Bleeding disorders /certified fixed orthodontic courses by Indian dental academy

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Bleeding disorders /certified fixed orthodontic courses by Indian dental academy

  1. 1. BLEEDING DISORDERS INDIAN DENTAL ACADEMY Leader in Continuing Dental Education www.indiandentalacademy.com
  2. 2. INDEX- PLATELETS: FORMATION MORPHOLOGY FUNCTIONS-HAEMOSTASIS: VASCULAR SPASM PLATELET PLUG FORMATION COAGULATION INHIBITORS OF COAGULATION www.indiandentalacademy.com HAEMOSTASIS DRUGS USED FOR OPPOSING
  3. 3. - THE LABORATORY TESTS FOR DIAGNOSIS OF BLEEDING DISORDERS- BLEEDING DISORDERS- PERIODONTAL TREATMENT OF BLEEDING DISORDERS- REFERENCES www.indiandentalacademy.com
  4. 4. PLATELETS• INTRODUCTION: Platelets are tiny cells that congregate around ruptures in bloodvessels to provide backbone of clot.the platelets essentially form a temporary plug to stop bleeding.active platelets also stimulate the action of other coagulation proteins. www.indiandentalacademy.com
  5. 5. • FORMATION OF PLATELETS MYELOID STEM CELLS www.indiandentalacademy.com
  6. 6. • Factors controlling thrombopoiesis:1.Interleukins(IL): IL-3,IL-6,IL-11,colony stimulating factors stimulate thrombopoiesis.2.thrombopoietin(TPO): Produced by liver & kidney.It helps the megakaryocyte to produce the platelets rapidly.3.TGFBeta: when excessive thrombopoiesis it is released from platelets and depress the platelet production. www.indiandentalacademy.com
  7. 7. • The life span of platelet is – 7 to 12 days Most of the platelets are destroyed in spleen.• The normal platelet count is 150000 – 400000 / ul of blood www.indiandentalacademy.com
  8. 8. MORPHOLOGY• SHAPE – disc shape ( inactive platelet) spherical (active platelet)• SIZE - 2-4 um in diameter• Platelets exist in red bone marrow,blood &spleen• Platelets have plasma membane , cytosol & no nucleus.• Plamamembrane has 2 layers Outer glycocalyx layer:contains glycoproteins Inner lipoprotein layer:contains phospholipids www.indiandentalacademy.com
  9. 9. PLATELET STRUCTURE www.indiandentalacademy.com
  10. 10. • The cytosol consists of 1.Granules: -Alpha granules contain fibronectin, factor V, factor VII, PF4, PDGF. -Dense granules contain ADP, ATP, histamine& Calcium 2.Tubules: -Open tubules: Communicate with extracellular fluid(ECF). During activation,ca++ from ECF enter the inside of platelets via these tubules -Dense tubules: donot communicate with the exterior.They store ca++. www.indiandentalacademy.com
  11. 11. • 3.contractile elements:actin, myosin.• 4.mitochondria & golgiapparatus www.indiandentalacademy.com
  12. 12. Functions of platelets• Primary haemostasis – vascular spasm platelet plug formation• Secondary haemostasis (blood coagulation) www.indiandentalacademy.com
  13. 13. HEMOSTASIS• 1.Vascular spasm• 2.Platelet plug formation• 3.Blood clotting or coagulation www.indiandentalacademy.com
  14. 14. • 1.Vascular spasm: www.indiandentalacademy.com
  15. 15. • 2.Platelet plug formation: a) platelet adhesion. b) plaetelet release reaction. c) platelet aggregation & formation of platelet plug. www.indiandentalacademy.com
  16. 16. * The substances involved in platelet plug formation:• TXA2• ATP• ADP• Ca++• Serotonin• Prostaglandin• Fibrin stabilizing factor• Lysozomes• Platelet derived growth factor (PDGF) www.indiandentalacademy.com
  17. 17. a) Platelet adhesionwww.indiandentalacademy.com
  18. 18. b)Platelet release reactionwww.indiandentalacademy.com
  19. 19. c) platelet aggregation & formation of platelet plug. www.indiandentalacademy.com
  20. 20. * 3.Blood clotting:• Within the vessels blood is in liquid form.when it is drawn from body it thickens and forms a gel.• The gel separates from the liquid.This straw colored liquid is called serum & the gel is called clot.• The process of gel formation – clotting or coagulation. www.indiandentalacademy.com
  21. 21. • Definition : Blood clotting is an complex cascade of enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence.finally a large quantity of product (clot) is formed. www.indiandentalacademy.com
  22. 22. • THE FACTORS INVOLVED IN CLOTTING:-Clotting factors (CF)-Ca++-Enzymes synthesized by hepatocytes-Molecules associated with platelets www.indiandentalacademy.com
  23. 23. Clotting factorswww.indiandentalacademy.com
  24. 24. * Clotting can be divided into 3 stages.• 1.Formation of prothrombinase by 2 pathways. Extrinsic pathway Intrinsic pathway• 2.Prothrombinase converts prothrombin into thrombin.• 3.Thrombin converts fibrinogen into soluble fibrin.Fibrinwww.indiandentalacademy.com forms the clot.
