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  2. 2. HEMOSTASIS <ul><li>The body’s intrinsic ability to slow down or stop hemorrhage </li></ul><ul><li>normal hemostasis involves a delicate balance between factors that promote blood coagulation and thrombus stabilization and factors that inhibit blood coagulation and promote thrombus dissolution </li></ul>clot RESOLUTION FORMATION
  3. 3. COAGULATION <ul><li>vascular wall </li></ul><ul><li>coagulation factors </li></ul><ul><li>platelet </li></ul>
  4. 4. COAGULATION FIRST STEP <ul><li>Smooth muscle </li></ul><ul><ul><li>muscle constriction </li></ul></ul><ul><ul><ul><li>luminal diameter reduction </li></ul></ul></ul><ul><ul><ul><li>retarding blood loss </li></ul></ul></ul><ul><ul><ul><li>enhancing platelet adherence </li></ul></ul></ul><ul><li>Endothelial cells </li></ul><ul><ul><li>VIII-vWF synthesis </li></ul></ul><ul><ul><li>thromboplastin (III) release </li></ul></ul><ul><ul><li>  activation of ext pathway </li></ul></ul><ul><ul><li>activation of Factor IX & X </li></ul></ul><ul><li>Subendothelium </li></ul><ul><ul><li>collagen  platelet adherence, activation </li></ul></ul>
  5. 5. PRIMARY HEMOSTASIS <ul><li>Platelet </li></ul><ul><ul><li>Adherence </li></ul></ul><ul><ul><li>Activation </li></ul></ul><ul><ul><li>Aggregation </li></ul></ul><ul><ul><li>(Contraction) </li></ul></ul><ul><ul><li>(Stabilization) </li></ul></ul>
  6. 6. C O L L A G E N von Willebrand Factor fibrinogen endothelial cells Platelet Adhesion mediated by GP-Ib on platelet surface and vWF C O L L A G E N GP-Ib
  7. 7. von Willebrand Factor <ul><li>Synthesized & stored in endothelial cells and megakaryocytes (also stored in platelets ) </li></ul><ul><li>Forming bridge between subendothelial collagen and Plt </li></ul><ul><li>Carrier molecule for Factor VIII Coagulant Protein (vWF is also known as Factor VIII Related Antigen) </li></ul><ul><li>Circulates as series of multimers (in various sizes) </li></ul><ul><li>Large, high molecular weight multimers required for normal hemostasis </li></ul>
  8. 8. <ul><li>Release of platelet’s cytoplasmic products </li></ul><ul><li>activation of platelet factor III (PF-3) </li></ul><ul><ul><li>PF-3 serves as a binding site for cofactor V & VIII </li></ul></ul><ul><li>production of thrombin </li></ul>C O L L A G E N Platelet Activation GP-IIb, IIIa release of  and electron dense granules
  9. 9. <ul><li>formation of primary plug </li></ul><ul><li>activated platelets synthesize and secrete TXA 2 </li></ul><ul><li>TXA 2 : </li></ul><ul><ul><li>1. promotes plt aggregation </li></ul></ul><ul><ul><li>2. vasoconstriction </li></ul></ul><ul><ul><li>3. release of plt factor (ADP) </li></ul></ul>C O L L A G E N Platelet Aggregation GP IIb-IIIa - fibrinogen interaction Aspirin inhibits TXA 2 and ADP
  10. 10.
