Causes prevention and consequences of DVT/PE Flashcards
Thrombosis
Blood clot within circulation
Thrombus
Blood clot in intact blood vessel fixed at a site
Thromboembolus
blood clot breaking free and occludes elsewhere in circulation
Pulmonary embolism
Deposition of a clot in the main branch/bifurcation of pulmonary artery
Patent foramen ovale and pulmonary embolism
Clot can pass from R to L - can enter systemic circulation
Virchow’s triad
- Endothelial injury - sepsis/toxins/oedema/trauma
- Blood stasis - impaired muscle pump/proximal occlusion/turbulence
- hyper-coagulability - protein C deficiency/factor 5 Leiden/pregnancy/hyperviscosity/malignancy
haemostasis
- Tissue damage exposes collagen
- Vasoconstriction to decrease blood flow - serotonin, thromboxane A2 etc
- Platelets stick to exposed collagen and release ADP, Ca2+ and serotonin, as well as vWF, fibrinogen and factors V/X111 (a granules)
- Fibrinogen and vWF promote platelet aggregation, ADP, thrombin and TXA2 cause platelet activation, factors V and XIII cause clotting
Function of activated protein C
Negative feedback - self-regulation of clotting cascade by inhibiting 5a and 8a
How are clots prevented from forming and spreading?
- Prostacyclin (PGI2) and NO from undamaged endothelium prevent platelet adhesion
- Fibrinolysis: plasminogen → plasmin (TPA), plasmin acts on fibrin by creating FDPs
Factor 5 leiden
Variant of factor 5 that is resistant to protein C - always activates clotting cascade
Treatment for DVTs
Compression stockings + heparin
Antidote to unfractionated heparin
Protamine
Side effects of heparin
Heparin induced thrombocytopenia - platelet destruction
Thrombolytics use
- Used in PE
- Impaired venous return
- Used in significant hypotension and systolic lower than 100
Reversal for rivaroxaban and apixaban
Andexanet alfa