Physiology of blood ppt

blood ppt dental

1. BLOOD PHYSIOLOGY By Dr MILIND RAJAN MDS PEDIATRIC DEPARTMENT CIDS VIRAJPET

2. Introduction Properties Functions Composition Plasma Erythrocytes Leukocytes Platelets Conclusion References CONTENTS

3. PROPERTIES 8% of body weight Colour : Red Volume : approximately 5 L ph : 7.4 ± 0.5 Specific Gravity : 1.052 to 1.061 Viscosity : 5 times more than water

4. FUNCTIONS Nutritive Respiratory Excretory Transport of hormones and enzymes Regulation of water balance Regulation of acid base balance Regulation of body temperature Storage function Defensive function

5. COMPOSITION

6. PLASMA

7. PLASMA PROTEINS Albumin : 55% Globulin : 38% Fibrinogen : 7%

8. 19- 9 Plasma Liquid part of blood Pale yellow made up of 91% water, 9% other Colloid : Liquid containing suspended substances that don’t settle out Albumin : Important in regulation of water movement between tissues and blood Globulins : Immune system or transport molecules Fibrinogen : Responsible for formation of blood clots

9. 19- 10 Formed Elements Red blood cells ( erythrocytes ) White blood cells ( leukocytes ) Granulocytes Neutrophils Eosinophils Basophils Agranulocytes Lymphocytes Monocytes Platelets ( thrombocytes )

10. FUNCTIONS OF PLASMA PROTEINS Coagulation of blood Immune function Transport function Maintain colloidal osmotic pressure Maintain acid-base balance in the body Maintain viscosity of blood Provides stability to blood

11. ERYTHROCYTES

12. Red blood cells Count - 4-5.5millions/cu mm of blood Shape -disk shaped, biconcave, central portion is thinner and periphery is thicker Diameter - 7.5u Thickness – 2.2u at periphery 1u at the centre. Rouleaux formation- Lifespan- about 120 days

13. E rythropoiesis It is the process of origin, development and maturation of erythrocytes In the early weeks of embryonic life, primitive, nucleated red blood cells are produced in the yolk sac . During the middle trimester of gestation in the liver Up to age of 20 years-RBC’S are produced from red bone marrow of all bones After the age of 20 years-produced from membranous bone like vertebra, sternum, ribs, scapula, iliac bones, skull bones

14. ERYTHROPOIESIS

15. FACTORS

16. GENERAL FACTORS Erythropoietin Thyroxine Hemopoietic Growth factors : IL-3,IL-6,IL-11 Colony stimulating factors Vitamins B, C, D

17. MATURATION FACTORS Vitamin B 12 ( Cynacobalamine ) Iron Folic acid

18. FACTORS FOR H b FORMATION Proteins and amino acids : globin Iron : heme Copper Cobalt and nickel Vitamins

19. HEMOGLOBIN Red O 2 carrying chromoprotein Birth : 22 - 25 gm% Males : 14 -18 gm% Female : 12 - 15.5 gm% Types of hemoglobin HbA HbF

20. Structure of hemoglobin Iron porphyrin globin Ferrous form ( F e++) pigment part Contain 4 polypeptide chains 2 alpha 2 beta

21. Hemoglobin synthesis

22. DESTRUCTION OF HEMOGLOBIN Iron porphyrin globin Utilisesd for resynthesis of Hemoglobin Stored as ferritin and hemosiderine Reutilised for synthesis of new Hemoglobin biliverdin bilirubin

23. Fate of Hemoglobin Erythrocytes

24. FUNCTIONS Transport of gases. Hb acts as an acid- base buffer.

25. E.S.R Rate at which the red blood cells settle down Male : 3-7 mm/hr Female : 5-9 mm/hr

26. PACKED CELL VOLUME Hematocrit value expressed as the percentage of cellular elements with that of whole blood. Males : 40-45% Female : 38-42%

27. Red Cell Indices Packed cell volume (PCV) Mean corpuscular volume (MCV) PCV x 10/ No. of RBCs per cu. mm. Normal value – 80 to 90 μ 3 Mean corpuscular hemoglobin (MCH) Hb in gm/lt/RBC count Normal value – 30 pg Mean corpuscular hemoglobin concentration (MCHC) Hb (in gm%) x 100 / PCV Normal value – 31 – 35 gm% Erythrocytes