  11. 11. Coagulation Factors XII XI IX VIII VII X V I extrinsic pathway intrinsic pathway PT aPTT XIII Stable clot II
  12. 12. Coagulation Factors <ul><li>Intrinsic Pathway </li></ul><ul><li>Extrinsic Pathway </li></ul><ul><li>Common Pathway </li></ul><ul><li>majorities are serine proteases </li></ul><ul><li>circulate as inactive forms (require activation to function) </li></ul><ul><li>majority produced in liver </li></ul>II XII XI IX VIII VII X V I extrinsic pathway intrinsic pathway PT aPTT XIII Stable clot negative charged surface tissue factor
  13. 13. Coagulation Factors <ul><li>Intrinsic Pathway </li></ul><ul><li>Extrinsic Pathway </li></ul><ul><li>Common Pathway </li></ul><ul><li>majorities are serine proteases </li></ul><ul><li>circulate as inactive forms (require activation to function) </li></ul><ul><li>majority produced in liver </li></ul><ul><li>many require vit K for synthesis </li></ul><ul><ul><li>II, VII, IX, X </li></ul></ul><ul><ul><li>protein C, S </li></ul></ul>II XII XI IX VIII VII X V I extrinsic pathway intrinsic pathway PT aPTT XIII Stable clot negative charged surface tissue factor
  14. 14. Secondary Hemostasis <ul><li>tissue factor </li></ul><ul><li>phospholipid complex </li></ul><ul><li>thrombin activation </li></ul><ul><li>fibrin polymerization </li></ul><ul><li>thrombin, ADP, TXA 2 </li></ul><ul><li>Contraction </li></ul><ul><li>contraction of intraplatelet actomyosin </li></ul><ul><li>formation of secondary plug </li></ul><ul><li>uncover plt membrane receptors (GPIb, IIIa) </li></ul><ul><li>Stabilization </li></ul><ul><li>activation of XII thrombin </li></ul><ul><li>cross linking of fibrin monomers </li></ul>
  15. 15. A A B B fibrinopeptide A & B D domain E domain Spontaneous aggregation fibrinogen fibrin monomer soluble fibrin polymer E D D E D D E D D E D D E D D E D D E D D E D D B A A B E D D E thrombin Factor XIIIa
  16. 16. Stabilization of Fibrin Clot Thrombin Factor XII I Factor XIIIa soluble fibrin clot stabilized fibrin clot E D D E D D E D D E D D E D D E D D E D E D E D D E D D E D D E D D E D D E D D E D E D
  17. 17. Other Proteins in Blood Coagulation <ul><li>Prekallikrein </li></ul><ul><li>activates XII and prekallikrein </li></ul><ul><li>High molecular wt. Kininogen (HMWK) (=binding protein) </li></ul><ul><li>supports reciprocal activation of XII, XI and prekallikrein </li></ul>
  18. 18.
  19. 19. ANTICOAGULATION & FIBRINOLYSIS <ul><li>Vascular Wall </li></ul><ul><li>Anti-Coagulation Factors </li></ul><ul><li>Fibrinolytic Factors </li></ul>
  20. 20. ANTICOAGULATION & FIBRINOLYSIS Vascular Wall <ul><li>Endothelial Cell </li></ul><ul><ul><li>prostacyclin (PGl2) </li></ul></ul><ul><ul><li>heparan sulfate </li></ul></ul><ul><ul><li>thrombomodulin </li></ul></ul><ul><ul><li>tissue plasminogen activator (tPA) </li></ul></ul><ul><li>Muscle </li></ul><ul><ul><li>muscular dilation </li></ul></ul>
  21. 21. ANTICOAGULATION & FIBRINOLYSIS Anti-Coagulation Factors <ul><li>Antithrombin III (with thrombin & heparin) </li></ul><ul><ul><li>negative feedback on thrombin </li></ul></ul><ul><ul><li>inactivates Xa (XIIa, XIa, IXa) </li></ul></ul><ul><li>Prostacyclin (PGl2) from endothelial cells </li></ul><ul><ul><li>vasodilation </li></ul></ul><ul><ul><li>conversion of ADP into products that inhibit plt aggregation </li></ul></ul><ul><li>thrombin + endothelial cells </li></ul><ul><ul><li>thrombomodulin binds & activates Protein C </li></ul></ul><ul><ul><li> inactivates Va & VIIIa </li></ul></ul><ul><ul><li>inhibits thrombin </li></ul></ul>II XII XI IX VIII VII X V I XIII Stable clot
  22. 22. <ul><li>Protein C </li></ul><ul><ul><li>vit K dependent zymogen </li></ul></ul><ul><ul><li>produced in liver </li></ul></ul><ul><ul><li>inactivates Va and VIIIa </li></ul></ul><ul><li>Protein S </li></ul><ul><ul><li>vit K dependent binding protein </li></ul></ul><ul><ul><li>co-factor for protein C </li></ul></ul><ul><ul><li>binds C4b-binding protein </li></ul></ul>II XII XI IX VIII VII X V I XIII Stable clot
