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Clotting factors

clotting factors

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Clotting factors

  3. 3. INTRODUCTION Hemostasis is the process of forming clots in the walls of damaged blood vessels and preventing blood loss while maintaining blood in a fluid state within the vascular system.
  4. 4. MECHANISMS  Vasoconstriction  Platelet plug formation  Blood coagulation or clotting  Clot retraction
  5. 5. BLOOD COAGULATION /CLOTTING Coagulation or clotting is the process in which blood looses its fluidity and becomes a jelly like mass in a few minutes after it is shed. HISTORY: 1720 JEAN LOUIS PETIT : Hemostasis was caused by blood clots. 1860 RUDOLF VIRCHOW described blot clots and their tendency to embolise. 1905 PAUL MORAWITZ assembled 4 coagulation factors . 1940 PAUL OWREN :Recognized the other factors.
  6. 6. FACTORS INVOLVED IN BLOOD COAGULATION Coagulation of blood occurs through a series of reactions due to activation of a group of substances. The substances necessary for clotting are called CLOTTING FACTORS. They are:
  7. 7. Factor VI Presence has not been proved Factor VII Stable factor Factor VIII Antihemophilic factor Factor IX Christmas factor Factor X Stuart Prower factor Factor XI Plasma thromboplastin antecedent Factor XII Hegman factor Factor XIII Fibrin stabilisng factor Factor I Fibrinogen Factor II Prothrombin Factor III Thromboplastin (tissue factor) Factor IV Calcium Factor V Labile factor (Proaccelerin or accelerator globulin) FACTORS INVOLVED IN BLOOD COAGULATION
  8. 8.  Clotting factors are proteins in the form of enzymes. Proenzymes enzymes clot formation.  Reactions involved in the conversion of proenzymes to active enzymes is explained by ENZYME CASCADE THEORY . 3 STAGES:  Formation of prothrombin activator  Conversion of prothrombin into thrombin  Conversion of fibrinogen into fibrin.
  10. 10. Clot is a mesh of thin fibrils entangling the blood cells. These fibrils consist of fibrin. The fibrin is formed from fibrinogen
  11. 11. FACTOR I /FIBRINOGEN • 3 polypeptide chains - alpha, beta and gamma. Fibrinogen Fibrin Prothrombin Fibrin forms a mesh around the wound leading - blood clot. INHERITED DISORDERS (MUTATIONS IN FIBRINOGEN ) INCLUDE :  Afibrinogenemia  Hypofibrinogenemia  Hyperfibrinogenemia The gene for factor I is located on the 4th chromosome.
  12. 12. FACTOR II /PROTHROMBIN Vitamin K-dependent serine protease. Prothrombin FACTOR Xa Thrombin. Soluble fibrinogen THROMBIN Insoluble fibrin. • Activates factors V, VIII, XI and XIII. • Thrombin along with thrombomodulin present on endothelial cell surfaces form a complex that converts protein C to activated protein C (APC). • Patients suffer from dysprothrombinemia or hypoprothrombinemia. • The gene for thrombin is located on the eleventh chromosome (11p11).
  13. 13. FACTOR III / THROMBOPLASTIN /TISSUE FACTOR:  Found in the tissue cell.  Surface glycoprotein.  This factor enables cells to initiate the blood coagulation cascades, and it functions as the high-affinity receptor for the coagulation factor VII.  Acts as a cofactor in the factor VIIa- catalysed activation of factor X to Xa.  The gene for tissue factor is located on the first chromosome (1p22) .
  14. 14. FACTOR IV /CALCIUM • Calcium ions are essential in low concentrations for normal blood coagulation • Binding of coagulation factor complexes to phospholipid • Acts as a co factor in the coagulation process • Essential for formation of intrinsic and extrinsic thromboplastin • Conversion of prothrombin to thrombin • No evidence that coagulation disorder results from pathological reduction in ionised calcium
  15. 15. FACTOR V / PROACCELERIN OR LABILE FACTOR  Enzymatically inactive cofactor to the serine protease FXa Ca + phosholipid activation of prothrombin to thrombin.  Factor V mutation  Factor V deficiency ( Parahemophilia)  Myocardial Infarction  Deep Vein Thrombosis.  first chromosome (1q23).