  25. 25. Clotting mechanism www.indiandentalacademy.com
  26. 26. www.indiandentalacademy.com
  27. 27. Thrombin has 2 +ve feedback mechanisms www.indiandentalacademy.com
  28. 28. Clot retraction• Clot retraction is the consolidation or tightening of the fibrin clot.As the clot retracts it pulls the edges of the damaged vessel close together.Fibroblasts from ruptured www.indiandentalacademy.com area &new epithelial cells repair the vessel lining.
  29. 29. www.indiandentalacademy.com
  30. 30. • Intra vascular clotting *Clotting in an undamaged bloodvessels – thrombosis. *The clot – thrombus. *A blood clot,bubble of air,fat from broken bones or a piece of debris transported by the blood stream -embolus www.indiandentalacademy.com
  31. 31. Inhibitors of coagulation• Circulatory anti coagulants• The fibrinolytic mechanism• Tissue factor pathway inhibitor (TFPI)• Thrombomodulin www.indiandentalacademy.com
  32. 32. • Role of Vitamin k• Role of VWF• Role of liver• Role of bloodvessels www.indiandentalacademy.com
  33. 33. • Circulatory anticoagulants: Antithrombin Heparin Protein C & protein S www.indiandentalacademy.com
  34. 34. CIRCULATORY ANTI COAGULANTS www.indiandentalacademy.com
  35. 35. • Fibrinolytic mechanism: www.indiandentalacademy.com
  36. 36. • Thrombomodulin www.indiandentalacademy.com
  37. 37. • TFPI : After the onset of coagulation mechanism, TFPI begins to be formed and inhibits the intrinsic pathway. www.indiandentalacademy.com
  38. 38. • Role of vitamin K : Vitamin K is required for synthesis of factors II,VII,IX&X Source of vitamin K:vegetables Vitamin k is synthesized by intestinal bacterial flora.*Vitamin K deficiency:-Vitamin K free nutrition-Antibiotics like cephalosporins-Newborns-Obstructive jaundice www.indiandentalacademy.com
  39. 39. • Role of blood vessels:-The subendothelium is highly thrombogenic.-The contact of blood with subendothelium triggers the formation of XIIa.-Vascular endothelium synthesize PGI2 (prostacyclin) opposes the action of TXA2 thus prevents the platelet activation. www.indiandentalacademy.com
  40. 40. • Role of liver:-Liver synthesizes prothrombin, fibrinogen, factors V,VII,IX,X & XI.Thus the liver failure causes failure of clot formation.-Liver also synthesizes antithrombin III, heparin, proteinsC & S.Thus liver failure also can cause excessive clotting. www.indiandentalacademy.com
  41. 41. • Role of VWF:- Synthesized by megakaryocytes & vascular endothelium.It acts as a bridge between platelet & denuded endothelium. www.indiandentalacademy.com
  42. 42. * The drugs used for opposing haemostasis:• 1.Anti thromboitics• 2.Anti coagulants• 3.Thrombolytic drugs www.indiandentalacademy.com
  43. 43. * 1.Anti thrombotics• Eg:Aspirin• Aspirin inhibits vasoconstriction & platelet aggregation by blocking synthesis of TXA2.• It reduces the chance of thrombus formation.• Indications : -Transient ischaemic attacks -Myocardial infarction -Angina pectoris -Blockage of peripheral arteries www.indiandentalacademy.com
  44. 44. * 2.Anti coagulants:• In vivo:-Heparin :potentiates the action of anti thrombinIII-Vitamin K antagonists :eg-warfarin Blocks the synthesis of CF II,VII,IX,X.-Indications: Deep venous thrombosis Myocardial infarction Pulmonary embolism www.indiandentalacademy.com
  45. 45. • In vitro: To prevent clotting in donated blood, blood banks and laboratories often add a substance which prevents coagulation by removing the ionized calcium of blood citrate.-Eg : EDTA CPD Oxalates. www.indiandentalacademy.com
