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  • 1. DJ COLLEGE OF DENTAL SCIENCES AND RESEARCH SEMINAR TOPIC – BLOOD AND BLOOD DISORDERS PRESENTED BY:Dr Venisha Pandita 1st Year Post Graduate Department of Public Health Dentistry
  • 2. CONTENTS:              Introduction Characteristics Composition Plasma proteins Blood cells : RBC WBC Platelets Haemoglobin Haemopoiesis Haemostasis Functions of blood Blood groups
  • 3. Disorders : Diseases of red blood cells  Anemia  Polycythemia Hemostasis and its disorders  Thrombocytopenia  Haemophilia  Disseminated intravascular coagulation Disorders of White Blood Cells  Agranulocytosis  Leukaemia  Conclusion  References 
  • 4. BLOOD: William Harvey- father of physiology discovered blood circulated through the body in 1628.  It is a fluid connective tissue which transports substance from one part of the body to another.  It provides nutrients and hormones to the tissues and removes their waste products. 
  • 5. CHARACTERISTICS OF BLOOD         Color: blood is red in color. Arterial blood is scarlet red and venous blood is purple Volume: Average volume of blood in a normal adult is 5 l In females it is slightly less and it is about 4.5 l Reaction and pH: Blood is slightly alkaline and its pH in normal conditions is 7.4
  • 6.       Specific gravity: total blood: 1.052 to 1.061 blood cells: 1.092 to 1.101 plasma: 1.022 to 1.026 Viscosity: blood is five times more viscous than water.
  • 7. COMPOSITION
  • 8. 1.PLASMA:   Straw colored, nonliving part of blood. Blood plasma is a mixture of proteins, enzymes, nutrients, wastes, hormones and gases.  It contains :  91% Water  9% Solids : that comprises :  1% inorganic molecules: Na+,Ca2+,Cl-, HCO3-,K+,Mg2+
  • 9. o 8% organic molecules :7% plasma proteins 1% NPN (non –protein nitrogenous) , Substances,sugar,fats,enzymes and hormones  The specific composition and function of its components are as follows:
  • 10. 1. PROTEIN :      Normal value: 6.4 -8.3 gm% There are three major categories of plasma proteins, and each individual type of proteins has its own specific properties and functions: Albumin: 55% 3-5gm% helps substances dissolve in the plasma by binding to them, hence playing an important role in plasma transport of substances such as drugs, hormones and fatty acids.
  • 11. Globulin : 38 %  2-3 gm %  alpha, beta and gamma globulins.  eg: immunoglobulins, transport globulins  immunoglobulins: antibiotics, attack foreign proteins & pathogens  transport globulins: bind small ions, hormones  Fibrinogen : functions in blood clotting  accounts for roughly 7% of plasma proteins 
  • 12. OTHER FORMS GLYCOPROTEIN  LIPOPROTEIN : HDL, LDL, VLDL, Chylomicrons  TRANSFERRIN : (mainly -globulin)-Iron binding property  HAPTOGLOBIN : 2 globulin - Regulates renal threshold for hemoglobin 
  • 13. CERULOPLASMIN -(mainly 2 globulin) – binds with copper and helps in its storage and transport .  FETUIN –present in FOETUS, growth promoting protein  COAGULATION FACTORS - , -globulin  ANGIOTENSIGEN - 2 globulin  HAEMAGGLUTININS -antibodies against red cells Ag  IMMUNOGLOBULIN (Ig) - globulin 
  • 14. 2. Nutrients:  These include glucose, amino acids, fats, cholesterol, phospholipids, vitamins and minerals. 3. Gases:  Some oxygen and carbon dioxide are transported by plasma. 4. Electrolytes:  The most abundant of these are sodium ions 5. Amino acids 6. Nitrogenous waste: o urea ,uric acid, creatine, creatnine
  • 15. FUNCTIONS OF PLASMA PROTEINS: 1. 2. 3. 4. 5. 6. 7. Helps in coagulation of blood Helps to maintain colloidal osmotic pressure. Helps in maintaining viscosity of blood Provides stability to blood Helps in maintaining the acid-base balance in the body Immune function Transport and reservoir function
  • 16. BLOOD CELLS:  Red blood cell  White blood cell  Platelet
  • 17. RED BLOOD CELLS The most abundant blood cells are the red blood cells (RBCs), which account for 99.9 percent of the formed elements.  These cells give whole blood its deep red color.  Red blood cells contain the red pigment hemoglobin .  No nucleus   Cell membrane : Lipids, Proteins, Spectrin, Glycophorin  No Mitochondria  No Ribosome  No Centriole In adult males,4.5–6.3 million per 1 cubic ml females,4.2–5.5 million per 1 cubic ml 
  • 18. HAEMOGLOBIN: Normal values: At birth: 23gm/dl At the end of 3 months: 10.5gm/dl At the end of 1 year 12.5gm/dl Adults- males: 14-18gm/dl females: 12-15 gm/dl
  • 19. STRUCTURE OF HAEMOGLOBIN : Red oxygen carrying pigment in the RBCs, there are two parts.  Globin (96%) and Heme (4%).  Each heme unit holds an iron ion in such a way that the iron can interact with an oxygen molecule, forming oxyhemoglobin . 
