Transcription of Coagulation Made Simple - Denver, Colorado
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Thomas A. Whitehill, of Vascular SurgeryCoagulation Made SimpleObjectives of This Presentation Identify and describe the critical elements of the hemostatic mechanisms of the body Develop and implement an effective diagnostic and therapeutic approach to the abnormally bleeding patientBlack Box View of HemostasisPlatelet/ Coagulation factor activationLots of exciting biochemistryCLOT!Key Points Hemostasis requires the interaction of platelets, Coagulation and fibrinolyticfactors, endothelium, proinflammatoryand anti-inflammatory mediators, and leukocytes Clot formation is typically initiated by vascular injury, in which a platelet plug forms and is reinforced with fibrin produced via the extrinsic pathway Physiologic anticoagulants such as AT-III and Activated Protein C oppose thrombosis, serving to localize it to sites of vascular injury Clot formation is balanced by plasmin-mediated fibrinolysis, resulting in the formation of D-dimersand other fibrin degradation productsVascular InjuryExposure of Subendothelial CollagenPlatelet Adhesion, Aggregation, and Activation(Primary Hemostasis)SecondStable Fibrin/Platelet ClotFibrinolysis [as needed]VasoconstrictionFirstRelease of Tissue FactorCoagulation Cascade(Secondary Hemostasis)
Acquired or Inherited Factor Disorder? • Inherited bleeding factor disorders – Present from birth until old age – Mild hemophilia or von Willebrand disease
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GUIDELINES FOR THE MANAGEMENT OF HEMOPHILIA, Guidelines for the Management of, Hemophilia, FOR THE TREATMENT OF HEMOPHILIA, For the Treatment of Hemophilia and von Willebrand Disease, ANNUAL GLOBAL SURVEY 2016, Neuraxial Techniques in Obstetric and, How Do I Administer LOVENOX, University of Colorado