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8. CP - Core Haematology > (44) Thrombosis and risk factors > Flashcards

(44) Thrombosis and risk factors Flashcards

1
Q

What are the 3 components of Virchow’s triad?

A
  • blood flow
  • vascular endothelium
  • blood composition
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2
Q

What is the primary pathological abnormality in arterial thrombosis?

A

Atherosclerosis of the vessel wall

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3
Q

What do you get in arterial thrombosis?

A
  • atherosclerosis
  • rupture of atheromatous plaque
  • endothelial injury
  • platelet aggregation and platelet thrombi
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4
Q

In arterial thrombosis, what plays an important role in final vessel occlusion?

A

Platelet aggregation and platelet thrombi

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5
Q

What are the risk factors for arterial thrombosis?

A
  • smoking
  • hypertension
  • hypercholesterolaemia
  • diabetes
  • family history
  • obesity
  • physical inactivity
  • age
  • male sex
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6
Q

What does the pathogenesis in venous thrombosis involve?

A
  • venous stasis

- hypercoagulable state

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7
Q

The thrombi in venous thrombosis are composed of what?

A

Predominantly composed of fibrin with a lesser role for platelet accumulation and aggregation

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8
Q

Venous thromboembolism (VTE) are frequently unrecognised. What percentage of DVT are clinically silent?

A

80%

VTE is a silent killer

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9
Q

In which vein is there a clot in DVT?

A

The femoral vein of the leg

PE in pulmonary artery

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10
Q

How many patients with proximal DVT have (asymptomatic) PE?

A

About 50%

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11
Q

DVT is found in how many patients with PE?

A

Over 80%

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12
Q

What is the incidence of VTE?

A

1 per 1000

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13
Q

How many cases of PE present as sudden death?

A

Up to 20%

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14
Q

30% of those with VTE develop what?

A

Recurrent VTE in 10 years

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15
Q

28% of those with VTE develop what?

A

Post thrombotic syndrome

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16
Q

What is the mortality of promptly diagnosed and adequately treated PE?

A

2% (direct)

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17
Q

How many deaths does VTE cause in the UK?

A

60,000

32,000 due to hospital admissions, 25,000 preventable

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18
Q

How is hospital-acquired VTE defined?

A

Any VTE within 90 days of discharge

  • 2/3rds of all VTE
  • markedly underestimated
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19
Q

Outline the strategies concerning VTE

A
  • prophylaxis (consistent risk assessment and appropriate prophylaxis)
  • treatment (prompt diagnosis and guideline-led unified care)
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20
Q

Describe the care pathway in hospital patients concerning VTE

A
  • patient admitted to hospital
  • assess VTE risk
  • assess bleeding risk
  • balance risks of VTE and bleeding and act appropriately
  • reassess risks of VTE and bleeding
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21
Q

How often should the risks of VTE and bleeding in hospital patients be reassessed?

A

Within 24 hours of admission and whenever the clinical situation changes

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22
Q

In hospital patients, the risk of VTE and bleeding should be balanced. What is the appropriate action after this?

A

Offer VTE prophylaxis if appropriate. Do not offer pharmacological VTE prophylaxis if patient has any risk factor for bleeding and risk of bleeding outweighs risk of VTE

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23
Q

What are the risk factors for VTE?

A
  • active cancer or cancer treatment
  • over 60 years
  • critical care admission
  • dehydration
  • thrombophilias
  • significant medical comorbidities
  • surgery
  • major trauma
  • personal history of VTE
  • use of HRT
  • use of oestrogen-containing contraceptive therapy
  • varicose veins with phlebitis
  • obesity
  • pregnancy and postnatal periods
  • immobility
  • first degree relative with VTE
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24
Q

What 2 things must be balanced? (concerning VTE and bleeding)

A
  • procoagulants

- anti-coagulants

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25
Q

What is involved in pro coagulation?

A
  • platelets

- clotting factors

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26
Q

What is involved in anticoagulation?

A
  • protein C
  • protein S
  • anti-thrombin III
  • fibrinolytic system
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27
Q

Give some general advice concerning hospital patients and VTE

A
  • do not allow the patients to become dehydrated unless clinically indicated
  • encourage patients to mobilise as soon as possible
  • do not regard aspirin or other anti-platelet drugs as prophylaxis for VTE
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28
Q

Describe the pressure differences at different parts of the leg (Doppler)

A 
upper thigh = 8mmHg
lower thigh = 10mmHg
popliteal = 8mmHg
calf = 14mmHg
ankle = 18mmHg
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29
Q

What are the pharmacological prophylaxis for VTE?

