Section B Thrombosis Thrombus Thrombi
Thrombosis Thrombus Thrombi
ANTITHROMBOTIC PROPERTIES Inhibition of platelet aggregation: PGI NO. ADPase Anticoagulant-binding and inhibition of thrombin: Antithrombin ii acceleration by heparin-like molecules, thrombomodulin activation of protein C/S, a2-macroglobulin. Fibrinlysis: Tissue plasminogen activator(tPA)
ANTITHROMBOTIC PROPERTIES • Inhibition of platelet aggregation: PGI2, NO, ADPase • Anticoagulant -binding and inhibition of thrombin: Antithrombin III acceleration by heparin-like molecules, thrombomodulin activation of protein C/S, 2 -macroglobulin. • Fibrinlysis: Tissue plasminogen activator (tPA)
PROTHROMBOTIC PROPERTIES Simulation of platelet aggregation (adhesion): von Willebrand factor, platelet-activating factor. Procoagulation factors: Tissue factor, binding factors IXa and Xa, Factor V. Inhibition of fibrinolysis: t-PA inhibitor
PROTHROMBOTIC PROPERTIES • Simulation of platelet aggregation (adhesion): von Willebrand factor, platelet-activating factor. • Procoagulation factors: Tissue factor, binding factors IXa and Xa, Factor V. • Inhibition of fibrinolysis: t-PA inhibitor
2shape chang 3Gnmuerul 0Pateetan (ADP, TXA) THrombin actator Tranomaro o tactor clocks coaglation
• Fig 5-5
FAVOR THROMBOSIS INHIBIT THROMBOSIS Extrinsic coagulation Inactivates thrombin, lactors Xa, IXa factors Va and villa ActiveproteinC-,ProteinC Exposure of membrane-bound Inhibit platelet tissue factor aggregation Platelet adhesion. Antithrombin Ill Held together by VWF PGl2, NO and Fibrinogen adenosine d phosphatase H lke Thrombomodulin molecule
• Fig 5 - 6
THREE INFLUENCES OF THROMBOSIS Endothelial injury(most important) Alone can induce thrombosis Alterations in normal flow Hypercoagulability. When the last two are both present, endothelial injury is not requisite
THREE INFLUENCES OF THROMBOSIS • Endothelial injury (most important). Alone can induce thrombosis. • Alterations in normal flow. • Hypercoagulability. When the last two are both present, endothelial injury is not requisite
Deficiency Bernard-Soulier Syndrome A Deficiency: GpIb Glanzmann Platelet Thrombasthenia Gpllb-llla Fibrinogen complex Endothelium G von Willebrands factor Deficiency von Willebrand's Subendothelium Disease
INTRINSIC PATHWAY EXTRINSIC PATHWAY (Hageman Facton Tisse Inury HMK ccnA 区x (Prothrombin Phospho pa surface Actie Inactin COMMON PATHWAY
• Fig 5-8
Endothelial iniury Ulcerative atherosclerosis Transmural myocardial infarction Vasculitis Trauma ● Radiation ● Bacterial toxins
Endothelial injury • Ulcerative atherosclerosis • Transmural myocardial infarction • Vasculitis • Trauma • Radiation • Bacterial toxins
Alterations in normal blood flow Platelets activated by contact with endothelium Slowed fow retards dilution of activated clotting factors and hepatic clearance. Stasis or turbulence retards the inflow of inhibitors Turbulence may induce endothelial iniur
Alterations in normal blood flow • Platelets activated by contact with endothelium. • Slowed flow retards dilution of activated clotting factors and hepatic clearance. • Stasis or turbulence retards the inflow of inhibitors. • Turbulence may induce endothelial injury