HTHSCI 2H03 Lecture Notes - Lecture 20: Tissue Plasminogen Activator, Bone Marrow Suppression, Coagulation
28 Nov 2017
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Document Summary
Vessel spasms, constricting the vessel and limiting blood flow to the site of injury. Platelets bind with high affinity to the damaged vessel. Activated platelets release adenosine diphosphate (adp) and thromboxane a2 which stimulate the activation of new platelets, platelet aggregation and vasoconstriction (begin the process of healing). Fibrin strands provide the scaffolding that forms the clot. Extrinsic pathway: triggered when tissue thromboplastin is released from damaged cells (outside the circulation, catalyzes formation of faxtor xa. Intrinsic pathway: triggered when collagen is exposed at the site of vascular injury to blood components, catalyzes formation of factor xa. Thromboembolic disorders: formation of non-therapeutic clots, occlusion of arterial vessels leads to mi & cva, embolus (i. e. : travelling clot, piece of stable thrombi breaks off and lodges in smaller blood vessels. Bleeding disorders: clients does not produce enough clots, thrombocytopenia (bone marrow suppression, hemophilia. Anticoagulants are the most commonly prescribed coagulation modifiers.