28. LEUKOCYTES

29. LEUKOCYTES Colourless nucleated formed element WBC count : 4000-11,000/mm 3

30. LEUKOPOIESIS

31. PROPERTIES Diapedesis Ameboid movement Chemotaxis Phagocytosis

32. FUNCTIONS Defence of the body Inflammation and acute hypersensitivity reactions Immunity

33. NEUTROPHILS 50-70%

34. GRANULOCYTES-WITH GRANULES Neutrophils – also known as polymorphs multilobed , 2-5 lobes 50-70 % , 10-12u diameter chemotaxis or cell mobilisation phagocytosis life span-2-5 days Neutrophil leukocytosis - increase in neutrophils above 7500/ ul Acute infections Acute haemorrhage malignancies Neutropenia-count falls below2500/ ul Infections- typhoid,influenza,measels,malaria Pernicious anaemia Anaphylactic shock

35. EOSINOPHILS 2-4 %

36. FUNCTIONS Major functions- detoxification,disintigration and removal of foreign proteins. prevents hypersensitivity to antigen antibody complexes ( anti allergic role ) Act against parasites

37. BASOPHILS 0-1 %

38. FUNCTIONS Healing after inflammation and acute hypersensitivity reactions

39. MONOCYTES 2-6 %

40. FUNCTIONS forms tissue macrophages and act as scavenger. Constitute the first line of defence.

41. LYMPHOCYTES 20-30 %

42. FUNCTIONS Immunity Cell mediated - T lymphocytes Humoral - B Lymphocytes

43. PLATELETS Small non-nucleated mass of protoplasm 2 – 4 µm Inactive : Disc like structure Active : Spherical Normal : 1.5 – 4 lakhs / mm 3 Critical count : < 40,000/ mm 3

44. MORPHOLOGY OF PLATELETS Membrane Structure

45. Microscopic structure

46. THROMBOPOESIS One megakaryocyte : 1000 – 1500 platelets

47. FACTORS IL-3, IL-6, IL-11, Cytokines, Colony stimulating factors Thrombopoietin TGF- β Life span : 8 -12 days Destruction : Spleen

48. PROPERTIES

49. FUNCTIONS Blood clotting Clot retraction Hemostasis Repair of ruptured blood vessels Defence mechanism

50. Hemostasis Haemostasis is prevention of blood loss Stages of haemostasis- Vasoconstriction Platelet plug formation Coagulation of blood

51. Hemostasis

52. Injury to the blood vessel and damage of endothelium Exposure of collagen Adherence of platelets to collagen Activation of platelets Secretion of serotonin Secretion of ADP and thromboxane A2 Formation of prothrombin activator Aggregation of platelets Formation of platelet plug vasoconstriction Blood clotting stage1 Stage 2 Stage 3

53. HEMOSTASIS Spontaneous arrest or prevention of bleeding by physiological processes

54. Primary hemostasis Entails platelet plug formation and lasts for 2–3 seconds . Predominant mechanism in capillaries and small-diameter vessels Secondary hemostasis Associated with fibrin synthesis and its deposition Provides stabilization of the hemostatic clot

55. CLOTTING FACTORS FACTORS NAME I Fibrinogen II Prothrombin III Thromboplastin IV Calcium V Proaccelerin , Labile factor VII Stable factor, Proconvertin VIII Antihaemophilic factor (AHF), IX Christmas factor X Stuart – Prower factor XI Plasma thromboplastin antecedent XII Hageman factor XIII Fibrin stabilizing factor

56. COAGULATION PHASE

57. Coagulation of blood Coagulation or clotting is defined as the process in which blood looses its fluidity and becomes a jelly like mass . stages Formation of prothrombin activator Conversion of prothrombin into thrombin Conversion of fibrinogen into fibrin Formation of prothrombin activator occurs through 2 pathways (1) by the extrinsic pathway that begins with trauma to the vascular wall and surrounding tissues and (2) by the intrinsic pathway that begins in the blood it self, initiated by platelets

58. Extrinsic Pathway Tissue factor dependent pathway Acts rapidly Produces a small quantity of thrombin, triggering the initiation of the intrinsic pathway

59. Intrinsic pathway Initiated when Factor XII is activated with surface contact Occurs more slowly Common pathway The steps in clotting after formation of activated factor X are the same in both pathways.