  • 20. VARIETIES OF HEMOGLOBIN: A haemoglobin molecule in which the iron has separated from the oxygen molecule is called deoxyhemoglobin .  The RBCs of an embryo or a foetus contain a different form of hemoglobin, known as fetal hemoglobin , which binds oxygen more readily than does the haemoglobin of adults.
  • 21. Methaemoglobin - Hb with ferrous to form ferric  Carboxyhaemoglobin -CO bound at O2 binding site  Sulphaemoglobin n- Sulphur containing Hb usually -Resulting from drug ingestion 
  • 22. FUNCTIONS OF HAEMOGLOBIN: 1. 2. 3. Facilitate transport of oxygen from lungs to tissues Facilitate transport of CO2 from the tissues to the lungs It acts as an excellent acid- base buffer, being a protein.
  • 23. VARIATIONS Sex :males > females  Diurnal variation: Lowest in morning; highest in evening  Altitude : Increased at higher altitude  Exercise : Increased  Excitement :Increased 
  • 24. VARIATIONS:             Poikilocytosis :variation in shape of RBC Anisocytosis:variation in size of RBC Phsiological: Diurnal variation – lowest during sleep maximum in evening Muscular exercise: increases Altitude: increases Pathological: increases Hypoxia Shock dehydration Life span : 120 days Destruction: Mainly in spleen; liver; bone marrow
  • 25. HAEMOPOEISIS In order to maintain the constant blood count it is necessary that new cells should be formed to replace these that are destroyed. This phenomenon of cell production is called hemopoeisis.  Erythropoeisis -dev of RBCs  Leucopoeisis -dev of WBCs  Megakaryocytopoeisis -dev of platelets
  • 26. HAEMOPOEISIS:
  • 27. RBC LIFE SPAN & CIRCULATION Erythropoiesis : development of RBCs During intrauterine life1. Mesoblastic stage:  Intravascular erythropoeisis: Upto 3 months RBC are formed from mesoderm of yolk sac, hence erythropoeisis occurs within the vessel. 2. Hepatic stage:  After 3 months, liver and spleen are the site of blood formation. 3. Myeloid stage : from middle of foetal life ,occur in bone marrow 
  • 28.           In Children, erythropoiesis occurs in : all bones with red marrow mainly liver spleen. In adults : after 18-20 yrs end of long bones like humerus and femur, because shaft is converted to yellow marrow Skull Vertebrae Ribs Sternum and pelvis.
