of a control not on warfarin

72
Q

What is prothrombin time?

A

Measurement in seconds of the extrinsic pathway

73
Q

What is the target INR? What can happen from an INR that is too low or high?

A
  • Target INR = 2-3
  • INR < 2 may lead to thrombotic complications
  • INR > 3 may lead to bleeding
74
Q

When are dabigatran and rivaroxaban used?

A
  • Percutaneous cardiac interventions
  • Venous thromboembolism prophylaxis and management
  • Post hip/knee replacement
75
Q

What are major advantages to dabigatran and rivaroxaban?

A
  • Rapid predictable response and orally active

- Doesn’t require monitoring

76
Q

What is the primary adverse effect of dabigatran and rivaroxaban?

A

Bleeding, particularly if co-administered w/ NSAIDs

77
Q

What is the function of plasmin?

A

Break down fibrin, so removes clots

78
Q

When is tPa used?

A

Tx of myocardial infarction, massive pulmonary embolism, and acute ischemic stroke

79
Q

What is the cutoff point for efficacy of tPa?

A

4.5 hours

80
Q

What is the relationship between anistreplase and streptokinase?

A

Anistreplase is a pro-drug for streptokinase

81
Q

What is the function of streptokinase?

A

Forms a stable complex w/ plasminogen, making it active

82
Q

Out of the thrombolytic agents, which has the greatest antigenicity?

A

Streptokinase

83
Q

Out of the thrombolytic agents, which has the greatest fibrin specificity?

A

tPa

84
Q

Out of the thrombolytic agents, which has the longest half-life?

A

Streptokinase

85
Q

What is a disadvantage to fibrinolytic agents?

A

Cannot distinguish between fibrin of a beneficial hemostatic plug or an unwanted thrombi, so may cause bleeding in an unknown lesion (ex: peptic ulcer)

86
Q

Which drugs are fibrinolytic inhibitors?

A
  • Tranexamic acid

- Aminocaproic acid

87
Q

What are the functions of fibrinolytic inhibitors?

A
  • Bind to and inhibit plasmin and plasminogen

- Stabilize clots

88
Q

When are fibrinolytic inhibitors used?

A

To reduce peri- and post-operative bleeding, especially in px w/ bleeding disorders

89
Q

Vitamin K activates ______

A

Carboxylase

90
Q

When is vitamin K used?

A
  • Hemorrhagic diseases of newborns
  • Bleeding due to overdose of anticoagulant drugs (ex: warfarin)
  • Vitamin K deficiencies

Pharmacology - Winter (18 decks)

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