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Week 7: Fibrinolysis and Thrombophilia

Secondary fibrinolysis Primary fibrinolysis Plasminogen FDP D-dimer DIC 3P test. Hypercoagulable state Thrombophilia Activated protein C resistance (APCR) Factor V Leiden Antithrombin deficiency Anticoagulant therapy. Week 7: Fibrinolysis and Thrombophilia. Fibrinolysis.

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Week 7: Fibrinolysis and Thrombophilia

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  1. Secondary fibrinolysis Primary fibrinolysis Plasminogen FDP D-dimer DIC 3P test Hypercoagulable state Thrombophilia Activated protein C resistance (APCR) Factor V Leiden Antithrombin deficiency Anticoagulant therapy Week 7: Fibrinolysis and Thrombophilia

  2. Fibrinolysis • Plasminogen Activators • Thrombin • Tissue plasminogen activator (t-PA) • Streptokinase • Urokinase • Kallikrein • Fibrinolysis Inhibitors • 2 antiplasmin • 2 macroglobulin

  3. Fibrin(ogen) Degradation Product • X fragment: D-E-D • Y fragment: D-E • Smallest fragments: D and E • D-dimers from fibrin degradation only (ie, 2o fibrinolysis, not 1o)

  4. Fibrin Degradation

  5. FDP Screen • Thrombo-Wellco • Anti-fibrinogen coated latex • D-dimers • Positive only with 2o fibrinolysis • Plasma protaminesulfate paracoagulation (3P) • Dissociate FM-FDP to allow FM to re-associate • Also specific to 2o fibrinolysis

  6. Triggering mechanism Trauma, injury, surgery Hemolysis AML M3 Snake venom Amniotic fluid Dead fetus Gram negative endotoxin Consumptive Low PLT Long PT/APTT Low fibrinogen FDP, D-dimer Schistocyte Treatment Remove source of Tpl Heparin to stop cascade Disseminated Intravascular Coagulation

  7. Disseminated Intravascular Coagulation

  8. DIC • Syndrome, not disease • 1:1,000 hospitalized patients, but many asymptomatic • Tx: removal of underlying cause if possible • Support with FFP, PLT, RBC, etc. • Low molecular weight heparin (LMWH)

  9. Plasminogen activation without clotting Unknown mechanism Labs similar to DIC but important differences PLT unaffected No schistocyte Long PT/APTT Low fibrinogen FDP but no D-dimer Primary Fibrinolysis

  10. Thrombophilia • Tendency to form thombi • Hereditary and acquired • Hypercoagulable state • Arterial thrombi: usually in areas of atherosclerotic plaques • Venous thrombi: thrombophlebitis, DVT, pulmonary embolism

  11. Venous Thromboembolism • Venous stasis • Activated protein C resistance, factor V Leiden • Protease inhibitor deficiency (antithrombin, protein C, protein S)

  12. Antithrombin deficiency Recurrent DVT Protein C deficiency Vitamin K dependent Inactivated Va and VIIIa Protein S deficiency Vitamin K dependent Protein C cofactor APCR Factor V Leiden Prothrombin gene mutation 20210 Hereditary Thrombophilia

  13. Acquired Thrombophilia • Antiphospholipid antibody: e.g., Lupus-anticoagulant • Malignancy • Oral contraceptives • Post-op and trauma • Myeloproliferative disorders

  14. Heparin Monitor with APTT LMWH no HIT Oral anticoagulants (e.g., Coumadin) Monitor with PT Thrombolytic agents (plasminogen activators) Streptokinase Urokinase t-PA Anti-platelet agents Aspirin Plavix IV inhibitors Direct thrombin inhibitors (e.g., hirudin - from leech saliva) Not dependent on AT-III Act on thrombin’s fibrin binding site Therapies

  15. Problems with Oral Anticoagulants • GI hemorrhage • Skin necrosis • Antidote: vitamin K

  16. Problems with Heparin • Unfractionated Heparin may cause heparin induced thrombocytopenia (HIT) due to antibody against heparin-PF4 complex • LMWH: almost exclusively against Xa, less osteoporosis, less HIT • Antidote: protamine sulfate

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