60. Intrinsic pathway

61. Extrinsic pathway

62. 19- 64 Determined by antigens ( agglutinogens ) on surface of RBCs Antibodies ( agglutinins ) can bind to RBC antigens, resulting in agglutination ( clumping ) or hemolysis ( rupture ) of RBCs Groups ABO and Rh Blood Grouping

63. BLOOD GROUPS ABO System Rh system Lewis system MNS system P system Kell system Duffy system Lutheran system

64. 19- 66 ABO Blood Groups

65. 19- 67 Agglutination Reaction

66. Rh BLOOD GROUP SYSTEM 6 types Of Rh Antigen i.e. Rh Factor C,D,E,c,d,e Type D : most prevalent and most antigenic. If D antigen present : Rh Positive If D antigen absent : Rh Negative

67. BLEEDING TIME Duke method The test is timed from the start of bleeding until bleeding is completely stopped Normal – Within 8 mins

68. Ivy method Normal : 1-6 mins

69. Increased bleeding time is associated with: Thrombocytopenic purpura Auto immune disease Vascular defects Coagulation defects Decreased platelet count

70. PROTHROMBIN TIME Prothrombin Time (PT) Increased in deficiency in extrinsic and common pathway Normal : 11-14 seconds PT is prolonged with: deficiencies of factors II, V, VII, X or fibrinogen liver disease Vitamin K deficiency Warfarin use

71. INTERNATIONAL NORMALIZED RATIO WHO, 1983 Measure of the extrinsic pathway of coagulation. Determines the clotting tendency of blood, in the measure of warfarin dosage, liver damage and vitamin K status. Normal range - 0.8-1.2

72. Increase INR= increase bleeding risks INR : < 3.0 : Infiltration anesthesia , scaling and root planing INR : < 2.0 - 2.5 : Block anesthesia , minor periodontal surgery, simple extractions INR : < 1.5 - 2.0 : Complex surgery or multiple extractions

73. ACTIVATED PARTIAL THROMBOPLASTIN TIME aPTT is prolonged only when the factor levels in the intrinsic and common pathways are < 30%. The values are altered Hemophilias A and B with the use of the anticoagulant heparin. Normal : 25-40 secs

74. CLOTTING TIME It measures all stages of coagulation in the intrinsic system. Method: Lee & White method, Wright’s capillary tube method. Normal range: within 10 minutes

75. RED BLOOD CELL DISORDERS

76. POLYCYTHEMIA Abnormal increase in erythrocyte count in peripheral blood, usually accompanied by an increase in hemoglobin and hematocrit

77. POLYCYTHEMIA VERA Myeloproliferative disorder After 50 years of age. Etiology : unknown / acquired genetic changes

78. ORAL MANIFESTATIONS A purplish red discoloration of the oral mucosa Gingiva : red bleed spontaneously Petechiae and ecchymoses Exaggerated Varicosities in the ventral tongue

79. DENTAL CONSIDERATIONS Complete blood count prior to treatment Hemoglobin < 16 g/ dL Hematocrit < 47% Local hemostasis

80. ANEMIA Abnormal reduction in the number of circulating red blood cells, the quantity of hemoglobin and the volume of packed red cells in a given unit of blood.

81. CLASSIFICATION

82. IRON DEFICIENCY ANEMIA Iron deficiency anemia : hypochromic microcytic ETIOLOGY Chronic blood loss Inadequate dietary intake Faulty iron absorption Increased requirements

83. ORAL MANIFESTATIONS Angular chelitis Pallor of the mucosa Atrophy of oral epithelial cells Atrophy of the filiform and fungiform papillae Glossodynia

84. DENTAL CONSIDERATIONS Consultation with physician Complete blood count (CBC) with differential. Elective oral surgical or periodontal procedures Hb < 10 g/ dL low oxygen tension interactions between the cellular components of blood decreasing their ability to clot effectively. General anaesthesia : not administered unless the hemoglobin is at least 10 g/ dL .

85. PLUMMER-VINSON SYNDROME Iron deficiency anemia, glossitis , ulceration of oral mucosa and oropharynx inducing dysphagia

86. HEMOLYTIC ANEMIA The hemolytic anemias : normocytic,normocromic Decreased survival of erythrocytes, either episodically or continuously

87. ORAL MANIFESTATIONS Pallor of oral mucosa Jaundice : Best seen in the sclera, but the skin, soft palate, tissues of the floor of the mouth also become icteric . Chronic increased erythropoietic activity and marrow hyperplasia : dental radiographs.

88. SICKLE CELL ANEMIA Autosomal recessive disorder

89. ORAL MANIFESTATIONS Pallor and jaundice Delayed eruption and hypoplasia of the dentition Ladderlike pattern “Hair on end” appearence

90. DENTAL CONSIDERATIONS Elimination of oral sources of infection - infection can precipitate an aplastic crisis. Periodontal infections can precipitate sickle cell crisis. General anaesthesia should be used with caution

91. THALASSEMIA Deficient synthesis of α or β chains of globin . Microcytic and hypocromic

92. ORAL MANIFESTATIONS Bimaxillary protrusion & other occlusal abnormalities - thalassemia major Poor spacing of teeth, a marked open bite, prominent malar bones, saddle nose. Pneumatization of the maxillary sinuses is delayed. “Chipmunk facies .”

