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Haematology > Haemostasis and bleeding disorders > Flashcards

Haemostasis and bleeding disorders Flashcards

1
Q

What are the three normal components of haemostasis?

A

Primary haemostasis
Secondary haemostasis
Fibrinolysis

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2
Q

What is primary haemostasis?

A

Formation of a platelet clot

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3
Q

What is secondary haemostasis?

A

Formation of a fibrin clot

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4
Q

What happens when endothelium is damaged?

A

Collagen is exposed
Von Willebrand factor is released
Platelets stick to collagen and Von Willebrand factor provides adhesion

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5
Q

What is the lifespan of a platelet?

A

7-10 days

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6
Q

What are the consequences of a lack of platelet plug formation?

A 
Spontaneous Bruising and Purpura
Mucosal Bleeding:
- Epistaxes
- Gastrointestinal
- Conjunctival
- Menorrhagia
Intracranial haemorrhage
Retinal haemorrhages
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7
Q

Do single clotting factor deficiencies tend to be inherited or acquired?

A

Inherited e.g. haemophilia

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8
Q

Do multiple clotting factor deficiencies tend to be inherited or acquired?

A

Acquired e.g. disseminated intravascular coagulation

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9
Q

Which clotting factors does prothrombin time assess?

A

Tissue factor, VII, II (prothrombin), V, X and fibrinogen

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10
Q

Which clotting factors does activated partial thromboplastin time assess?

A

XII, XI, IX, VIII

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11
Q

What is a blood vessels response to damage?

A

Vasocontstriction

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12
Q

What are the causes of peripheral platelet destruction?

A

Coagulopathy: Disseminated intravascular coagulation
Autoimmune: Immune thrombocytopenic purpura (ITP)
Hypersplenism

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13
Q

What acquired functional platelet defects are there?

A

Drugs (eg Aspirin, non-steroidal anti inflammatory drugs)

Renal failure

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14
Q

What mode of inheritance is Von Willebrand Factor deficiency?

A

Autosomal dominant

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15
Q

What are petechiae?

A

Small spots on the skin caused by bleeding - very specific to platelet disorders

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16
Q

What is the most common cause of immune mediated thrombocytopenia?

A

Immune thombocytopenia purpura

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17
Q

What is the acute syndrome of immune thrombocytopenia purpura?

A

Affects children between ages of 2-6
Symptomatic thrombocytopenia occurs post infection
Resolves spontaneously

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18
Q

What is the chronic syndrome of immune thombocytopenia purpura?

A

Affects middle aged women usually
No preceding infection
Must be treated with steroids and splenectomy if severe

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19
Q

What drugs have been indicated to precede immune thrombocytopenia?

A

Penecillin
Oral thiazides
Heparin
Transfusion

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20
Q

What chronic conditions may cause immune thrombocytopenia?

A

HIV

SLE

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21
Q

What is disseminated intravascular coagulation?

A

Excessive and inappropriate activation of the haemostatic system: primary, secondary and fibrinolysis

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22
Q

How might DIC present?

A

Bruising, purpura and generalised bleeding

Organ failure

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23
Q

What are the complications of DIC?

A

Microvascular thrombus formation causing organ death

Clotting factor consumption

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24
Q

How do disorders of coagulation typically present?

A

Delayed bleeding after surgery

Deep muscle bleeding or bleeding into joints

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25
Q

What is haemophilia A and haemophilia B?

A

Both are congenital deficiencies of clotting factors
Haemophilia A - clotting factor 8
Haemophilia B - clotting factor 9

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26
Q

What mode of inheritance does haemophilia have?

A

X-linked recessive

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27
Q

Which haemophilia is more common?

A

Haemophilia A

28
Q

What is the APTT and PT like in haemophilia?

A

APTT increased

PT normal

29
Q

What is type 1 Von Willebrand disease?

A

Partial reduction in the amount of Von Willebrand factor

30
Q

What is type 2 Von Willebrand disease?

A

Reduction in the quality of the Von Willebrand factor

31
Q

What is type 3 Von Willebrand disease?

