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 – factor 2a inhibitor (oral – NOAC-non vit k antag oral anti coag)

Rivaroxaban – factor 10a inhibitor (oral – NOAC)

Heparin – potentiates antithrombin III – less 2a + 10a (IV/SC)

Low Molecular Weight Heparin (e.g. Dalteparin) – activates antithrombin III – preferentially targets factor 10a

Warfarin – vitamin K antagonist– inhibits the production of factors 2, 7, 9 and 10

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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

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

Clopidogrel – irreversible ADP (P2Y12) receptor antagonist

Abciximab – monoclonal antibodies directed at GlpIIb/IIIa

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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 or other anticoagulants (and potentially thrombolytics if PE)

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 would you administer if Clot suspected:

a. in arteries
b. in veins

A

Thrombolytics for both if already formed,
if high risk of forming in future:
a. for arteries: anti-platelets
b. for veins: anti-coagulants