HAEM: Venous Thrombosis Flashcards
What % of hospital deaths does PE account for?
5-10%
25000 deaths per annum related to VTE, difficult to reverse but preventable
What is the recurrence rate of VTE?
20% within 2 years and 4% pa after
What is the death rate from VTE?
5% die
What is the occurence of pulmonary hypertension with VTE?
4% at 2 years
What is Virchow’s triad?
- blood - hypercoagulability
- vessel wall - damage
- blood flow - stasis
What factors in blood increase risk of VTE?
- Viscosity
- Haematocrit
- Protein/paraprotein
- Platelet count
- Coagulation system - net excess of procoagulant activity
List some procoagulant and anticoagulant factors.
Procoagulant - V, VIII, XI, IX, X, II, Fibrinogen, Platelets
Anticoagulant - TFPI, Protein C, Protein S, Thrombomodulin, EPCR, Antithrombin, Fibrinolysis
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Reduced protein C
Is VTE preventable in thrombophilias?
In thrombophilias, VTE is precipitated in 50% of cases so these are still preventable e.g. Factor V leiden, Protein C/S deficiency, antithrombin deficiency
What factors in vessel wall increase risk of VTE?
- Expresses anticoagulant molecules
- Thrombomodulin
- Endothelial protein C receptor (ERCP) - helps protein C become activated
- Tissue factor pathway inhibitor - FT usually kept outside the circulation
- Heparans - co-factor for antithrombin
- Does not express tissue factor
- Secretes antiplatelet factors e.g. Prostacyclin, NO
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How does inflammation make the endothelium prothrombotic?
Inflammaton/injury makes the vessel wall prothormbotic e.g. infection, malignancy, vasculitis, trauma
Effects:
- Anticoagulant molecules (eg TM) are down regulated
- TF may be expressed
- Prostacyclin production decreased
- Adhesion molecules upregulated
- Von Willebrand factor release –> platelet and neutrophil capture –> neutrophil extracellular traps (NETS) form
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Describe the role of neutrophils in ‘immunothrombosis’.
How neutrophils contribute to thrombosis has been termed “immunothrombosis” highlighting that inflammation is an important drive for thrombosis.
Neutrophils - under stimuli release DNA forming neutrophil extracellular traps which…
- captures vWD,
- releases histones which activates platelets,
- provides a surface for contact activation of coagulant pathways (FXII –> XIIa)
- contains neutrophil elastase which can break down TFPI
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How does blood flow/stasis increase risk of thrombosis?
Stasis –> thrombosis because..
- Accumulation of activated factors
- Promotes platelet adhesion
- Promotes leukocyte adhesion and transmigration
- Hypoxia produces inflammatory effect on endothelium - adhesion, release of VWF
What are the causes of blood stasis?
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How does flight distance/time affect PE occurrence?
The longer the flight the higher the risk of PE.
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How does taking the OC and having FVL increase risk of thrombosis compared to the general population?
RR of VTE with FVL + OC = x35
OC alone = ~x5
FVL alone = ~x7
Which of the inherited thrombophilias has the highest risk of thrombosis?
Antithrombin deficiency
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Antithrombin - decline in antithrombin curve was steepest for this out of all the thrombophilias