Coagulation Abnormalities - 哥伦比亚大学.ppt

HEMOSTASIS I A Primer to Interpreting Clotting Testing Coagulation Abnormalities History is critical to assessment of lab studies Has patient had spontaneous bleeding problems? Has patient had surgery in the past? Does patient have easy bruising? Does patient have heavy menses? Has patient had a tooth extracted? Has patient required a blood transfusion? Physical exam helpful only in severe cases eg Hemophilia, severe von Willebrand disease Laboratory essential for determining of specific defect Necessary for designing specific therapy CIRCULATORY SYSTEM Low volume, high pressure system Efficient for nutrient delivery to tissues Prone to leakage 2o to endothelial surface damage Small volume loss ? large decrease in nutrient delivery Minimal extravasation in critical areas? irreparable damage/death of organism HEMOSTASISPrimary vs. Secondary vs. Tertiary Primary HemostasisPlatelet Plug FormationDependent on normal platelet number functionInitial Manifestation of Clot Formation Secondary HemostasisActivation of Clotting Cascade ?Deposition Stabilization of Fibrin Tertiary HemostasisDissolution of Fibrin ClotDependent on Plasminogen Activation PLATELETS Anucleate cellular fragmentsMultiple granules, multiple organelles Synthesis controlled by IL-6, IL-3, IL-11, thrombopoietin Circulate as inactive, non-binding concave discs On stimulation, undergo major shape change Develop receptors for clotting factors Develop ability to bind to each other subendothelium PLATELET ACTIVATION PLATELET ACTIVATION PLATELET ACTIVATION COAGULATION CASCADEGeneral Features Zymogens converted to enzymesby limited proteolysis Complex formation requiring calcium,phospholipid surface, cofactors Thrombin converts fibrinogen to fibrin monomer Fibrin monomer crosslinked to fibrin Forms glue for platelet plug COAGULATION CASCADE COAGULATION CASCADE COAGULATION CASCADE COAGULATION TESTINGBasic Tests Prothrombin time (PT) Lipid Source + Plasma; Calcium added, then time to clot Extrins