  46. 46. • 3.Thrombolytic drugs: These are injected into the body to dissolve clots that have already formed to restore circulation. -The mechanism of action: activate plasminogen. -Eg: Streptokinase Tissue plasminogen activator Urokinase www.indiandentalacademy.com
  47. 47. * The common laboratory tests for diagnosis of bleeding disorders:• 1.Bleeding time(BT)• 2.Clotting time(CT)• 3.Prothrombin time(PT)• 4.Partial thromboplastin time(PTT)• 5.Platelet count www.indiandentalacademy.com
  48. 48. BLEEDING DISORDERS www.indiandentalacademy.com
  49. 49. I) BLEEDING DISORDERS CAUSED BY VESSEL WALL ABNORMALITIES• Called non thrombocytopenic purpura.• They induce small haemorrhages such as petchiae and purpura in the skin,mucous membranes,particularly in gingivae.• The platelet count,BT,CT,PTT are normal. www.indiandentalacademy.com
  50. 50. CAUSES:* 1.Infections: Meningococcemia Septicaemia Infective endocarditis. Rickettsia Measles* 2.Drug reactions:The vascular injury is mediated by drug induced Abs and deposition of immune complexes in vessel walls leading to hypersensitivity vasculitis. www.indiandentalacademy.com
  51. 51. • 3.Scurvy & Ehlers - Danlos Syndrome: -Impaired formation of collagens causes microvascular bleeding. -Cushings syndrome-Protein wasting effects of excessive corticosteroid production cause loss of perivascular supporting tissues. www.indiandentalacademy.com
  52. 52. • 4.Amyloid infiltration of blood vessels: Systemic amyloidosis associated with perivascular deposition of amyloid and consequent weakening blood vessel walls. www.indiandentalacademy.com
  53. 53. 5.Henoch-Schonlein purpura: (senile purpura)- Systemic hypersensitivity disease characterizedby a purpuric rash, ployarthralgia,acute glomerulonephritis www.indiandentalacademy.com
  54. 54. * 6.Heriditary haemorrhagic telangiectasia:• is an autosomal dominant disorder characterized by dilated,tortuous blood vessels that have thin walls and hence bleed readily.most commonly occurs under the mucous membranes of the nose,tongue,mouth,eyes,GIT. www.indiandentalacademy.com
  55. 55. • II.BLEEDING DISORDERS DUE TO FAULT OF PLATELETS:A.Related to reduced platelet number (thrombocytopenic purpura)B.Related to defect in platelet function www.indiandentalacademy.com
  56. 56. A.Related to reduced platelet number: (Thrombocytopenic purpura)• Platelet count is < 100000/ul.• post traumatic bleeding is aggravated-when platelet count is 20000-50000/ul.• BT is prolonged.• PT,PTT – normal.• The common sites involved are: -skin -Mucous membrane of GIT & genito urinary tract www.indiandentalacademy.com
  57. 57. CAUSES:1.Decreased production of platelets - Generalized diseases of bonemarrow a) Aplastic anaemia b) Leukaemia - Selective impairment of platelet production a) Drug induced : Alcohol,thiazides,cytotoxicdrugs. b) Infections: measles,HIV. - Infective Megakaryopoiesis a) Megaloblastic anaemia b) Myelodisplastic syndrome c) Paroxysmal nocturnal haemoglobinuria. www.indiandentalacademy.com
  58. 58. 2.Sequestration: - Spleen normally sequesters30-40% of platelets. -In case of hypersplenism orsplenomegaly it sequesters 90% of all platelets. -Treatment: splenectomy3.Dilutional: -Massive transfusions may producethrombocytopenia.Blood stored for longer than24hrs contains virtually no viableplatelets.Thus,plasma volume &RBC arereconstitued by transfusion,but the number ofcirculating platelets is reduced. www.indiandentalacademy.com
  59. 59. 4.Decreased platelet survival:i)Immunologic destuction:a.Auto immune: Idiopathicthrombocytopenic purpura Systemic lupus erythematosis.b.Iso immune: Post transfusion Neonatalc.Drug associated:heparin,quinidine,sulfa compounds.d.Infections: Infectious mononucleosis HIV Cytomegalovirus. www.indiandentalacademy.com
