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Pathological Processes > 5. Haemostasis > Flashcards

5. Haemostasis Flashcards

1
Q

Define haemostasis.

A

The process of preventing or stopping bleeding in cases of trauma or disease while maintaining blood in its fluid state.

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2
Q

What are the 3 major steps in haemostasis?

A
  1. Vasoconstriction
  2. Primary haemostatic plug - friable platelet plug
  3. Secondary haemostatic plug - stable fibrin clot
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3
Q

What cell are platelets derived from?

A

Megakaryocytes

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4
Q

What blood components are essential for haemostasis?

A

Platelets
Coagulation factors - clotting proteins
Anticoagulation factors

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5
Q

What is the first step of formation of a platelet plug following vessel damage?

A

Exposure of underlying tissue containing collagen with vWF. Platelets bind to the exposed collagen via vWF.

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6
Q

Once bound to vWF, what happens to the platelets in order to form a plug?

A

They secrete ADP, thromboxane and other substances to become activated and change shape. They then cross-link to form a platelet plug.

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7
Q

Other than the formation of the platelet plug, what else do platelets do in response to vessel injury?

A

Activate the clotting cascade

Provide some coagulation factors (V) by secreting from internal stores.

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8
Q

What properties does the primary haemostatic clot have?

A

Weak, friable

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9
Q

What are the benefits of the primary haemostatic plug?

A

Forms very quickly - seconds to minutes and may control bleeding.

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10
Q

What is the key action of thrombin in coagulation?

A

Converts soluble fibrinogen to insoluble fibrin which enmeshed the platelet plug to form a stable clot

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11
Q

What factors contribute to the control of the clotting cascade?

A

Clot destroying proteins are activated by the clotting cascade
Natural anticoagulants inhibit unnecessary activation

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12
Q

What are some examples of natural anticoagulants?

A

Protein C
Protein S
Antithrombin
Tissue factor

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13
Q

What coagulation factors are synthesised in the liver?

A

Fibrinogen
Prothrombin
Factors 5,7,8,9,10,11,13
Tissue factor

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14
Q

What pathway does prothrombin time measure?

A

Extrinsic pathway

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15
Q

What pathway does APPT measure?

A

Intrinsic pathway

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16
Q

If a patient has a deficiency in factor VIII,IX,XI or XII will APPT or PT be prolonged?

A

APPT

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17
Q

If a patient has a deficiency in factor VII, will APPT or PT be prolonged?

A

PT

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18
Q

If a patient has a deficiency in factor V, which test will be prolonged?

A

Both APPT and PT

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19
Q

What is the thrombin burst?

A

When thrombin comes into contact with exposed tissue factor, it initiates the coagulation cascade and has a positive feedback loop to produce more thrombin. Extrinsic pathway.

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20
Q

What are the roles of vWF?

A
  • platelet adhesion and aggregation

- carrier and ‘protector’ of factor VIII, preventing it from premature destruction

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21
Q

Explain fibrinolysis.

A

Plasminogen is converted to plasmin by plasminogen activator. Plasmin breaks down fibrin into fragments called D-dimers.

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22
Q

Other than plasmin, what else contributes to preventing further clot formation?

A

Natural anticoagulants: Protein C, Protein S, Anti-thrombin

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23
Q

What will does deficiency in natural anticoagulants lead to?

A

Thrombophilia

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24
Q

What could lead to an aquired coagulation disorder?

A

Vitamin K deficiency
Liver disease
Anticoagulant medication - warfarin

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25
Q

What are some congenital causes of coagulation factor disorders?

A

Haemophilia A and B

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26
Q

What is the difference between haemophilia A and B?

A

Haemophilia A is more common- deficiency in factor VIII

B- factor IX

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27
Q

What inheritance pattern does haemophilia A demonstrate?

A

X-linked recessive

28
Q

How is haemophilia A treated?

A

Recombinant factor VIII

29
Q

What symptoms and signs would you expect in haemophilia A?

A

Bleeding into muscles and joints (haematomas and haemarthroses)
Post operative bleeding

30
Q

How is Von Willebrands disease inherited?

A

Autosomal dominant

31
Q

How does VWD affect clotting?

A

Abnormal platelet adhesion to the vessel wall

Reduced factor VIII activity

32
Q

How would the presentation of vWD differ to haemophilia?

A

Platelet-associated bleeding in VWF- skin and mucous membranes, epistaxis, gum bleeding, heavy periods
Spontaneous muscle bleeds are rare

Haemophilia - muscle haematomas and haemarthroses

33
Q

What symptoms would you expect in patients with vessel wall abnormalities?

A

Easy bruising - mainly skin

34
Q

What is a congenital vessel wall abnormality?