  23. 23. Anticoagulation Heparin <ul><li>Heparin activates Antithrombin III (AT III) </li></ul><ul><li>AT III inactivates Thrombin and Factor Xa </li></ul><ul><li>rapid onset of action </li></ul><ul><li>Laboratory monitoring: </li></ul><ul><ul><li>aPTT : ~1.5X – 2.5X normal mean </li></ul></ul><ul><ul><li>heparin level : </li></ul></ul><ul><ul><ul><li>0.2 – 0.4 U/mL by protamine titration </li></ul></ul></ul><ul><ul><ul><li>0.35 – 0.70 by Factor Xa inactivation assay </li></ul></ul></ul>II XII XI IX VIII VII X V I XIII Stable clot aPTT
  24. 24. Anticoagulation Heparin AT AT
  25. 25. II
  26. 26. II AT
  27. 27. II AT
  28. 28. II AT
  29. 29. II AT
  30. 30. II AT
  31. 31. Coumadin (Warfarin) Anticoagulants <ul><li>inhibits hepatic synthesis of vit K-dependent clotting factors (II, VII, IX, X) </li></ul><ul><li>competitive inhibition of g-carboxylation </li></ul><ul><ul><ul><ul><li>inactivate “acarboxy” forms synthesized </li></ul></ul></ul></ul><ul><li>onset delayed 3 to 5 days </li></ul><ul><li>also inhibits synthesis of protein C & S </li></ul>II XII XI IX VIII VII X V I PT XIII Stable clot
  32. 32. Thrombolytic (Fibrinolytic) Factors <ul><li>Urokinase : released from endothelial cells and monocytes </li></ul><ul><li>Tissue plasminogen activator (tPA) </li></ul><ul><li>conversion of plasminogen to plasmin </li></ul><ul><li>cleavage of fibrinogen & fibrin into fibrin split products </li></ul><ul><li>inhibit plt aggregation </li></ul><ul><li>thrombin activity </li></ul><ul><li>fibrin strands cross linking </li></ul>
  33. 33.
  34. 34. Plasmin Degradation of Fibrin Clot plasmin plasmin plasmin D-dimer E-fragment DED complex Fibrin Degradation Products E D D E D D E D D E D D E D D E D D E D E D E D E D E D D D D E D D D D E
  35. 35. Bleeding Disorders
  36. 36. Procoagulant Platelets Factors Fibrinogen von Willebrand Factor Anticoagulant Antithrombin III Protein C Protein S Profibrinolytic Plasminogen tPA Fibrin Fragment D-dimer Antifibrinolytic PAI-1 Alpha-2 Antiplasmin clot RESOLUTION FORMATION
  37. 37. Vessel Abnormalities increased vascular fragility <ul><li>manifested by petechial hemorrhages of skin/mucous membranes </li></ul><ul><li>bleeding time, plt count, PT, aPTT --- normal </li></ul><ul><li>not life threatening bleeding </li></ul><ul><li>1. congenital </li></ul><ul><li>a. Ehlers-Danlos syndrome (AD) </li></ul><ul><li>b. hereditary hemorrhagic telangiectasia (AD) </li></ul><ul><li>2. acquired </li></ul><ul><li>a. hypersensitivity vasculitis </li></ul><ul><li>(1) drug reaction : immune complex deposit in vessel walls </li></ul><ul><li>(2) Henoch-Schonlein purpura </li></ul><ul><li>b. scurvy (vit C deficiency) </li></ul>
  38. 38. Henoch-Schonlein purpura <ul><li>generalized hypersensitivity vasculitis </li></ul><ul><li>uncertain cause </li></ul><ul><li>clinical Sx: </li></ul><ul><ul><li>purpura </li></ul></ul><ul><ul><li>colicky abdominal pain </li></ul></ul><ul><ul><li>polyarthralgia </li></ul></ul><ul><ul><li>acute glomerulonephritis </li></ul></ul>
  39. 39. Coagulation Factor Abnormality <ul><li>hematomas/ecchymoses after minor trauma </li></ul><ul><li>often severe bleeding </li></ul><ul><li>1. congenital : usually single factor deficiency </li></ul><ul><li>a. sex-linked </li></ul><ul><li>(1) hemophilia A (Factor VIII def.) </li></ul><ul><li>(2) hemophilia B (Christmas disease, Factor IX def.) </li></ul><ul><li>b. autosomal dominant </li></ul><ul><li>(1) von Willebrand’s disease </li></ul><ul><li>c. autosomal recessive </li></ul><ul><li>2. acquired : usually multi-factor deficiency and clotting abnormalities </li></ul><ul><li>a. vitamin K deficiency </li></ul><ul><li>b. severe liver disease </li></ul>
  40. 40.
