Bleeding timeclotting-time-pt-and-ptt

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  • 1. COGULATIONPROFILEBleeding time, clotting time,PT, and PTTPresented ByHUSSAIN AKHTAR
  • 2. WHAT IS COAGULATION?Coagulation is a complex process by which blood forms clots.Blood must be remain fluid with in the vasculature and yet clotquickly when expose to non endothelial surface at a site ofvascular injury.It is an important part of haemostasis (the cessation of bloodloss from a damaged vessel), where in a damaged blood vesselwall is covered by a platelet and fibrin-containing clot to stopbleeding and begin repair of the damaged vessel.Disorders of coagulation can lead to an increased risk ofbleeding (hemorrhage) or clotting (thrombosis).
  • 3. Hemostasis is maintained in the body via threemechanisms:Vascular spasm - Damaged blood vessels.constrictPlatelet plug formation - Platelats adhere todamaged endothelium to form platelet plug(primary hemostasis) and then degranulate.Blood Coagulation - Clots form upon theconversion of fibrinogen to Fibrin, and itsaddition to the platelet plug (secondaryhemostasis).
  • 4. Factor I Fibrinogen Factor VIII AntihemophilicglobulinFactor II Prothrombin Factor IX PartialthromboplastincomponentFactor III Thromboplastin Factor X Stuart-ProwerfactorFactor IV Calcium Factor XI PlasmathromboplastinantecedentFactor V Labile orproaccelerinFactor XII Hageman factorFactor VII Stable factor orproconvertinFactor XIII Fibrin-stabilizing factor
  • 5. THE CLOTTING MECHANISMINTRINSIC EXTRINSCPROTHROMBIN THROMBINFIBRINOGENFIBRIN(II) (III)(I)VXTisue ThromboplastinCollagenVIIXIIXIIXVIII
  • 6. FIBRINOLYTIC PHASEANTICLOTTING MECHANISMS AREACTIVATED TO ALLOW CLOTDISINTEGRATION AND REPAIR OF THEDAMAGED VESSEL.
  • 7. HEMOSTASISDEPENDENT UPON:Vessel Wall IntegrityAdequate Numbers of PlateletsProper Functioning PlateletsAdequate Levels of Clotting FactorsProper Function of Fibrinolytic Pathway
  • 8. So What Causes Bleeding Disorders?VESSEL DEFECTSPLATELET DISORDERSFACTOR DEFICIENCIES
  • 9. VESSEL DEFECTSVITAMIN C DEFICIENCYBACTERIAL & VIRAL INFECTIONSACQUIRED
  • 10. PLATELETDISORDERSTHROMBOCYTOPENIA (INADEQUATENUMBER OF PLATELETS)CausesDRUG INDUCEDBONE MARROW FAILUREHYPERSPLENISMOTHER CAUSES
  • 11. THROMBOCYTOPATHY) ADEQUATE NUMBER BUT ABNORMAL FUNCTION )causesUREMIAINHERITED DISORDERSMYELOPROLIFERATIVE DISORDERSDRUG INDUCED(ASPIRIN, NSAIDS)
  • 12. FACTOR DEFICIENCIES Inherited:1. HEMHHHHOPHILIA A2. HEMOPHILIA B3. VON WILLEBRAND’SDISEASE Acquired:1. Anticoagulant therapy2. Liver diseases3. DIC
  • 13. LABORATORY EVALUATIONPLATELET COUNTBLEEDING TIME (BT)Clotting time (CT)PROTHROMBIN TIME (PT)Activated PARTIAL THROMBOPLASTIN TIME(APTT)
  • 14. PLATELET COUNT (CBC)NORMAL 100,000 - 400,000 CELLS/MM3< 100,000 Thrombocytopenia50,000 - 100,000 Mild Thrombocytopenia< 50,000 Sever Thrombocytopenia
  • 15. BLEEDING TIMEPROVIDES ASSESSMENT OF PLATELET COUNTAND FUNCTIONNORMAL VALUE2-8 MINUTES
  • 16. Clotting time - capillary method Material1. Sterile disposable pricking needle or lancet.2. Stop watch3. Dry glass capillary tube (narrow diameter 1 top 2 mm,minimum 10 cm long.)4. Cotton Swab of absorbent cotton.5. Spirit wetted, cotton swab.6. 70 % v/v ethyl alcohol
  • 17. Clotting time of whole blood
  • 18. Clotting Time - Slide Method• The surface of the glass tubeinitiates the clotting process.This test is sensitive to thefactors involved in the intrinsicpathway• The expected range for clottingtime is 4-10 min.
