北京大学：《病理学》课程PPT教学课件（英文版）Section B Thrombosis Thrombus Thrombi

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