  • 29. STAGES OF ERYTHROPOIESIS Stem cell Committed cell Haemocytoblast Proerythroblast Developmental pathway Early intermediate Late Reticulocyte Erythrocyte normoblast normoblast Normoblast
  • 30. REGULATION OF ERYTHROPOIESIS  for erythropoiesis to proceed normally myeloid tissues must receive adequate supplies of amino acids, Fe, & vitamins required for protein synthesis  essential coenzymes: B6, B12, folic acid – necessary for DNA replication (mitosis)  vitamin B12: obtained from dairy products & meat; its absorption requires presence of intrinsic factor produced in stomach
  • 31. LEUKOCYTES (WBCS) Leukocytes found in blood in the following proportions:  Granulocytes–WBC with granules in their cytoplasm  60% Neutrophils  1-4% Eosinophils  <1% Basophils  Agranulocytes–lack visible cytoplasmic granules  20 - 40% Lymphocytes  2 - 8% Monocytes
  • 32.  TLC: At birth is 20000/ ul In adults is 4000-11000/ ul  Leucopenia : decreases less than 4000/ cumm Causes:  starvation  Typhoid fever  Viral/ protozoal infection
  • 33. Leucocytosis : increases above 11,000/ cumm Causes:  newborn  Evening  Exercise  Stress  Pregnancy  Menstruation  Any pyogenic / pyrogenic infections 
  • 34. 1. NEUTROPHILS Size: 10-12 diam  Nucleus: Multilobed (2-6)-PMNL  Cytoplasm: Granular, Neutrophilic  Granules: pin point granules  neutrophilic in nature  Contains proteins and lipids  These granules are regarded as lysosomes as they can lyse any type of substances using varieties of enzymes like nucleases,glycosidases 
  • 35. Functions:  Phagocytosis : whenever the body gets invaded by bacteria, neutrophils are the first to seek out to ingest and kill bacteria. (First line defense)
  • 36. 2. EOSINOPHIL Size: 10-12 diam  Nucleus : Bilobed spectacle appearance  Cytoplasm : Acidophilic, granular  Granules: coarse, acidic  High peroxidase content  Lysosomal enzymes 
  • 37. Functions Mild phagocytic Anti-allergic effect: collect at the site of the tissues where allergic reactions occur by degrading the effects of mediators (histamine,bradykinin) Inhibits Kills Mast cells degranulation parasites
  • 38. Eosinophilia: increase in eosinophils Causes:  Allergic reactions ( bronchial asthma)  Skin diseases  Eosinopenia: decrease  After injection of corticosteroids 
  • 39. 3. BASOPHIL Size: 10-12 m  Nucleus : Bilobed  Cytoplasm : Basophilic  Granules: Coarse,basic  Plenty in no., overcrowd the nucleus  Contain- Histamine, Heparin Eosinophil chemotactic factor (ECF-A): chemical mediator of immediate hypersensitivity reactions. 
  • 40. Functions:  Liberates Histamine and ECF-A: which leads to allergic manifestations  Liberates Heparin : which acts as Anticoagulant and keeps the blood in fluid state Mild phagocytosis Basophilia: increase Chickenpox Tuberculosis Influenza Basopenia : decrease After administration of gluco-corticoids 
  • 41. 4. MONOCYTE Largest WBC  Size :12-18 diam  Nucleus : Kidney shaped eccentric in position  Cytoplasm : Clear Enzymes- proteolytic, hydrolytic 
  • 42. Functions  Active Phagocytosis : second line defence  Enter the tissues to become tissue macrophage  Kill tumor cells after sensitization by Lymphocytes. Monocytosis: Tuberculosis Some leukaemia Monocytopenia: Hypoplastic bone marrow
  • 43. 5. LYMPHOCYTES 2 types:  Large Lymphocyte : 10-14 diam, precursor of small lymphocyte  Small Lymphocyte : 7-10 diam
  • 44. Nucleus : Single, round, oral or indented central, occupies whole of the cell Nuclear chromatin is coarse and lumpy  Cytoplasm: Only narrow ring around nucleus 
  • 45. Functions  produce antibodies and hence responsible for Immunity  Immunity: Resistance exhibited by the host towards the injury caused by bacteria or foreign proteins.  Humoral Immunity: Antibodies which are -globulins produced by B-Lymphocytes  Cell-mediated Immunity: Due to T-Lymphocytes Lymphocytosis: In children : 60 % more than neutrophils (relative Lymphocytosis) Lymphopenia: AIDS Hypoplastic bone marrow
  • 46. LIFE SPAN AND FATE OF WBC  Neutrophils  : 2-4 days Eosinophils : 8-12 days (Last through GIC or Resp. tract)  Monocyte : 1 day in circulation  B-Lymphocytes : Few days or weeks  T-Lymphocytes : 2-4 years
  • 47. PLATELETS (THROMBOCYTES) Structure : General  smallest blood cells, colorless  disc shaped (in activated from) to sphere shaped (activated) granulated bodies.  Size : 2-5 m in diameter, average volume 5.8 m3  Leishman staining : faint blue cytoplasm with distinct reddish purple granules.  Nucleus is not present.
