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CLINICAL PATHOLOGY > Thrombosis and risk factors for thrombosis > Flashcards

Thrombosis and risk factors for thrombosis Flashcards

1
Q

What does Virchow’s triad define as the causes of thrombosis?

A

1) Changes to blood flow
2) Changes to blood composition
3) Changes to the vascular endothelium

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2
Q

What is the normal cause of arterial thrombosis?

A

Endothelial injury

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3
Q

What kind of thrombus forms in arterial thrombosis?

A

Platelet rich thrombus

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4
Q

What are the 9 risk factors for arterial thrombosis?

A

1) Smoking
2) Hypertension
3) Hypercholesterolaemia
4) Diabetes
5) Family history
6) Obesity
7) Physical inactivity
8) Age
9) Male sex

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5
Q

What are the main pathogenic processes about venous thrombosis?

A

1) Venous stasis - changes to blood flow

2) Hypercoagulable states - changes to blood constituents

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6
Q

What kind of thrombus forms in venous thrombosis?

A

Predominantly made up of fibrin with a lesser role for platelets

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7
Q

How does a DVT present? 3

A

1) Swollen legs
2) Hot legs
3) Painful legs

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8
Q

What percentage of DVTs are clinically silent?

A

80%

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9
Q

What percentage of patients with DVT have asymptomatic PE?

A

50%

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10
Q

DVT is found in what percentage of patients with PE?

A

> 80%

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11
Q

What percentage of patients with VTE develop recurrent VTE in 10 years?

A

30%

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12
Q

What percentage of patients with VTE develop post thrombotic syndrome?

A

28%

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13
Q

What is post thrombotic syndrome?

A

Chronic leg swelling due to damage to veins when the clots form

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14
Q

Why is it important that VTE gets treated?

A

Mortality of promptly diagnosed and adequately treated from PE is 2%

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15
Q

Why is hospital VTE so significant?

A

Hospital admission is an important predisposing factor for VTE - mixture of immobility and the sorts of things that bring people into hospital

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16
Q

What are the 2 strategies for treating VTE?

A 
Prophylaxis:
1) Consistent risk assessment 
2) Appropriate prophylaxis
Treatment
1) Prompt diagnosis
2) Guideline led unified care
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17
Q

What are the 5 steps in the care pathway for VTE?

A

1) Patient admitted to hospital
2) Assess VTE risk
3) Assess bleeding risk
4) Balance risks of VTE and bleeding - offer prophylaxis if appropriate
5) Reassess risk of VTE and bleeding within 24 hours of admission and whenever clinical situation changes

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18
Q

What are the 16 risk factors for VTE?

A

1) Active cancer or cancer treatment
2) Personal history of VTE
3) Age over 60
4) Use of hormone replacement therapy
5) Critical care admission
6) Used of oestrogen containing contraceptive therapy
7) Dehydration
8) Varicose veins with phlebitis
9) Known thrombophilias
10) Obesity
11) One or more significant medical comorbidities (heart disease, metabolic, endocrine or resp pathologies, acute infectious diseases and inflammatory conditions)
12) Pregnancy and post natal period
13) Surgery
14) Immobility
15) Major trauma
16) First degree relative with VTE

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19
Q

Name the 2 procoagulant substances in the body?

A

Platelets and clotting factors

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20
Q

Names the 4 anticoagulant substances in the body?

A

1) Protein C
2) Protein S
3) Anti thrombin III
4) Fibrinolytic system

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21
Q

Are aspirin and other antiplatelets appropriate prophylaxis for VTE?

A

No - remember venous thrombus is fibrin and erythrocyte rich with few platelets

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22
Q

What are the 3 important pieces of general advice for avoiding VTE in hospital patients?

A

1) Do not allow patients to become dehydrated unless it is clinically indicated
2) Encourage patients to mobilise ASAP
3) Do not regard aspirin or other anti platelet drugs as adequate prophylaxis for VTE

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23
Q

How do compression stockings work as prophylaxis for VTE?

A

Graduated compression
From ankle to knee with decreasing compression
Popliteal break
From lower to upper thigh with decreasing compression

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24
Q

What are the drugs used as VTE prophylaxis?

A

1) Low dose low molecular weight heparin
2) Fondaparinux (synthetic pentasaccharide)
Newer anticoagulants:
3) Direct inhibitors of factor Xa - rivaroxaban
4) Direct thrombin inhibitors - dabigatran

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25
Q

What is the rough mechanism of action of unfractionated heparin, LMW heparin and Fontaparinox?

A

Unfractionated heparin, LMW heparin and Fontaparinox work through anti thrombin, they bind to anti thrombin and enhance its effects on thrombin (FII) and/or factor 10a.

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26
Q

What is Fontaparinox?

A

Synthetic pentasaccharide - enhances the effect of anti thrombin on factor 10a

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27
Q

How do the actions of unfractionated heparin, LMW heparin and Fontaparinox differ?