A
  • “low dose” low molecular weight heparin
  • fondaparinux (synthetic pentasaccharide)
  • newer anticoagulants (rivaroxaban, dabigatran)
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30
Q

Which drug is a direct inhibitor of factor Xa? (an anticoagulant)

A

Rivaroxaban (apixaban)

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31
Q

Which drug is a direct thrombin inhibitor? (an anticoagulant)

A

Dabigatran

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32
Q

What is fondaparinux?

A

An anticoagulant medication chemically related to low molecular weight heparins

  • a synthetic pentasaccharide
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33
Q

What are low molecular weight heparins?

A

Class of anticoagulant medications - used in the prevention and treatment of venous thromboembolism

34
Q

What is the Wells score/Wells criteria used for?

A

Used for clinical prediction

  • diagnosing DVT
  • diagnosing PE
35
Q

What is a D-dimer test used for?

A

Used to help exclude thrombus (exclude DVT/VTE)

36
Q

What does a positive D-dimer indicate?

A

The presence of an abnormally high level of cross-linked fibrin degradation products in your body. Shows there has been significant thrombus formation and breakdown in the body, but it does not identify the location or cause. An elevated D-dimer may be due to a VTE or DIC but it may also be due to a recent surgery, or trauma, infection etc

A negative result practically rules out thrombosis

37
Q

What is a D-dimer?

A

A fibrin degradation product, present after a clot is degraded by fibrinolysis.
- contains D fragments of the fibrin protein

38
Q

What do you look for on ultrasound to detect DVT?

A
  • loss of flow signal
  • intravascular defects
  • non-collapsing vessels in the venous system

Duplex scanning with compression will aid to detect any thrombus

39
Q

Is ultrasound useful for diagnosing thrombi?

A

Highly sensitive and specific for diagnosing DVT

40
Q

What types of scans can be used for diagnosing DVT?

A
  • ultrasound
  • spiral/multislice CT
  • VQ scan
41
Q

What might a V/Q mismatch indicate?

A

A potential pulmonary embolism

42
Q

Describe how low molecular weight heparin (LMWH) is used in treatment for VTE?

A
  • doses fixed by body weight
  • usually once a day by s/c injection
  • treat for at least 5 days
  • overlap with warfarin until INR >2.0 for 2 consecutive days
43
Q

Give 2 examples of LMWH and how they are used

A
  • enoxaparin 1.5mg/kg subcutaneous one daily

- tinzaparin 175u/kg subcutaneous once daily

44
Q

Describe the treatment pathway for uncomplicated DVT/PE in whom pregnancy excluded

A
  • suspected DVT/PE (check contraindication to anticoagulation)
  • treat with single dose LMWH (sub cut - see enoxaparin dosing chart)
  • confirm diagnosis
  • LMWH (min. 5 days)
  • start warfarin (see dosing chart)
  • start patient-held anticoagulant book + inpatient warfarin chart
  • overlap warfarin and heparin until 2 therapeutic INR results (>2)
45
Q

What should you use instead of LMWH if there is a need for quick anticoagulation or the rapid reversal of is required?

A

Unfractionated heparin intravenously

46
Q

Name a parenteral anticoagulant

A

Fondaparinux

47
Q

What does parenteral mean?

A

Administration by injection

48
Q

Name an oral anticoagulant

A
  • rivaroxaban
  • apixaban
  • dabigatran
49
Q

Name a direct thrombin inhibitor

A

Dabigatran

50
Q

Name anticoagulants that have direct anti-Xa activity

A
  • rivaroxaban
  • apixaban
  • endoxaban
51
Q

What does NOAC stand for?

A

New oral anticoagulant

52
Q

How much does the dose of warfarin vary?

A

40 fold

53
Q

How do the does of NOACs vary?

A
  • dose is uniform in most patients
  • no need for routine monitoring: predictable effect
  • all agents have dose reduction recommend in specific populations
54
Q

In which groups is the dose of NOAC recommended to be lowered?