93. Radiographic changes : generalized rarefaction of the alveolar bone thinning of cortical bone enlarged marrow spaces coarse trabeculae P arietal bones- “hair on end” appearance.

94. MEGALOBLASTIC ANEMIAS Impaired DNA synthesis Maturation of nucleus delayed relatively to that of cytoplasm

95. PERNICIOUS ANEMIA

96. ORAL MANIFESTATIONS “Beefy red tongue” Hunter’s / Moeller’s glossitis Erythematous macular lesions involving buccal and labial mucosa. Dysphagia and taste aberrations Discomfort by denture wearers Burning mouth sensation due to a neuropathy

97. FOLIC ACID DEFICIENCY ANEMIA Oral manifestations Angular cheilitis Ulcerative stomatitis Pharyngitis Severe cases

98. APLASTIC ANEMIA Aplastic anemia : normochromic normocytic Bone marrow failure Cause is frequently unknown Term “ anemia ” : a misnomer Pancytopenia

99. ORAL MANIFESTATIONS Pale discoloration of oral mucosa Increased susceptibility to infections Bleeding from gingival margin ( Alty 1962, Stamps 1974 ) Severe periodontal destruction ( Stamps 1974 )

100. FANCONI ANEMIA Brown skin pigmentation Hypoplasia of the kidney and spleen Absent or hypoplastic thumb or radius Microcephally Mental and sexual retardation Several teeth lost, severe bone loss, pockets > 10mm, blue red gingiva , bleeding on probing, suppuration ( Opinya et al, 1988 )

101. DENTAL CONSIDERATIONS Two major problems : Infection Bleeding

102. LEUKOCYTES DISORDER

103. WBC DISORDERS

104. GRANULOCYTOPENIA Absolute reduction in the number of circulating WBCs Results from a decrease in neutrophils, and most cases of granulocytopenia are known as neutropenia . The degree of neutropenia predicts the risk of serious bacterial infections.

105. NEUTROPENIA Normal absolute number of neutrophils in the peripheral blood : 3000/mm 3 - 6000/mm 3

106. NEUTROPENIA Associated with periodontal problems Cyclic neutropenia Chronic benign & severe familial neutropenia Chronic idiopathic neutropenia

107. AGRANULOCYTOSIS Reduction in the number of circulating granulocytes Often restricted to a syndrome characterized by extremely severe neutropenias fever malaise ulceration and necrosis of tissues

108. AGRANULOCYTOSIS 1922 : Werner Schultz : Syndrome of unknown cause in a middle aged old women Agranulocytosis Fulminate form of severe neutropenia : “ Schultz disease ”

109. AGRANULOCYTOSIS Medication that interferes with cell formation or enhances cell destruction Drug idiosyncrasy

110. Oral changes in leukemia bleeding,petechiae,ecchymosis,ulcer,gingival hyperplasia & bone resorption Generalized gingival swelling, mostly involving interdental papilla .

111. ORAL & DENTAL CONSIDERATIONS Ulceration of the oral mucosa Neutropenic ulcers Isolated necrotic black and gray patches

112. ORAL & DENTAL CONSIDERATIONS Fetid odor Gingival margin may or mat not be involved Gingival hemorrhage, necrosis, increased salivation

113. ORAL & DENTAL CONSIDERATIONS Oral ulcers, advanced periodontal disease, pericoronitis , and pulpal infections bacteremia , septicemia Topical application of antibacterial mouth rinses An individualized soft splint : covers palatal lesions and carries medication

114. ORAL & DENTAL CONSIDERATIONS Combination of topical neomycin, bacitracin , nystatin Topical anesthetic mouth rinses : A solution containing 5% diphenhydramine hydrochloride with magnesium hydroxide or kaolin with pectin

115. CYCLIC NEUTROPENIA Transient severe neutropenia - occurs approximately every 21 days. Oral ulceration, rapid periodontal breakdown, alveolar bone loss ( Rylander and Ericsson 1981 ) Occurrence of aggressive periodontitis with cyclic neutropenia ( Scully et al,1982 )

116. CHEDIAK-HIGASHI SYNDROME Rare autosomal recessive trait Partial oculocutaneous albinism with photophobia and nystagmus , frequent pyogenic infections, intermittent febrile episodes. Presence of abnormal giant granules in the peripheral circulating leukocytes.