A

Unfractionated heparin has equal effect on thrombin and F10a
LMW heparin has more effect on F10a than thombin
Fontaparinox only acts of factor 10a

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28
Q

How does the action of direct thrombin inhibitors differ to other anticoagulants?

A

Directly inhibit thrombin in an antithrombin-independent way - ie unlike the others do not act by enhancing the effect of anti thrombin but bind directly to thrombin

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29
Q

Which is the only anticoagulant which has effect on clot bound thrombin?

A

Direct thrombin inhibitors

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30
Q

What is the function of exclusion tests in diagnosing VTE?

A

Useful in working out which patients with suspected VTE need to be investigated further and which patients do not

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31
Q

What 2 exclusion tests are used in diagnosis of VTE?

A

1) Wells score: validated numerical clinical probability score
2) Sensitive quantitative D-dimer with high negative predictive value
These are used in an agreed algorithm

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32
Q

What are D dimers, how does the test work?

A

D dimers are break down products of fibrin clot, they are cross link products
They are specific to plasma acting on fribin (ie. don’t get D dimer with plasmin acting on fibrinogen), D dimer tells you a clot has formed and plasmin has broken down the fibrin clot
High D dimer suggests a VTE

33
Q

In patients that need further investigation following exclusion test, what investigation is used?

A

Duplex scanning (US) with compression to detect and thrombus, it is highly sensitive and specific for diagnosing DVT. Look for loss of flow signal, intravascular defects or non collapsing vessels (a vein with a clot in it will not compress with pressure for US probe) in the venous system

34
Q

What 2 investigations can be used when looking for PE, which is used most commonly?

A

1) CT PA (pulmonary angiogram)
2) VQ scan
CT PA is most commonly used

35
Q

How does a VQ scan work?

A

Compare the radio-isotope pattern of injected radio-isotope (perfusion) with inhaled radio-isotope (ventilation)
If the patterns don’t match, ie there is a defect in perfusion but not ventilation there is a V/Q mismatch and this is diagnostic of PE

36
Q

Give 2 LMW heparin drug names?

A

1) Enoxaparin

2) Tinzaparin

37
Q

How is LMW heparin used to treat VTE? 4

A

1) Dose fixed by body weight
2) Once daily s/c injection
3) Treat for atleast 5 days
4) Overlap with warfarin until INR >2 for 2 consecutive days (must thus overlap for atleast 2 days)

38
Q

Why is INR a useful measurement when switching from LMW heparin therapy to warfarin?

A

INR is unaffected by LMW heparin and thus all effect is due to warfarin

39
Q

What are the 5 steps in treatment of uncomplicated in-patient with DVT or PE in whom pregnancy is excluded?

A

1) Suspect DVT/PE
2) Treat with single does of LMW heparin
3) Confirm diagnosis
4) LMWH for 5 days and start warfarin
5) Overlap LMWH treatment and warfarin until INR is >2 on 2 consecutive days

40
Q

Name 3 oral novel anticoagulants, what is the action of each?

A

1) Rivaroxaban - Direct 10a inhibitors
2) Apixaban - direct 10a inhibitor
3) Dabigatran - direct 2a (thrombin) inhibitor
(all anti thrombin independent)

41
Q

What are the 4 novel parenteral anticoagulants?

A

1) Fondaparinux
2) LMWH
3) Argatroban
4) Bivalirudin

42
Q

What is the main advantage of new oral anticoagulants?

A

Have predictable pharmacokinetics - thus require no monitoring

43
Q

What is the mechanism of action of the oral novel anticoagulant endoxaban?

A

Direct anti-10a activity

44
Q

What are the 4 main advantages of novel oral anticoagulants over warfarin?

A

1) Dose is uniform for most patients (warfarin dose can vary 40 fold)
2) No need for monitoring - predictable effect
3) All agents have does reduction recommendations for specific populations eg. very elderly, renal impairment for VTE prevention and for AF
4) Rapid onset of action

45
Q

What is the management for first episode of proximal vein DVT or PE?

A

Treat for 3-6 mnths

For warfarin target INR = 2.5

46
Q

What is the management for recurrent episodes of VTE?

A

Treat with long term anticoagulation

47
Q

How does management of DVT or PE which has occurred in the absence of a reversible risk factor differ?

A

Consider long term anticoagulation

48
Q

What is the management for recurrent VTE on therapeutic anticoagulation?

A

Increase target INR to 3.5 for warfarin

49
Q

What is the definition of thrombophilia?

A

Familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis (inherited abnormalities must co-segregate with clinical thrombosis in the pedigree)

50
Q

There are many families where many members have suffered DVT but there is no abnormality identifiable on investigation (about 50%) of cases, based on this what is the alternative definition of thrombophilia?

A

Patients who develop DVT:

1) Spontaneously
2) Of disproportionate severity
3) Recurrently
4) At an early age

51
Q

Name the 6 heritable thrombophilias?

