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POM > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

The stopping of flow of blood.

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2
Q

Three steps of haemostasis?

A

Vasoconstriction. Formation of unstable platelet plug. Formation of stable fibrin mesh. Breakdown of clot and vessel repair.

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3
Q

What is primary haemostasis?

A

Formation of unstable platelet plug.

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4
Q

What is secondary haemostasis?

A

Formation of stable fibrin mesh.

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5
Q

What are platelets?

A

Discoid (lens shaped), non-nucleated, granule-containing cells that are derived from myeloid stem cells.

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6
Q

Circulating lifespan of a platelet?

A

10 days.

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7
Q

What is the first way platelets can bind to collagen?

A

Directly using their glycoprotein Ia receptor.

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8
Q

What is the second way platelets can bind to collagen?

A

Indirectly using their glycoprotein Ib receptor to bind to Von Willebrand factor (VWF).

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9
Q

Where is Von Willebrand factor (VWF) found?

A

Produced and released from endothelial cells. Produced in megakaryocytes and released from alpha granules in platelets.

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10
Q

What happens after platelet adhesion to collagen?

A

They become activated.

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11
Q

What happens after platelets become activated?

A

They become more rounded and form spicules to encourage platelet-platelet interaction. Contents of platelet granules are also released.

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12
Q

How are the contents of platelet granules released?

A

Platelet membrane is invaginated to form a surface-connected cannalicular system through which the contents of platelet granules are released.

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13
Q

What are released from platelet granules?

A

ADP, fibrinogen and von Willebrand factor.

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14
Q

What else along with content from granules is produced and released from platelets?

A

Thromboxane A2

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15
Q

What does thromboxane A2 do?

A

Vasoconstrictor and aids with platelet aggregation.

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16
Q

What 2 main molecules encourage platelet platelet aggregation?

A

ADP and Thromboxane A2

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17
Q

What are the two main steps of primary haemostasis?

A

Platelet adhesion and platelet aggregation.

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18
Q

What receptor does ADP bind to promote platelet aggregation?

A

P2Y12 receptor found on platelets.

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19
Q

What receptor does Thromboxane A2 bind to promote platelet aggregation?

A

Thromboxane A2 receptor

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20
Q

What does fibrinogen do in primary haemostasis?

A

Binds to glycoprotein IIb/IIIa which further activates platelets. Also has a key role in linking platelets together to form a platelet plug.

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21
Q

How is platelet activation and aggregation counterbalanced?

A

Active flow of blood and the release of prostacyclin (PGI2) from endothelial cells; prostacyclin is a powerful vasodilator and suppresses platelet activation, thus preventing inappropriate platelet aggregation.

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22
Q

How does aspirin work as an anti platelet drug?

A

Aspirin inhibits the production of thromboxane A2 by irreversibly blocking the action of cyclo-oxygenase (COX) in platelets, resulting in a reduction in platelet aggregation.

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23
Q

How does clopidogrel work?

A

Blocks P2Y12 Receptor and so ADP can’t bind therefore reducing platelet aggregation.

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24
Q

VWF role apart from helping platelets with adhesion to collagen?

A

Carrier for factor VIII.

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25
Q

Where are most clotting factors made?

A

In the liver

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26
Q

What clotting factors aren’t produced in the liver?

A

Factor VIII and VWF.

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27
Q

Why is vitamin K essential?

A

Carboxylation of glutamic acid residues which is essential for clotting factor function.

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28
Q

Which factors require vitamin K?

A

Factors II (prothrombin), VII, IX and X

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29
Q

What factor initiates coagulation?

A

Tissue factor (TF).

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30
Q

What is important about tissue factor (TF)?

A

TF is mainly located at sites that are not usually exposed to the blood under normal physiological conditions. As a result, blood only encounters TF at sites of vascular injury.

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31
Q

What are the three phases of coagulation?

A

Initiation, amplification and propagation.

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32
Q

What does TF bind to?

A

Factor VIIa.

33
Q

What does binding of TF do?

A

Activates factors IX,X. This leads to factor II (prothrombin) being converted to small amounts of factor IIa (thrombin).

34
Q

What do calcium ions do?

A

Aid in binding of activated clotting factors to the phospholipid surfaces of platelets.

35
Q

What happens in the amplification step?

A

Small amount of thrombin mediates the activation of the co-factors V and VIII, the zymogen factor XI and platelets.

36
Q

What happens in the propagation phase?

A

Factor XI converts more factor IX to IXa, which in concert with factor VIIIa,amplifies the conversion of factor X to Xa, and there is consequently a rapid burst in thrombin generation which cleaves the circulating fibrinogen (soluble) to form the insoluble fibrin clot.

37
Q

What are the three main natural anticoagulant molecules?

A

Protein C, Protein S and antithrombin.

38
Q

What activates protein C?

A

Thrombin binding to thrombomodulin on the endothelial cell surface.

39
Q

What does activated protein C do?

A

Inactivates factors Va and VIIIa in the presence of a co-factor protein S.

40
Q

What does antithrombin do?

A

Inactivates thrombin and factor Xa.

41
Q

What makes antithrombin work?

A

Binding of antithrombin to endothelial cell-associated heparins.

42
Q

Main anticoagulant drugs?