  41. 41. Hemophilia A (Factor VIII deficiency) <ul><li>bleeding into joints  crippling arthropathy </li></ul><ul><li>sex-linked inheritance </li></ul><ul><li>high rate of spontaneous mutation </li></ul><ul><ul><li>25% of pt’s do not have family history of hemophilia </li></ul></ul><ul><li>decreased VIII-C, near normal VIII-vWF </li></ul><ul><li>>50% severe deficiency </li></ul><ul><li>increased aPTT </li></ul><ul><li>normal bleeding time, plt, PT </li></ul>II XII XI IX VIII VII X V I XIII Stable clot aPTT
  42. 42. hemophilia A
  43. 43. Hemophilia B (Christmas disease, Factor IX def.) <ul><li>less common than hemophilia A </li></ul><ul><li>similar clinical Sx and inheritance pattern as hemophilia A (sex-linked) </li></ul>II XII XI IX VIII VII X V I XIII Stable clot
  44. 44. von Willebrand’s disease <ul><li>easy bruisability (no bleeding into joints) </li></ul><ul><li>unable to release VIII-vWF </li></ul><ul><li>intact VIII-vWF synthesis </li></ul><ul><li>VIII-C level is also decreased (unknown reason) </li></ul><ul><li>autosomal dominant </li></ul><ul><ul><li>1 in 30,000 population </li></ul></ul><ul><li>usually diagnosed in childhood or young adults </li></ul><ul><li>increased bleeding time </li></ul><ul><li>normal plt, PT </li></ul><ul><li>normal or increased aPTT </li></ul>
  45. 45. Vitamin K Deficiency vitamin K dependent factors : II, VII, IX, X <ul><li>acquired disorder </li></ul><ul><ul><li>may occur in malnutrition, malabsorption, biliary obstruction, drug </li></ul></ul><ul><li>increased PT </li></ul><ul><li>normal bleeding time, plt </li></ul><ul><li>normal or increased aPTT </li></ul>II XII XI IX VIII VII X V I PT XIII Stable clot
  46. 46. Severe Liver Disease factors synthesized in liver : II, V, VII, IX, X, fibrinogen <ul><li>increased PT, aPTT </li></ul><ul><li>normal bleeding time, plt </li></ul>II XII XI IX VIII VII X V I PT XIII Stable clot aPTT
  47. 47. PLATELET ABNORMALITIES <ul><li>1. Thrombocytopenia </li></ul><ul><li>a. decreased production </li></ul><ul><li>b. increased utilization </li></ul><ul><li>c. increased destruction </li></ul><ul><li>(1) isoimmune thrombocytopenia </li></ul><ul><li>(2) idiopathic thrombocytopenic purpura (ITP) </li></ul><ul><li>(3) thrombotic thrombocytopenic purpura (TTP) </li></ul><ul><li>(4) drug reaction </li></ul><ul><li>(5) mechanical destruction </li></ul><ul><li>(6) hypersplenism </li></ul><ul><li>2. Functional abnormalities </li></ul><ul><li>a. congenital </li></ul><ul><li>(1) defective adhesion (Bernard-Soulier) </li></ul><ul><li>(2) defective aggregation (thrombasthenia) </li></ul><ul><li>b. acquired </li></ul><ul><li>(1) aspirin </li></ul><ul><li>(2) thrombocythemia </li></ul>
  48. 48. Thrombocytopenia <ul><li>decreased in number of platelets </li></ul><ul><li>bleeding from small vessels (skin, GI, mucous membrane, GU, brain) </li></ul><ul><li>normal or increased bleeding time </li></ul><ul><li>decreased platelet </li></ul><ul><li>normal PT, aPTT </li></ul>
  49. 49. Thrombocytopenia <ul><li>decreased production </li></ul><ul><li>diffuse bone marrow disease (aplastic anemia, tumor) </li></ul><ul><li>megakaryocyte disorder </li></ul><ul><li>increased utilization </li></ul><ul><li>DIC </li></ul>
  50. 50. Thrombocytopenia increased destruction <ul><li>isoimmune thrombocytopenia </li></ul><ul><ul><li>neonatal </li></ul></ul><ul><ul><li>[PLA 1 neg. mother] + [PLA 1 pos. baby] </li></ul></ul><ul><ul><li>production of anti-PLA 1 Ab (IgG) </li></ul></ul><ul><ul><li>post-transfusion </li></ul></ul><ul><ul><li>[PLA 1 neg. recipient] + [PLA 1 pos. platelet] </li></ul></ul><ul><ul><li>destruction of PLA 1 platelets and recipient's own platelets </li></ul></ul>
