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Pharmacology > Antiplatelet and Antithrombotics > Flashcards

Antiplatelet and Antithrombotics Flashcards

1
Q

What is aspirin?

A

COX I and II inhibitor

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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 LMW heparin?

A

Antithrombin III activator

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6
Q

What is protamine sulfate?

A

Binds heparin and LMW heparin

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7
Q

What is warfarin?

A

Vitamin K antagonist

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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

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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

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12
Q

What is tissue plasminogen activator

A

Activates plasminogen

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13
Q

What is hemostasis?

A

The process of arresting the loss of blood from injured vessels

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14
Q

What is hemostatic plug?

A

Formed by aggregated platelets and then stabilized by cross-linked fibrin fibres

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15
Q

What is thrombosis?

A

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

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16
Q

What is good and bad about the formation of a clot in a blood vessel?

A

It is beneficial to stop bleeding (normal hemostasis)

But may also obstruct blood flow

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17
Q

What is a thrombus?

A

Blood clot attached to a blood vessel
It may obstruct flow
Pieces may break off which then “plug” capilllaries

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18
Q

What is an emboli?

A

Portion of thrombus that breaks away
Clot floating in the blood
If “mobilized” it will get stuck in the capillaries
The damage depends on where it lodges (heart, brain, lung)

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19
Q

How are the arterial and venous sides of circulation different (from a blood clotting perspective)?

A

Arterial side is platelet rich

Venous side is rich in red blood cells

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20
Q

What is atherosclerosis? Why is it problematic?

A

It the build of cholesterol and it may partially obstruct blood flow in the arteries. Eventually the plaque damages the endothelium (thrombus forms)
Blood flow is blocked by the atherosclerosis and the thrombus.
If the thrombus ruptures it’s called an embolus and it can lodge in the capillary and block flow

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21
Q

What happens if there is damaged endothelium in the parties? What damages the endothelium?

A

The damaged endothelial layer stimulates thrombus formation
Atherosclerosis damages the endothelial layer
Physical damage can be caused by ballon angioplasty, stenting

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22
Q

What happens if an artery perfuses a the brain and there’s thrombosis?

A

The emboli can lodge in the cerebral capillaries and cause an acute ischemic stroke

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23
Q

What happens if an artery perfuses the heart muscle and there’s thrombosis?

A

The emboli can lodge in coronary arteries and cause an acute myocardial infarction

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24
Q

Describe venous thrombosis

A

It involves red blood cells and not platelets
It is more related to stagnant flow in the veins and/or atria
Problems post surgery, long term bed rest or just sitting (long plane rides)
Clots form and if dislodges (emboli) the flow in the capillaries in the lungs can be obstructed (pulmonary embolism)

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25
Q

What are the two major sites of venous clot formation?

A 
Lower leg veins (deep vein thrombosis)
Right atria (if atria is not contracting properly)
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26
Q

What is the platelet response to vascular injury?

A
  1. Formation of a platelet plug
  2. Coagulation (clot formation)
  3. Fibrinolysis
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27
Q

How does a platelet plug form?

A

Platelet adhesion
Platelet activation
Platelet aggregation

28
Q

Describe coagulation

A

It stabilizes the clot (platelet plug)

Thrombin increases fibrin formation (re-infroces platelet plug)

29
Q

What is fibrinolysis?

A

Clot dissolving (as would heals the clot is removed)

30
Q

What drugs affect the formation of a platelet plug?

A

Platelet inhibitors

  • COX inhibition (aspirin)
  • ADP receptor blockers (clopidogrel)
  • GPIIb/IIIa block (abciximab)
31
Q

What drugs affect coagulation?

A

Anticoagulants

  • thrombin inhibition (heparin)
  • vitamin K antagonist (warfarin)
  • thrombin antagonist (dabigatran)
  • factor Xa inhibitor (rivaroxaban)
32
Q

What drugs affect fibrinolysis?

A

Thrombolytic agents

-fibrin breakdown (tissue plasminogen activator)

33
Q

How does prostacyclin affect platelet aggregation?

A

Healthy, intact endothelium releases prostacyclin (PGI2) into the plasma
It binds to the platelet membrane receptors, causing the synthesis of cAMP
cAMP stabilizes inactive GPIIb/IIIa receptors and inhibits platelet aggregation agents or calcium

34
Q

What are platelet activating mediators?

A

Thromboxane A2
ADP
Serotonin
PAF

35
Q

What are the steps to the formation of a platelet plug?

A

Damaged endothelium causes the exposure of collagen
Platelets stick to exposed collagen
Platelets are activated and release mediators to excite other platelets
Released mediators activate resting platelets and recruit to the platelet plug
Activation of GPIIb/IIIa receptors binds fibrinogen linking platelets
Avalanche of platelet aggregation (which releases more mediators)

36
Q

How do we prevent plug formation?

A

Selective change in prostaglandin levels
-increase/maintain endothelial prostacyclin
-decrease thromboxane A2 levels in platelets
Block effects of released mediators (block ADP receptor)
Prevent GPIIb/IIIa receptor coupling (block the receptor)

37
Q

How does aspirin prevent the formation of platelet plugs?

A

Aspirin inhibits cyclo-oxygenase (irreversibly blocks it)
COX is the enzyme necessary for the formation of prostaglandins
Prostaglandins are ubiquitous and do many things

38
Q

Why does the inhibition of COX enzymes prevent platelet formation?

A

In platelets, COX produces thromboxane A2 which promotes aggregation
In vascular endothelium, COX produces PGI2, which acts on platelets to increase stability (less likely to aggregate)
A balance between TxA2 and PGI2 determines how “sticky” the platelets will be

39
Q

If COX produces TxA2 and PGI2, how does aspirin impede aggregation?

