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Bleeding tendency






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Bleeding tendency

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1. Bleeding tendency Normal haemostasis Factors involved in normal haemostasis

2. Bleeding: Clinical Features Local - Vs - General, spontaneous . . Hematoma & Joint bleed - Coagulation Skin/Mucosal Petechiae & Purpura ? PLT wound / surgical bleeding ? Immediate - (PLT) Delayed - (Coagulation)

3. Hemostasis

4. Platelet Coagulation

5. Primary Hemostatic Disorders Defect of platelet plug formation platelets small vessels or capillaries plasma proteins required for adhesion to subendothelium

6. Primary Hemostatic Disorders Vascular defect - ? fragility Petechiae, purpura, ecchymoses senile purpura vitamin C deficiency (scurvy) connective tissue disorders Osler-Weber-Rendu syndrome - hereditary malformations

8. Primary Hemostatic Disorders Vascular defect - cont. Infectious and hypersensitivity vasculitides - Rickettsial and meningococcal infections - Henoch-Schonlein purpura (immune)

9. Primary Hemostatic Disorders Platelet disorders: ? platelets (thrombocytopenia) petechiae spontaneous bleeding after trauma CNS bleeding (severe ? plt) Platelet dysfunction - mucocutaneous bleeding Prolonged bleeding time (BT)

11. Thrombocytopenia - Causes Marrow injury/failure - aplastic or myelophthesic anemia - drugs, infections - megaloblastic anemia, PNH Decreased survival - immune (ITP, drugs, infections) - nonimmune (DIC, TTP) Splenic sequestration

12. Idiopathic Thrombocytopenic Purpura (ITP) Acute - children (post infection) Chronic - adults (? females, 20-40 yrs) - autoimmune disorder - antiplatelet antibodies (IgG against platelet glycoproteins) - IgG coated platelets removed by spleen (? platelet survival) Usually ? megakaryocytes in BM

13. Primary Hemostatic Disorders Platelet dysfunction: Inherited - autosomal recessive Bernard-Soulier disease - large platelets - lack of glycoproteins (1b-IX complex) - failure of platelet adhesion Glanzmann?s thrombasthenia - normal platelet morphology - lack of glycoproteins (IIb-IIIa complex) - defect of platelet aggregation

14. Primary Hemostatic Disorders Platelet dysfunction: Acquired - common Aspirin and NSAID - cyclo-oxygenase inhibitors - lack of thromboxane A2 and PGE - failure of platelet aggregation Systemic disorders - i.e. uremia

15. Primary Hemostatic Disorders Plasma proteins required for adhesion to subendothelium: von Willebrand disease - quantitative or qualitative deficiency of vWF molecule - binds to exposed subendothelial collagen - mediates initial platelet adhesion

17. Secondary Hemostasis Consolidates initial platelet plug into stable clot Disorders - deficiencies of plasma clotting factors Clinical - bleeding from large vessels into joints (hemarthroses), muscles, deep soft tissues (hematomas, large ecchymoses) Onset - delayed after trauma

18. Secondary Hemostatic Disorders Laboratory findings: Normal bleeding time, platelet count Prolonged prothrombin time (PT) deficiencies of II, V, VII, X Prolonged activated partial thromboplastin time (aPTT) all factors except VII, XIII Mixing studies - normal plasma corrects PT or aPTT

20. Factor VIII Deficiency Classic hemophilia (hemophilia A) X-linked disorder (affects 1? males) Most common hereditary disease with severe bleeding 30% new mutations (not hereditary) Spontaneous hemorrhages

21. Factor VIII Deficiency Classic hemophilia - cont. Clinically severe if <1% circulating factor VIII (moderate 1-5%, mild 5-75%) Abnormal aPTT Diagnosis - factor assays Treatment - factor VIII concentrate - cryoprecipitate (less desirable)

22. Factor IX Deficiency Christmas disease (hemophilia B) X-linked recessive disorder Indistinguishable from classic hemophilia Requires evaluation of factor VIII and IX activity levels to diagnose Treatment - factor IX concentrate - cryoprecipitate if factor IX unavailable

23. Secondary Hemostatic Disorders Acquired coagulation disorder: Vitamin K deficiency - neonates - decreased intestinal flora and dietary intake - oral anticoagulants (coumadin) - fat malabsorption syndromes Required for factors II, VII, IX, X Prolonged PT and aPTT

24. Combined Primary and Secondary Hemostatic Disorders von Willebrand?s Disease Autosomal dominant (or recessive) Primary defect - platelet adhesion (prolonged bleeding time) Secondary defect - deficiency of factor VIII; normally stabilizes factor VIII in circulation (prolonged aPTT)

