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APPROACH TO BLEEDING DISORDERS

APPROACH TO BLEEDING DISORDERS. History of Bleeding. Spontaneous vs. trauma/surgery-induced Ecchymoses without known trauma Medications or nutritional supplements. Clinical Presentations. Spontaneous hemarthroses - factors VIII and IX deficiency

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APPROACH TO BLEEDING DISORDERS

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  1. APPROACH TO BLEEDING DISORDERS

  2. History of Bleeding • Spontaneous vs. trauma/surgery-induced • Ecchymoses without known trauma • Medications or nutritional supplements

  3. Clinical Presentations • Spontaneous hemarthroses - factors VIII and IX deficiency - severe deficiencies of fibrinogen, prothrombin, and FV, VII, and X • Mucosal bleeding symptoms - platelet disorders - von Willebrand disease (vWD)

  4. Clinical Presentations • Subcutaneous bleeding - Cushing's syndrome - Chronic steroid use - Senile purpura • Epistaxis - hereditary hemorrhagic telangiectasia - vwd

  5. Clinical Presentations • Menorrhagia - vWD ,factor XI deficiency and symptomatic carriers of hemophilia A

  6. Prohemorrhagic medications and dietary supplements • NSAID’s • Aspirin • Fish oil (omega 3 FA) • Vitamin E

  7. Systemic Diseases that Cause or Exacerbate Bleeding • Bruising or mucosal bleeding may be a presentation of: - liver disease, renal impairment, hypothyroidism, paraproteinemias or amyloidosis, and bone marrow failure

  8. History of Thrombosis • Risk Factors • Arterial : Atherosclerosis • Venous: Immobility, surgery, medical conditions, HRT, Obesity, Genetic. • Idiopathic event is the stongest predictor of recurrence of venous thromboembolis • Age is an important risk factor for thromboembolism • Thrombotic events often has more than one contributing event

  9. SCREENING ASSAYS • PT • aPTT • Platelet count

  10. MIXING STUDIES • Evaluate prolonged Aptt or less commonly PT • Factor deficiency vs presence of inhibitor • Normal plasma and patient plasma in a 50:50 ratio • Incubate ar 37oC for 30, 60, and/or 120 min • Factor deficiencies –with corection • Lupus anticoagulant - no correction

  11. Specific Factor Assay • Requested based on clinical situation and the results of coagulation screening tests • Precise diagnosis and effective management • patient's plasma is mixed with plasma deficient in the factor being studied

  12. Antiphospholipid Antibodies • Antibodies to phospholipids (cardiolipin) or phospholipid-binding proteins (β 2-microglobulin detected by ELISA

  13. OTHER COAULATION TESTS • Thrombin time and Reptilase Time • Fibrinogen conversion to fibrin • Anti-Factor Xa Plasma Inhibitory Activity • LMWH activity • UFH activity

  14. Platelet Function • Bleeding time • PFA-100 • vWF assays • platelet aggregometry

  15. Hemostatic Disorders and Coagulation Test Abnormalities • Prolonged (aPTT) • No clinical bleeding – factors XII, high-molecular-weight kininogen, protein kinase  •  Variable, but usually mild, bleeding – factor XI, mild FVIII and FIX  •  Frequent, severe bleeding – severe deficiencies of FVIII and FIX • Heparin

  16. Hemostatic Disorders and Coagulation Test Abnormalities • Prolonged prothrombin time (PT) • Factor VII deficiency   • Vitamin K deficiency – early •   Warfarin anticoagulation

  17. Hemostatic Disorders and Coagulation Test Abnormalities • Prolonged aPTT and PT • Factor II, V or X deficiency   • Vitamin K deficiency – late   • Direct thrombin inhibitors

  18. Hemostatic Disorders and Coagulation Test Abnormalities • Prolonged thrombin time • Heparin or heparin-like inhibitors   • Mild or no bleeding – dysfibrinogenemia   • Frequent, severe bleeding – afibrinogenemia

  19. Hemostatic Disorders and Coagulation Test Abnormalities • Prolonged PT and/or aPTT not correct with mixing with normal plasma • Bleeding – specific factor inhibitor   • No symptoms, or clotting and/or pregnancy loss – lupus anticoagulant   • Disseminated intravascular coagulation   • Heparin or direct thrombin inhibitor

  20. Hemostatic Disorders and Coagulation Test Abnormalities • Abnormal clot solubility • Factor XIII deficiency    • Inhibitors or defective cross-linking • Rapid clot lysis   • Deficiency of 2-antiplasmin or plasminogen activator inhibitor 1 • Treatment with fibrinolytic therapy

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