Blood coagulation

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This presentation will help you to understand the physiology of blood coagulation and various factors involved in it.

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Blood coagulation

  1. 1. ContentsHaemostasisVascular PhasePlatelet PhaseClot formationClot retractionFibrinolysisBleeding DisordersDiagnosis of bleeding disordersClinical implication in periodontology
  2. 2. Haemostasis
  3. 3. Haima + Stasis Prevent blood loss
  4. 4. Maintains blood flowPrevents bleeding
  5. 5. • Stages of Hemostasis
  6. 6. Vascular Phase
  7. 7. PLATELET Phase
  8. 8. Platelets• Thrombocyte = “ thrombos” + “ Kytos” •1,50,000 to 400,000 per cu mm Lifespan is 9 – 12 days
  9. 9. • Membrane• Outer glycocalyx layer— glycoproteins• Inner lipoprotein layer— phospholipid
  10. 10. Platelet PLUG
  11. 11. Blood coagulation
  12. 12. Role of thrombin
  13. 13. Fibrin formation
  14. 14. SEM of clot
  15. 15. • Release of fibrin stabilizing factor• Contractile protein of platelets• Activated and accelerated by thrombin and Ca ions.
  16. 16. ROLE OF ENDOTHILIUM
  17. 17. Approach to the diagnosis of bleedingdisorder Clinical Evaluation History Physical Examination Family history Laboratory Evaluation Screening test Specific test
  18. 18. Clinical Features of Bleeding Disorders Platelet disorders Coagulation disorders Site of bleeding Skin Deep in soft tissues (epistaxis, gum, Mucous vaginal, GI tract) membranes, joints, muscles) Petechiae Yes No Ecchymoses (“bruises”) Small, superficial Large, deep Hemarthrosis / muscle bleeding Extremely rare Common Bleeding after cuts & scratches Yes No Bleeding after surgery or trauma Immediate, Delayed (1-2 days), usually mild often severe
  19. 19. Platelet CoagulationPetechiae, Purpura Hematoma, Joint bl.
  20. 20. Tests for Primary Hemostasis• Bleeding time platelet & vascular phases• PFA – 100 system Platelet function• Platelet count Quantification of platelets• Blood smear Quantitative & morphological abnormalities of platelets , Detection of underlying haemotological disorder
  21. 21. Tests for Secondary hemostasis• Clotting factor Crude test of coagulation phase• Prothrombin factor Extrensic & common pathway• Activated partial thromboplastin time Intrensic & common pathway
  22. 22. PLATELET COUNT NORMAL 150,000 - 400,000 CELLS/MM3 < 100,000 Thrombocytopenia 50,000 - 100,000 Mild Thrombocytopenia < 50,000 Sev Thrombocytopenia
  23. 23. BLEEDING TIME  PROVIDES ASSESSMENT OF PLATELET COUNT AND FUNCTIONNORMAL VALUE 2-8 MINUTES
  24. 24. PROTHROMBIN TIME Measures Effectiveness of the Extrinsic Pathway Measures the activity of V, VII, X, II , INORMAL VALUE 11-16 SECS
  25. 25. Prothrombin time prolongs..Extrinsic pathway factor deficiencies(FII, V, VII, X)– Inherited or acquired– Consumption (DIC)– oral anticoagulant therapy
  26. 26. INRINR: International normalized ratio-was established by the WHO and the International Committee on Thrombosisand Hemostasis for reporting the results of prothrombin tests-All PT results are standardized by this calculation:INR= ( Patient PT / Control PT) ISIISI= International sensitivity index- Given by the manufacturer for each particular thromboplastin reagent andinstrument combination
  27. 27. ACTIVATED THROMBOPLASTIN TIME Measures Effectiveness of the Intrinsic Pathway & common pathway NORMAL VALUE 25-40 SECS
  28. 28. APTT prolongs..1. Intrinsic pathway factor deficiencies (FXII, XI,VIII, IX, HMWK, prekallikrein )- Inherited or acquired- Consumption (DIC)- PIVKA factors in cumarin therapy2. Specific inhibitors against FXII, XI, VIII, IX, HMWK, prekallikrein3. Lupus anticoagulant4. Non-fractionated heparin therapy
  29. 29. THROMBIN TIME Time for Thrombin To Convert Fibrinogen Fibrin A Measure of Fibrinolytic Pathway NORMAL VALUE 9-13 SECS
  30. 30. TT Prolongs..1. Hypo- afibrinogenaemia2. Dysfibrinogenaemia3. Non fractionated heparin4. Fibrinogen/ fibrin degradation product s5. Chronic liver disease
  31. 31. SPECIFIC TESTSTests for specific Platelet Functions1. Platelet aggregration test2. Flow cytometry3. Test for platelet secretion4. Clot retraction test5. Platelet procoagulant activityTest for Coagulation Phase1. Quantitative estimation of Fibrinogen2. Coagulation factor assays3. F XIII Qualitative assayLatex agglutination test for Fibrinolysis
  32. 32. BleedingDisorders Inherited • Vascular • Platelet • coagulation • Fibrinolytic Acquired • Vascular • Platelet • coagulation
  33. 33. HEMORRHAGIC DISORDERS Hemorrhagic syndromes are characterized by a disorder of one or more factors that participate in hemostasis. The majority of hemorrhagic syndromes are blood vessel disorders, platelet number and function disorders, or coagulation factor disorders:• vasculopathies• thrombocytopenias• thrombocytopathies• coagulopathies.