  16. 16. FACTOR VII (STABLE OR PROCONVERTIN)  Vitamin K-dependent Serine Protease.  Activates factors IX and X simultaneously with tissue factor in the extrinsic pathway.  Deficiency is rare (congenital Proconvertin deficiency) and inherits recessively.  The gene for factor VII is located on the thirteenth chromosome (13q34).
  17. 17. FACTOR VIII ANTI-HEMOPHILIC FACTOR (AHF).  It is a cofactor in the activation of factor X to FXa, which is catalyzed by factor IXa in the presence of calcium and phospholipids.  Mutations in the factor VIII gene results in HEMOPHILIA A.  CLASSICAL HEMOPHILIA, an X-linked recessive coagulation disorder.  The gene for factor VIII is located on the long arm of X chromosome (Xq28).
  18. 18. FACTOR IX ( CHRISTMAS FACTOR)  It is a proenzyme serine protease, which in the presence of calcium activates factor X.  Deficiency cause Hemophilia B or Christmas disease.  High antigen or activity levels of factor IX is associated with an increased risk of thromboembolism.  X chromosome (Xq27).
  19. 19. FACTOR X ( STUART-PROWER FACTOR)  Both intrinsic and extrinsic pathway of blood coagulation.  Factor X is activated to FXa by factors IX and VII.  It is the first member of the common pathway of blood coagulation. FXa cleaves prothrombin to thrombin.  Deficiency :Bleeding diathesis and hemorrhages.  The gene for factor X is located on the thirteenth chromosome (13q32).
  20. 20. FACTOR XI / PLASMA THROMBOPLASTIN ANTECEDENT  It is a serine protease zymogen which is activated to factor XIa by factor XIIa.  Hemophilia C.  Individuals with severe deficiency do not show excessive bleeding conditions and hemorrhage normally occurs after trauma or surgery.  Gene in chromosone 4
  21. 21. FACTOR XII /HAGEMAN FACTOR .  Zymogen form of factor XIIa, which activates factor XI and Prekallikrein.  Deficiency does not cause excessive hemorrhage due to lack of involvement of factor XIIa in thrombin formation.  Increases the risk of thrombosis, due to inadequate activation of the fibrinolytic pathway.  Long arm of the fifth chromosome (5q33).
  22. 22. FACTOR XIII ( FIBRIN STABILIZING FACTOR)  Composed of two subunits- Alpha (A) and Beta (B).  Activated by thrombin into factor XIIIa in presence of calcium.  Forms ε-(γ-glutamyl)-lysyl bonds between the fibrin chains & stabilizes the blood clot.  Reduces the sensitivity of the clot to degradation by proteases.  Genetic defects in the factor XIII gene leads to life long bleeding diathesis.  F13A is located on the sixth chromosome (6p24).  F13B gene is located on the long arm of first chromosome (1q32).
  23. 23. VON WILLEBRAND FACTOR (vWF)  Binding of platelets to the site of injury by forming a bridge between collagen matrix and platelet-surface receptor complex.  Hereditary or acquired defects of vWF lead to von Willebrand disease  The gene for vWF is located on short arm of the twelfth chromosome.
  24. 24. Kallikrein is a serine protease. Inactive form called prekallikrein kallikrein by factor XIIa. High-molecular-weight kininogen (HMWK) is also called as the Williams- Fitzgerald-Flaujeac factor. It is enzymatically inactive and functions as a cofactor for the activation of kallikrein and factor XII
  25. 25. Plasminogen is a glycoprotein which circulates as proenzyme. It is converted to plasmin by tissue plasminogen activator in the presence of a fibrin clot. Dissolve the fibrin of blood clots. Wound healing and the maintenance of liver homeostasis.
