BIOM3010 Lecture Notes - Lecture 7: Deep Vein Thrombosis, Intracerebral Hemorrhage, Hemostasis
Document Summary
Lecture 7 haemostasis: antiplatelet and anticoagulant drugs. The stopping of blood loss from damaged vessels and protect against haemorrhage (highly complex, regulated process) Mechanisms involved in haemostasis following a wound include: vasoconstriction, platelet adhesion to the exposed tissue, platelet activation to form a haemostatic plug, reinforcement of plug by fibrin blood coagulation (thrombosis) Times we want to promote haemostasis: haemophilia, haemorrhage after surgery or trauma. Times we want to inhibit haemostasis: myocardial infarct, stroke (arterial thrombosis-emboli) White clots made up of platelet aggregates and form under conditions of high flow so are usually associated with atherosclerosis (cholesterol) Heart and brain: deep vein thrombosis (venous thrombosis) Red clots that are made up of erythrocytes and fibrin that usually lodge in the lungs causing a pulmonary embolism. Thrombosis - haemostasis in the wrong place: formation of a haemostatic plug within the vasculature in the absence of bleeding.