  • 19. PROTHROMBIN TIMEPROTHROMBIN TIMEMeasures Effectiveness of the ExtrinsicMeasures Effectiveness of the ExtrinsicPathwayPathwayNORMAL VALUENORMAL VALUE10-15 SECS10-15 SECS
  • 20. PTThe prothrombin time: is therefore the time required for the plasmato clot after an excess of thromboplastin and an optimal concentrationof calcium have been added.Measures the function of the Extrinsic Pathway.Sensitive to Factors I, II, V, VII, X.The PT evaluates patients suspected of having an inherited oracquired deficiency in these pathways.
  • 21. THE CLOTTING MECHANISMINTRINSIC EXTRINSCPROTHROMBIN THROMBINFIBRINOGENFIBRIN(II) (III)(I)VXTisue ThromboplastinCollagenVIIXIIXIIXVIII
  • 22. When is it ordered?Used to monitor oral anticoagulant therapy (Warfarin /Coumadin).When a patient who is not taking anti-coagulant drugshas signs or symptoms of a bleeding disorder.When a patient is to undergo an invasive medicalprocedure, such as surgery, to ensure normal clottingability.
  • 23. An elevated prothrombin timemay indicate the presence of: Vitamin K deficiency(Vitamin K is needed to make prothrombin and other clotting factors) DIC liver disease a deficiency in one or more of the following factors: I, II, V, VII, X. Anticoagulant (warfarin)
  • 24. INRA PT test may also be called an INR test. INR (international normalized ratio) stands for a way ofstandardizing the results of prothrombin time tests, nomatter the testing method.So your doctor can understand results in the same wayeven when they come from different labs and differenttest methods. Using the INR system, treatment with (anticoagulanttherapy) will be the same. In some labs, only the INR isreported and the PT is not reported
  • 25. An INR of 1.0 means that the patient PT is normal.An INR greater than 1.0 means the clotting time iselevated.INR of greater than 5 or 5.5 = unacceptable high risk ofbleeding,whereas if the INR=0.5 then there is a highchance of having a clot. Normal range for a healthy person is 0.9–1.3, and forpeople on warfarin therapy, 2.0–3.0, although the targetINR may be higher in particular situations, such as forthose with a mechanical heart valve.
  • 26. PARTIAL THROMBOPLASTIN TIMEMeasures Effectiveness of the IntrinsicPathwayNORMAL VALUENORMAL VALUE25-40 SECS25-40 SECS
  • 27. PTTThe partial thromboplastin time (PTT) or activated partialthromboplastin time (aPTT or APTT( is a performanceindicator measuring the efficacy of both the "intrinsic" andthe common coagulation pathways.It is also used to monitor the treatment effects withheparin a major anticoagulant.Kaolin cephalin clotting time (KccT) is a historic name forthe activated partial thromboplastin time
  • 28. THE CLOTTING MECHANISMINTRINSIC EXTRINSCPROTHROMBIN THROMBINFIBRINOGENFIBRIN(II) (III)(I)VXTisue ThromboplastinCollagenVIIXIIXIIXVIII
  • 29. Normal PTT times require the presence of thefollowing coagulation factors:I, II, III, IV, V, VI, VIII, IX, X, XI, & XII
  • 30. When is it ordered?When a patient presents with unexplained bleeding orbruising,It may be ordered as part of a pre-surgical evaluation forbleeding tendencies,When a patient is on intravenous (IV) or injection heparintherapy, the APTT is ordered at regular intervals tomonitor the degree of anticoagulation.