  26. 26. INHIBITORS: ANTITHROMBIN III/ANTITHROMBIN Natural inhibitor of the activated serine proteases of the coagulation system. Inhibits factors Xa, IXa and thrombin. PROTEIN C is a serine protease enzyme. Its function is to inactivate factors Va and VIIIa. It is activated by thrombin to activated protein C (APC). APC along with protein S degrades factors Va and VIIIa.
  27. 27. Protein S -Vitamin K-dependent plasma glycoprotein. Cofactor to protein C, thus enhancing the inactivation of factors Va and VIIIa . Protein Z : Degradation of factor Xa. Heparin cofactor II - Serine protease inhibitor. Inhibits thrombin and factor X.
  29. 29. TEST NORMAL RANGE Bleeding time Clotting time <7 min 4 – 9 min Prothrombin time/ international normalised ratio PT: 11-13 s/INR 1.0 Activated partial thromboplastin time 15 – 30 s Thrombin time 3 – 6 s Fibrin degradation products < 10 µg/dL Fibrinogen assay 200 – 400 mg/dL Von Willebrands antigen 60 – 150% v WF activity Coagulation factor assay 60 – 100% F VIII ACTIVITY DIAGNOSTIC TESTS
  31. 31. FACTOR I DEFICIENCY Factor I deficiency is an umbrella term for several related disorders known as congenital fibrinogen defects.  Afibrinogenemia  Hypofibrinogenemia  Dysfibrinogenemia
  32. 32. Hypodysfibrinogenemia is a combined defect that involves both low levels of fibrinogen and impaired function. Afibrinogenemia : Autosomal recessive disorder Hypofibrinogenemia, dysfibrinogenemia and hypodysfibrinogenemia Recessive or dominant . Males and females.
  33. 33. SYMPTOMS OF AFIBRINOGENEMIA • Nosebleeds (epistaxis) • Easy bruising • Menorrhagia • Muscle bleeds • Cutaneous ecchymoses and hematomas
  34. 34. •Bleeding from the umbilical cord stump at birth • Bleeding in the mouth, particularly after dental surgery or tooth extraction •Gingival bleeding • Abnormal bleeding during or after injury, surgery •Problems during pregnancy
  35. 35. HYPOFIBRINOGENEMIA Symptoms are similar to those seen in afibrinogenemia. DYSFIBRINOGENEMIA • Symptoms depend on how the fibrinogen (which is present in normal quantities) is functioning. • Bleeding (similar to those seen in afibrinogenemia) • Signs of thrombosis (abnormal blood clots in blood vessels) instead of bleeding. HYPODYSFIBRINOGENEMIA Symptoms are variable and depend on the amount of fibrinogen that is produced and how it is functioning.
  36. 36. TREATMENT:  Fibrinogen concentrate  Cryoprecipitate  Fresh frozen plasma (FFP)
  37. 37. FACTOR II (PROTHROMBIN) DEFICIENCY/ HYPOPROTHROMBINEMIA • Autosomal recessive disorder • Males and females. • Very rare • Inherited bleeding disorder • It can also be acquired later in life as a result of liver disease, vitamin K deficiency, or certain medications such as Coumadin. • Acquired factor II deficiency is more common.
  38. 38. SYMPTOMS • Epistaxis • Easy bruising • Menorrhagia • Hemarthrosis • Muscle bleeds • Bleeding in the mouth, particularly after dental surgery or tooth extraction • LAB FINDINGS: P rothrombin time is increased.
  39. 39. TREATMENT  MADE FROM HUMAN PLASMA. • Prothrombin complex concentrate (PCC) • Fresh frozen plasma (FFP)  ANTIFIBRINOLYTIC DRUGS.
  40. 40. FACTOR V DEFICIENCY  Inherited bleeding disorder  PARAHEMOPHILIA  Autosomal recessive disorder.  Affects both males and females.  Rare LAB FINDINGS: Clotting and Prothrombin time prolonged
  41. 41. SYMPTOMS  Epistaxis  Easy bruising  Menorrhagia  Bleeding in the mouth  Bleeding in the gut  Gingival bleeding  Cutaneous ecchymoses and hematomas  Intraocular and CNS hemorrhages. TREATMENT :Fresh frozen plasma, platelet transfusions
  42. 42. COMBINED FACTOR V AND FACTOR VIII DEFICIENCY  Combined factor V and factor VIII deficiency is an inherited bleeding disorder.  Autosomal recessive disorder.  Affects both males and females.  Rare  Normally the disorder is caused by a single gene defect that affects the body’s ability to transport factor V and factor VIII outside the cell and into the bloodstream, and not by a problem with the gene for either factor.
