Haemostasis and Thrombosis Flashcards

1
Q

2 initial stages of thrombin production

A

TF bearing cells activate factors V and X to form prothrombinase complex

Prothrombinase complex activates factor II to IIa (prothrombin to thrombin)

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2
Q

endogenous antithrombus mechanism?

A

AT-III which inactivates fica and fXa

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3
Q

4 pharmacological targets for anticoagulants?

A

1) inhibition of fIIa
2) inhibition of fXa
3) up regulation of ATIII
4) reduce levels of vit K

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4
Q

factor IIa inhibitor?

A

Dabigatran

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5
Q

What is dabigatran

A

factor IIa inhibitor

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6
Q

factor Xa inhibitor?

A

Rivaroxaban

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7
Q

What is Rivaroxaban

A

factor Xa inhibitor

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8
Q

What is heparin

A

ATIII activator

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9
Q

An ATIII activator?

A

Heparin

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10
Q

What does warfarin do?

A

Reduce vit K levels

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11
Q

What is vit K necessary for?

A

Generation of factors II, VII, IX and X

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12
Q

What is needed for. Generation of factors II, VII, IX and X

A

Vit k

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13
Q

What can reduce vit K levels

A

Warfarin

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14
Q

Why is dabigatran rarely used.

A

Dabigatran can cause bad GI bleeding

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15
Q

Treatment for DVT, pre and post full diagnosis?

A

Dalteparin pre, and warfarin and rivaroxaban post

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16
Q

what is dalteparin an example of

A

LMW heparin

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17
Q

Treatment for a pulmonary embolism?

A

Dalterparin/heparin and rivoroxaban and warfarin

18
Q

example of LMW heparin

A

Dalteparin

19
Q

3 risk factors for DVT

A

rate of blood flow, consistency (constituents) of blood, blood vessel wall integrity

20
Q

What is given as anti-platelet therapy

A

Aspirin and clopidogrel

21
Q

thrombus in veins colour?

22
Q

Thrombus in artery colour? and why?

A

White because of foam cells

23
Q

What is always offered in NSTEMIs

A

Warfarin and clopidogrel, Antiplatelets

24
Q

What is used to treat NSTEMIs

A

Antiplatelets

25
What is used to treat STEMIs
Antiplatelets and thrombolytics
26
Difference between STEMI and NSTEMI
STEMI is a fully occluded coronary artery, NSTEMI is a partially occluded coronary artery
27
What factor activates platelets
IIa
28
Explain platelet activation molecular level (7/8)
thrombin binds to protease activated receptor PAR. this causes rise in intracellular Ca. this causes exocytosis of ADP from dense granules. ADP activates P2Y12 receptors which activates and aggregates platelets. PAR also liberates arachidonic acid (AA). Cyclooxygenase generates thromboxane A2 from AA. TXA2 activation causes expression of GPIIb/IIIa receptor on platelet surface which is involved in platelet aggregation
29
What does PAR stand for and do
Protease activates receptor Causes rise in intracellular Ca. this causes exocytosis of ADP from dense granules. PAR also liberates arachidonic acid (AA). Cyclooxygenase generates thromboxane A2 from AA.
30
What does clopidogrel do
Platelet inhibitor, P2Y receptor antagonist and so prevents activation and aggregation of platelets.
31
What does aspirin do
COX1 inhibitor so prevents AA from becoming TXA2
32
What does abciximab do
Binds to GpIIb/IIIa prevents aggregation
33
What drug Binds to GpIIb/IIIa prevents aggregation
Abciximab
34
What drug is a COX1 inhibitor so prevents AA from becoming TXA2
aspirin
35
What drug us a P2Y receptor antagonist and so prevents activation and aggregation of platelets.
Clopidogrel
36
How is fibrin generated
Large scale thrombin production, this binds to fibrinogen and makes fibrin strands
37
What do thrombolytics to
Convert plasminogen to plasmin which is a protease that degrades fibrin
38
Example of thrombolytic?
Alteplase
39
Alteplase is a?
thrombolytic
40
3 main antiplatelet drug categories?
COX inhibitors, P2Y receptor antagonists, and GpIIb/IIIa antagonists