A

Total loss of Von Willebrand factor - most severe form

32
Q

What other clotting factor deficiency may also be present in Von Willebrand disease?

A

Factor 8

33
Q

How does Von Willebrand disease usually present?

A

Petechiae
Eccymoses
Mucocutaneous bleeding

34
Q

How might coagulation tests be altered in Von Willebrand disease?

A

May be normal

May have both increased APTT and PT

35
Q

How is Von Willebrand disease treated?

A

Desmopressin

36
Q

How is haemophilia managed?

A

Lifelong replacement with frozen factor concentrate

37
Q

Why is vitamin K important?

A

Required for carboxylation of factors II, VII, IX and X

38
Q

How might coagulation tests be altered in vitamin K deficiency?

A

Both PT and APTT raised

39
Q

What are the causes of vitamin K deficiency?

A

Malnutrition and malabsorption
Warfarin therapy
Obstructive jaundice
Haemorrhagic disease of the newborn

40
Q

How is vitamin K deficiency managed?

A

Give vitamin K

41
Q

How does liver disease cause a coagulation disorder?

A

Coagulation factors are produced in the liver

Also causes platelet problems as platelets pool in enlarged spleens caused by portal hypertension

42
Q

What are the causes of DIC?

A 
Disseminated gram negative sepsis
Placental abruption
Mismatched blood transfusions
End stage malignancy
Hypovolaemic shock
43
Q

How might coagulation tests be altered in liver disease?

A

Prolonged PT and APTT as all factors are affected

44
Q

How is DIC managed?

A 
Treat the underlying cause
Replacement therapy:
- Platelet transfusions
- Plasma transfusions
- Fibrinogen replacement
45
Q

Why is aspirin not helpful in the prevention of venous thrombus formation?

A

Platelets are not activated - it is all the coagulation cascade

46
Q

What is thrombophilia?

A

Familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis

47
Q

By what mechanism does thrombophilia predispose to clot formation?

A

Decreased anticoagulant activity

48
Q

What naturally occuring anticoagulants are there?

A

Serine protease inhibitors e.g. antithrombin III
Protein C
Protein S
Factor V leiden

49
Q

When should screening for thrombophilia be offered?

A

Venous thrombosis

50
Q

What is factor V leiden?

A

A point mutation in factor V that may be present in up to 10% of the population
This causes normal procoagulin activity but an altered response to inhibition by anticoagulant factors

51
Q

What is the pathogenesis of antiphospholipid syndrome?

A

Antibodies lead to a conformational change in β2 glycoprotein 1 (a protein with unknown function in health) which leads to activation of both primary and secondary haemostasis and vessel wall abnormalities

52
Q

How is antiphospholipid syndrome managed?

A

Aspirin
Warfarin
(since both arterial and venous thrombosis)

53
Q

What is the action of unfractionated heparin?

A

Stabilises bond between antithrombin 3 and fibrinogen

54
Q

What is the action of LMWH?

A

Stabilises bond between antithrombin 3 and factor Xa

55
Q

What monitoring is required for unfractionated heparin?

A

APTT

56
Q

What is a complication associated with long term use of heparin and why?

A

Osteoporosis - heparin interferes with osteoclast activity

57
Q

How can heparin be reversed?

A

Stop heparin - has short half life

Severe bleeding - protamine sulphate

58
Q

Does protamine sulphate completely reverse heparin?

A

Completely reverses unfractionated heparin

Partially reverses LMWH

59
Q

Where is vitamin K absorbed?

A

Upper intestine

60
Q

What is required for vitamin K absorption?

A

Bile salts (hence obstructive jaundice can cause vitamin K deficiency)

61
Q

Why is calcium required in haemostasis?

A

Activation of fibrin clot

62
Q

How is INR calculated?

A

(patients PT time/mean normal PT)^ISI

63
Q

How can bleeding on warfarin be reversed?

A

Give Vit K - 6 hours

Give clotting factors - immediate

64
Q

What are rivaroxiban and apixiban?

A

Direct factor Xa inhibitors

65
Q

What is dabigatran?

A

Direct thrombin inhibitor

Haematology (9 decks)

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