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This document summarizes key aspects of hemostasis and thrombosis. It describes the three main responses that form blood clots: vascular reaction, platelet reaction, and biochemical reaction. Platelets play an important role by forming platelet plugs through adhesion, aggregation, and release of coagulation factors. The coagulation cascade is made up of thirteen coagulation factors and is tightly regulated by natural anticoagulants and fibrinolysis. Fibrinolysis breaks down clots through a system involving plasminogen and plasminogen activators.
Originalbeschreibung:
HEMOSTASIS PPT HEMATOLOGI modul hematologi
mekanisme hemostasis
This document summarizes key aspects of hemostasis and thrombosis. It describes the three main responses that form blood clots: vascular reaction, platelet reaction, and biochemical reaction. Platelets play an important role by forming platelet plugs through adhesion, aggregation, and release of coagulation factors. The coagulation cascade is made up of thirteen coagulation factors and is tightly regulated by natural anticoagulants and fibrinolysis. Fibrinolysis breaks down clots through a system involving plasminogen and plasminogen activators.
This document summarizes key aspects of hemostasis and thrombosis. It describes the three main responses that form blood clots: vascular reaction, platelet reaction, and biochemical reaction. Platelets play an important role by forming platelet plugs through adhesion, aggregation, and release of coagulation factors. The coagulation cascade is made up of thirteen coagulation factors and is tightly regulated by natural anticoagulants and fibrinolysis. Fibrinolysis breaks down clots through a system involving plasminogen and plasminogen activators.
to prevent spontaneous bleeding to keep the fluidity of blood Vascular reaction primary hemostatic barrier Cellular reaction Biochemical reaction / secondary hemostatic barrier vaso constriction Stimulates coagulation factors and platelets Substances synthesized by endothelial cells: von Willebrand factor tissue plasminogen activator (t-PA) plasminogen activator inhibitor -1 (PAI-1) prostacyclin (PGI 2 ) Thrombomodulin (PC activation) Glycosaminoglycan (heparan sulphate, dermatan sulphate) Originated from cytoplasm of megakariocyte (fragmentation) Morphology : discoid, biconvex, 2 4 m Cytoplasm contains: a-granule (PF 4 , b-thromboglobulin, platelet derived growth factor, vWF, fibrinogen, F V) Dense granule (Ca, ADP, ATP) Membrane: phospholipid bilayer, glycoprotein (receptor)
Megakaryoblast Megakaryocytes Platelets 1/3 of platelets: stored in spleen
2/3 of plateletes: blood circulation half-lime 3-4 days 15% use daily for haemostasis normal platelet count 140-360 x 10 9 /l The Platelets Platelet plug formation: Platelet adherent (need von Willebrand Factor) Platelet aggregation stimulated by ADP, thrombin, thromboxan A 2 , epinephrine, collagen Platelet release reaction (from a granule and dense granule) Stabilization of the plug : platelet factor 3 (flip flop of membrane phospholipid) phospholipid Arachidonic acid PGG2, PGH2 Thromboxan A2 Phospholipase A2, C cyclooxygenase Thromboxan synthetase Aspirin Prostacyclin PGI2 synthetase Factor I Fibrinogen precursor of fibrin Factor II Prothrombin serine protease Factor III Tissue thrombo initiate extrinsic path. plastin Factor IV Calsium ion bridge between Gla - phospholipid Factor V Proaccelerin Cofactor of Xa Factor VII Proconvertin serine protease Factor VIII Anti hemophilic f. Cofactor of IXa Factor IX Christmas factor serine protease Factor X Stuart Prower factor serine protease Factor XI Antihemophilic C serine protease Factor XII Hageman factor serine protease Factor XIII Fibrin stabilizing f. transglutaminase Prekallikrein Fletcher factor serine protease HMW kininogen Fitzgerald factor cofactor of Kall.
Vit. K is required for carboxylation of glutamic acid g carboxy glutamate Vitamin K dependent protein : prothrombin, VII, IX, X, protein C, protein S, protein Z Deficiency of vit. K PIVKA (protein induced by vitamin K absence or antagonist) Residue Glutamic acid (GLU) Precursor of II, VII, IX, X Prothrombin VII, IX, X Residue g Carboxy glutamat (GLA) carboxylase Vitamin KH2 Vitamin K epoxide Oral Anticoagulant
Ca ++ FPA FPB + F1.2 +
Mechanism of coagulation factor activation Local: fibrin, blood flow Humoral: - Antithrombin - Protein C - Protein S - Heparin cofactor II - TFPI Cellular : liver cell, RES Synthesized in the liver Function : neutralize thrombin and other serine protease (XIIa, XIa, Xa, IXa, VIIa, Kallikrein,plasmin) Heparin cofactor Activities enhanced by heparin Both are vitamin K dependent protein Thrombin with thrombomodulin as cofactor activates Protein C activated Protein C (APC) APC with Protein S as cofactor inactivates F Va and F VIIIa.
Function : inhibit F Xa and F VIIa Mechanism of action: First F Xa + TFPI F Xa-TFPI complex F Xa-TFPI complex + F VIIa-TF complex quartener complexed Mechanism of action of TFPI Fibrinolysis is a physiologic response to the deposition of intra or extra vascular fibrin Function : to destroy fibrin by enzymatic process Consist of : Plasminogen Plasminogen Activator Inhibitor Plasmin : proteolytic enzyme, substrates : fibrin, fibrinogen, V, VIII, hormon, complement PLasminogen : proenzyme of plasmin, found in plasma and other body fluid Plasminogen activator Inhibitor Physiologic plasminogen activators: Tissue-type plasminogen activator (t-PA) Urinary- type plasminogen activator (u-PA) Contact-phase dependent activators: F XIIa, Kallikrein Exogen: Streptokinase (SK) Staphylokinase (SAK) Vampire bat plasminogen activator
Antiplasmin: a 2 plasmin inhibitor a 2 macroglobulin antithrombin a 1 antitrypsin TAFI Transamin Plasminogen activator inhibitor PAI-1 PAI-2 PAI-3 (?)