血栓与止血基础理论课件.ppt

思考 血小板活化指标的临床应用 Thank You For Your Attention! * Multiple pathways are responsible for platelet activation. Platelets adhere to damaged blood vessels via cell surface adhesion molecules and their membrane receptors such as glycoprotein Ib/IX (GP Ib/IX), the ligand for von Willebrand factor (VWF), which in turn can activated platelets and cause conformational changes. Further, other activators including thrombin, adrenaline, ADP, and collagen can also activate platelets. When activation occurs, the glycoprotein IIb/IIIa membrane receptor (GP IIb/IIIa) is exposed. This receptor forms bridges using fibrinogen resulting in aggregation. Platelet activation also exposes a phospholipid surface (meeting place) upon which coagulation proteins carry out their reactions. The sequential activation of these coagulation factors ultimately leads to the formation of fibrin, which is a critical component in stabilizing the hemostatic plug. Thrombin when generated, plays a pivotal role in hemostasis, via both fibrin conversion and platelet activation. * * * As ADP, thrombin, and thromboxane as previously mentioned are some of the agonists that bind to a specific receptor site on the platelet and initiates intracellular signals that amplify platelet activation, recruit other platelets, and activate the fibrinogen binding site, namely the Gp IIb/IIIa complex which, once activated, undergoes a conformational change that allows fibrinogen to bind to the activated sites. The multivalent fibrinogen molecule attaches to the Gp IIb/IIIa complex on one platelet and links to other platelets that have been activated by ADP from the circulation or released from other activated platelets. Numerous platelets are bound together and form a platelet plug that serves as the nidus for further steps in the process of thrombus formation that result in the thrombin-mediated conversion of fibrinogen to fibrin and incorporation of red cells to form a thrombus that may become occlusive. At ma