  43. 43. SYMPTOMS • Skin bleeding • Menorrhagia • Bleeding in the mouth • Abnormal bleeding during or after injury, surgery, or childbirth TREATMENT: Desmopressin Factor VIII concentrate Fresh frozen plasma
  44. 44. FACTOR VII DEFICIENCY • Inherited bleeding disorder . • Produces less factor VII • Autosomal recessive disorder • Rare. • It can also be acquired later in life as a result of liver disease, vitamin K deficiency, or certain medications such as Coumadin.
  45. 45. SYMPTOMS • Nosebleeds (epistaxis) . • Easy bruising . • Menorrhagia. • Bleeding in the mouth, particularly after dental surgery or tooth extraction. • Bleeding in the head (newborns) . TREATMENT: • Recombitant factor VII • Prothrombin complex conc. factor VII • Factor VII conc • Fresh frozen plasma
  46. 46. FACTOR VIII DEFICIENCY (Bleeder s disease, disease of Hapsburg,Disease of Kings)  Hemophilia A - most common hereditary disease associated with factor VIII  Reduction in the amount or activity of factor VIII.  This protein serves as a cofactor for factor IX in the activation of factor X in the coagulation cascade  Hemophilia A is inherited as an X-linked recessive trait  Occurs in males.
  47. 47. Genetic abnormality includes: • Deletion of variable size • Abnormalities of stop codon • Frame shift defects • 45% of severe Hemophilia A results from inverse mutation
  48. 48. ETIOLOGY AND PATHOGENESIS OF HEMOPHILIA FACTOR IX a activates Factor X in the presence of Factor VIII a , phospholipids, activated platelets and calcium. Factor X a converts prothrombin to thrombin In patients with HEMOPHILIA the clot formation is delayed as thrombin generation is markedly decreased.
  50. 50. CLINICAL FEATURES: • Bleeding into muscle, degeneration & contracture of the muscle. • Compression of the peripheral nerve by large haematoma peripheral nerve lesions. • Haemophilic cysts & pseudotumour is common in pelvic & knee region enlarge & sometime erode through skin & cause ulceration on the skin. • Haematuria is common in severe haemphilia. Bilateral obstruction by clots acuteoliguric renal pain. • Spontaneous intracranial & intraspinal haemorrhage is common
  51. 51. Retroperitoneal and mesentric bleeding Gastrointestinal bleeding Epistaxis Menorhhagia Oral Manifestation: Oral hematoma Bleeding gums during tooth shedding Bleeding after extraction Palatal and tongue purpura Ecchymosis TMJ hemarthrosis Mandibular pseudo tumour
  52. 52. Muscle hematoma (pseudotumor) Hemarthrosis (joint bleeding) COMPLICATIONS OF HEMOPHILIA
  53. 53. Claw hand deformity of hand Atrophy of muscles
  54. 54. LABORATORY FINDINGS: Prothrombin time is normal Clotting time prolongd APTT is prolonged Specific assay for factorVIII lowered activity Treatment: Desmopressin Cryoprecipitate Fresh frozen plasma Factor VIII concentrate Antifibrinolytics
  55. 55. HAEMOPHILIA – B 1X DEFICIENCY (Christmas Disease/ Plasma thromboplastin component deficiency)) • Christmas disease is a congenital sex-linked disorder due to absence reduction or functional abnormality of factor IX • Incidence 1 per 50,000 male • Clinical features are same as Haemophilia – A • Factor IX coagulation activities is reduced or absent. • X linked disorder • Occurs one fifth as frequently as hemophilia A • Prolonged APTT level • Bioassay of Factor IX has lowered activity
  56. 56. FACTOR X DEFICIENCY  Inherited bleeding disorder  Autosomal recessive disorder  Males and females.  Rare TREATMENT Prothrombin complex concentrate containing factor X. Fresh frozen plasma.  Antifibrinolytic drugs.
