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Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Under normal conditions, in what form are platelets and coagulation factors present in the blood?

A

Unactivated

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2
Q

What is the physiological/pathological response when you cut yourself?

A

Bleed at site of injury
Clot is formed to stop the bleeding - platelets, Von Willebrand Factor and coagulation factors become activated (remain unactivated under normal conditions)
Clot remains confined to site of injury, it does not spread from site of injury so further clot formation has been switched off - natural anticoagulants, switch coagulation factors off which allows clot to be formed only where needed
Eventually, the clot disappears - fibrinolytic system

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3
Q

What natural heparins does the endothelium produce?

A

Tissue factor pathway inhibitor and thrombomodulin

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4
Q

How does the endothelium prevent things from sticking to it?

A

By producing chemicals such as nitric oxide and prostacyclin

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5
Q

Why are diseases associated with diffuse widespread endothelial injury often severe?

A

As you get widespread micro thromboses and endothelium failure leading to organ failure

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6
Q

What activates platelets and coagulation factors?

A

Emergence of an abnormal endothelial surface at the site of an injury

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7
Q

When vessel damage occurs, platelets become activated and stick to

A

subendothelial collagen, when they stick here they become activated

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8
Q

vWF has a receptor for some substances which it brings into the area of tissue damage, what are these?

A

Subendothelial collagens
Platelet glycoproteins
Factor 8

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9
Q

What is the physiological activator of coagulation?

A

Production of a small amount of clotting factor

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10
Q

What class of drugs are a large proportion of the population taking due to thrombotic disease?

A

Anti-platelets

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11
Q

What are glycoproteins IIb and IIIa receptors for?

A

Plasminogen

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12
Q

What are glycoprotein Ia and VI receptors for?

A

Collagen

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13
Q

How is clot formation activated?

A

Through binding of ADP, epinephrine and thrombin on the cell surface receptors

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14
Q

What contains products which have significant roles in clotting?

A

Granules

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15
Q

What allows granules to be released onto the platelet surface?

A

Degranulation into the canalicular system

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16
Q

What do glycoproteins IIb/IIIa, Ib, Ia/IIa and VI bind to?

A

GP IIb/IIIa binds fibrinogen
GP Ib binds vWF
GP Ia/IIa and GP VI bind collagen

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17
Q

Once the platelet clot is formed, platelets bind fibrinogen and hold it up waiting for

A

coagulation to cleave peptides off of the fibrinogen so that it can be converted into fibrin

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18
Q

What are the roles of platelets in haemostats?

A

Adhere to surface
Become activated
Become aggregated
Provide phospholipid surface for coagulation

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19
Q

Mobilisation of arachidonic acid makes

A

thromboxane A2 which causes aggregation

20
Q

What is the main aggregant?

A

Product of mobilisation of arachidonic acid by COX - thromboxane A2

21
Q

What are lots of the coagulation activations dependent on?

A

Phospholipid membrane

22
Q

What will mutations in the binding site of von Willebrand Factor cause?

A

Molecule failure and a form of von Willebrand disease

23
Q

What does failure of haemostasis result in clinically?

A

Bleeding

24
Q

When is the primary haemostatic (platelet) plug formed?

A

When platelets adhere to damaged endothelial surface

25
Q

What needs to happen once a clot has been formed and bleeding has stopped?

A

Entire coagulation cascade needs to be stopped as further clot formation is not necessary

26
Q

What are the three main natural anticoagulants?

A

Tissue factor pathway inhibitors
Proteins C (and co-factor protein S)
Antithrombin

27
Q

Tissue factor pathway inhibitor switches off

A

activated factor X and VIIa

28
Q

What is protein C activated by?

A

Thrombin

29
Q

What do protein C and co-factor protein S switch off?

A

Activated factor VIIIa and Va

30
Q

Antithrombin switches off

A

activated factor XIa, IXa, Xa, VIIIa and thrombin

31
Q

If a patient doesn’t have enough antithrombin, TFPI, protein C and S, they are at higher risk of

A

developing venous thromboembolism

32
Q

When a clot is formed, what forms t-PA?

A

Endothelium

33
Q

What does t-PA do?

A

Tissue plasminogen activator

Cleaves plasminogen into plasmin

34
Q

What does plasmin do in clots?

A

Starts to break down fibrin clot into fibrin degradation products

35
Q

What are D-dimers made by?

A

Activity of plasmin breaking down the clot and reorganising the vessel wall

36
Q

What is plasmin regulated by?

A

Alpha 2 antiplasmin and alpha 2 macroglobulin

37
Q

What is the the degradation of the fibrin clot known as?

A

Fibrinolysis

38
Q

How does aspirin work?

A

By preventing the enzyme cyclo-oxygenase from converting arachidonic acid into thromboxane A2
Thromboxane A2 is a key molecule in platelet aggregation

39
Q

How do clopidogrel, prasugrel and ticagrelor work?

A

Block ADP receptor on platelet which causes activation of arachidonic acid
High use in patients with stents

40
Q

How do abciximab, tirofiban and eptifibatide work?

A

Prevent binding of fibrinogen to GP IIb/IIIa receptor

41
Q

How does warfarin work?

A

Anti-coagulant
Inhibits activation of vitamin K
Vitamin K is required for the ultimate production of factors II, VII, IX and X
Effectively reduces these factors and produces an anti-coagulated state

42
Q

In what patients is warfarin most beneficial?

A

Patients with atrial fibrillation

43
Q

What are the functions of heparin?

A

Treatment and prophylaxis of thrombosis
Parenteral - injected forms of therapy
Indirectly inhibit activated factor Xa and thrombin
Bind to anti-thrombin, increases avidity of anti-thrombin and so enhances its natural activity

44
Q

How do rivaroxaban, edoxaban and apixaban work?

A

Sit on and inhibit activated factor X

When inhibited, it decreases thrombin production and therefore conversion of fibrinogen to fibrin

45
Q

How does dibigatran work?

A

Direct thrombin inhibitor

Reduces cleavage of fibrinogen to fibrin

46
Q

What needs to be normal to have an appropriate localised clot at the site of injury?

A

Platelets
Von Willebrand Factor
Coagulation factors

Haematology (11 decks)

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