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Y2 Clinical Pathology > Thrombosis & Risk Factors for Thrombosis > Flashcards

Thrombosis & Risk Factors for Thrombosis Flashcards

1
Q

What are the 3 components of Virchow’s triad?

A

this describes the 3 broad categories of factors that are thought to contribute to thrombosis

  1. hypercoagulability
  2. haemodynamic changes (e.g. stasis, turbulence)
  3. endothelial injury / dysfunction
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2
Q

What causes arterial thrombosis?

What is the primary pathological abnormality?

A

atherosclerosis of the vessel wall is the primary pathological abnormality

rupture of atheromatous plaques causes endothelial injury

platelet aggregation and platelet thrombi play an important role in final vessel occlusion

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3
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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4
Q

What is involved in the pathogenesis of venous thrombi?

What are the thrombi composed of?

A

pathogenesis mainly involves venous stasis and hypercoagulable states

thrombi are predominantly composed of fibrin with a lesser role for platelet accumulation and aggregation

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5
Q

What % of venous thromboemobolism are unrecognised?

A

80% of VTEs are clinically silent

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6
Q

What are the 2 main consequences of venous thromboemobolism?

A

deep vein thrombosis:

  • this is a large thrombus (usually) in the femoral vein of the leg
  • 50% of patients with proximal DVT have asymptomatic PE

pulmonary embolism:

  • the embolus originates in the femoral vein and travels into a pulmonary artery
  • DVT is found in >80% of patients with PE
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7
Q

What is the incidence of VTE?

How may it present?

A

incidence is 1 person per 1000

it may present as sudden death (20% of PE)

30% develop recurrent VTE in 10 years

28% develop post-thrombotic syndrome

mortality of promptly diagnosed and treated PE is 2%

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8
Q

What is the definition of hospital-acquired VTE?

A

any VTE within 90 days of discharge

hospital-acquired clots account for 2/3 of all VTE

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9
Q

What are the strategies to prevent hospital-acquired VTE?

A

prophylaxis:

  • involves constant risk assessment and appropriate prophylaxis

treatment:

  • requires prompt diagnoses and guideline-led unified care
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10
Q

What are the stages involved 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
  5. reassess risks of VTE and bleeding within 24 hours of admission and whenever clinical situation changes
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11
Q

Why is it important to balance risks of VTE and bleeding?

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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12
Q

What are the significant medical comorbidities that increase risk of VTE?

A
  • heart disease
  • metabolic, endocrine or respiratory pathologies
  • acute infectious diseases
  • inflammatory conditions
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13
Q

What are the 16 risk factors for VTE?

A
  • active cancer or cancer treatment
  • age over 60 years
  • critical care admission
  • dehydration
  • known thrombophilias
  • one or more significant medical comorbidities
  • surgery
  • major trauma
  • personal history of VTE
  • use of hormone replacement therapy
  • use of oestrogen-containing contraceptive therapy
  • varicose veins with phlebitis
  • obesity
  • pregnancy and postnatal period
  • immobility
  • first degree relative with VTE
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14
Q

What are the procoagulant and anticoagulant factors that need to be balanced?

A

procoagulant:

  • platelets
  • clotting factors

anti-coagulant:

  • protein c
  • protein s
  • anti-thrombin III
  • fibrinolytic system
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15
Q
A
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16
Q

What is general advice that is given to avoid development of VTE?

A
  • do not allow patients to become dehydrated unless clinically indicated
  • encourage patients to mobilise as soon as possible
  • do not regard aspirin or other antiplatelet drugs as adequate prophylaxis for VTE
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17
Q

What is involved in the pharmacological prophylaxis for VTE?

A

“low dose” low molecular weight heparin

fondaparinux (synthetic pentasaccharide)

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18
Q

What are newer anticoagulants that are used as pharmacological prophylaxis for VTE?

A

direct inhibitors of factor Xa:

  • rivaroxaban
  • apixaban

direct thrombin inhibitors:

  • dabigatran
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19
Q

How does rivaroxaban work?

A

it is a direct inhibitor of activated factor X (factor Xa)

this prevents FXa from cleaving prothrombin to yield active thrombin

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20
Q

How does dabigatran work?

A

it is a direct inhibitor of thrombin

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21
Q

How do the parenteral oral anticoagulants work?

A

Fondaparinux and LMWH inhibit factor Xa

Argatroban and Bivalirudin inhibit thrombin

22
Q

What are the exclusion tests for diagnosing VTE?

A

wells score:

  • this is a validated numerical clinical probability score

D-dimer:

  • sensitive quantitative D-dimer with high negative predictive value

both of these tests are used in an agreed algorithm

23
Q

What is D dimer?

What do high levels of D dimer in the blood suggest?

A

it is a fibrin degradation product

it is a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis

high levels of D-dimer suggest a major clot, such as DVT

24
Q

How can ultrasound be used to look for and diagnose DVT?

A

duplex scanning with compression will aid to detect any thrombus

it is highly sensitive and specific for diagnosing DVT

look for loss of flow signal, intravascular defects or non-collapsing vessels in the venous system

25
Q

What other type of scan can be used to detect a thrombus?

A

spiral / multislice CT

26
Q

What type of scan is used to look for pulmonary embolism?

A

VQ scan

27
Q

How is the dose of LMWH for treatment of VTE decided?

How often is the dose taken for?