  • 48. Under Electron Microscope: Platelet membrane: Features  Identical structure with cells membranes thickness: 60 nm  Main lipids in lipo-protein layer of cell membrane: Phospholipids. Cholesterol, and glycolipids  Contains various receptors meant for combining with specific substances like:  Collagen  Fibrinogen  Von-Willebrand’s factor: important role in platelet adhesion
  • 49. Cytoplasm : contains  Golgi apparatus  Endoplasmic reticulum  Few mitochondria  Microvesicles and microtubules:  Contractile protein –actin and myocin : helps in clot retraction.  Glycogen  Lysosomes
  • 50. Granules - 2 types.  Dense granules- contains  Non-proteins substances like phospholipid, triglycerides. Cholesterol etc.  Serotonin - Vasoconstrictor agent  ADP- helps platelet aggregation  ATP- stores energy  Other adenine nucleotides  -Granules- contains secreted proteins including  Clotting factors  Platelet derived growth factor (PDGF)- stimulates wound healing, helps in repair of damaged vessel wall
  • 51.  Count Normal count: 1.5 to 4 lacs /cumm (average 2.59 lac/cumm)  Life span : 8-12 days  Destruction : Mainly in spleen
  • 52. VARIATIONS: Thrombocytosis :increase in platelet count  after administration of epinephrine  After trauma  Splenectomy  Stress  Thrombocytopenia :decrease in platelet count  Bone marrow depression  Hypersplenism
  • 53. FUNCTIONS OF PLATELET 1. Hemostasis: Spontaneous arrest of bleeding by physiological process.    Platelet adhesion Platelet activation Platelet aggregation : Hemostatic plug that prevents blood loss 2 . Blood coagulation- release of clotting factors, Prostaglandins, Phospholipids
  • 54. 3. Clot Retraction- 40% of original volume and release of Thrombosthetin 4. Phagocytic functions – helps in phagocytosis of carbon particles,viruses.
  • 55. MECHANISM OF HAEMOSTASIS      Injury to vessel wall initiates series of events A. Constriction of injured blood vessel. B. Formation of a 'temporary haemostatic plug' of platelets. C. Conversion of temporary haemostatic plug into the 'definitive haemostatic clot'. Formation of clot Seals off the damaged blood vessel prevents further loss of blood
  • 56. PHYSIOLOGY OF CLOTTING MECHANISM  The clotting mechanism responsible for the formation of fibrin involves a 'complex series' or 'cascade' of reactions. Here 'inactive' enzymes are activated, and the activated enzymes in turn activate other inactive enzymes.
  • 57. ANTICOAGULANTS Types  Natural Anticoagulants  Synthetic Anticoagulants 1. Heparin  A powerful anticoagulant first isolated from liver (hence its name)  present in many other organs e.g. lungs.  It facilitates the action of antithrombin III, thereby inhibiting the active forms of clotting factors IX, X, XI and XII.
  • 58. Origin: Heparin is secreted by (i) granules of circulating basophils (ii) granules of "mast cells". These cells are found in large numbers in tissues that are rich in connective tissue;  Destruction: by an enzyme "Heparinase" in the liver. 2. Anti-Thrombin or Heparin co-factor II: It inhibits thrombin. 3. Protein C: It inactivates factors V and VIII. 
  • 59. Synthetic Anticoagulants 1. Vitamin K Antagonists: effective orally  These include coumarin derivatives dicoumarol. and warfarin. 2. Malayan (Malaysian) Pit Viper 3. Arvin (Ancord) e.g.
  • 60. FUNCTIONS OF BLOOD Transport of Respiratory gases:  Blood and particularly red cells are responsible for transport of O2 from lungs to the tissues.  This is done due to the presence of hemoglobin, which combines with O2 to form oxy-Hb; Co2 from tissue is taken up by the blood and released in the lungs.  Transport of Nutrition:  The substances such as glucose, fatty acids, amino acids, vitamins, electrolytes and trace metals are absorbed from the intensive transported to all parts of the body for utilization and storage via blood. 
  • 61. Excretory: Blood transports urea, uric acid, creatinine to kidney, lungs, skin, and gastrointestinal tract for excretion.  Regulation of Body Temperature:  Blood forms internal environment of the cell i.e. MILLIEU INTERIUER in terms of volume, composition, concentration, pH and temperature which is regulated to normal physiological limits with respect to miner changes in the body.  This mechanism is called Homeostasis. (W. E. Cannen). 
