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Haematology > Anticoagulants and Bleeding Disorders > Flashcards

Anticoagulants and Bleeding Disorders Flashcards

1
Q

What is primary haemostasis?

A

The process which recruits platelets to the site of vessel damage

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2
Q

What is secondary haemostasis?

A

The process of activating coagulation factors

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3
Q

Primary and secondary haemostasis occur simultaneously. T/F?

A

True

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4
Q

The exposure of collagen in a damaged vessel allows the binding of which factor to facilitate platelet plug formation?

A

Von Willebrand factor

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5
Q

What two factors are required in every step of the process of coagulation cascade?

A

Phospholipids

Calcium

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6
Q

In the clotting cascade, tissue factor activates which factor?

A

Factor 7

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7
Q

In the clotting cascade factor ten works alongside which other factor to activate prothrombin?

A

Factor 5

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8
Q

What is the main action of thrombin in the clotting cascade?

A

The convert fibrinogen to fibrin

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9
Q

In the clotting cascade, which factor allows cross binding of fibrin?

A

Factor 13

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10
Q

Which factor in the clotting cascade activates factor 13?

A

Thrombin or factor 2

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11
Q

In the intrinsic pathway of the clotting cascade, which factor does factor 11 activate?

A

Factor nine

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12
Q

In the intrinsic pathway of the clotting cascade, which factor works alongside factor nine to activate factor ten?

A

Factor eight

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13
Q

The production of thrombin in the coagulation cascade stimulates the activation of antithrombin. Which factors are inhibited by antithrombin?

A

Factors 2, 7 and 10

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14
Q

Which molecule does thrombin bind to to activate protein C in the coagulation cascade?

A

Thrombomodulin

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15
Q

Protein C alongside protein S act. to inhibit which coagulation factors?

A

Factors 5 and 8

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16
Q

What action does tissue factor pathway inhibitor have on the coagulation cascade?

A

Inhibits the activation of factor 7

Inhibits factor 10

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17
Q

How does the production of fibrin lead to the production of plasmin in the clotting cascade?

A

Fibrin formation results in the inactivation of plasminogen activation inhibitors which results in the conversion of plasminogen to plasmin

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18
Q

Plasmin acts to dissolve the clot which creates fibrin degradation products including…?

A

D-dimers

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19
Q

How is primary haemostasis assessed in vivo?

A

Bleeding time

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20
Q

How is primary haemostasis assessed ex vivo?

A

FBC and platelet function tests

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21
Q

What technique is used to test platelet function?

A

Light transmission aggregometry

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22
Q

What tests are used to assess secondary haemostasis?

A

APTT, PT, TCT, individual clotting factor assays

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23
Q

Why is citrate added to a blood sample before a PT, APTT or TCT test?

A

To chelate all the calcium to prevent clotting

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24
Q

At what temperature are PT, APTT and TCT tests performed at?

A

37 degrees Celsius

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25
Q

Which part of the clotting cascade does prothrombin time stimulate?

A

Extrinsic pathway

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26
Q

Which part of the clotting cascade does activated partial thromboplastin time stimulate?

A

Intrinsic pathway

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27
Q

What Is the international normalised ratio?

A

A standardised form of prothrombin time used particularly to monitor oral anticoagulants

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28
Q

The INR for any given patient should be identical in any laboratory. T/F?

A

True

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29
Q

Briefly describe the procedure used in a prothrombin test

A

Patients plasma added to thromboplastin (tissue factor and phospholipids), warmed to 37 degrees celsius and the calcium added and the time taken to clot measured

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30
Q

Briefly describe the procedure used in a activated partial thromboplastin test

A

Patients plasma added to contact factor (kaolin or silica) and phospholipid, warmed to 37 degrees celsius and then calcium added and the time taken to clot measured

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31
Q

What does thrombin clotting time measure?

A

The conversion of fibrinogen to fibrin

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32
Q

Briefly describe the procedure used in a thrombin clotting time test

A

At 37 degrees C, patient’s plasma and bovine thrombin are added and the time to clot is measured

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33
Q

Which of the three tests of the coagulation cascade is less dependent on calcium and phospholipid?

A

Thrombin clotting time

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34
Q

What is the general mechanism of action of anticoagulants?

A

Inhibit one or several components of the coagulation cascade

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35
Q

What is the mechanism of action of heparins?

A

These enhance the activity of endogenous antithrombin to inhibit factors 2, 7 and 10

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36
Q

Discuss the pros and cons of using low molecular weight heparin as opposed to unfractionated heparin?

A

LMWH has a reduced risk of heparin induced thrombocytopenia, osteoporosis and hyperkalaemia
LMWH has the same clinical efficacy as UFH
LMWH is more expensive
LMWH does not require monitoring so can be used in out-patients

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37
Q

When are heparins used?