A

Heparin, Warfarin and direct oral anticoagulants.

43
Q

How does heparin work?

A

Works indirectly by potentiating the action of antithrombin leading to the inactivation of factors Xa and IIa (thrombin).

44
Q

How is heparin administered?

A

Intravenously or by subcutaneous injection.

45
Q

How does warfarin work?

A

Vitamin K antagonist that works by interfering with protein carboxylation. It therefore reduces synthesis of functional factors II, VII, IX and X by the liver.

46
Q

How is warfarin administered?

A

Given as an oral tablet and its anticoagulant effect needs to be monitored by regular blood testing

47
Q

Why does warfarin take longer to take effect compared to heparin?

A

Reduces synthesis of coagulation factors in the liver rather than inhibiting existing factor molecules.

48
Q

How do direct oral anticoagulants?

A

Directly inhibit either thrombin or factor Xa.

49
Q

What lyses fibrin?

A

Plasmin.

50
Q

What is key for fibrin to be lysed?

A

Both plasminogen and t-PA need to bind to lysine residues on fibrin.

51
Q

Why do plasmin levels need to be regulated?

A

Plasmin isn’t specific for fibrin. They can cause break down fibrinogen, factor Va and VIIIa.

52
Q

What inhibits plasmin?

A

alpha 2 macroglobulin and anti-plasmin.

53
Q

When would thrombolytic agents like t-PA be used?

A

To treat PE or ischaemic stroke.

54
Q

Risks of thromobolytic agents?

A

Bleeding.

55
Q

When would anti-fibrinolytic drugs be used?

A

Trauma, surgical patients and patients with bleeding disorders.

56
Q

Examples of anti-fibrinolytic drugs?

A

Tranexamic acid and aminocaproic acid.

57
Q

How do anti-fibrinolytic drugs work?

A

Competitive inhibition. Bind to plasminogen and so plasminogen can’t bind to fibrin and so fibrin isn’t lysed.

58
Q

When is prothrombin time used?

A

To evaluate extrinsic pathway and common pathway.

59
Q

What factors does pro thrombin test for?

A

VII, X, V, II and fibrinogen.

60
Q

When performing a pro thrombin time test, sodium citrate is used. Why is sodium citrate used?

A

To prevent clotting by chelating calcium.

61
Q

When performing a pro thrombin time test, the sample is centrifuged. Why?

A

To produce platelet poor plasma.

62
Q

How is prothrombin time done?

A

A source of TF and phospholipid is added to the citrated plasma sample, together with calcium to start the reaction; the length of time taken for the mixture to clot is recorded.

63
Q

What does recombinant thromboplastin contain?

A

Tissue factor and phospholipids.

64
Q

How is APTT done?

A

Contact activator, together with phospholipid, is added to the citrated plasmasample followed by calcium; the time taken for this mixture to clot is measured

65
Q

What pathway does APTT (Activated partial thromboplastin time) test for?

A

Intrinsic and common pathway.

66
Q

What factors does APTT (Activated partial thromboplastin time) test for?

A

XII, XI, IX, VIII, X, V, II and fibrinogen.

67
Q

Why is international normalised ratio (ITR) used as a way to express prothrombin time results?

A

INR is used because different thromboplastin reagents are used by different laboratories. All laboratories would be expected to obtain the same INR result for a given sample irrespective of the source of thromboplastin.

68
Q

Difference in preparation of PT and APTT?

A

PT tissue factor is used. APTT a contact activator is used.

69
Q

Prolonged APTT causes?

A

Haemophilia A (Factor VIII deficiency). Haemophilia B (Factor IX deficiency). Haemophilia C (Factor XI deficiency)

70
Q

Increased bleeding causes?

A

Thrombocytopenia. Use of anti platelet drugs (e.g aspirin). Reduction in coagulation factors. Increased fibrinolysis (Use of t-PA).

71
Q

What is disseminated intravascular coagulation (DIC)?

A

Generalised and uncontrolled activation of coagulation followed by marked activation of the fibrinolytic system. This activation results from the expression of TF within the circulation.

72
Q

Causes of reduction of clotting factors?

A

Liver disease, Disseminated intravascular coagulation

73
Q

Increased fibrinolysis causes?

A

Disseminated intravascular coagulation or use of t-PA.

74
Q

3 principle causes of thrombosis (Virchow’s triad)

A

Stasis of blood flow (veins). Endothelial injury (artery). Hyper-coagulability (both).

75
Q

Causes of thromobosis?

A

Inherited thrombophilia (reduced levels of anticoagulant proteins such as antithrombin). Reduced fibrinolytic activity (seen in pregnancy). Hyperviscocity (polycthaemia).

76
Q

Why can’t anti thrombin activated by low molecular weight heparin inhibit thrombin (factor IIa), but can only inhibit clotting factor Xa?

A

Inactivation of IIa (thrombin)
requires longer chains of heparin
chains, which are able to wrap
around both the antithrombin and
thrombin. LMW heparin mainly
inactivates Xa.

77
Q

What factor is increased in pregnancy?

A

Factor VIII

78
Q

What does the single point mutation causing factor V Leiden result in?

A

Factor V Leiden makes factor V more resistant to inactivation by protein C. Type of inherited thrombophilia.

POM (41 decks)

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