A
  • very elderly
  • renal impairment
  • for VTE prevention
  • for AF
55
Q

Do NOACs have a slow of fast onset of action?

A

Rapid onset of action

initiation may be done directly with rivaroxaban and apixaban with no need for LMWH

56
Q

Briefly describe the management of the first episode of proximal vein DVT or PE

A

Treat for 3-6 months

For warfarin, target INR = 2.5

57
Q

Briefly describe the management of recurrent episodes of VTE

A

Treat with long term anticoagulation

58
Q

Briefly describe the management of proximal DVT or PE that has occurred in the absence of reversible risk factor

A

Consider long term anticoagulation

59
Q

How should the target INR change in recurrent VTE on therapeutic anticoagulation

A

Increase target INR to 3.5 for warfarin

60
Q

In which conditions should you consider long term anticoagulation?

A

For recurrent episodes of VTE, and in proximal DVT or PE that has occurred in the absence of reversible risk factor

61
Q

What does INR show?

A

The higher the INR, the thinner the blood

The lower the INR, the thicker the blood

1 = normal blood

62
Q

Define 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

63
Q

Give an alternative definition of thrombophilia

A

Patients who develop VTE

  • spontaneously
  • of disproportionate severity
  • recurrently
  • at an early age
64
Q

Name 6 heritable thrombophilias

A
  • antithrombin deficiency
  • protein C deficiency
  • protein S deficiency
  • activated protein C resistance/FV Leiden
  • dysfibrinogenaemia
  • prothrombin 20210A
65
Q

Name a type of acquired thrombophilia

A

Antiphospholipid syndrome (APS - also known as Hughes syndrome)

66
Q

What are the clinical features of thrombophilia?

A
  • DVT
  • PE
  • superficial thrombophlebitis
  • thrombosis of cerebral, axillary, portal, mesenteric veins
  • arterial thrombosis (APS, only)
  • coumarin induced skin necrosis (PC deficiency)
  • obstetric complications: foetal wastage (APS)
67
Q

What converts fibrinogen to fibrin?

A

Thrombin

68
Q

What converts prothrombin to thrombin?

A

Factor Va

69
Q

What does the activated protein C/protein S complex?

A

Degrades factors Va and VIIIa by proteolysis

70
Q

What does the factor V Leiden mutation cause?

A

Protein C is unable to inactivate factor Va when the factor V Leiden mutation is present

71
Q

Factor V Leiden is associated in most cases with which mutation?

A

A single point mutation in the factor V gene: G to A1691

72
Q

What amino acid change occurs in factor V Leiden?

A

Arg506 is replaced by Gln (glutamine), rendering FV relatively resistant to cleavage by APC

73
Q

What is the most common familial thrombophilia?

A

Factor V Leiden

74
Q

Geographically, where is factor V Leiden found?

A

5-8% European population are heterozygous

Not found in Far East and Africa

75
Q

What increased risk do heterozygotes of factor V Leiden have of venous thrombosis?

A

3-5 fold OR for venous thrombosis

76
Q

What increased risk do homozygotes of factor V Leiden have of venous thrombosis?

A

30-50 fold OR for venous thrombosis

77
Q

What is prothrombin 20210A?

A
  • point mutation in 3’ untranslated region of prothrombin gene
  • associated with increased prothrombin levels
  • 3 fold increase in venous thrombosis
78
Q

Geographically, where do prothrombin 20210A occur?

A
  • occurs in 1-2% health UK population

- rare in Asia and Africa

79
Q

What is antiphospholipid syndrome?

A

An autoimmune, hypercoagulable state caused by antiphospholipid antibodies. Predisposed to thrombi in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, and severe preeclampsia

80
Q

How is antiphospholipid syndrome defined?

A

Antiphospholipid antibodies (lupus anticoagulant or anticardiolipid antibody) on at least 2 occasions 8 weeks apart in association with venous thrombosis or arterial thrombosis or recurrent foetal loss

May be primary or secondary

81
Q

For selected patients with arterial events of recurrent miscarriage, which thrombophilia screening tests should you do?

A

Antiphospholipid antibody screen only

82
Q

In which situations should you not do thrombophilia screening?

A

In acute VTE

When the patient is already on anticoagulants

Pregnancy and oral contraceptive pills also have an effect

8. CP - Core Haematology (11 decks)

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