A 
Treatment of acute DVT or PE
During cardiac bypass surgery
Acute coronary syndrome
medium term after VTA in cancer patients
Prophylaxis against VTE in medical- post-op and obstetric patients
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38
Q

Heparin is administered orally. T/F?

A

False - it is administered paraenterally

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39
Q

Heparin does not cross the placenta. T/F?

A

True

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40
Q

What is the mechanism of action of warfarin?

A

Inhibits vitamin K oxide reductase which is used in the production of factors 2, 7, 9 and 10 in the liver

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41
Q

Warfarin has a delayed onset and a long half-life. T/F?

A

True

42
Q

Warfarin has a narrow therapeutic window. T/F?

A

True

43
Q

DOACs are generally preferred compared to warfarin. In what group of patient would warfarin be particularly useful?

A

Patient’s who are non-compliant due to its long half-life

44
Q

How can the effects of warfarin be rapidly reversed?

A

Infusion of clotting factors and vitamin K

45
Q

When is warfarin used?

A

Treatment of AF, acute DVT or PE and prosthetic heart valves

46
Q

What is one disadvantage of DOACs compared to warfarin?

A

There is no rapid reversing agent for DOACs

47
Q

Give an example of a DOAC which inhibits thrombin.

A

Dabigatran

48
Q

Give an example of a DOAC which inhibits factor 10

A

Apixaban
Rivaroxaban
Edoxaban

49
Q

What is the general mechanism of action of fibrinolytic agents?

A

Enhance lysis of the fibrin clot

50
Q

What are the two main classes of fibrinolytic agents?

A

Kinases

Tissue plasminogen activators

51
Q

What are the indications for the use of catheter directed thrombolysis?

A

Acute limb ischaemia
Massive DVT
blocked central line

52
Q

What are the advantages of using catheter directed thrombolysis?

A

Drug is administered directly into the vessel containing the thrombosis, this has a lesser systemic effect

53
Q

What is the mechanism of action of kinases?

A

These bind to plasminogen and release plasmin to enhance the breakdown of fibrin

54
Q

Systemic fibrinogenolysis results in a significant bleeding risk in patients treated with kinases. T/F?

A

True

55
Q

Streptokinase is an antigenic drug. What are the implications of this?

A

The drug will be ineffective if the patient has previous used it or if the patient has had a recent streptococcus infection

56
Q

Give an example of a kinase which is not antigenic.

A

Urokinase

57
Q

What is the mechanism of action of tissue plasminogen activators?

A

Enhance the activation of plasminogen to plasmin

58
Q

Tissue plasminogen activators have a significant systemic effect. T/F?

A

False - they are relatively selective for clot bound plasminogen

59
Q

Give examples of tissue plasminogen activators which have a short half life and so are given as a bolus and then as an infusion.

A

Alteplase

Tenectplase

60
Q

Give examples of tissue plasminogen activators which have a longer half life and so are given as a bolus only .

A

Reteplase

61
Q

What are the indications for the use of alteplase (a tissue plasminogen activator)?

A

Acute MI for patients not suitable for percutaneous coronary intervention, within 12 hours of onset of symptoms
within 4.5 of onset of symptoms of ischaemic stroke
Massive PE with haemodynamic instability

62
Q

There is a significant risk of haemorrhage, particularly in which organ, with the use of tissue plasminogen activators?

A

The brain

63
Q

Describe the mechanism of action of clopidogrel and ticlopidine?

A

Irreversibly bind to a block the ADP receptor on platelets to disrupts the arachidonic pathway and inhibit platelet binding of fibrinogen by decreasing the expression of GP11B/IIIA

64
Q

Describe the mechanism of action of abciximab and tirofiban?

A

Monoclonal antibodies with antagonist the GP11B/111A receptor to reduce platelet aggregation and the binding of fibrinogen

65
Q

Describe the mechanism of action of aspirin

A

Irreversibly inhibits cyclooxyrgenase to block the conversion of arachidonic acid to thromboxane A2 which results in decreased platelet activation

66
Q

What is the mechanism of action of dipyridamole?

A

Increases platelet concentration of cAMP which decreases the platelets responsiveness to ADP to reduce platelet aggregation

67
Q

What is the mechanism of action of Picotamide?

A

Thromboxane synthesis inhibitor and receptor blocker

68
Q

What is the mechanism of action of ifetroban?

A

Thromboxane receptor blocker

69
Q

How are anti-platelet agents used in the treatment of an acute MI?

A

Aspirin is used indefinitely
Clopidogrel is for up to 12 months after an acute MI
Tirofiban can be used acutely for an acute MI

70
Q

Which anti-platelet agent is used for the secondary prevention of cardiovascular disease?

