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LCRS Pharmacology and Therapeutics > Haemostasis and thrombosis > Flashcards

Haemostasis and thrombosis Flashcards

1
Q

What percentage of blood volume is made up by red blood cells?

A

45%

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2
Q

Where are clotting factors found?

A

All within the plasma

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3
Q

What is the difference between haemostasis and thrombosis?

A

Haemostasis- physiological process that prevents excessive blood loss
Thrombosis- Pathophysiological- a blood clot is forming but this doesn’t always involve the rupture of the blood vessel itself

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4
Q

What is thrombosis normally only caused by?

A

Damage to the tunica intimate- it’s not stopping blood from leaking out because there is no hole in the first place so it’s pathophysiological

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5
Q

What are red thrombi?

A

Venous clots because they contain lots of erythrocytes and thrombin

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6
Q

What are white thrombi?

A

Arterial clots- they have a higher platelet component and are white because of macrophages entering the lesion and becoming foam cells

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7
Q

What is virchow’s triad which offers explanations for increased probability of thrombus formation?

A

Rate of blood flow
Consistency of blood
Vessel wall integrity

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8
Q

Why does rate of blood flow affect risk of thrombus formation?

A

Slow blood flow increases likelihood of thrombosis

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9
Q

What is slow blood flow a common explanation for?

A

DVT in legs because BP is very low

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10
Q

What affects the consistency of blood?

A

Balance between procoagulants and anticoagulants

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11
Q

What are the three main stages of coagulation?

A

Initiation
Amplification
Propagation

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12
Q

What types of drugs target each stage of coagulation?

A

Initiation- anticoagulants
Amplification- antiplatelets
Propagation- thrombolytics

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13
Q

Initiation starts with a tissue factor bearing cell, what is on a tissue factor bearing cell?

A

Tissue factor and prothrombinase complex

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14
Q

What does the prothrombinase complex consist of?

A

Factor 5a and factor 10a

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15
Q

What does the prothrombinase complex do?

A

Converts prothrombin (zymogen) to thrombin (active enzyme)

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16
Q

Where is antithrombin (AT-III) found and what does it do?

A

It is present within the blood and it inactivates factors 2a and 10a

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17
Q

In terms of thrombin generation and breakdown, what happens normally?

A

Thrombin will be formed by prothrombinase complex and broken down by anti-thrombin

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18
Q

Under pathological conditions, what can happen to thrombin?

A

Too much thrombin being formed

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19
Q

What is dabigatran?

A

Factor 2a inhibitor- direct thrombin inhibitor and first oral anticoagulant

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20
Q

What is the problem with dabigatran?

A

It can cause more bleeding than anticipated

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21
Q

What is rivaroxaban?

A

Factor 10a inhibitor

Direct inhibitor of factor 10a- also taken orally

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22
Q

What are dabigatran and rivaroxaban classified as?

A

Novel oral anticoagulant (NOAC)

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23
Q

What does heparin do?

A

Increases activity of antithrombin (AT-III)

Very effective anticoagulant that can be given IV or SC

24
Q

What is different about low MW heparin than normal?

A

It has a longer half life and it activates the portion of antithrombin that is more concerned with breakdown of 10a more so than 2a

25
Q

What is an example of low MW heparin?

A

Dalteparin

26
Q

What does warfarin do?

A

Vitamin K antagonist- orally active

27
Q

What is vitamin K important for?

A

Gamma-carboxylation of factor 2,7,9 and 10 which is important for these to function

28
Q

When are anticoagulants mainly used?

A

Treat venous thromboses
During surgery
In atrial fibrillation to prevent stroke

29
Q

What does thrombin do to platelets?

A

It interacts with platelets and causes platelet activation

30
Q

What happens to a platelet when it becomes activated?

A

The platelet changes shape and becomes more sticky and they aggregate around the area of thrombus formation

31
Q

What sort of receptors are found on the surface of a platelet?

A

G protein coupled receptors called protease activated receptors (PAR)

32
Q

How does thrombin activate platelets?

A

It binds to PAR

33
Q

What happens once thrombin binds to PAR?

A

It causes an increase in intracellular calcium which causes a change in shape of the platelets and also causes exocytosis of ADP

34
Q

What does ADP do after being exocytosed by a platelet?

A

It either has an autocrine effect on same platelet or a paracrine effect on neighbouring platelets by binding to P2Y12 receptors (ADP receptors)

35
Q

What does ADP binding to the ADP receptor cause?

A

Platelet to become more sticky and more activated which also causes the liberation of arachidonic acid

36
Q

What happens to arachidonic acid once it is liberated?

A

It is acted upon by COX to convert it to prostaglandins and thromboxane A2

37
Q

What does thromboxane A2 do?

A

It increases the expression of GlpIIb/IIIa on the surface of the platelet- this makes the platelet sticky

38
Q

What is clopidogrel?

A

Oral P2Y12 receptor antagonist- prevents platelet activation/aggregation

39
Q

What is aspirin?

A

Irreversible COX-1 inhibitor- reduces the production of thromboxane A2

40
Q

What is abciximab?

A

Monoclonal antibody that is directed against GlpIIb/IIIa

41
Q

Why is abciximab not used that often?

A

Aspirin and clopidogrel are very effective

42
Q

When are antiplatelets commonly used?

A

Arterial thrombosis
Acute coronary syndromes- clots in coronary arteries
Atrial fibrillation

43
Q

What is there large scale production of on the surface of platelets?

A

Thrombin

44
Q

What does thrombin do apart from activating platelets?

A

Converts fibrinogen to fibrin

45
Q

What does fibrin do?

A

It traps all the platelets within it like a net

46
Q

What are thrombolytics also known as?

A

Clot busters

47
Q

How do thrombolytics work?

A

They activate plasmin (anticoagulant factor) which breaks down preformed clots

48
Q

What is an example of thrombolytic drug?

A

Alteplase (IV)- A recombinant tissue type plasminogen activator (tPa)

49
Q

What is the problem with thrombolytics?

A

They are a little too effective and cause a lot of bleeding- only used in life threatening and dangerous conditions within a certain time period

50
Q

What are thrombolytics used for?

A

First line treatment of stroke

STEMI

51
Q

Where are you most likely to get venous thromboses?

A

In the popliteal veins where there is stasis

52
Q

How do you prevent DVT?

A

Restore the balance and increase amount of anticoagulants:
Prophylactically- anticoagulant drugs
After a PE- heparin or low MW heparin

53
Q

What is the difference between NSTEMI and STEMI?

A

NSTEMI- Non-ST elevated myocardial infarction
STEMI- ST elevated myocardial infarction
STEMI is more dangerous

54
Q

What causes NSTEMI?

A

Partial occlusion of a coronary artery- can lead to stable angina

55
Q

What is used to treat NSTEMI?

A

Antiplatelets

56
Q

What causes STEMI?

A

Full occlusion of a coronary artery- causes unstable angina

57
Q

What is used to treat STEMI?

A

Anti platelet drugs but in severe cases you may use thrombolytics to dissolve the clot before there is too much damage to the heart muscle

LCRS Pharmacology and Therapeutics (33 decks)

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