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Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis

A

The arrest of bleeding and

the maintenance of vascular patency

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2
Q

List the key steps of the haemostatic system

A

Primary haemostasis - formation of platelet plug
Secondary haemostasis - formation of fibrin clot
Fibrinolysis
Anticoagulant defence - switch off the mechanism

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3
Q

What is fibrinolysis

A

Breaking down of a blood clot

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4
Q

Why is fibrinolysis vital to the haemostatic system

A

Need to keep the clot an appropriate size so that the vessel isn’t blocked
Balance between haemostasis and this

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5
Q

How do platelets form

A

Platelets bud off from the megakaryocyte in the bone marrow

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6
Q

Describe the structure of a platelet

A

Small discs without a nucleus

Have a lifespan of 7-10 days

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7
Q

How does endothelial damage lead to platelet aggregation at the site

A

The damage exposes collagen and releases Von Willebrand Factor (VWF), and other proteins to which platelets have receptors – platelet adhesion at the site of injury.
There is then secretion of various chemicals from the platelets, which leads to aggregation of platelets at the site of injury (more are signalled to come to site)

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8
Q

What can cause a failure of formation of the platelet plug

A

Thrombocytopaenia - reduced number of platelets
Reduced platelet function
Lack of collagen in vessels - age or Vit C deficiency
Collagen disorders - SLE, anti-phospholipid
Aspirin use
VWF diseases

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9
Q

What happens if the platelet plug fails to form at a damaged site

A

Spontaneous Bruising and Purpura ( mainly on lower limbs)
Mucosal Bleeding - epistaxis, GI, conjunctival and menorrhagia
Intracranial haemorrhage
Retinal haemorrhages

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10
Q

How can you screen for primary haemostasis

A

Platelet count

Part of the FBC

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11
Q

How does the fibrin clot form

A

Platelets release calcium – it is positive charged so sits on the negative phospholipid layer
This attracts negatively charged clotting factors
Tissue factors is released when tissue is damaged and activates factor 7 – starts haemostasis
This activates 5 and 10 which cleave prothrombin to its active form – thrombin (2a)
Thrombin then cleaves fibrinogen to fibrin which forms the clot
Thrombin activates 8 and 9 which amplify the 5/10 which acts as positive feedback to produce more fibrin

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12
Q

What can cause a failure of fibrin clot formation

A

Single clotting factor deficiency - haemophilia
Multiple clotting factor deficiency - DIC
Increased fibrinolysis

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13
Q

What causes haemophilia

A

Inherited defect
Haemophilia A – clotting factor 8 is missing
In B, clotting factor 9 is missing

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14
Q

What is Disseminated Intravascular Coagulation

A

Occurs when there is massive tissue damage
You release lots of TF which causes lots of blood clots
The clotting factors are used up and eventually haemorrhage occurs

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15
Q

Why can liver disease affect the clotting mechansms

A

Clotting factors are made in the liver

If production is affected then the system doesn’t work as well

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16
Q

How can you measure fibrinolysis

A

Measure degradation products in a blood test
D-dimers are the ones used
Can screen for DVT and PE

17
Q

What is the pattern of bleeding in haemophilia

A

More likely to bleed into muscles and joints - leads to pain and swelling
Delayed bleeds
Knees and ankles most often affected

18
Q

How do you screen for fibrin clot formation (secondary haemostasis)

A

Prothrombin time - measures extrinsic path
Activated partial thromboplastin time - APTT
This measures intrinsic

19
Q

Which clotting time is affected in haemophilia

A

The APTT would be prolonged in haemophilia

It measures the action of factors 8 and 9

20
Q

What are the naturally occurring anticoagulants

A

Anti-thrombin = neutralizes thrombin (binds to it)

Protein C and S = switch off factor 8 and 5 to stop haemostasis

21
Q

How does heparin function

A

Heparin helps anti-thrombin do its job to neutralise thrombin – stabilizes the complex

22
Q

How does a failure of primary haemostasis present

A

Usually problems with superficial bleeds
Easy bruising (petechiae)
Prolonged bleeding after dental work/surgery
Mucosal bleeding
Menorrhagia

23
Q

How long before surgery should aspirin be stopped

A

7 days

Platelets live for around 7 days so need to be sure you have outlived the anti-platelet effect

24
Q

What is the function of secondary haemostasis?

A

It reinforces the plug through the formation of a fibrin clot

25
Q

Describe the extrinsic coagulation pathway

A

It involves the activation of tissue factor and factor 7 complex. This then activates the factor 5/10a complex which can convert prothrombin to its active form of thrombin.

26
Q

Describe the intrinsic coagulation pathway

A

The intrinsic pathway starts with thrombin activating the factor 8/9a complex which in turn can amplify the activation of the 5/10a complex which contributes to the final pathway.

27
Q

Describe the final, common steps in the coagulation pathway

A

The final common pathway involves thrombin converting fibrinogen to its active form of fibrin which can form the fibrin clot.

28
Q

What does a raised PT and normal APTT suggest

A

Factor 7 deficiency

29
Q

How does warfarin work

A

It is a vitamin K antagonist which affects factors 2,7,9 and 10

30
Q

How do you monitor warfarin use

A

Measure the INR which is a standardised measurement

PT will be affected

31
Q

How do you monitor heparin use

A

APTT

Will also affect PT

32
Q

How do you manage DIC

A

Find the underlying cause and treat it
You also have to support them through the coagulopathy which often involves platelet transfusion, FFP to replace clotting factors and cryoprecipitate to replace fibrinogen

33
Q

What would happen to D-dimers in DIC

A

They would be raised

Lots of clots being broken down

34
Q

How can liver disease lead to hypersplenism

A

Liver disease leads to portal hypertension

This causes hypersplenism - backs up

35
Q

Describe the process of DIC

A

Excessive and inappropriate activation of the haemostatic system
Microvascular thrombus formation - leads to end organ failure
Clotting factor consumption leads to Bruising, purpura and generalised bleeding

36
Q

What can cause DIC

A

Sepsis
Obstetric emergencies
Malignancy
Hypovolaemic shock

37
Q

What can raise D-dimers

A 
DVT/PE 
Malignancy 
Pregnancy 
Sepsis 
Post-op period

Haematology (8 decks)

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