V. Hyper Coagulation State

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Hyper Coagulation State

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V. Hyper Coagulation State

  1. 2. Hyper coagulation state Najmeh Vaghef Msc student in Tarbiat modares university
  2. 3. <ul><li>Introduction </li></ul><ul><li>Definition of thrombus </li></ul><ul><li>Review of coagulation triangular and it ’ s relation with hyper coagulation </li></ul><ul><li>Categories of thrombosis ( arterial and venous ) and review of their etiology and their treatments </li></ul><ul><li>The importance of getting case report properly and familial history of thrombosis </li></ul><ul><li>Review of lab tests for diagnostic of hyper coagulation state </li></ul>
  3. 5. <ul><li>Introduction </li></ul><ul><li>Definition of thrombus </li></ul><ul><li>Review of coagulation triangular and it ’ s relation with hyper coagulation </li></ul><ul><li>Categories of thrombosis( arterial and venous ) and review of their etiology and their treatments </li></ul><ul><li>The importance of getting case report properly and familial history of thrombosis </li></ul><ul><li>Review of lab tests for diagnostic of hyper coagulation to state </li></ul>
  4. 6. Thrombus: A mass consist of blood elements that exist in circulation .
  5. 7. <ul><li>Introduction </li></ul><ul><li>Definition of thrombosis </li></ul><ul><li>Review of coagulation triangular and it ’ s relation with hyper coagulation </li></ul><ul><li>Categories of thrombosis ( arterial and venous ) and review of their etiology and their treatments </li></ul><ul><li>The importance of getting case report properly and familial history of thrombosis </li></ul><ul><li>Review of lab tests for diagnostic of hyper coagulation to state </li></ul>
  6. 9. Procoagulant role of Elndothelial cells
  7. 10. Anticoagulant role of Endothelial cells <ul><li>No </li></ul><ul><li>Ecto ADPase </li></ul><ul><li>PGI2 </li></ul><ul><li>Heparan sulfate </li></ul><ul><li>Thrombomadulin </li></ul><ul><li>tpA </li></ul>
  8. 12. Platelet <ul><li>Number </li></ul><ul><li>Function </li></ul>
  9. 13. Platelet Activation Pathways ADP Adrenaline Platelet GpIb THROMBIN Exposed Collagen Endothelium vWF Adhesion Adhesion GpIIb/IIIa GpIIb/IIIa Aggregation
  10. 14. Coagulation Factors and inhibitors
  11. 16. <ul><li>Introduction </li></ul><ul><li>Definition of thrombosis </li></ul><ul><li>Review of coagulation triangular and it ’ s relation with hyper coagulation </li></ul><ul><li>Categories of thrombosis (arterial and venous) and review of their etiology and their treatments </li></ul><ul><li>The importance of getting case report properly and familial history of thrombosis </li></ul><ul><li>Review of lab tests for diagnostic of hyper coagulation to state </li></ul>
  12. 17. Thrombosis: <ul><li>Arterial </li></ul><ul><li>Ischemia and Infarctus </li></ul><ul><li>Venous </li></ul><ul><li>Edema and emboli </li></ul>( white thrombus ) ( red thrombus )
  13. 18. Thrombosis Inherited hypercoagulable states Acquired hypercoagulable states
  14. 19. Etiology of arterial thrombosis <ul><li>Atherosclerosis </li></ul><ul><li>Hypertension </li></ul><ul><li>Hyper vescositemia </li></ul><ul><li>Diabetic mellitus </li></ul><ul><li>Hyper lypemia </li></ul><ul><li>Vacuities </li></ul><ul><li>Anti phospholipids syndrome </li></ul>
  15. 20. <ul><li>Some hematological syndromes: TTP , HUS , HITTS , Myeloprotive disorders , </li></ul><ul><li>Increase some proteins and amino acids: Lpa (LDL+Apoa), Homocystein ( aquired and hereditary) , Factor VII </li></ul>Etiology of arterial thrombosis
  16. 21. Homocysteinemia and hyper coagulation state <ul><li>Increase connection of Lpa to fibrin </li></ul><ul><li>Bad functional of Endothelial Cells ( Anticoagulant surface change to procoagulant surface ) </li></ul><ul><li>Reduced thrombomadulin </li></ul><ul><li>Reduced tpA </li></ul><ul><li>Reduced APC </li></ul><ul><li>Increase factor (V) </li></ul>
  17. 22. Treatment of arterial thrombosis <ul><li>Anti platelet </li></ul><ul><li>Anticoagulant </li></ul><ul><li>If homocysteinemia exists with thrombosis + foliate </li></ul>
  18. 23. Etiology of venous thrombosis <ul><li>Stasis </li></ul><ul><li>Hyper coagulability </li></ul><ul><li>Endothelial injury </li></ul>
  19. 24. Virchow ’ s Triad <ul><li>Hypercoagulability </li></ul><ul><li>Endothelial injury </li></ul><ul><li>Venous flow disturbance (stasis or turbulence) </li></ul>
  20. 25. Hyper coagulability <ul><li>Protein defects: </li></ul><ul><li>Factor (V) Leiden ( 20-40%) </li></ul><ul><li>G to A mutation at base pair 1691 results in amino acid 506,Glu instead of Arg </li></ul><ul><li>Prothrombin 20210 (6%)(G to A) </li></ul><ul><li>Defect or deficiency of protein C (4%) </li></ul><ul><li>(outozomal dominant) </li></ul>