A

Aspirin irreversibly blocks COX, so a cell needs to produce new COX to be able to synthesize TxA2 and prostaglandins
Platelets lack a nucleus so they cannot generate new COX. The lifespan of a platelet is 7-10 days, so throughout, there won’t be any new TxA2
Vascular endothelial cells have nucleus and are able to generate more COX and therefore more PGI2
So the balance shifts towards PGI2

40
Q

What are the problems associated with the use of aspirin?

A

Can cause problems associated with increased bleeding

  • hemorrhagic stroke
  • GI bleeding
  • easy bruising
41
Q

What does clopidogrel do?

A

It prevents ADP from binding to platelets (ADP binding to platelets activates the GPIIb/IIIb receptors)
Fibrinogen is now unable to link platelets and aggregation is significantly decreased
It is effective in preventing ischemic stroke and myocardial infarction
It is given routinely during stent insertion during a MI

42
Q

What is the problem with clopidogrel?

A 
Bleeding may be prolonged and hard to stop
Easy bruising (bleeding)
43
Q

What does abciximab do?

A

It’s a monoclonal antibody against the GPIIb/IIIa receptor. This prevents fibrinogen from binding and “joining” platelets and aggregation of platelets can not occur
Potential problems for bleeding and bruising
Given IV

44
Q

What is the goal of the coagulation pathway?

A

There are two pathways that result in thrombin activation and ultimately fibrin formation. Both pathways involve a number of coagulation factors and the purpose of both it to convert prothrombin into thrombin. Thrombin in turn converts fibrinogen into fibrin

45
Q

What activates the intrinsic pathway of coagulation?

A

Factors released from the site of damage

46
Q

What activates the extrinsic pathway of coagulation?

A

Tissue factors released from elsewhere (not the site of damage)

47
Q

Why is vitamin K important?

A

Vitamin K is an important factor in the synthesis of many of the coagulation factors (factors II, VII, IX and X)
Low vitamin K is associated with bleeding disorders

48
Q

What does antithrombin III do?

A

It naturally inactivates thrombin and Factor Xa (decreasing fibrin formation)

49
Q

What does heparin do?

A

It is usually given as unfractionated heparin and low molecular weight heparin
Heparin leads to thrombin inactivation by binding to antithrombin and increasing its activity
It prevents expansion of the thrombi by blocking fibrin formation

50
Q

When do we use heparin?

A

Used in the prevention of arterial and venous thrombosis (post-op venous thrombosis, coronary re-thrombosis following thrombolytic treatment)
Used in the treatment of pulmonary embolism and acute MI
Anticoagulant choice in pregnancy (does not cross the placenta)

51
Q

How do we treat excessive bleeding (due to heparin)?

A

Antidote: protamine sulfate, given IV

52
Q

How is heparin given (not LMWH)? What is the IV half life? When is the anticoagulant response? What is the bioavailability? What is the major adverse effect? What is the setting for therapy?

A 
IV or SC
2 hours
Variable
20%
Frequent bleeding
Hospital
53
Q

How is low molecular weight heparin given? What is the IV half life? When is the anticoagulant response? What is the bioavailability? What is the major adverse effect? What is the setting for therapy?

A 
IV or SC
4 hours
Predictable
90%
Less frequent bleeding
Hospital and outpatient
54
Q

What is warfarin?

A

It is a vitamin K antagonist

55
Q

Why is warfarin losing popularity?

A

It requires constant monitoring and visits to the clinic (International Normalized Ratio needs to be measured)
LMWH is given easily SC and has predicable/reproducible effects
Newer oral anticoagulants are now available (NOACs)

56
Q

What are the adverse effects of warfarin?

A 
Effects are variable
Bleeding disorders (major problem)
Many drug interactions
Dietary interactions
Avoid during pregnancy (teratogenic and may cause abortion)
57
Q

What are dabigatrin and rivaroxaban?

A

They are novel oral anticoagulants (NOACs)
Dabigatran directly inhibits thrombin
Rivaroxaban directly inhibits factor Xa

58
Q

When do we use novel oral anticoagulants?

A 
Percutaneous cardiac interventions
Venous thromboembolism (prophylaxis and management)
Hip/knee replacement (post surgery)
59
Q

Why are NOACs superior to heparin and warfarin?

A

Heparin and warfarin have very narrow therapeutic windows

These can be used without measuring drug levels or coagulation times

60
Q

Why are dabigatrin and rivaroxaban so great?

A

They are orally active direct thrombin inhibitors (decrease in fibrin formation, natural dissolution of clot)
Used post-op for knee and hip replacements to prevent/manage venous thromboembolism
Rapid, predictable response and orally active

61
Q

What is the response to excessive bleeding due to dabigatrin?

A

Intravenous antidote: idarucizumab

It’s monoclonal antibody fragment that binds to dabigatrin

62
Q

What is the response to excessive bleeding due to rivaroxaban?

A

Andexanet alfa

It’s a modified Factor Xa molecule that binds directly to to factor Xa inhibitors

63
Q

What does plasmin do?

A

It breaks down fibrin, dissolving the clot

64
Q

What is tPA?

A

Tissue plasminogen activator

Can be used as a fibrinolytic drug (alteplase)

65
Q

What does tPA do?

A

It activates tissue plasminogen that is bound to fibrin

The increase in plasmin breaks down the clot

66
Q

What do we use tPA for?

A

MI
Massive pulmonary embolism
Acute ischemic stroke

Pharmacology (15 decks)

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