117. PERIODONTAL FEATURES Severe gingival inflammation ( Gilling and Cladwell 1970, Hamilton and Giansanti 1974 ) Excessive and early periodontal destruction resulting in premature loss of permanent dentition.

118. LAZY LEUKOCYTE SYNDROME Defect in leukocyte chemotaxis and random mobility Marked gingivitis Susceptibility to aggressive periodontitis

119. LEUKOCYTE ADHESION DEFICIENCY Inability to produce or failure to express cell surface integrin ( CD 18) Extremely acute gingival inflammation and proliferation of gingival tissues with rapid destruction of bone.

120. PAPILLON LEFEVRE SYNDROME Hyperkeratotic skin lesions, severe destruction of the periodontium , calcification of the dura Periodontal involvement : early inflammatory changes that lead to bone loss and exfoliation of teeth By 15 yrs: edentulous except 3 rd molars

121. DOWN SYNDROME High prevalence of periodontal disease Deep periodontal pockets Moderate gingivitis Poor chemotaxis and phagocytosis

122. LEUKEMIA Malignant neoplasia of WBC precursors characterized by : Diffuse replacement of the bone marrow with proliferating leukemic cells Abnormal number and forms of immature WBCs in the circulating blood Widespread infiltrates in the liver, spleen, lymph nodes and other body sites

123. LEUKEMIA Displace normal components of bone marrow elements with leukemic cells

124. PERIODONTIUM IN LEUKEMIA LEUKEMIC INFILTRATION Gingiva > alveolar bone Highest incidence : Acute monocytic leukemia ( Dreizen et al ) Gingival involvement Pdl and alveolar bone involvement

125. PERIODONTIUM IN LEUKEMIA BLEEDING : Bleeding gingiva early sign Thrombocytopenia and anemia : pallor of the mucosa petechiae ecchymoses gingival bleeding

126. PERIODONTIUM IN LEUKEMIA ORAL ULCERATION AND INFECTION: Discrete punched out ulcers penetrating deeply into the submucosa and covered by a firmly attached white slough Acute gingivitis and lesions resembling necrotizing ulcerative gingivitis : more frequent in acute leukemias Acute herpetic gingistomatitis : common infection

127. MANAGEMENT OF PERIODONTAL PROBLEMS Mechanical plaque control with antiplaque agents where possible Antimicrobials for acute infections Drainage and application of topical antimicrobial agent Gingival hemorrhage : Direct pressure Absorbable gelatin or collagen sponges, topical thrombin, placement of microfibrillar collagen held in place by packing or splints

128. MANAGEMENT OF PERIODONTAL PROBLEMS Gingivectomy : in periods of remission Physician consulted before surgery

129. CLASSIFICATION OF BLEEDING DISORDERS COAGULATION FACTOR DEFICIENCIES Congenital Haemophilia A & B von Willebrand’s disease Other factor deficiencies (rare) Acquired Liver disease Vitamin K deficiency Warfarin therapy Disseminated intravascular coagulation

130. PLATELET DISORDERS Quantitative disorders (thrombocytopenia) Immune mediated Non – immune mediated Qualitative disorder Congenital Glanzmann thrombasthenia Von Willebrand’s disease Acquired Drug –induced Liver disease Alcoholism

131. VASCULAR DISORDERS Scurvy Purpura Hereditary hemorrhagic telangiectasia Cushing syndrome Ehlers – Danlos syndrome FIBRINOLYTIC DEFECTS Streptokinase therapy Disseminated intravascular coagulation

132. A clinicians’ thorough understanding of physiology of blood, blood dyscrasias, their management and the various diagnostic tests is essential for treatment planning as well as avoiding any untoward complications while treating the patients. conclusion

133. REFERENCES 1. Consice medical physiology, Chaudhari , 5 th edition 2. Shafer’s text book of oral pathology 5 th edition 3. Burkets Oral medicine-10 th edition 4. Guyton and hall. Texbook of medical Physiology 11 th edition 5. Essentials of medical physiology, K Sembulingam 2 nd edition 7. Essential Pathology for Dental Students, Harsh Mohan,4 th edition

134. 8. Anuragh Gupta; Joel B Epestin et al . Bleeding disorders of Importance in Dental Care and Related Patient Management. JCDA 2007;73(1):77-83 9. Philip Vassilopoulos & Kent Palcanis . Bleeding disorders and periodontology Periodontology 2000 2007; 44: 211-223 10. James W. Little, Craig S. Miller et al. Antithrombotic agents: Implications in dentistry. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002; 93: 544- 551