A

Aspirin

71
Q

Which anti-platelet agent is used for the treatment of secondary prevention of an acute stroke or TIA?

A

Clopidogrel or dipyridamole is clopidogrel is not tolerated

72
Q

Which anti-platelet agent is used for the treatment of peripheral vascular disease?

A

Clopidogrel

Or aspirin if clopidogrel is not tolerated

73
Q

Disseminated intravascular coagulation is an acquired consumptive process. T/F?

A

True

74
Q

What can caused disseminated intravascular coagulation?

A 
Sepsis
Malignancy
Massive haemorrhage
Severe trauma
Pregnancy complications e.g. pre-eclampsia, placental abruption, amniotic. fluid embolism
75
Q

When would protein C be given in the treatment of disseminated intravascular coagulation?

A

Meningococcal sepsis

76
Q

How is disseminated intravascular coagulation treated?

A

By treating underlying cause
Fresh frozen plasma if there is bleeding
Activated protein C, protein c concentrate or AT concentrate can be used
Heparin is thrombotic phenotype

77
Q

Explain the pathophysiology of disseminated intravascular coagulation

A

Acquired, consumptive process where there is abnormal activation of the coagulation cascade causing the formation of mciro thrombi and later exhausting the cascade and causing bleeding

78
Q

How does liver disease cause coagulopathy?

A

Clotting factors are produced. in the liver
Vit K deficiencies can contribute
Poor clearance of activated coagulation factors can lead to DIC, hypersplenism and reduced thrombopoietin synthesis

79
Q

Haemophillia A is a deficiency in which clotting factor?

A

Factor 8

80
Q

Severe haemophilia A causes spontaneous bleeds, What level of factor 8 is classified as ‘severe haemophilia’?

A

<1iu/dl

81
Q

Moderate haemophilia A causes bleeding with minor trauma. What level of factor 8 is classified as ‘moderate haemophilia’?

A

1-5iu/dl

82
Q

Mild haemophilia A causes bleeding with surgery, What level of factor 8 is classified as ‘mild haemophilia’?

A

6-10iu/dl

83
Q

What mode of inheritance is exhibited by haemophilia A?

A

X linked recessive

84
Q

What effect will haemophilia A have on PT, APTT and TCT?

A

PT and TCT normal

APTT prolonged

85
Q

If a patient with haemophilia A is still capable of producing some factor 8, how is this treated?

A

Desmopressin.

86
Q

What mode of inheritance is exhibited by von willebrand disease?

A

Autosomal dominant

87
Q

Which clotting factor is commonly reduced in von willebrand disease?

A

Factor 8

88
Q

What pattern of bleeding results from von willebrand disease?

A

Mucosal bleeding pattern

89
Q

Describe types 1, 2 and 3 of von willebrand disease?

A

Type 1 - partial quantitative deficiency of vWF
Type 2 - qualitative deficiency of vWF
Type 3 - virtually complete deficiency of vWF

90
Q

What is the cause of glansmanns thromboplasthenia?

A

Absent or defective GPIIB/IIIA

Normal platelet count but platelets cannot function properly

91
Q

What is the cause of Bernard soupier syndrome?

A

Absent of defective GPIB/V/IX which causes macrothrombocytopaenia

92
Q

How can severe inherited platelet disorders such as Bernard soupier syndrome and glansmanns thromboplasthenia be treated?

A 
Applying pressure
Tranexamic acid
Desmopressin
Platelet transfusion
rFVIIa
93
Q

How does the Factor V Leiden mutation result in thrombophillia?

A

APC and prothrombin gene resistance

94
Q

Antithrombin deficiency increases the chances of developing DVT. T/F?

A

True

95
Q

What causes thrombophillia?

A

A deficiency of natural anticoagulants such as antithrombin, protein C and protein S

96
Q

The presence of lupus anticoagulant will falsely prolong which test of secondary haemostasis?

A

APTT

97
Q

Lupus anticoagulant antibody is associated with an increased bleeding risk. T/F?

A

False - this is associated with a prothrombotic state

98
Q

What is antiphospholipid syndrome?

A

Combination of persisting lupus anticoagulant and thrombosis or recurrent foetal. loss

99
Q

Why is it important not to use blood or blood products to treat DIC caused by meningitis?

A

DIC is a consumptive process and so given blood would worsen the process and cause thrombus

100
Q

What is a heterophiles antibody?

A

An antibody developed by a human which has the capability to react to antigens in a different species

101
Q

What test is used to diagnose infectious mononucleosis?

A

Monospot test

102
Q

What is the causative organism of infectious mononucleosis?

A

Epstein barr virus

Haematology (6 decks)

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