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Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

The arrest of bleeding with the maintenance of vascular patency

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2
Q

What are the requirements for well functioning haemostasis?

A

Permanent state of readiness
Prompt response
Localised response
Protection against unwanted thrombosis

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3
Q

What is primary haemostasis?

A

Formation of platelet plug

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4
Q

What is secondary haemostasis?

A

Formation of fibrin clot

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5
Q

What are the components of normal haemostasis?

A

Primary haemostasis; platelet plug
Secondary haemostasis; fibrin clot
Fibrinolysis
Anticoagulant defences

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6
Q

How are platelets formed?

A

Budding of megakaryocytes in bone marrow

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7
Q

What is the life span of a platelet?

A

7-10 days

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8
Q

Do platelets have a nucleus?

A

No

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9
Q

How does platelet adhesion occur?

A

Endothelial damage exposes collagen and releases von Willebrand factor (VWF) which results in platelet adhesion at the site of injury

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10
Q

How do platelets know where the site of injury is?

A

Once initial platelet adhesion has occurred, degranulation occurs leading to aggregation of platelets

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11
Q

What can cause failure of platelet plug formation?

A

Vascular; scurvy, old age
Thrombocytopenia
Reduced function; antiplatelets
VWF

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12
Q

What are the consequences of failure of primary haemostasis?

A

Spontaneous bruising and purpura
Mucosal bleeding; epistaxis, GI, conjunctival, MENORRHAGIA
Severe; intracranial haemorrhage, retinal haemorrhage

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13
Q

What is the screening test for primary haemostasis?

A

Platelet count

In VWF; there will be decreased platelets and a low factor 8 (prolonged APTT)

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14
Q

Descibe the mechanism of fibrin clot formation

A

Tissue Factor binds with factor 7a (initiation)
This leads to the activation of factors 5 and 10a.
Factors 5 and 10a will result in the cleavage of prothrombin (2) to thrombin (2a)
Thrombin results in the cleavage of fibrinogen to fibrin
Thrombin will also act to activate factors 8 and 9 (amplification)
Which will act to further increase factors 5 and 10a (propagation) to increase thrombin levels
Formation of a stable fibrin clot

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15
Q

What is initiation in fibrin clot formation?

A

Activation of tissue factor and clotting factor 7a

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16
Q

What is amplification in fibrin clot formation?

A

Thrombin acts to activate clotting factors 8 and 9

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17
Q

What is propagation in fibrin clot formation?

A

Activated clotting factors 8 and 9 act on 5 and 10a to increase thrombin levels via cleavage of prothrombin

18
Q

What can cause failure of fibrin clot formation?

A

Single clotting factor deficiency; haemophilia
Multiple clotting factor deficiencies; DIC
Increased fibrinolysis

19
Q

What is haemophilia A (more common)?

A

Deficiency of clotting factor 8

20
Q

What is haemophilia B?

A

Deficiency of clotting factor 9a

21
Q

Describe fibrinolysis

A

Plasmin is formed from plasminogen via tPA

Plasmin will act on fibrin to break it down into FDPs

22
Q

How are FDPs measured?

A

D-dimer

Indication of excess fibrinolysis; DIC and DVT/PE

23
Q

Is there a clinical syndrome for failure of secondary haemostasis?

A

No

If haemophilia; bleeding into joints (haemarthrosis) and muscles

24
Q

What are the screening tests for fibrin clot formation?

A

Prothrombin time

Activated Partial Thromboplastin Time (APTT)

25
Q

What does prothrombin time assess?

A

Extrinsic Pathway
Add tissue factor and phospholipid thromboplastin) to patients serum to activate factor 7a
Measures factor 7a, 5, 10a and prothrombin

26
Q

What does APTT assess?

A

Intrinsic Pathway
Clotting factors 8 and 9a
And 5, 10a and prothrombin

27
Q

What will increase prothrombin time?

A

Deficiency in factor 7

28
Q

What will increased APTT time?

A

Deficiency in factors 8 or 9a (haemophilia)

29
Q

What will increase both prothrombin and APTT?

A

Deficiency in 5, 10a, prothrombin, fibrinogen or both 8/9a and 7
Multiple clotting factor deficiency or the main pathway that links both (5, 10a, prothrombin, fibrinogen)

30
Q

What is the clinical approach to bleeding disorders?

A

History; bleeding, bruising, duration(? life-long)
Previous surgery/ dental extractions
Drug hx
FMHx
Exam; fundal haemorrhages, mouth, purpura (primary haemostasis), muscles and joints (secondary haemostasis), splenomegaly

31
Q

What is the action of anti-thrombin?

A

Serine protease inhibitor
Naturally occuring anti-coag
Deactivates TF/7a, 5/10a and 8/9a along with thrombin inactivation

32
Q

What drug acts to increase anti-thrombin action?

A

Heparin

33
Q

What is the action of protein C and S?

A

Act to deactivate 5/10a and 8/9a

Thrombin will also bind to thrombomodulin to have a positive feedback to increase levels of protein C and S

34
Q

What is thrombophilia?

A

Deficiency of naturally occuring anticoagulants

Tendency to develop DVT/ PE

35
Q

In primary haemostasis; what will activated platelets release and what is the result of that?

A 
Thromboxane A2 (TXA2) 
Acts to release serotonin and ADP which will result in platelet aggregation and vasoconstriction
36
Q

What component of the platelet cell membrane allows for adhesion?

A

Pseudopodia

37
Q

What role does ADP specifically have in primary haemostasis?

A

Aggregation to form soft plug

Expose acidic phospholipids on platelet surface to initiate coagulation and solid clot formation

38
Q

What is virchows triad?

A

Injury to vessel wall
Abnormal blood flow
Increased coagulability of blood

39
Q

Describe an arterial thrombus

A

White; mainly platelets in a fibrin mesh
Forms an embolus
ANTIPLATELET THERAPY

40
Q

Describe a venous thrombus?

A

White head, jelly like red tail, fibrin rich

ANTICOAG THERAPY

Haematology (31 decks)

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