  60. 60. ii)Non immunologic destruction: Disseminated intravascular coagulation(DIC) Thrombotic thrombocytopenic purpura Giant haemangiomas Microangiopathic haemolytic anaemias www.indiandentalacademy.com
  61. 61. i)Immune thrombocytopenic purpura(ITP):• Primary ITP – Acute Chronic (common)• Secondary ITP – Systemic lupus erythomatosis AIDS Viral infections Drug therapy www.indiandentalacademy.com
  62. 62. PRIMARY ITP: CHRONIC:• Most common• Cause:the formation of auto Abs against platelet membrane glycoproteins,most often IIb-IIIa or Ib-IX• Prevalence: F:M=3:1• Age : <40yrs• C/F: -Insidious in onset. -Bleeding into skin,mucousal surface -Petechiae prominent in the dependent areas where the capillary pressure is high.Petechiae become confluent & give rise to ecchymosis. -Long history of easy bruising ,epitaxis,bleeding gums. www.indiandentalacademy.com
  63. 63. • The disease may be manifested first by malena,haematuria and increased menstrual flow.• Subarachnoid haemorrhage & intracerebral haemorrhage very rarely seen.• Diagnosis: -Decreased platelet count -Normal or Megakaryocytes in bone marrow. -Prolonged BT* Treatment:Glucocorticoids & splenectomy www.indiandentalacademy.com
  64. 64. ACUTE ITP:• Occurs in children• M:F=1:1• C/F: -Abrupt in onset -The interval between infection & onset is 2wks -Usually selflimited and resolves spontaneously within 6months. -20% of children may develop chronic ITP. www.indiandentalacademy.com*Treatment:corticosteroid therapy
  65. 65. Secondary ITP:• Drug induced:Heparin Quinidine Sulfa compounds -Heparin induced : occurs in 5% of cases receiving heparin. Two types: TypeI-occurs rapidly after onset of therapy TypeII-5-14 days after onset of therapy. www.indiandentalacademy.com
  66. 66. • HIV associated thrombocytopenia: CD4, the receptor for HIV on T cells demonstrated on megakaryocytes,making it possible for these cells to be infected by HIV.Infected megakaryocytes undergo apoptosis causing impaired platelet production. www.indiandentalacademy.com
  67. 67. • Non immunologic thrombocytopenia -Cause:by mechanical injury. Eg:Thrombotic microangiopathies-thrombotic thrombocytopenic purpura Haemolytic-uremic syndrome www.indiandentalacademy.com
  68. 68. • B.Bleeding disorders related to defective platelet function:1.Congenital2.Acquired www.indiandentalacademy.com
  69. 69. 1.Congenital• On the basis of specific functional abnormalitya)Defect in platelet adhesion to sub endothelial matrix.eg:Bernard-Soulier syndrome. Platelet membrane glycoprotein is a receptor for VWF and is essential for platelet adhesion.b)Defect in platelet aggregation Eg:Glanzmann’s thrombasthenia. Platelets fail to aggregate in response to ADP,collagen,thrombin,fail to form glycoprotein complex which forms bridges between platelets. www.indiandentalacademy.com
  70. 70. c)Disorders of platelet secretion:Eg: storage pool disorders. -Characterized by normal initial aggregation withcollagen ADP, but the secretion ofTXA2,prostaglandins, & granule bound ADP areimpaired. www.indiandentalacademy.com
  71. 71. 2.Acquired:a)Ingestion of aspirin & other NSAIDS which increase BT.b)Uremia: Impaired platelet function www.indiandentalacademy.com
  72. 72. • III)BLEEDING DISORDERS RELATED TO ABNORMALITIES IN CLOTTING FACTORS: (FAULT IN SECONDARY HAEMOSTASIS)-The Bleeding is manifested by large post traumatic ecchymosis or haematomas-Prolonged BT-Bleeding into GIT,UT & joints. www.indiandentalacademy.com
  73. 73. • Two types 1.Congenital:deficiency of fac VIII-haemophilia A deficiency of fac IX- haemophilia B 2.Acquired: DIC VitaminK deficiency Liver disorders www.indiandentalacademy.com