  57. 57. FACTOR XI DEFICIENCY  Hemophilia C  Autosomal recessive  Both sexes  Resembles mild to moderate haemophilia  Rare  No bleeding into joints and muscles.
  58. 58. FACTOR XII DEFICIENCY: •Absence of clinical haemorrhage •Prolonged coagulation time •Prolonged APTT •Discovered on routine laboratory testing •No treatment required
  59. 59. FACTOR XIII DEFICIENCY: •Congenital deficiency •Clinical findings similar to mild to moderate haemophilia •Characteristic feature: bleeding from umbilical stump after birth •Acquired form seen in hepatic failure, inflammatory bowel disorder •Healing of wounds poor •BT, CT is normal •XIII α and XIII β antigen level by ELISA technique TREATMENT: Fresh frozen plasma, factor XIII concentrate
  60. 60. FLETCHER FACTOR AND FLITZGERALD FACTOR: •Show similar laboratory abnormalities •No clinical significance •Rare
  61. 61. von Willebrand’s Disease (vWD)(Pseudohemophilia, Vascular purpura) Composite of two disorders: 1. An inherited disorder of platelet adhesion, which involves a deficiency and or a qualitative defect in von Willebrand’s tissue factor (vWF) 2. Deficient or low levels of Factor VIII. Hence, this bleeding disorder leads to “a combined defect in platelet plug formation and fibrin formation.” •Most common disorder •Autosomal dominant •Affects both sexes
  62. 62. Classification of von Willebrand disease • Type 1 vWD- the most common variant • autosomal dominant in inheritance • normal vWF in structure and function but decrease in quantity- range 25- 50% of normal • Type 2 vWD • autosomal dominant in inheritance • vWF is abnormal in structure and/or function • Type 3 vWD • autosomal recessive in inheritance • the most severe form characterized by very low or undetectable level of vWF
  63. 63. Von-Willebrand’s disease It is a autosomally transmitted congenital haemorrhagic disorder in which there is prolongation of bleeding time in addition to reduction of factor VIII coagulation activity.
  64. 64. Clinical manifestations: •Asymptomatic •Epistaxis •Mucous membrane bleeding •Gingival bleeding •Menorrhagia •Echymosis LABORATORY FINDINGS: •Prolonged bleeding count •Reduced plasma vWF concentration •Defective platelet aggregation with ristocetin •Reduced Factor VIII activity
  65. 65. TREATMENT: •Desmopressin •Cryoprecipitate •Fresh frozen plasma
  66. 66. Acquired coagulation disorders may occur due to one of the following causes. • Vit-K deficiency • Liver diseases • Anticoagulant therapy • Disseminated intravascular coagulation • Acute primary fibrinolysis • Circulating inhibitors of coagulation
  67. 67. VITAMIN K DEFICIENCY: • VIT K deficiency occurs in 3 disorders: DISORDERS THAT IMPAIR FAT ABSORPTION • Obstructive jaundice and biliary fistula • Coeliac disease , pancreatic disease and related disoders STERILISATION OF THE BOWEL BY ANTIBIOTIC DRUGS • Caused due to combined effects of low diet and vit k • Loss of the normal bowel flora which synthesises the vitamin.
  68. 68. HAEMORRHAGIC DISEASE OF THE NEWBORN • Occurs during the first few days of life Causes: • Reduced stores of Vit K • Functional immaturity of the liver • Lack of bacterial synthesis of Vit K • Ingestion of oral anticoagulants and anticonvulsants by the mother.
