Cardiovascular Pathology 1 Flashcards
What forms a haemtostatic plug
Platelets
Fibrin
Red blood cells
How is a haemostatic plug formed?
Endothelial injury leads to adhesion and aggregation of platelets
Platelets adhere to collagen by vWF and RBC becomes enmeshed with the platelets forming a loose platelet plug
At the same time, exposure of tissue factor initiates the coagulation cascade forming insoluble fibrin stabilising the loose plug
Fibrinolysis
Ensures the haemostatic plug does not become too big
Fibrinolysis is activated by the same injury that initiates haemostasis
TPA cleaves plasminogen
Plasmin is formed and this breaks down insoluble fibrin to soluble products
Thrombosis
Inappropriate activation of haemostasis which overwhelms the capacity of the fibrinolytic system leading to a solid plug-thrombus
This is pathological
Clot vs. Thrombus
Both are made from RBC and fibrin, but thrombus also have platelets
Clots: Forms outside cardiovascular system and in stationary life
Thrombus: Forms within the cardiovascular system and flowing blood
Virchow’s Triad
Endothelial Injury
Abnormal blood flow
Hypercoagulability
Causes of endothelial injury
Atherosclerosis
Vasculitis
Direct trauma e.g. heat, chemical injury
Causes of abnormal blood flow
Turbulence:
Atherosclerosis, artificial valves, stents, implanted devices
Stasis:
Recent surgery, trauma, immobilisation, pelvic obstruction
Causes of hypercoagulability
Too many blood cells:
Erythrocytosis, thrombocytosis
Coagulation factor defects:
Hereditary e.g. Factor V Leiden, prothrombin mutation
Acquired: DIC, active cancer, anti-phospholipid syndrome
Most important risk factor for thrombosis in an artery
Atherosclerosis
Most important risk factors for thrombosis in a vein
Stasis and hypercoagulability
Complications of Thrombosis
Partial occlusion of the vessel at the site of thrombosis
Complete occlusion of the vessel at the site of thrombus
Embolism to a distant site
Modifiable risk factors for developing atherosclerosis
Smoking
Hypertension
DM
Dyslipidemia
What happens to damaged endothelial cells?
They become dysfunctional
Increased permeability
Produce adhesion molecules and cytokines which attract inflammatory cells and prothrombotic molecules
e.g. VCAM-1 binds monocytes and T cells
What happens when inflammatory cells are recruited?
Monocytes and T cells adhere to the endothelium and migrate into the intima
Monocytes differentiate into macrophages