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Year 3 CardioResp > Coag Cascade, Antiplatelet, Anticoagulatns & Thrombolytics > Flashcards

Coag Cascade, Antiplatelet, Anticoagulatns & Thrombolytics Flashcards

1
Q

What is naturally released by the endothelial cells of blood vessels to prevent clotting?

A

Nitric oxide & prostaglandins

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2
Q

What is nitric oxides job?

A

Dilate blood vessels

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3
Q

What is prostacylin’s job?

A

Bind to receptors on platelets, binding triggers reactions to prevent platelet activation and aggregation

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4
Q

What happens when there is a damaged blood vessel?

A

Less nitric oxide and less prostacyclin

  1. Blood vessels become more constricted and platelets become activated
  2. Platelets adhere to expose collagen with help of VWF = change shape
  3. Activated, different shaped platelets released ADP thrombin, thrombosis A2, 5HT, TA2
  4. Fibrinogen causes agglutination
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5
Q

Example of a popular antiplatelet?

A

Aspirin

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6
Q

How do platelets work?

A
  1. Platelet activated
  2. AA released from membrane phospholipid —> prostaglandin H2 (via COX-1)
  3. Prostaglandin H2 —> thromboxane A2
  4. TXA2 stimulates new platelets and aggregation
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7
Q

What stimulates aggregation of platelets and forms new platelets

A

TXA2 (thromboxane A2)

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8
Q

Aspirin MOA?

A

Irreversibly Inhibits COX-1 = no clot formation

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9
Q

Other examples of anti platelet drugs? (4)

A
  1. Clopidogrel
  2. Ticagrelor
  3. Ticlopidine
  4. Prasurgel
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10
Q

What (that is important) in platelet formation/aggregation does platelet release? (2)

A

Arachidonic Acid + ADP

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11
Q

What does ADP bind to in platelets?

A

P2Y12

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12
Q

What drugs are P2Y12 inhibitors?

A

Clopidogrel, tricagrelor

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13
Q

Why is ADP important in platelet aggregation? (MOA)

A

ADP binds to P2Y12, this activates GPIIb/IIIa receptors needed for fibrin-platelet linking and aggregation.

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14
Q

What drugs inhibit the GPIIb/IIIa receptors also causing anti platelet aggregation? (3)

A

Abciximab, eptifibatide and tirofiban

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15
Q

what pathways are in the clotting cascade?

A

Intrinsic and extrinsic

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16
Q

What is the intrinsic pathway?

A

Damage to the blood vessel wall directly

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17
Q

What is the extrinsic pathway?

A

Damage to the blood vessel wall plus surrounding tissues

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18
Q

Explain the intrinsic pathway?

A

XII activated when blood comes into contact with collagen = XIIa

XIIa activates XI = XIa

XIa activates IX = IXa

IXa activates X = Xa

Xa converts prothrombin = thrombin

Thrombin converts fibrinogen = fibrin

Fibrin = mesh that forms the clot

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19
Q

Explain the extrinisc pathway?

A

VII is activated by tissue factor released by damaged cells —> VIIa

VIIa activates X = INTRINSIC/COMMON PATHWAY

20
Q

What is the common pathway?

A

Xa = prothrombin = thrombin = fibrinogen = fibrin = clot

21
Q

3 Examples of anticoagulants?

A

Heparin, LMWH (enoxapasin & daltepasin)

22
Q

Anticoagulants bind to natural anticoagulants floating in blood called?

A

Antithrombin III

23
Q

What part of the coagulation cascade does antithrombin III attach to?

A

Xa and Thrombin

24
Q

How does anticoagulants affect antithrombin III

A

Rapidly increases its activity

25
Q

What does antithrombin III do to coag cascade Xa and thrombin?

A

Inactivates

26
Q

MOA of heparin

A

Bind to antithrombin III increasing its activity, increasing inactivation of Xa and Thrombin and CLOTS

27
Q

MOA of LMWH

A

Don’t bind to antithrombin they bind to Xa selectively, no affect on thrombin!!!

28
Q

Thrombin is not affected by what drug?

A

LMWH

29
Q

Major Side effect of heparin?

A

HIT (heparin induced thrombocytopenia)

30
Q

What happens in HIT

A

Antibody complexes formed when heparin bound to platelet factor 4

31
Q

MOA of apixaban and Rivaroxaban

A

Inhibits Xa preventing prothrombin —> thrombin

32
Q

Risk of apixaban?

A

BLEEDING

33
Q

When is protamine sulfate used?

A

When bleeding is excessive but cant be used for fondaparinux

34
Q

With which anticoagulants cant bleeding be controlled

A

Fondaparinux

35
Q

What is one of the oldest anticoagulants?

A

Warfarin

36
Q

What coag factor is prothrombin?

A

2

37
Q

What coag factors does vitamin K carboxylate/activate

A

2, 7 , 9, 10

38
Q

when does carboxylation of coag factors occur?

A

When reduced Vit K is present

39
Q

How does warfarin work?

A

Inhibits vit K epoxied reductase
- this stops vitamin K epoxide being recycled back into reduced vit K and being re-used to make more clotting factors

40
Q

Vit k is reduced into what?

A

Vit k epoxide

41
Q

What recycles vit k epoxide?

A

Vit k epoxide reductase

42
Q

3 disadvantages of warfarin?

A
  1. Many drug drug interactions
  2. Many drug food interactions
  3. Small therapeutic range
43
Q

How is patients on wafarin measured?

A

INR

44
Q

How is bleeding from warfarin managed?

A

Vitamin K - but takes up to 24 hours to reverse

Fresh frozen plasma preferred in emergencies

45
Q

What do thrombolytics act on?

A

Acts on current clot!

46
Q

Examples of thrombolytics? (3/2)

A

Alteplase
Rete please
Tenetecteplase
Urokinase/streptokinase (less selective)

47
Q

How to reverse thrombolytics?

A

Aminocaproic acid
Tranexamic acid

Stop fibrinolytic but Inhibit binding of plasminogen to fibrin + conversion of plasminogen to plasmin

Year 3 CardioResp (3 decks)

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