  21. 26. <ul><li>Defect or deficiency of Protein S (3-4%) ( outozomal dominant) pregnancy and estrogens reduced protein S </li></ul><ul><li>Dysfibrinogenemia ( 3% ) </li></ul><ul><li>Antithrombin deficiency ( 1% ) (outozomal dominant ) acquired deficiency of it happened in sever obesity , liver disease , chronic renal failer , using ocp ,immature neonates </li></ul>Hyper coagulability
  22. 27. <ul><li>Dysplasminogenemia ( <1% ) </li></ul><ul><li>Reduced Heparin cofactor II </li></ul><ul><li>Elevation of PAI-1 </li></ul><ul><li>Elevation of Coagulation factors VII,VIII,IX,X,XI and II </li></ul><ul><li>Reduction of protein Z </li></ul><ul><li>Xa </li></ul>Z X vitK Hyper coagulability
  23. 28. <ul><li>Hematologic diseases : </li></ul><ul><li>DIC </li></ul><ul><li>HITTS </li></ul><ul><li>Anti phospholipid syndrome </li></ul><ul><li>TTP </li></ul><ul><li>HUS </li></ul><ul><li>Platelet disorders </li></ul><ul><li>Homocysteinemia </li></ul>Hyper coagulability
  24. 29. Risk factors for venous thrombosis <ul><li>Age </li></ul><ul><li>Prolonged immobility </li></ul><ul><li>Obesity </li></ul><ul><li>Neurological disease </li></ul><ul><li>Cardiac disease </li></ul><ul><li>Pregnancy </li></ul><ul><li>Oral contraceptive (ocp) if the patient has the factor ( V ) leiden mutation the risk is increased 28-fold </li></ul><ul><li>Surgery </li></ul><ul><li>Malignancy </li></ul>
  25. 30. Treatment of venous thrombosis <ul><li>Anti fibrin-generating agents (Heparin, Hirudin, argatroban, LMW Heparin, Warfarin ) </li></ul><ul><li>Lyses of cloths with thrombolytic therapy ( tpA, Streptokinase, Urokinase) </li></ul>
  26. 31. <ul><li>Introduction </li></ul><ul><li>Definition of thrombosis </li></ul><ul><li>Review of coagulation triangular and it ’ s relation with hyper coagulation </li></ul><ul><li>categories of thrombosis ( arterial and venous ) and review of their etiology and their treatments </li></ul><ul><li>The importance of getting case report properly and familial history of thrombosis </li></ul><ul><li>Review of lab tests for diagnostic of hyper coagulation to state </li></ul>
  27. 32. 3 questions in thrombosis <ul><li>Thrombosis is venous or arterial ? </li></ul><ul><li>Cause of thrombosis : </li></ul><ul><li>acquired or hereditary ? </li></ul><ul><li>Acquired: </li></ul><ul><ul><li>Vascular disorders ( atherosclerosis , diabetic mellitus , vacuities , homocysteinemia ) </li></ul></ul>
  28. 33. Acquired <ul><li>Blood flow disorders : </li></ul><ul><li>Stasis (immobility , CHF) </li></ul><ul><li>Hypervescoshtemia ( P.V ,Leukemia , plasma cell disorders , sickle cell anemia </li></ul><ul><li>Platelet disorders </li></ul><ul><li>Myeloprolifrativedisorders , thrombocytosis , hyper lypemia , PNH </li></ul>
  29. 34. Acquired <ul><li>Coagulation and Fibrinolytic disorders </li></ul><ul><li>Malignancies , nephritic syndrome , trauma , hyperthyroidism , liver disease , operation </li></ul><ul><li>Hematological disorders </li></ul><ul><li>TTP , HUS , HITTS , DIC </li></ul>
  30. 35. <ul><li>What cases need to follow up ? Answer : </li></ul><ul><ul><ul><li>Familial thrombosis </li></ul></ul></ul><ul><ul><ul><li>Recurrent autonomous thrombosis </li></ul></ul></ul><ul><ul><ul><li>Thrombosis in youth </li></ul></ul></ul><ul><ul><ul><li>Surface migrant thrombofelebits </li></ul></ul></ul><ul><ul><ul><li>Thrombosis in unusual sites </li></ul></ul></ul><ul><ul><ul><li>Recurrent abortions </li></ul></ul></ul>Cases that need to follow up for hyper coagulation state
  31. 36. <ul><li>Introduction </li></ul><ul><li>Definition of thrombosis </li></ul><ul><li>Review of coagulation triangular and it ’ s relation with hyper coagulation </li></ul><ul><li>Divided thrombosis tow categories ( arterial and venous ) and review of their etiology and their treatments </li></ul><ul><li>The importance of getting case report properly and familial history of thrombosis </li></ul><ul><li>Review of lab tests for diagnostic of hyper coagulation to state </li></ul>
  32. 37. Lab tests for diagnostic of hyper coagulation state <ul><li>Factor ( V ) leiden </li></ul><ul><li>Antithrombin III </li></ul><ul><li>Prothrombin 20210 </li></ul><ul><li>Protein C </li></ul><ul><li>Protein S </li></ul><ul><li>Protein Z </li></ul><ul><li>Homocystein </li></ul><ul><li>Specific platelet protein and increase of it ’ s metabolism </li></ul><ul><li>Decrease of fibrinolytic action </li></ul><ul><li>ACLA, LACT, dRWVT </li></ul><ul><li>D-dimmer , PTT </li></ul>
  33. 39. Thank you for your attention
  34. 40. Thank you

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