Please enable JavaScript.
Coggle requires JavaScript to display documents.
Aiman, 7 year-old, Mechanism of hemostasis, Laboratory Investigations, PBL…
Aiman, 7 year-old
Treatment
-
-
Chemotherapy
Cell cycle specific agents
-Act during specific phase of cell cycle
-Effective for high-growth fraction malignancies
-S phase: Doxorubicin, antimetabolites
-M phase: Vinca alkaloids, taxanes
-G2 phase: Bleomycin
Cell cycle non-specific agent
-Active throughout the cell cycle
-Effective for high and low growth fraction malignancies
-Alkylating agents (cyclophosphamide,cisplatin)
-
-
-
-
-
Neutropenia, lymphocytosis, thrombocytopenia, leukocytosis
PBF: Normochromic, normocytic anemia
-
Mechanism of hemostasis
- Constriction of blood vessels -Tiny platelets rush to the site of injury and bunch together around the wound. This will also attract other platelets and help for a plug to close up the break at the site. Clotting factors producefibrin that surrounds the platletsplug and ultimately the fibrin clot become as a mesh which keeps the plug firm and stable
- Extrinsic: Tissue factor bind to factor VII then activate activate factor VIIa.It then activate factor X and IX by proteolysis. Activated factor X binds to activated factor V and generate prothrombinase complex that cleaves the prothrombin into thrombin
- Intrinsic: With thrombin production, conversion of factor XI toXIa. Factor Xia with activated VIIa and tissue factor converts factor IX to activated IXa. IXa combines with with VIIIa to activate X. Xa bind to Va and converts prothrombin to thrombin. Thrombin acts as cofactor and catalyzes and enhances the bioactivity of the proteolytic pathways
Fibrin clot formation: Final step in coagulation cascade. Involve conversion of fibrinogen to fibrin monomers. That will polymerize and forms fibrin polymer mest -> cross linkfibrin clot -> catalyzed by activated XIII.
-
-
-