25. Von Willebrand?s Disease Clinical - often mild - excessive bleeding from wounds - spontaneous bleeding from mucous membranes Different types - ? quantity or loss of selective multimers Diagnosis - ristocetin induced plt aggregation or multimer analysis

27. Combined Primary and Secondary Hemostatic Disorders Disseminated Intravascular Coagulation Primary - platelet consumption (? bleeding time, ? platelets) Secondary - factor consumption (? PT, aPTT) Major pathologic processes - obstetric complications, neoplasms, infection (sepsis), major trauma

28. Disseminated Intravascular Coagulation

29. Disseminated Intravascular Thrombosis (DIC) Acute DIC - ? bleeding - i.e. major trauma - give fresh frozen plasma Chronic DIC - ? thrombosis - i.e. cancer - give heparin or anticoagulant Treat underlying disease

30. Combined Primary and Secondary Hemostatic Disorders Severe Liver Disease Primary - dysfunctional platelets and/or thrombocytopenia (? BT) Secondary - decrease in all coagulation factors except vWF (? PT, aPTT) Vitamin K will promote synthesis of factors II, VII, IX, X

31. Summary Hemostatic Disorders BT Plt PT PTT 1o hemostasis -? -? - - 2o Factor VIII/IX deficiency - - - ? 2o Vitamin K deficiency - - ? ? Combined ? ? -? ?

32. Approach to bleeding disorders Personal history of bleeding With surgery Tonsillectomy, circumcision Epistaxis a Immediate bleeding after trauma or surgery suggest platelet or severe protein deficiency. Bleeding 2-5 days post trauma or surgery suggest plasma protein deficiency .

33. Family history X linked Autosomal al * Drug history Oral anticoagulant, Heparin, Aspirin * Physical examination

34. Initial lab works CBC : Platelet count PT (INR) APTT Bleeding time

35. Signs and Symptoms of Coagulation Disorders Bleeding Ecchymoses Petechiae Hemarthroses Hematomas

36. Petechiae

37. Platelets versus Coags Petechiae?platelets low or dysfunctional Ecchymoses, hematomas, hemarthroses?seen more frequently with low clotting factors or dysfunction Bleeding can be seen with either

38. Hematoma

39. Hemarthrosis

40. Hematoma

41. Ecchymosis

42. Management : Always be on the safe side Don?t do invasive procedures if you are in doubt. Always check with haematology/ internal medicine. Check the above tests if normal you can proceed Remember some cases of bleeding tendency might go first to you, like AML with gingival hyper trophy. Always check Drugs

43. HEPARIN THERAPY Enhances activity of AT III Parenteral administration required Onset of action immediate Monitor aPTT Lower dose may work in patients without active thrombosis

44. HEPARIN THERAPY Low Molecular Weight Heparin-Advantages Less heterogeneous than heparin Less inhibition of platelet function Longer half life - Can give 1-2x/day Much less thrombocytopenia ? safer, equally effective

45. HEPARIN Low Molecular Weight Heparin-Disadvantages Bleeding-? Less than with heparin (probably not) Most cross react with heparin RE: thrombocytopenia Each preparation is different Less overall experience with the drug

46. COUMADIN (warfarin) Mechanism of Action Inhibits Vitamin K dependent carboxylase activity Prevents reduction of Vitamin K Humans secrete des-?-carboxyglutamic acid, an inactive protein DOES NOT AFFECT PROTEINS ALREADY SYNTHESIZED Monitor using prothrombin time Multiple interactions with other drugs Antidote-Vitamin K

47. What do if no help if INR< 1.5 safe to do procedures, so if patient on Warfarin , stop Warfarin 2 days before surgery. Heparin stop if unfractionated 2 hours before SX. If low MW Heparin 4-6 hours stop surgery

48. Platelet defect: Count : Thrombocytopenia = low platelet count Thrombocytosis = High platelet count Safe procedure if platelet count above 50,000. Thrombosthenia : The count is normal but the function is abnormal.

49. Systemic illnesses can predispose to bleeding like liver diseases, Chronic renal failure.

50. Depending on the underlying cause abnormalities of the platelet should be corrected before any procedure . How to correct depends on the underlying cause either with platelets transfusion or other modalities to increase the count ,like steroids , IVIg in ITP.

51. If on Aspirin please stop Aspirin at least one week before SX. If urgent please check bleeding time if prolonged please give platelets. Which should be 1-2 hour before SX.

52. For congenital causes of bleeding please contact haemtology.

53. leukaemias Can predispose to bleeding due to 1- low platelets count 2- DIC 3-Hyerviscosity syndrome. Oral manifestations of acute leukaemia Includes : gingival hypertrophy, bleeding , and ulcers.

54. Oral manifestations of leukaemia


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