  • 31. Prolonged APTT may indicate:Use of heparin.antiphospholipid antibody:especially lupus anticoagulant,which paradoxically increases propensity to thrombosiscoagulation factor deficiency ,e.g hemophiliaDICLiver disease
  • 32. FACTOR DEFICIENCIES Inherited:1. HEMOPHILIA A2. HEMOPHILIA B3. VONWILLEBRAND’SDISEASE Acquired:1. Anticoagulanttherapy2. Liver diseases3. DIC
  • 33. HEMOPHILIA A (Classic Hemophilia) 80-85% of all Hemophiliacs Deficiency of Factor VIII Lab Results - Prolonged PTT
  • 34. HEMOPHILIA B (Christmas Disease) 10-15% of all Hemophiliacs Deficiency of Factor IX Lab Test - Prolonged PTT
  • 35. VON WILLEBRAND’S DISEASE Deficiency of VWF & amount of Factor VIII Factor VIII is bound to vWF while inactive in circulation;Factor VIII degrades rapidly when not bound to vWF Lab Results - Prolonged BT, PTT
  • 36. ANTICOAGULANTS An anticoagulant is a substance that preventscoagulation; that is, it stops blood from clotting This prevents deep vein thrombosis, pulmonarembolism, myocardial infarction and stroke.ANTICOAGULANTS1. Coumadins (Vitamin K antagonists)2. Heparin
  • 37. CoumadinsThese oral anticoagulants that antagonize the effects ofvitamin K. Examples include warfarin. It takes at least 48 to 72 hoursfor the anticoagulant effect to develop. Where animmediate effect is required, heparin must be givenconcomitantly.Monitored by PT timesThese anticoagulants are used to treat patients with deep-vein thrombosis (DVT), pulmonary embolism (PE), atrialfibrillation (AF), and mechanical prosthetic heart valves.
  • 38. HeparinHeparin is a biological substance.It works by activating antithrombin III, which blocksthrombin from clotting blood.Heparin Therapy is Monitored by PTT times Low molecular weight heparin is a more highly processedproduct that is useful as it does not require monitoring ofthe APTT coagulation parameter (it has more predictableplasma levels) and has fewer side effects.
  • 39. Liver DiseaseLiver Disease can Result in ReducedProduction of Coagulation Factors(I,II,V,VII,IX,X).
  • 40. DICDisseminated intravascular coagulation (DIC is apathological activation of coagulation) blood clotting)mechanisms that happens in response to a variety ofdiseasesDIC leads to the formation of small blood clots inside theblood vessels throughout the bodyThe small clots also disrupt normal blood flow to organs(such as the kidneys), which may malfunction as a result
  • 41. As the small clots consume coagulation proteins andplatelets, normal coagulation is disrupted and abnormalbleeding occurs from the skin the gastrointestinal tract,the respiratory tract and surgical wounds.The PT and APTT are usually very prolonged and thefibrinogen level markedly reducedHigh levels of fibrin degradation products, including D-dimer, are found owing to the intense fibrinolytic activitystimulated by the presence of fibrin in the circulation.
  • 42. Definitive diagnosis depends on the result of DIC: Thrombocytopenia) prolonged bleeding time) Prolongation of prothrombin time and activated partialthromboplastin time A low fibrinogen concentration Increased levels of fibrin degradation products
  • 43. Pre-analytic errors Problems with blue-top tube Partial fill tubes Vacuum leak and citrate evaporation Problems with phlebotomy Heparin contamination Wrong label Slow fill Underfill Vigorous shakingBiological effects•Hct ≥55 or ≤15•Lipemia, hyperbilirubinemia,hemolysisLaboratory errors•Delay in testing•Prolonged incubation at 37°C•Freeze/thaw deterioration