A

Hereditary haemorrhagic telangiestasia (HTT)

CT disorders - Ehlers-danlos

35
Q

How is HTT inherited?

A

Autosomal dominant

36
Q

How would a bone marrow biopsy help to determine the cause of thrombocytopenia?

A

If lots of megakaryocytes present then it suggests that production is normal and cause is increased removal.

37
Q

What disease is characterised by immune destruction of platelets?

A

Immune thrombocytopenic purpura (ITP) - antibodies against glycoproteins on surface of platelets

38
Q

How is ITP treated?

A

Immunosuppression

39
Q

Why would a blood transfusion be inappropriate in patients with ITP?

A

Autoimmune disease, so transfused platelets will be destroyed too.

40
Q

Suggest some reasons for non-immune destruction of platelets.

A

Miceoangiopathic haemolytic states - TTP, DIC, HUS

Cardiopulmonary bypass surgery can consume platelets

41
Q

What could cause decreased platelet production?

A

B12 or folate deficiency
Infiltration of bone marrow by cancer cells or fibrosis
Drugs- chemotherapy, antibiotics
Viruses - HIV, EBV, CMV

42
Q

Why does the artery contract in haemostasis?

A

Decrease the pressure downstream (arteries only), isn’t enough to stop the bleeding.

43
Q

Which coagulation factors require vitamin K for their synthesis?

A

II, VII, IX and X

Anticoagulants - protein C and protein S

44
Q

What properties of coagulation factors enables control of the coagulation cascade?

A

They are pro-enzymes which have to become activated, and then act as endopeptidases to active other proenzymes in signal amplification

45
Q

What co-factor is required for clotting?

A

Calcium - allows negative exposed membrane to bind to negative gla residues on thrombin.

46
Q

How is this intrinsic pathway triggered?

A

By a negatively charged surface, e.g subendothelium

The vessel does not need to be broken for it to occur

47
Q

How is the extrinsic pathway activated?

A

It needs a ‘tissue factor’ which is present outside of the blood. This is triggered by thromboplastin released from damaged cells adjacent to haemorrhage.

48
Q

Which factors are secreted by the endothelium to oppose clotting?

A

Plasminogen activator

Thrombomodulin

49
Q

Plasmin activates as an inactive precursor. How is it activated?

A

Tissue plasminogen activator
Urokinase
Streptokinase (from streptococci)

50
Q

How does the clotting cascade initiate fibrinolysis?

A

Fibrin increases the activity of tissue plasminogen activator which activated plasmin to break down fibrin.

51
Q

What happens after resolution of a clot?

A

Fibrous repair, granulation tissue and a tiny scar

52
Q

Why do people with haemophilia suffer from bleeding?

A

They cannot produce an adequate amount of fibrin as they have impaired clotting

53
Q

Are petechiae a symptom of haemophilia?

A

No, they are caused by blood leaking from capillaries, which is the result of platelet abnormalities.

54
Q

What would the PT of a patient with haemophilia show?

A

No change - factor VIII is not a part of the extrinsic pathway

55
Q

What affect does haemophilia have on APPT?

A

Prolongs APPT as this measures the intrinsic pathway which involves factor VIII.

56
Q

What is the cause of vWD?

A

Deficiency or abnormality in von Willebrand factor

57
Q

In vWD, what changes would you see in bleeding time and APTT?

A

Raised because it affects platelet adhesion and factor VIII which is involved in the intrinsic pathway.

58
Q

What changes to bleeding time,PT and APPT would you see in thrombocytopenia?

A

Prolonged bleeding time but normal AP and APPT as these assess the clotting cascade and not platelet function

59
Q

Would you expect to see petechiae in patients with thrombocytopenia?

A

Yes

60
Q

What is the pathophysiology of DIC?

A

Microthrombi are formed throughout the circulation, which consumes platelets, fibrin and coagulation factors and activates fibrinolysis. The patient may then experience haemorrhage.

61
Q

How is DIC usually caused?

A

Never occurs as a disease in itself but is always a complication of another condition

  • sepsis (gram negative endotoxin activates clotting)
  • severe trauma
  • extensive burns
  • malignancy
62
Q

How can you measure the fibrinolytic systems activity in the blood?

A

Presence of D-dimers

63
Q

What is factor V Leiden an example of?

A

Thrombophilia

64
Q

What clotting tests will be affected by DIC?

A

Raised PT
Raised APPT
Low fibrinogen
Raised D-dimers

65
Q

What is a thrombophilia?

A

Thrombophilias are inherited or acquired defects of haemostasis resulting in a predisposition to thrombosis

66
Q

What is the function of thrombomodulin?

A

Thrombin binding to thrombomodulin (endothelial receptor) activates protein C

Pathological Processes (12 decks)

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