1 / 33

Approach to bleeding Disorders

Approach to bleeding Disorders. By Mohannad Ibn Homaid. A few points. Content Structure 1 st half 2 nd half. Overview. Why is it important ? Why is it so confusing ? Basic Science Clinical manifestations Laboratory tests . Basic Science Review. Blood is gold

gerek
Download Presentation

Approach to bleeding Disorders

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Approach to bleeding Disorders By MohannadIbnHomaid

  2. A few points • Content • Structure • 1st half • 2nd half

  3. Overview • Why is it important ? • Why is it so confusing ? • Basic Science • Clinical manifestations • Laboratory tests

  4. Basic Science Review • Blood is gold • The 2 arms of Heamostasis • Platelets • Clotting Factors • Small Vessel Response To Injury

  5. Normal Response • Always Goes Through the following: • Vascular Phase • Platelet Phase • Coagulation Phase • Fibronlytic Phase • Pointless ? Or useful ?

  6. Vascular Phase Not Very important for understanding Vasoconstriction TXA2 and Aspirin

  7. Platelet Phase

  8. Platelet Phase • Unfortunately Very important • The following occurs: • Platelet Adhesion (vWF later) • Platelet Release Reaction • ADP • TXA2 • Temporary Plug < < BLEEDING STOPS HERE • Bleeding time • The Tile

  9. Coagulation Phase

  10. Coagulation Phase • VERY IMPORTANT and VERY CONFUSING • Why is it Confusing ? • Not Tangible • Coagulation Phase and 12 factors • Cofactors Ca and PF3 • Extrinsic vs intrinsic • Vitamin K factors • Anti-Thrombin 3 • And last but not least….

  11. THE ROMAN NUMBERS

  12. Coagulation Cascade • What do you need to know ? • Simple Steps : extrinsic vs intrinsic • Content of both • How to test them • Where they are made ( liver ) • Vitamin K • AT-3

  13. CONFUSING

  14. THIS SLIDE HAS BEEN INTENTIONALLY LEFT BLANK

  15. Extrinsic System: 7 Intrinsic System: 12-11-9-8 Final Common Pathway :10-5-2-1 Vitamin K : 2-7-9-10 AT-3 : 12 -11-10-9 PTT vs PT

  16. Coagulation Studies

  17. Fibrinolytic Phase

  18. Fibrinolytic Phase • Kinnnd of important but very easy • Tissue plasminogen Activator • Plasmin • Test • Fibrin Degradation Products • D-Dimer Assay

  19. Back to the clinical world • Presentation of platelet Defects • Blood leaks out of vessels • Skin and mucosal surfaces • Prolonged bleeding ( temporary plug plug ) • Presentation • Deep Tissue Bleeding • Late Rebleeding ( permanent plug Defect )

  20. Laboratory Test • Platlets • Count • Bleeding Time • Aggregation Test • Clotting Factors • PT and PTT • Factor Assay • Fibrinolysis • FDP • D-Dimer

  21. Platelet Disorders Quantitative vs Qualitative Thrombocytopenia Immune Thrombocytopenic Prupura Bernard Soulier Syndrome GlanzmannsThrombasthenia Thrombotic thrombocytopenic Purpura

  22. Thrombocytopenia Pathology :Increase Destruction or decrease Productions > > Clinical Features : depend on degree Labs: Treatment:

  23. ITP Pathology : Auto antibodies AgainsPlatlets Clinical Features: Labs: Treatment:

  24. Bernard Soulier Syndrome Pathology :GP1B receptor Defiency Clinical Features: Labs:

  25. GlanzmannThromboasthenia Pathology :GPIIb-IIIaDefiency Clinical Features: Labs: Treatment:

  26. TTP Pathology :Unkown Clinical Features: Pentad : HUS + Fever Neurological Labs: Treatment :Plasmapharesis

  27. Diorders of Coagulations Hemophilia Von Willebrand Disease

  28. Hemophilia • Pathology :Factor 8 or 9 • Clinical Features: • Acute Hemoarthrosis • Intracranial Bleeding • Hematomas • Labs: • Treatment: • Factor Replacement • DDAVP

  29. Von willebrand Disease • Function of vWF • Made in platelets and endothelium • Adhesion of platelets to exposed Collagen • Protection of Circulating Factor 8 • Pathology • Deficiency of vWF • Secondary decrease in Factor 8

  30. Von Willebrand Disease • Pathology : Mentioned • Clinical Features: • Labs: • Treatment: • DDAVP And factor concentrates

  31. DIC • Pathology :Inappropriate Activation of platelets and clotting Factors due to : • Sepsis ( 50%) • Obstetric Complications • Malignancy • Trauma • Clinical Features: • Labs: • Treatment: ICU and supportive = Treatment of underlying Cause

  32. Questions

More Related