1 / 45

Fisiologia del processo emostatico. Modificazioni della coagulazione e della fibrinolisi Sergio Siragusa Professore A

Definition of hemostasis.

dash
Télécharger la présentation

Fisiologia del processo emostatico. Modificazioni della coagulazione e della fibrinolisi Sergio Siragusa Professore A

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


    2. Definition of hemostasis “Normal hemostasis … controlled activation of clot formation and lysis to prevent hemorrhage without [inappropriate] thrombosis …” (Laposata et al.) Normal hemostasis has been defined as the controlled activation of clot formation and clot lysis in an effort to prevent hemorrhage without the inappropriate formation of thrombosis or clots. Normal hemostasis requires the maintenance of a balance between clot formation processes and clot breakdown processes, permitting blood to flow through blood vessels unimpeded. An imbalance due to vascular injury, disease, or drugs can result in either hemorrhage or inappropriate clot formation. Normal hemostasis has been defined as the controlled activation of clot formation and clot lysis in an effort to prevent hemorrhage without the inappropriate formation of thrombosis or clots. Normal hemostasis requires the maintenance of a balance between clot formation processes and clot breakdown processes, permitting blood to flow through blood vessels unimpeded. An imbalance due to vascular injury, disease, or drugs can result in either hemorrhage or inappropriate clot formation.

    4. The classical ‘twin pathway’ mechanism of coagulation was derived from in vitro investigations into the factors necessary for the process to occur. However, it fails to explain several important clinical observations, such as why a patient lacking FVIII should be capable of bleeding so profusely, when they have an intact ‘extrinsic’ pathway…The classical ‘twin pathway’ mechanism of coagulation was derived from in vitro investigations into the factors necessary for the process to occur. However, it fails to explain several important clinical observations, such as why a patient lacking FVIII should be capable of bleeding so profusely, when they have an intact ‘extrinsic’ pathway…

    37. Monitoring hemostasis: cascade vs. cell-based model Cascade model Common coagulation tests (PT, aPTT, platelet counts) do not reflect the roles of cells or contributions of local vascular and tissue conditions Cell-based model The need of whole blood tests (that measure the interaction of platelets, coagulation factors, and other cellular or plasma factors present during clot formation) Routine coagulation tests are based on the cascade model of hemostasis and do not reflect the roles of cells or the contributions of local vascular and tissue conditions. PT and aPTT are plasma-based assays that miss the impact of platelet activation on thrombin generation. Because these tests use static end points such as initial fibrin formation, they also miss the impact of alterations in thrombin generation on platelet function and clot structure. Monitoring hemostasis using the cell-based model requires a whole blood test in order to measure the effect of the interactions among platelets, coagulation factors, and other cellular or plasma factors. In vitro tests are not able to measure the effect of the vascular endothelium on hemostasis, a limitation in all in vitro tests. The thrombelastograph (TEG®) hemostasis analyzer is an example of a whole blood coagulation analyzer that can be used to monitor the cell-based model of hemostasis.Routine coagulation tests are based on the cascade model of hemostasis and do not reflect the roles of cells or the contributions of local vascular and tissue conditions. PT and aPTT are plasma-based assays that miss the impact of platelet activation on thrombin generation. Because these tests use static end points such as initial fibrin formation, they also miss the impact of alterations in thrombin generation on platelet function and clot structure. Monitoring hemostasis using the cell-based model requires a whole blood test in order to measure the effect of the interactions among platelets, coagulation factors, and other cellular or plasma factors. In vitro tests are not able to measure the effect of the vascular endothelium on hemostasis, a limitation in all in vitro tests. The thrombelastograph (TEG®) hemostasis analyzer is an example of a whole blood coagulation analyzer that can be used to monitor the cell-based model of hemostasis.

    39. Patterns of TEG

More Related