  69. 69. LABORATORY FINDINGS: Decreased plasma levels of Vit K dependent factors. Prolonged PT Prolonged APTT TREATMENT: Parental administration of Vit K
  70. 70. L IVER DISEASES: LIVER: •Major site for synthesis and metabolism of clotting factors •Produces inhibitors •Helps in clearance of activated factor and fibrinolytic enzymes FACTORS THAT CONTRIBUTE TO HAEMOSTATIC DEFECT IN LIVER DISEASES: • Defective synthesis of coagulation factors • Thrombocytopenia • Increased fibrinolytic activity • Intravascular coagulation
  71. 71. LAB FINDINGS: •Prolonged PT and APTT •Mild thrombocytopenia •Decreased hepatic stores of Vit K TREATMENT: •Fresh frozen plasma, •EACA to be administered •Transfusion of plasma and platelet conc.
  72. 72. HAEMORRHAGIC DISORDERS DUE TO CIRCULATING INHIBITOR OF COAGULATION Circulating natural inhibitors : Ig heavy chain class activity directed against a coagulation protein 2 MAJOR TYPES OF INHIBITORS Congenital haemophilia or congenital coagulation disorder Acquired or in the course of some other disease state Lupus inhibitor does not normally cause bleeding tendencies but clinical expression is paradoxically a striking tendency to thrombosis. Rare in occurence
  73. 73. LAB FINDINGS: Prolonged PT, APTT TREATMENT: Blood transfusion Doses of concentrate of appropriate factors Immunosuppressives
  74. 74. DISSEMINATED INTRAVASCULAR COAGULATION: (DEFRIBRINATION SYNDROME/CONSUMPTION COAGULOPATHY) A hemorrhagic disorder in which diffuse intravascular cloting causes a hemostatic defect resulting from utilisation of coagulation factors and platelets in the clotting process. ETIOLOGY: 1. Infections Acute DIC: Bacteria and their toxins, fungi, viruses, Chronic DIC: Any chronic infection (eg, tuberculosis, abscesses, osteomyelitis) 2. Noninfectious inflammatory diseases Inflammatory bowel disease: Crohn's disease and similar disorders 3. Obstetrical complications Acute DIC: Abruptio placentae, abortions ,amniotic fluid embolism, hemorrhagic shock Chronic DIC: Dead fetus syndrome
  75. 75. 4. Malignancy Acute DIC: Acute promyelocytic leukemia, acute myelomonocytic or monocytic leukemia, disseminated prostatic carcinoma Chronic DIC: Lung, breast, gastrointestinal malignancy 5. Vascular disease Acute DIC: Brain infarction or hemorrhage Chronic DIC: Aortic aneurysm, giant hemangioma 6. Venoms Acute DIC: Snake, spider (rare) 7. Trauma Acute DIC: Massive tissue destruction, brain damage 8. Others Acute DIC: Heparin-induced thrombocytopenia with thrombosis (HITT),
  77. 77. CLINICAL FEATURES: •Bleeding: localised or generalised •Organ damage: due to ischaemia in kidney and brain • Microangiopathic hemolytic anemia and thrombosis LAB FINDINGS: •Platelet low •PT,TT, APTT all prolonged •Plasma fibrinogen level are reduced •Fibrin degradation products raised TREATMENT: •Elimination of precipitating factor •Replacement of coagulation factors and platelets •Inhibition of clotting process: Heparin, EACA , aprotinin
  78. 78. ANTICOAGULANT DRUGS: Heparin : Inhibits formation of thromboplastin and the action of thrombin Vit k antagonists: coumarin and indanedione derivatives: suppress the synthesis of active Vit K dependent clotting factors. These drugs can cause hypersensitivity reaction or an overdose can cause clotting disorder.
  79. 79. . POTENTIATING INHIBITING Salicylates Barbiturates Sulindac Carbamazepine Phenylbutazone Chloral hydrate Indomethacine Griseofulvin Sulphonamides Sprironolactone Amiodarone Cimetidine FACTORS THAT INTERFERE WITH CONTROL OF ORALANTICOAGULANT THERAPY: DRUGS
  81. 81. FIBRINOLYTIC DEFECTS: Fibrinolysis consisting of plasminogen – plasmin and fibrin degradation products Essential protective physiologic mechanism to limit blood coagulation in the body. Excessive fibrinolysis leads to bleeding Causes of primary pathologic fibrinolysis leading to haemorrhagic defects: def of α 2 plasmin inhibitor following trauma and surgery Impaired clearance of tissue plasminogen activator such as in liver cirrhosis.