A

doses are fixed by body weight

they are given once daily by subcutaenous injection

patient is treated for at least 5 days

overlap with warfarin until INR > 2.0 for 2 consecutive days

28
Q

What are the stages involved in treatment of uncomplicated in-patient with DVT or PE when pregnancy is excluded?

A
  1. suspected DVT / PE
  2. treat with a single dose of LMWH subcutaenously
  3. confirm diagnosis
  4. LMWH for 5 days

start warfarin

start patient-held anticoagulation book and inpatient warfarin chart

  1. overlap warfarin and heparin until two consecutive therapeutic INR results (>2.0)
29
Q

When should unfractionated heparin be used instead of LMWH?

A

it should be given intravenously if there is a need for quick anticoagulation

30
Q

What are examples of direct thrombin and direct factor Xa inhibitors?

A

direct thrombin inhibitors:

  • dabigatran

direct anti-Xa activity:

  • rivaroxaban
  • apixaban
  • endoxaban
31
Q

What is meant by predictable dose-response?

A

for direct oral anticoagulants, the dose is uniform in most patients

there is no need for routine monitoring as there is a predictable effect

32
Q

In which populations is a dose reduction of direct acting oral anticoagulant recommended?

A
  1. very elderly
  2. renal impairment
  3. VTE prevention
  4. atrial fibrillation
33
Q

What is the difference in the dose of DAOC given usually and given for VTE?

A

rivaroxaban and apixaban have a rapid onset of action and initiation may be done directly with no need for LMWH

for VTE, the recommended dose at initiation is greater

34
Q

How should a first episode of proximal vein DVT be treated compared to recurrent episodes?

A

first episode of proximal vein DVT or PE should be treated for 3-6 months

for warfarin, target INR is 2.5

long-term anticoagulation is used to treat recurrent episodes of VTE

35
Q

What is the treatment for a proximal VTE or PE that has occurred in absence of a reversible risk factor?

A

consider long term anticoagulation

when someone has recurrent VTE on therapeutic anticoagulation, increase target INR to 3.5 for warfarin

36
Q

What is the definition of thrombophilia?

A

familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis

37
Q

What is the alternative definition of thrombophilia?

A

patients who develop VTE:

  • spontaneously
  • of disproportionate severity
  • recurrently
  • at an early age
38
Q

What are the 6 heritable thrombophilias?

A
  • antithrombin deficiency
  • protein c deficiency
  • protein s deficiency
  • activated protein c resistance / factor V Leiden
  • dysfibrinogenaemia
  • prothrombin 20210A
39
Q

What is an example of an acquired thrombophilia?

A

antiphospholipid syndrome

40
Q

What are the clinical features of thrombophilia?

A
  • deep vein thrombosis
  • pulmonary embolism
  • superficial thrombophlebitis
  • thrombosis of cerebral, axillary, portal & mesenteric veins
  • arterial thrombosis
  • coumarin induced skin necrosis
  • obstetric complications
41
Q

What is thrombophlebitis?

A

an inflammatory process that causes a blood clot to form and block one or more veins

42
Q

What happens in protein c and s deficiency?

A

there is increased risk of developing abnormal blood clots

protein c and s are vitamin-K-dependent plasma proteins that work as a natural anticoagulant system

43
Q

How does factor V Leiden work?

A

there is a gene mutation which leads to an abnormal Factor V

the mutation means that Protein C cannot bind to and inhibit the pro-clotting activity of Factor V

this leads to a hypercoagulable state

44
Q

What is the role of antithrombin?

A

it is a small protein that inactivates several clotting factors

45
Q

What mutation is usually responsible for Factor V Leiden?

A

APC resistance is associated with a single point mutation in the factor V gene

Arg506 is replaced by GIn rendering FV relatively resistant to cleavage by APC

46
Q

What is the increased risk of VTE in factor V Leiden?

A

heterozygotes:

  • 3-5 fold increased risk for venous thrombosis

homozygotes:

  • 30-50 fold increased risk for venous thrombosis
  • risk of recurrent VTE is not increased
47
Q

What causes prothrombin 20210A?

What is it associated with?

A

point mutation in 3’ untranslated region of the prothrombin gene

associated with increased prothrombin levels

3 fold increase in venous thrombosis risk

48
Q

How is antiphospholipid syndrome diagnosed?

A

antiphospholipid antibodies (lupus anticoagulant or anticardiolipin antibody) on at least 2 occasions 8 weeks apart in association with:

venous thrombosis

arterial thrombosis

or recurrent foetal loss

49
Q

What are the confounding factors in thrombophilia testing?

A
  • acute phase of thrombosis
  • anticoagulation
  • warfarin
  • heparin
  • liver disease
  • acute major illness (e.g. sepsis)
  • pregnancy
  • COCP/oestrogen use
50
Q

How does a diagnosis of heritable thrombophilia affect management of VTE?

A

a diagnosis of heritable thrombophilia rarely changes acute management of VTE

51
Q

When are people screened for thrombophilia?

A

Who?

  • not indicated in unselected patients with VTE
  • younger patients
  • positive family history
  • if management will change

When?

  • avoid confounding factors
  • e.g. acute VTE, anticoagulants, pregnancy, COCP

Which tests?

  • for selected patients with arterial events or recurrent miscarriage, antiphospholipid antibody screen only

Y2 Clinical Pathology (76 decks)

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