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LCRS 1 > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

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

A

Around 45%

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2
Q

What normally has to be damaged for a thrombus to form?

A

Tunica intima

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3
Q

What is the difference between red and white thrombi?

A

Red – forms in veins – rich in fibrin and red blood cells

White – forms in arteries – rich in platelets and macrophages (foam cells)

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4
Q

What are the three parts of Virchow’s triad?

A

Stasis
Vessel wall injury
Hypercoagulability/consistency of blood (balance between procoagulants and anti-coagulants)

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5
Q

What are the three stages in the cell based theory of coagulation? State which types of drugs target each of the different stages.

A

Initiation – small-scale production of thrombin – ANTI-COAGULANTS
Amplification – large-scale thrombin production on the surface of platelets – ANTI-PLATELETS
Propagation – thrombin mediated generation of fibrin strands - THROMBOLYTICS

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6
Q

What does the tissue factor-bearing cell contain?

A

Tissue Factor

Prothrombinase Complex = Factor 5a + Factor 10a

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7
Q

Describe the process of initiation.

A

TF bearing cells activate factor 5 and factor 10 forming the prothrombinase complex (5a + 10a)
The prothrombinase complex converts prothrombin to thrombin

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8
Q

What is responsible for the inactivation of factors 2a and 10a?

A

Antithrombin (AT-III)

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9
Q

State some drugs that target the initiation stage of coagulation.

A 
Dabigatran  
Rivaroxaban   
Heparin 
Low Molecular Weight Heparin (e.g. Dalteparin)   
Warfarin
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10
Q

What are the indications of these anti-coagulants?

A

Venous thromboembolism (DVT + PE)
Prevent thrombosis during surgery
Atrial fibrillation – prophylaxis of stroke

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11
Q

Describe the amplification stage of coagulation.

A

Thrombin activates platelets and makes them more sticky so that they aggregate

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12
Q

Explain, in detail, how thrombin causes platelet activation.

A

Thrombin binds to PAR (platelet activated receptor) on the platelet membrane
This causes an increase in intracellular Ca2+ concentration from intracellular stores
This stimulates ADP exocytosis from dense granules
The ADP then binds to P2Y12 receptors (ADP receptor) on the same platelet or on neighbouring platelets, which leads to platelet activation/aggregation
Thrombin binding to the PAR also liberates arachidonic acid The arachidonic acid is converted by COX to thromboxane A2
Thromboxane A2 increases expression of GlpIIb/IIIa (which is involved in platelet aggregation)

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13
Q

State three drugs that target the amplification stage of coagulation and explain how they act.

A

Aspirin
Clopidogrel
Abciximab

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14
Q

What are the indications of these anti-platelet drugs?

A

Arterial thrombosis:  Acute coronary syndromes – myocardial infarction  Atrial fibrillation – prophylaxis of stroke

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15
Q

Describe the propagation stage of coagulation.

A

Thrombin converts fibrinogen to fibrin so fibrin strands are generated

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16
Q

Name an important thrombolytic and explain how it acts.

A

Alteplase – it is a recombinant tissue plasminogen activator (tPA)
Plasminogen is converted to plasmin, which is a protease that degrades fibrin

17
Q

What are the indications of thrombolytics?

A

First line treatment for stroke

STEMI

18
Q

What is a common site for the formation of deep vein thrombosis?

A

Popliteal veins

19
Q

How can DVT and PE be treated, either prophylactically and after it has happened?

A

Prophylactically – anticoagulants

After it happens – heparin or low MW heparin

20
Q

What is an acute coronary syndrome?

A

Any condition brought on by sudden, reduced blood flow to the heart

21
Q

What is NSTEMI?

A

Non-ST elevation myocardial infarction

This is caused by partial occlusion of a coronary artery and it can lead to stable angina

22
Q

Describe the management of NSTEMI.

A

Anti-platelets (e.g. clopidogrel and aspirin)

23
Q

What is STEMI?

A

ST-elevation myocardial infarction

This is caused by FULL occlusion of a coronary artery

24
Q

Describe the management of STEMI.

A

Anti-platelet drugs

Sometimes thrombolytics if the clot needs to be dissolved

25
Q

What is IIa

A

Thrombin

26
Q

Role of abciximab

A

Monoclonal antibodies directed at GlpIIb/IIIa

27
Q

Role of aspirin

A

Irreversible COX1 inhibitor – it reduces the production of thromboxane by platelets

28
Q

Role of clopidogrel

A

Irreversible ADP (P2Y12) receptor antagonist

29
Q

Role of dabigatran

A

factor 2a inhibitor

30
Q

Role of Rivaroxaban

A

factor 10a inhibitor

31
Q

Role of heparin

A

Potentiates antithrombin – less 2a + 10a

32
Q

Role of low molecular weight heparins

A

activates antithrombin – preferentially targets factor 10a

33
Q

Role of warfarin

A

Vitamin K epoxide reductase inhibitor – inhibits the production of factors 2, 7, 9 and 10

LCRS 1 (58 decks)

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