  51. 51. Thrombocytopenia increased destruction <ul><li>idiopathic thrombocytopenic purpura (ITP) </li></ul><ul><ul><li>acute ITP </li></ul></ul><ul><ul><ul><li>children following a viral infection </li></ul></ul></ul><ul><ul><ul><li>self-limiting disease </li></ul></ul></ul><ul><ul><ul><li>? platelet as an “innocent bystander” </li></ul></ul></ul><ul><ul><li>chronic ITP </li></ul></ul><ul><ul><ul><li>adults (often premenopausal females) </li></ul></ul></ul><ul><ul><ul><li>may be associated with other “autoimmune diseases” </li></ul></ul></ul><ul><ul><ul><li>production of autoantibody against Pt’s own platelets </li></ul></ul></ul><ul><ul><ul><li>removal of opsonized platelets by reticuloendothelial system </li></ul></ul></ul><ul><ul><ul><li>decreased circulating platelet, but increased BM megakaryocytes </li></ul></ul></ul>
  52. 52. <ul><li>idiopathic thrombocytopenic purpura (ITP) </li></ul><ul><ul><li>clinical: </li></ul></ul><ul><ul><ul><li>easy bruising and bleeding after minor trauma </li></ul></ul></ul><ul><ul><li>treatment: </li></ul></ul><ul><ul><ul><li>steroid </li></ul></ul></ul><ul><ul><ul><li>splenectomy </li></ul></ul></ul>
  53. 53. Thrombocytopenia increased destruction <ul><li>thrombotic thrombocytopenic purpura (TTP) </li></ul><ul><ul><li>abnormal platelet aggregation in microcirculation </li></ul></ul><ul><ul><li>microangiopathic hemolytic anemia </li></ul></ul><ul><ul><li>fever </li></ul></ul><ul><ul><li>transient neurologic deficits </li></ul></ul><ul><ul><li>renal failure </li></ul></ul><ul><ul><li>hemolytic uremic syndrome (HUS) </li></ul></ul><ul><ul><li>platelets start to aggregate in small vessels without particular reason </li></ul></ul> HUS
  54. 54. Disseminated Intravascular Coagulation (DIC) <ul><ul><li>- an acute, subacute, or chronic thrombohemorrhagic disorder occurring as a secondary complication in a variety of diseases </li></ul></ul><ul><ul><li>- activation of clotting system resulting in wide spread formation of microthrombi throughout the microcirculation </li></ul></ul><ul><ul><li>- as a consequence, causing consumption of platelets, fibrin and coagulation factors, and activation of thrombolytic mechanism </li></ul></ul><ul><ul><li>Two major triggering mechanisms </li></ul></ul><ul><ul><li>1. release of tissue factor or thromboplastic substance </li></ul></ul><ul><ul><li>2. widespread endothelial injury </li></ul></ul>
  55. 55. DIC <ul><ul><li>Triggering Mechanisms </li></ul></ul><ul><ul><li>1. release of tissue factor or thromboplastic substance </li></ul></ul><ul><ul><li>- placental tissue </li></ul></ul><ul><ul><li>- granules from leukemic cells </li></ul></ul><ul><ul><li>- bacterial endotoxin </li></ul></ul><ul><ul><li>- mucus from adeno CA </li></ul></ul><ul><ul><li>2. widespread endothelial injury </li></ul></ul><ul><ul><li>- Ag-Ab immune complex deposit </li></ul></ul><ul><ul><li>- extreme temperature </li></ul></ul><ul><ul><li>- microorganisms </li></ul></ul>
  56. 56. DIC <ul><ul><li>Pathology: - wide spread thrombi </li></ul></ul><ul><ul><li> (brain, heart, lungs, kidneys, adrenals, spleen , liver) </li></ul></ul><ul><ul><li>- microinfarcts </li></ul></ul><ul><ul><li>Clinical: - ~50% associated with obstetric complications </li></ul></ul><ul><ul><li>- ~30% with carcinomatosis </li></ul></ul><ul><ul><li>- microangiopathic anemia </li></ul></ul><ul><ul><li>- dyspnea, cyanosis </li></ul></ul><ul><ul><li>- convulsions, coma </li></ul></ul><ul><ul><li>- oliguria, acute renal failure </li></ul></ul><ul><ul><li>- shock, circulatory failure </li></ul></ul>
