thrombosis and embolism Flashcards
thrombosis
the process leading to the formation of thrombus
thrombus
a solid mass composed of blood constituents which have aggregated together in flowing blood in the lumen of a blood vessel. the main constituents are platelets and fibrin
physiological thrombosis- primary haemostasis
- vessel wall is breached
- circulating platelets aggregate to plug gap
- platelets release factors which trigger coagulation cascade
physiological thrombosis- secondary haemostasis
- coagulation cascade converts fibrinogen to large molecules of insoluble fibrin
- long fibrin molecules bind together platelets and entrapped red and white cells
fibrinolysis
fibrin holds the thrombus together. if fibrin is broken down, the thrombus dissolved = fibrinolysis. plasmin is the active enzyme which fragments fibrin. the fragmented fibrin are called ‘fibrin degradation products’ or FDPs
plasminogen in fibrinolysis
plasma contains the inactive proenzyme plasminogen.
plasminogen is converted to plasmin by plasminogen activators, particularly tissue plasminogen activator (t-PA) secreted by endothelial cells and Urokinase.
when fibrin is formed, plasminogen and t-PA secreted by endothelial cells and Urokinase.
when fibrin is formed, plasminogen and t-PA bind to it. the t-PA convert nearby plasminogen to plasmin, which binds to degrade the fibrin. this controls the size of the thrombus.
pathological thrombosis .
pathological thrombosis occurs when the thrombus enlarges beyond vessel healing requirements, and continues to grow. beyond a certain thrombus size and rate of development, the intrinsic fibrinolytic system is incapable of controlling the size to which the thrombus grows
D-dimer test
D-Dimers are FDBs. detected by monoclonal antibody test to D fragment. increased blood levels in thrombosis.
positive test in presence of active thrombosis:
- pulmonary embolus
- deep vein thrombosis
- aortic dissection.
best used as a test of exclusion rather than inclusion.
what factors predispose thrombus formation?
virchow’s triad:
1) damage to vessel wall, especially endothelium
2) stasis- slow or turbulent blood flow
3) hypercoagulability- change in character of blood especially increased platelets, increased red cell numbers, increased viscosity
pathological thrombosis- where does it occur?
arteries- main predisposing factors are vessel wall damage.
veins- stasis most important
heart- ventricles: chamber wall damage most important. Atrium- stasis most important. heart valves- valve surface damage most important
thrombo-embolism
thrombus fragments/ detaches completely and travel elsewhere in the circulation.
what happens when a thrombus occludes a vessel?
artery- thrombotic occlusion stops flow of blood, cuts off oxygen to tissues -> infarction.
vein- occlusion prevents venous drainage of tissues, blood pools, cannot escape –> congestion and infarction (that is often haemorrhagic)
organisation and recanalisation of pathological thrombus
new vessel grow into the thrombus. vascular granulation tissue develops. fibroblasts invade and deposit collagen. fibrovascular granulation tissue develops.
embolism
the transference of abnormal material by the blood stream with eventual impaction of the material in a vessel distal to its site of origin.
the most important materials to embolise are thrombus and cancer cells (metastasis)
embolism (non-thrombotic)
thrombus and malignant tumour are the most important materials to embolize. others: fat and marrow air nitrogen amniotic fluid