  34. 34. Vasculopathies• Vasculopathies may be inherited or acquired. Inherited forms result from blood vessel structure disorders (inherited telangiectasia,Rendu-Osler-Weber’s disease) while acquired disorders can be a consequence of inflammatory or immune processes that damage blood vessel walls.• In clinical practice, acquired disorders are found more frequently (secondary purpuras, infections, effects of some drugs, allergic purpura, effect of aspirin, vitamin C deficiency, etc.).
  35. 35. Thrombocytopenias• Thrombocytopenia, or reduced circulating platelet count, can be inherited or acquired; the acquired form being more frequent.• Thrombocytopenia occurs as a result of:– decreased platelet formation with normal platelet survival time (effects of irradiation, drugs, malignant tissue pressure on bone marrow, leukemias, aplastic anemias) or− increased platelet degradation or platelet deposit in spleen with decreased platelet survival (DIC, effects of drugs, bacterial or viral infections, inherited idiopathic thrombocytopenic purpura, chronic leukemias, lupus erythematosus,Hodgkin’s disease, massive transfusions and liver cirrhosis).
  36. 36. Thrombocytopathies• Inherited Qualitative Platelet Disorders may be due to abnormalities of1. platelet membrane glycoproteins,- Glanzmann Thrombastenia, abnormal GPIIb/IIIa– Bernard-Soulier Syndrome, abnormal GPIb, GPIX and GPV– platelet-type of vWD, abnormal GPIb2. platelet granules,• These may occur due to absence of granules in platelets, storage pool disorder (characterized by disturbed platelet aggregation to collagen, adrenaline and thrombin), or disturbed release (absence of T A2).
  37. 37. 3. platelet coagulant activity, or4. signal transduction and secretion.• defects in arachidonic acid metabolism,• cyclooxigenase deficiency, platelets unable to produce thromboxane; endothelium may not produce prostacyclin,• thromboxane synthesis deficiency, and• defects in platelet secretion and the second wave of platelet aggregation, found in response to epinephrine or ATP.
  38. 38. Coagulopathies
  39. 39. ACQUIRED BLOOD CLOTTINGDISORDERSThey occur in:– vitamin K deficiency,– liver diseases,– liver transplantation,– disseminated intravascular coagulation,– renal diseases,– primary pathological fibrinolysis– during the course of anticoagulant therapy.
  40. 40. • The extent and severity of periodontal disease determines the necessity for a surgical or nonsurgical treatment approach in its management.• The nature and severity of an acquired bleeding disorder, and the degree of invasive dental procedures, determines the need to modify the treatment to be provided.• Various Illnesses, along with pharmacotherapy,may contribute to the tendency for excessive bleeding.
  41. 41. Pre-operative management of patients starts with a medicalhistory focusing on the previous bleeding history of thepatient and medical conditions associated with bleeding.Presence of following illness may need a modification intreatment protocol to minimize the risk of intra-operativeand postoperative bleeding.• Chronic renal failure• Lack of vitamin K• Liver failure• Aspirin• Antiplatelet medication• Anticoagulant therpay
  42. 42. Intra-operative measures include a number of systemic and localmeasures administered prior to, or during, the procedure to preventunlikely bleeding diathesis. Surgeries • Platelet count should be assessed • Iv infusion 1 hr before • Level should be 50% higher in plasma forMissing factors Regional anesthesiaScaling and root planing • Antifibrinolytic mouthwash (Lee , Boyle) LA • regional anesthesia should be avoided • Conservative design Flap • Mandibular molar Prevention of • Curettage of extraction socket infection • Granulation tissue
  43. 43. Hemostatic agent Other means Hard tissue• Absorbable • Sponge • Bone burnishing gelatin • Surgical splint • Bone wax• Absorbable • Electrocautery collagen • Laser• Microfibrillar • Moistened or collagen hemostatic• Oxidised soaked gauze cellulose• Thrombin• Tranexamic acid• Fibrin glue• PRP
  44. 44. General recommendations is crucial for preventingbleeding, postoperatively.Prohibition of Liquid , high Antifibrinolytic Rinsing protein diet mouthwash Pain Antibiotics medication
  45. 45. References :-• Textbook of Medical Physiology ,10th edition,Hall & Guyton• Essentials of hematology , Shirish M Kawthalkar• Periodontal Medicine, Rose• Bleeding disorders and periodontology, Philip Vassilopoulos & Kent Palcanis , Periodontology 2000, Vol. 44, 2007, 211–223.• Coagulation Pathway and Physiology, Jerry B. Lefkowitz• Hemostasis And Hemorrhagic Disorders, R. Baklaja, M. C. Pešic´, J. Czarnecki• Platelet function analysis,Paul Harisson, Blood Reviews (2005) 19, 111–123
  46. 46. Thank You

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