  74. 74. • Haemophilia A :-Most common heriditary disorder.-Caused by reduction in amount or activity of fac VIII.-It is inherited as an X-linked recessive trait.-Occurs in males & homozygous females.-30% of pts-no family history.caused by new mutations. www.indiandentalacademy.com
  75. 75. -The severity correlates with the level of fac VIII activity.• <1% of normal activity – severe• 2-5% of normal activity- moderate• 6-50% of normal activity- mild-C/F:Easy bruising & massive haemorrhage after truama or operative procedures.spontaneous haemorrhages occurs in regions of body normallly subject to trauma,particularly in joints(haem arthroses)-Normal BT,platelet count & PT but prolonged PTT.-Treatment:Recombinant fac VIII www.indiandentalacademy.com
  76. 76. • Haemophilia B (Christmas disease):-It is inherited as an X linked recessive trait.-Caused by a wide sprectrum of mutations involving- the fac IX gene.-Clinically indistinguishable from haemophilia A.-14% of pts fac IX is present but non functional.-Prolonged PTT,normal PT& BT. www.indiandentalacademy.com-Treatment: Recombinant fac IX.
  77. 77. • VONWILLEBRAND DISEASE• Caused by an inherited defect in involving platelet adhesion.• C/F:Spontaneous bleeding from mucous membranes,excessive bleeding from wounds,menorrhagia.• Prolonged BT,normal platelet count.• Types:Type1 Type2 Type3 www.indiandentalacademy.com
  78. 78. Type 1&3 are associated with a reduced quantity of circulating VWF.• Type1:mild&autosomal dominant.• Type3:severe&autosomal recessive haemarthroses is common Severe deficiency of VWF has a marked effect on stability of fac VIII.• Type 2 is characterized by qualitative defects in VWF. -Because of mutations the VWF is abnormal. C/F:mild to www.indiandentalacademy.com moderate bleeding.
  79. 79. • Patients with Vonwillebrands disease have a compound defect involving platelet function & coagulation pathway. www.indiandentalacademy.com
  80. 80. * Acquired haemophilia• Disseminated intravascular clotting:• It occurs as a secondary complication in a vareity of diseases.• It results from pathologic activation of the extrinsic and/or intrinsic pathways or impairment of clot inhibiting influences.• The mechanisms trigger DIC - release of TF into the circulation www.indiandentalacademy.com - wide spread of injury to endothilial cells.
  81. 81. Release of TF into the circulationCauses Obstetrics complications. - retained dead foetus - septic abortion - amniotic fluid embolism - toximia neoplasms - adenocarcinoma, leukemia infections – gm-ve species, malaria, histoplasmosis www.indiandentalacademy.com aspergillosis
  82. 82. wide spread of injury to endothelial cells Endothelial injury ↓ release TF ↓ promotes platelet aggregation ↓ activates intrinsic pathway www.indiandentalacademy.com
  83. 83. • Consequence of DIC widespread deposition of fibrin ↓ ischemia ↓ microangiopathic haemolytic anaemia. www.indiandentalacademy.com
  84. 84. Haemostatic failure consumption of platelets and CF, ↓ activation of plasminogen ↓ plasmin→ fibrinolysis → inhibition of thrombin ↓ platelet aggregationproteolysis of clotting factors ↓ ↓ bleeding bleeding www.indiandentalacademy.com
  85. 85. SPONTANEOUS BRUISING IN HAEMOPHILIA www.indiandentalacademy.com
  86. 86. PERIODONTAL TREATMENT OF HAEMORRHAGIC DISORDES• Identification of the pt via the health history,clinical examination and lab tests.1.H/O bleeding after previous surgery or trauma.2.Past & present drug history.3.H/O bleeding problems among relatives. www.indiandentalacademy.com4.Illness associated with potential bleeding problems.
