Pathophysiology of thrombosis and embolism Flashcards
normal blood flow is described as
laminar
process of thrombosis.
endothelial injury, stasis or turbulent blood flow, hyper coagulability of blood
significance of Virchow’s triad.
change in blood vessel wall (eg atheromatous artery), blood constituents and pattern of blood flow. these are factors of thrombosis NOT clot
relationship between atheroma and thrombosis.
arterial thrombosis most commonly superimposed on atheroma due to virchows triad. hypercholesterolaemia due to virchows triad
factors causing thrombosis.
change in the heart eg vessel wall, hyper viscosity, post traumatic hyper-coagulability, stasis eg economy class syndrome, turbulence eg atheromatous plaque, aortic aneurysm
factors causing embolism.
defects in blood flow
atheroma, spasm, vasculitis, vascular steal syndrome, external compression, hyperviscosity, thromboembolism
clinical consequences of thrombosis
deep vein thrombosis, ischaemic limb, myocardium infarction
outcomes of thrombosis
resolution, organisation, recanalisation
outcomes of thrombosis
resolution, organisation, recanalisation, death, propagation
embolus
detached intravascular solid, liquid or gaseous mass. most are dislodged thrombi
types of embolus
systemic thromboembolus, venous thromboembolus, fat embolus, gas embolus, tumour, trophoblast, septic material, amniotic fluid, bone marrow, foreign bodies
mural thrombus
thrombus of the heart
systemic thromboembolus
travel to other sites eg lower limbs or brain. consequences depend on vulnerability of affected tissues to ischaemia, calibre of occluded vessel, collateral circulation but usually infarction occurs
consequences of pulmonary thromboembolism
depends on size of embolus but can be silent, pulmonary haemorrhage/infarction, right heart failure, sudden death. multiple PE over time leads to pulmonary hypertension and right ventricular failure