  57. 57. DIC <ul><ul><li>Clinical: acute DIC with a predominance of thrombin generation and consumption of coagulation factors </li></ul></ul><ul><ul><li>bleeding tendency </li></ul></ul><ul><ul><li>(oozing from venopuncutres or operating site) </li></ul></ul><ul><ul><li>subacute and chronic DIC </li></ul></ul><ul><ul><li>thrombotic tendency </li></ul></ul>
  58. 58. DIC <ul><ul><li>Lab: - fibrinogen </li></ul></ul><ul><ul><li>- platelet </li></ul></ul><ul><ul><li>- PT </li></ul></ul><ul><ul><li>- aPTT </li></ul></ul><ul><ul><li>- fibrin degradation product </li></ul></ul><ul><ul><li>acute DIC: - prolongation of aPTT, PT and TT </li></ul></ul><ul><ul><li>- reduction of platelets, AT III and protein C </li></ul></ul><ul><ul><li>- decreased fibrinogen </li></ul></ul><ul><ul><li>- elevated fibrin degradation products </li></ul></ul><ul><ul><li>chronic DIC: - aPTT and PT may be within normal ranges </li></ul></ul><ul><ul><li>- slightly decreased platelets </li></ul></ul><ul><ul><li>- elevated fibrin degradation products and D-dimer </li></ul></ul>
  59. 59. Platelet Functional Abnormalities congenital <ul><li>Bernard-Soulier syndrome </li></ul><ul><ul><li>defect in platelet adhesion </li></ul></ul><ul><ul><li>autosomal recessive </li></ul></ul><ul><ul><li>defect in platelet membrane glycoprotein (GP Ib) </li></ul></ul><ul><li>thrombasthenia </li></ul><ul><ul><li>defect in platelet aggregation </li></ul></ul><ul><ul><li>autosomal recessive </li></ul></ul><ul><ul><li>defect in platelet membrane glycoprotein (GP IIb & IIIa) </li></ul></ul><ul><ul><li>no fibrinogen linking of platelets </li></ul></ul><ul><ul><li>easy bleeding and no clot retraction </li></ul></ul>1 2
  60. 60. Platelet Functional Abnormalities acquired <ul><li>aspirin </li></ul><ul><ul><li>inhibits cyclooxygenase </li></ul></ul><ul><ul><ul><ul><li>suppression of TXA 2 synthesis </li></ul></ul></ul></ul><ul><ul><li>effect lasts for 72 hours </li></ul></ul><ul><li>thrombocythemia </li></ul><ul><ul><li>platelet : >3,000,000/ml </li></ul></ul><ul><ul><li>functionally abnormal platelets </li></ul></ul><ul><ul><li>occasionally seen in myeloproliferative disorders </li></ul></ul>
  61. 61. Coagulation Tests <ul><li>1. Bleeding Time : in vivo test </li></ul><ul><li>measures adequacy of plt function </li></ul><ul><li>normal : <6 min. </li></ul><ul><li>2. Platelet Count normal : >200,000/mL </li></ul><ul><li>3. aPTT : intrinsic pathway (XII, XI, IX, VIII, X, V) </li></ul><ul><li>used to guide heparin therapy </li></ul><ul><li>4. 50/50 mixing study </li></ul><ul><li>pt’s plasma + nl. plasma </li></ul><ul><li>if mixing correct aPTT = Pt is deficient in intrinsic factor(s) </li></ul><ul><li>no correction = circulating anticoagulants or inhibitors </li></ul><ul><li>5. Prothrombin Time (PT) : extrinsic pathway (II, VII, V, X) </li></ul><ul><li>monitoring warfarin/coumadin effects </li></ul>
  62. 62. Coagulation Tests <ul><li>6. Fibrinogen Level normal : 200 – 500 mg/dL </li></ul><ul><li>7. ADP platelet aggregation </li></ul><ul><li>8. Ristocetin aggregation test </li></ul><ul><ul><li>test for presence or activity of vWF </li></ul></ul><ul><li>9. Thrombin Time (TT) normal : 20 – 30 sec </li></ul><ul><ul><li>measures 3 rd stage of coagulation </li></ul></ul><ul><ul><li>prolonged if </li></ul></ul><ul><ul><ul><li>def or abnormality of fibrinogen </li></ul></ul></ul><ul><ul><ul><li>presence of fibrin split products </li></ul></ul></ul><ul><ul><ul><li>presence of heparin </li></ul></ul></ul>
  63. 63. History & Physical Exam are most important most sensitive most specific Tests of Hemostasis
  64. 64.
  65. 65.
  66. 66.