  82. 82. LAB FINDINGS: •Decreased fibrinogen •Increased FDP TREATMENT: •Fresh frozen plasma •Antifibrinolytics
  83. 83. CONSIDERATIONS FOR DENTAL TREATMENT The most important objective is the prevention of complications. The following principles apply in this sense: 1. Identification of the patient based on a thorough clinical history 2. Counseling 3. Consultation with the specialist to determine the type of congenital disorder 4. Replacement therapy in necessary cases. Replacement may comprise coagulation factors (hemophilia A and B, and vW disease) or vitamin K (lack of ingestion or poor absorption and liver disease) 5. Avoidance of brusque maneuvers during dental treatment
  84. 84. 6. Evaluation of the advisability of hospital admission when complex surgery is required. 7. Aspirin and its derivatives are to be avoided as pain treatment. In this sense, paracetamol is a safe alternative. 8. Reabsorbable sutures. 9. Local haemostatic measures. 10. Avoid regional block injections.
  85. 85. RECENT ADVANCES The quick development and commercialization of recombinant clotting factors was facilitated by the catastrophic impact of viral contamination of plasma-derived clotting factor concentrates . Since their transition into the clinic, the recombinant versions of both factor VIII and IX have proven to be remarkable facsimiles of their plasma derived counterparts. ( Recombinant clotting factor Steveen W. PipThromb Haemost 2008; 99: 840– 850)
  86. 86. Presumptive diagnosis of factor XIII deficiency was by clot solubility test in 5M urea or 1% monochloroacetic acid environments. In patients with abnormal screening clot solubility test, the disease can be confirmed by more specific tests such as quantitative factor XIII activity assay andFXIIIAg assay. M Naderial Current understanding in diagnosis and management of factor XIII deficiency, Iran J Ped Hematol Oncol. 2013; 3(4): 164–172.
  87. 87. Family studies were performed and molecular analysis, using a Short Tandem Repeat (STR) marker closely linked to the factor XIII A subunit gene, allowed antenatal exclusion diagnosis to be undertaken in a subsequent pregnancy. C. Killick, C. Barton, S.Aslam and G.Standen Prenatal diagnosis in factor XIII-A deficiency Arch Dis Child Fetal Neonatal Ed. 1999 May; 80(3): F238–F239.
  88. 88. REFERENCES • Shafer’s Text Book Of Oral Pathology 7th Edition • Neville Oral And Maxillofacial Pathology 3rd Edition • Guyton’s Text Book Of Medical Physiology 11th Edition • Review of Medical Physiology: Ganong.21st Edition • Robbin’s Basic Pathology 7th Edition • Davidsons Principles And Practice Of Medicine 20th Edition • Burket’s Oral Medicine Diagnosis And Treatment 10th Edition
  89. 89. • Harrison’s Principle Of Internal Medicine 18th Edition • De Gruchys Clinical Hematology In Medical Practice 6th Edition • Practical Haematology: Dacie and Lewis 11th Edition • Wintrobe’s Clinical Hematology 12th Edition • James P. Riddel Jr, MS, RN,et AL Theories of Blood Coagulation Journal of Pediatric Oncology Nursing, Vol 24, No 3 (May-June), 2007: 123-131 • What are rare clotting factor deficiencies? WHF
  90. 90. • Godkars Text Book Of Medical Laboratory Technology 2nd Edition • Jover-Cervero A, Poveda-Roda R, Bagan JV, Jimenez-Soriano Y. Dental treatment of patients with coagulation factor alterations: An update. MedOral Patol Oral Cir Bucal 2007 • Hematology Clinical hemostasis review / July-August 2004 • Dental Management of Patients with Bleeding Disorders. Sandra D’Amato-Palumbo, RDH, MPS Continuing Education Units.

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