  87. 87. • Clinical examination : Ecchymosis Jaundice Spider telangiectasia Haemarthrosis Petechiae Haemorrhage vesicles Spontaneous gingival bleeding Gingival hyperplasia www.indiandentalacademy.com
  88. 88. • LABORATORY TESTS : BT CT PT PTT Complete bloodcell count Torniquet test www.indiandentalacademy.com
  89. 89. * Haemophilia A:• To prevent surgical haemorrhage fac VIII levels of atleast 30% are needed.• Parentral 1-deamino-8-D-arginine vasopressin (DDAVP) can be used to raise fac VIII levels in mild to moderate haemophilia.• In severe case preoperative infusion of fac VIII or cryoprecipitate form is recommended.• Advantage of DDAVP:Avoids the risk of viral disease transmission from fac VIII infusion. www.indiandentalacademy.com
  90. 90. * Haemophilia B:• To prevent surgical haemorrhage fac VIII levels of atleast 30%-50% are needed.• Purified prothrombin complex concentrates or fac IX concentrates can be used to raise fac IX levels .• Mild-DDAVP before periodontal surgery or toothextraction.• Severe-preoperative infusion of www.indiandentalacademy.com fac IX or cryoprecipitate form.
  91. 91. • Probing scaling and prophylaxis – without medical modification.• More invasive treatment such as block local anesthesia,root planning or surgery – prior physician consultation.• Local haemostatic measures:to enhance clot formation. Pressure packs Electro cautery www.indiandentalacademy.com Splints&dressings
  92. 92. • Anti haemostatic agents:may be placed over surgical sites or extraction sockets. -Oxidized cellulose -Gel foam -Surgicel -Avitene -Purified bovine collagen.• Anti fibrinolytic agents: -Epsilon-aminocaproic acid(EACA)-systemically -Amicar systemically -Tranexamic acid-systemically, also available in a mouthrinse. -100mg / kg – preoperatively continued towww.indiandentalacademy.comat a dose 50mg/kg 8-10 days postoperatively qid.
  93. 93. • TREATMENT OF LIVER DISEASES OPPOSING HAEMOSTASIS-physician consultation-Lab tests-Conservative,non surgical periodontal therapy-If surgery is required may require hospitalization-Platelet count should be >80000/mm3-PT <2.5 www.indiandentalacademy.com
  94. 94. * TREATMENT IN PTS TAKING ANTI COAGULANT THERAPY• The effectiveness of anticoagulant therapy is monitored by PT.• The recommended INR-2to3.-INR < 3- infiltration anesthesia,scaling & rootplaning.-INR < 2-block anesthesia, minor surgery & simple extractions. www.indiandentalacademy.com-INR <1.5-complex surgeries,multiple extractions.
  95. 95. • Physician consultation to determine the degree of required anticoagulation & dicontinuation of the drug until the desired PT is achieved.May be discontinued for 2-3 days.• The pts taking aspirin <325 mg / day – discontinued for atleast 7-10 days before periodontal therapy in consultation with physician.• NSAIDS like ibuprofen – the effect is transitory,lasting only a short time after the last drug dose. www.indiandentalacademy.com
  96. 96. *Thrombocytopenic purpura• Removal of local irritants to reduce the inflammation & to avoid the aggressive therapy.• Oral hygiene instructions & frequent recall visits.• Platelet count < 60000/mm3-scaling &rootplaning is safe.• Platelet count >80000/mm3-surgical procedures safely can be performed.• Platelet transfusion may be required before surgery. www.indiandentalacademy.com• Atraumatic surgical techniques&local haemostatic measures
  97. 97. * Non thrombocytopenic purpura• Surgical therapy should be avoided unless qualitative & quantitative platelet problems are resolved.• Local haemostatic pressure&atraumatic technique should be applied. www.indiandentalacademy.com
  98. 98. REFERENCES1.Concise medical physiology-Choudhuri2.Principles of anatomy&physiology-Tortora3.Pathologic basis of disease-Robbins4.Clinical periodontology-Carranza5.Management of dental pts with bleeding disorders:Review and Update (Oral surg Oral med Oral pathol 1988;66:297-303.6.Haematology text book-Martin & Peter www.indiandentalacademy.com
  99. 99. THANK YOUwww.indiandentalacademy.com

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