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HEMOSTASIS & BLEEDING

HEMOSTASIS & BLEEDING. Professor Anwar Sheikha MD, FRCP, FRCPath ., FCAP, FRCPA, FRCPI, FACP Senior Consultant Clinical & Lab. Hematologist Clinical Professor of Hematology University of Mississippi Medical Center, Jackson, Mississippi Professor of Hematology,

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HEMOSTASIS & BLEEDING

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  1. HEMOSTASIS & BLEEDING

  2. Professor Anwar Sheikha MD, FRCP, FRCPath., FCAP, FRCPA, FRCPI, FACP Senior Consultant Clinical & Lab. Hematologist Clinical Professor of Hematology University of Mississippi Medical Center, Jackson, Mississippi Professor of Hematology, University of Salahaddin, Erbil, Kurdistan, IRAQ

  3. HEMOSTASIS ARREST OF BLEEDING Hemostasis is a highly integrated process involving Blood Vessels, Platelets and a number of plasma proteins that are collectively responsible for Coagulation and Fibrinolysis

  4. HEMOSTASIS ARREST OF BLEEDING Hemostasis is a highly integrated process involving Blood Vessels, Platelets and a number of plasma proteins that are collectively responsible for Coagulation and Fibrinolysis DEFECT IN ANY OF THESE COMPONENTS  BLEEDING TRIGGERING OF ANY OF THESE COMPONENTS  THROMBOSIS

  5. HEMOSTASIS ARREST OF BLEEDING Hemostasis is a highly integrated process involving Blood Vessels, Platelets and a number of plasma proteins that are collectively responsible for Coagulation and Fibrinolysis      

  6. HEMOSTASIS Hemostasis is a highly integrated process involving Blood Vessels, Platelets and a number of plasma proteins that are collectively responsible for Coagulation and Fibrinolysis

  7. HEMOSTASIS CEMENT “Clotting” BRICKS “Platelets”

  8. HEMOSTASIS

  9. HEMOSTASIS Blood Vessel ﮔﻪﺭﻩﻻﻮﮊﻩ Clotting Platelet

  10. BLOOD VESSEL Collagen Nitric Oxide Microfibrils

  11. von Willebrand Factor

  12. BLEEDING PURPURIC BLEEDING DEEP SEATED BLEEDING ﻛﻪﭘﺮ ﻛﯚﺷﻚ

  13. BLEEDING PURPURIC BLEEDING DEEP SEATED BLEEDING BLEEDING TIME CLOTTING SCREEN ﻛﻪﭘﺮ ﻛﯚﺷﻚ

  14. How to do Bleeding Time? Simplate

  15. BLEEDING DUE TO VESSEL WALL ABNORMALITIES

  16. HEREDITARY HEMORRHAGIC TELENGIECTASIA

  17. EHLERS- DANLOS SYNDROME

  18. SENILE PURPURA

  19. SCURVEY

  20. MULTIPLE MYELOMA

  21. HENOCH-SCHONLEIN PURPURA

  22. ALLOPURINOL INDUCED PURPURA

  23. SLE SYSTEMIC LUPUS ERYTHEMATOSUS

  24. WISKOTT-ALDRICH SYNDROME

  25. PURPURA PETICHAE BRUISES MENORRHAGIA METRORRHAGIA EPISTAXIS GI BLEEDING HEMATOMA ECCHYMOSIS

  26. The old practice of Bleeding Time & Clotting Time! Do Platelet count  If Low  Do Bleeding Time  If Prolonged, give Platelets

  27. Do Platelet count  If Low  Do Bleeding Time  If Prolonged, give Platelets

  28. BLEEDING DUE TO PLATELET ABNORMALITIES

  29. Megakaryocytes • Largest hemopoietic marrow cells (~100 um) • Multi-lobulated nuclei; no mitosis but nuclear duplication • Abundant cytoplasm with azurophilic granules • Each Produces 3000 platelets SHEIKHA

  30. Megakaryocytes The committed platelet progenitor cells do not undergo classical mitosis; instead they will develop nuclear duplications & cytoplasmic expansion. The rapid increase in cytoplasm is accommodated by progressive folding, or invaginations, of megakaryocytic membrane. These demarcation membranes will eventually produce individual platelet membranes. MK pseudopodia penetrates marrow sinusoids. Blood flow breaks off large platelets that are finally fragmented to individual platelets in the pulmonary microcirculation. SHEIKHA

  31. Megakaryocytes EACH MK CAN PRODUCE 3000 PALETLETS In stressed thrombopoiesis, cytoplasm matures quicker than nucleus so that low ploidy MK start to produce platelets that are larger, denser and metabolically more active SHEIKHA

  32. THROMBOCYTOPENIA ↓ PRODUCTION APLASTIC ANEMIA LEUKEMIAS CHEMOTHERAPY MARROW INFILTRATION

  33. THROMBOCYTOPENIA ↓ PRODUCTION APLASTIC ANEMIA LEUKEMIAS CHEMOTHERAPY MARROW INFILTRATION ↓ SURVIVAL ITP EVANS’ SLE DIC TTP/HUS SEPSIS

  34. THROMBOCYTOPENIA ↓ PRODUCTION APLASTIC ANEMIA LEUKEMIAS CHEMOTHERAPY MARROW INFILTRATION ↓ SURVIVAL ITP EVANS’ SLE DIC TTP/HUS SEPSIS LOSS FROM CIRCULATION SPLENOMEGALY MASSIVE TRANSFUSION

  35. ITP IMMUNE THROMBOCYTOPENIC PURPURA

  36. Old View: Increased Platelet Production with High Platelet Turnover New Concept: Decreased Platelet Production!!

  37. Spleen in ITP

  38. ITP

  39. EVANS’ SYNDROME

  40. MANAGEMENT OF ITP STEROID IV IMMUNOGLOBULIN Anti-D SPLENECTOMY ?Platelet Transfusion

  41. Rituximab “Anti CD20”

  42. WAS

  43. DRUG-INDUCED THROMBOCYTOPENIA

  44. TTP/HUS THROMBOTIC THROMBOCYTOPENIC PURPURA HEMOLYTIC UREMIC SYNDROME TP MAHA RENAL FEVER CNS ICU BROKEN RBCs A PHONE CALL SAVE A LIFE

  45. Mortality Rate 85%

  46. Mortality Rate 85% Recovery Rate 85%

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