A 
Deficiencies of natural anticoagulants:
1) Anti thrombin deficiency
2) Protein C deficiency
3) Protein S deficiency
Abnormalities of pro-coagulant factors:
4) Activated protein C resisitance/ factor V leiden
Abnormalities of fibrin:
5) Dysfibrinogenaemia
6) Prothrombin 20210A
52
Q

What is the difference between activated protein C resistance and factor V leiden?

A

Factor V leiden is the genotype which leads to the phenotype of activated protein C resistance

53
Q

Name the 1 acquired thrombophilia?

A

Anti phospholipid syndrome

54
Q

Arterial thrombosis is a clinical feature of which thrombophilia?

A

Anti phospholipid syndrome

55
Q

Coumarin induced skin necrosis is a clinical feature of which thrombophilia?

A

Protein C deficiency (warfarin induced skin necrosis)

56
Q

Obstetric complications are a clinical feature of which thrombophilia?

A

Anti phospholipid syndrome

57
Q

What is thought to be the cause of obstetric complications (recurrent miscarriage) in thrombophilia?

A

Thrombosis in placental circulation

58
Q

What are the 7 clinical features of thrombophilia?

A

1) DVT
2) PE
3) Superficial thrombophlebitis
4) Thrombosis of cerebral, axillary, portal and mesenteric veins
5) Arterial thrombosis (APS only)
6) Coumarin induced skin necrosis (PC deficiency)
7) Obstetric complications (APS)

59
Q

What is the action of anti thrombin?

A

Inhibits factor 10a and 2a (thrombin)

60
Q

How does Protein C become activated?

A
  • Protein C exists in inactive form
  • Aswell as cleaving fibrinogen thrombin also binds to thrombomodulin (vascular endothelial protein)
  • The thombin-thrombomodulin complex activates Protein C
61
Q

What is the role of activated Protein C?

A
  • Has a co factor called Protein S
  • Protein C is responsible fro degrading protein 5 and 8 by proteolysis (which are the co factors in the coagulation cascade)
62
Q

How common are protein C, S and anti thrombin deficiencies?

A

Altogether account for less than 5% of patients presenting with VTE

63
Q

What is the inheritance pattern of natural anticoagulant deficiencies?

A

Autosomal dominant

64
Q

What is the genetic defect in Factor V leiden and what is the result of this defect?

A

Point mutation in factor V gene right at the point where it is cleaved by protein C - thus resistant to activated protein C

65
Q

What is the most common familial thrombophilia?

A

Factor V leiden

66
Q

How common is Factor V leiden?

A

European gene - 5-8% of the population heterozygous

Not found in Far east and Africa

67
Q

How does Factor V leiden increase clotting risk?

A

Heterozygotes - 3-5 fold increase for venous thrombosis
Homozygotes = 30-50 fold increase for venous thrombosis
Interacts with other risk factors for VTE

68
Q

What is prothrombin 20210A?

A

Point mutation in 3’ untranslated region of prothrombin gene - its an enhancer region responsible for turning on prothrombin synthesis
Associated with increased pro thrombin levels

69
Q

How does prothrombin 20210A increase clotting risk?

A

3 fold increase in venous thrombosis

70
Q

How common is prothrombin 20201A?

A

occurs in 1-2% of healthy UK population

Rare in Asia and Africa

71
Q

What is the diagnostic criteria for antiphospholipid syndrome?

A

Antiphospholipid Ab on atleast 2 occasions 8 weeks apart in association with venous thrombosis or arterial thrombosis or recurrent fetal loss (>2)

72
Q

What is the difference between primary and secondary APS?

A

APL can be associated with other connective tissue disorders eg. SLE
Primary is APL not in association with other connective tissue disorders

73
Q

Why must a patient have to have evidence of antiphospholipid Ab on more than one occasion to have APS?

A

They can often be an incidental finding, it is thought we all make these Ab from time to time and most get rid of it
Thus only have APS if they cause a problem and can be identified more than once

74
Q

What 2 test are used to identify antiphospholipid Abs?

A

1) Lupus anticoagulant

2) Anticardiolipin Ab

75
Q

Is a thrombophilia screen indicated in all patients with VTE?

A

No

76
Q

Which 3 groups of patients with VTE should have a thrombophilia screen?

A

1) younger patients
2) Positive family history
3) if discovery of a thrombophilia will change management

77
Q

When should a thrombophilia screen be undertaken?

A

Not in acute VTE - this will affect results
Not when patient still on Anticoagulant
Preferably not when patient is pregnant or taking OCP
Ie. when patient has recovered from VTE and stopped therapy

78
Q

Which is the only type of thrombophilia which should be screened for in patient with arterial events or recurrent miscarriage?

A

Anti phospholipid Ab screen only

CLINICAL PATHOLOGY (56 decks)

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