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HEMOSTASIS

BIOCHEMISTRY DEPARTMENT
UNIVERSITAS MUHAMMADIYAH SUMATERA UTARA
Major Components of Hemostasis
Vasoconstriction (vascular phase)
Platelet activation

Coagulation cascade/ antithrombotic control


mechanisms

Fibrinolysis
Endothelial cells normally inhibit thromus
formation through multiple mechanism:
1. Secretion of prostacyclin inhibits
platelet activation and aggregation
2. Secretion of nitric oxide vasodilates
and inhibits platelet activation
aggregation
3. Expression of heparine sulfate
activates antithrombin
4. Thrombomodulin changes thrombins
affinity away from activation of
proclotting factors, and toward
activation of anticoagulants factors
5. Tissue factor pathway inhibitor
inhibits the Tf/viiA/Xa complex
Vasoconstriction reduce blood getting out

Cells around area send signals


Nerve reflex

Myogenic spasm

Smooth muscle constriction


Primary
hemostatic
mechanism
Coagulation
Intrinsic
and extrinsic pathway (clotting factors), lead to
prothrombinase (prothrombine activator)
Prothrombinase and calsium catalyze prothrombine
thrombine
Thrombine and calsium acts as an enzyme to convert
fibrinogen fibrin

Erythrocyte, platelet, fibrin meshwork stable clot


Proteins of Blood Coagulation
A cell-based model of coagulation
THE FIBRINOLYTIC PATHWAY. Plasminogen is converted enzymatically to plasmin by t-PA or by u-
PA. Plasmin cleaves fibrin and fibrinogen into fibrin degradation products. Major inhibitors of the
fibrinolytic pathway are depicted. PAI-1 and PAI-2 inhibit t-PA. Plasmin activity is inhibited by 2-
AP. Abbreviations: t-PA, tissue plasminogen activator; u-PA, urokinase; PAI-1, plasminogen activator
inhibitor 1; PAI-2, plas- minogen activator inhibitor 2; 2-AP, 2 antiplasmin. = inhibition
Screening tests of coagulation and the coagulation parameters
they measure. Ptt, partial thromboplastin time; pt, prothrombin
time.

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