  • 62. Defensive Action: Blood acts as a great defensive mechanisms through WBC s , lymphocytes  Transport of Other Substances: Blood acts as a vehicle through hormones, vitamins, and other essential chemicals are transported to the various tissues.  Coagulation Property: It is a mechanism by which various factors present in the blood form a cell and thus prevent blood less  Plasma Proteins: The plasma proteins of blood have various functions which will be discussed subsequently 
  • 63. BLOOD GROUPS     The chief blood groups are : Classical ‘ABO’ blood group Rhesus (Rh) blood group M and N blood group
  • 64. 1.CLASSICAL ‘ABO’ BLOOD GROUP RELATIONSHIPS BETWEEN BLOOD TYPES AND ANTIBODIES Blood Type Antigens on Red Blood Cell Can Donate Blood To Antibodies in Serum Can Receive Blood From A A A,AB Anti-A A,O B B B.AB Anti-B B,O AB A and B AB None AB,O O None A,B,AB and O Anti-A and Anti-B O
  • 65. Blood typing is a laboratory test done to discover a person's blood type. If the person needs a blood transfusion, cross-matching is done following blood typing to locate donor blood that the person's body will accept. (Illustration by Electronic Illustrators Group.)
  • 66. 2.RHESUS (RH) BLOOD GROUP Landsteiner and Weiner (1940)  Present in > 85% of individuals Rh + Ve  No corresponding Agglutinin in plasma  Rh antigen is called D and its antibody is called Anti-D also known as warm antibodies. 
  • 67. Rh incompatibility
  • 68. 3. M N SYSTEM Significance in the determination of paternity in medico legal cases.  M and N factors depend on two minor genes.  Each person carries of the two of the genes of the M and N group.  i.e. M + M = M N +N = N M+ N =MN o These are antigenic to rabbits 
  • 69. USES OF BLOOD GROUPING TESTS Blood transfusion  In pregnancy (Rh Incompatibility)  Investigating cases of paternity dispute  In forensic medicine  Medico legal value 
  • 70. BLOOD DISORDERS DISEASES OF RED BLOOD CELLS (ERYTHROCYTES): Anaemia  Iron Deficiency Anaemia  Anaemia Of Chronic Disease  Sideroblastic Anaemia
  • 71. megaloblastic anaemia  haemolytic anaemia  sickle cell anaemia  thalassemia  aplastic anaemia  Polycythemia 
  • 72. ANAEMIA  At birth, haemoglobin is 20g/dl and at 3 months lower limit of normal is taken as 9.5g/dl. A haemoglobin level of 12g/dl or less is usually regarded as anaemia in adult males and less than 11g/dl is taken as anaemia in females.
  • 73. SYMPTOMS Pallor or lack of color  fatigue, dizziness, headaches  decreased exercise tolerance  rapid heartbeat, and shortness of breath  haemic murmurs  Untreated anemia may progress to death from heart failure 
  • 74. ETIOLOGICAL CLASSIFICATION OF ANEMIA  Blood loss: Acute Post hemorrhagic  Chronic blood loss   Deficiency of Hemopoetic factors:Iron deficiency  Folate and vitamin b12deficiency  Protein deficiency.   Bone marrow aplasia:Aplastic anemia  Pure red cell aplasia 
  • 75.  Anemia due to systemic infections:     Anemia due to bone marrow infiltration:      Due to chronic infection Due to chronic renal disease Due to chronic liver disease Endocrinal diseases Leukemia’s Lymphomas Myelofibrosis Multiple myeloma Congenital sideroblastic anemia Anemia due to increased red cell destruction:Intra-corpuscular defect  Extra-corpuscular defect 
  • 76. Morphological classification of anemia:- Microcytic hypochromic  Normocytic normochromic   Macrocytic normochromic
  • 77. TYPES OF ANAEMIA     Macrocytic anemia: Megaloblastic anemia and nonmegaloblastic macrocyctic anemia. Primary cause of this sort of anemia is collapse of DNA synthesis with kept RNA synthesis that occurs due to the division of the divisional cells. Microcytic anemia: Sort of anemia occurs due to hemoglobin synthesis shortage or collapse. Normcytic anemia: Occurs when Hb levels decreases overall. Size of RBC is often normal. Heinz Body anemia: Considered a cell abnormality that usually occurs in cells under anemia.
  • 78.    Iron-deficiency anaemia – hypochromic microcytic anemia characterized by low serum iron, increased serum iron-binding capacity, decreased serum ferritin, and decreased marrow iron stores. Megaloblastic (pernicious) anaemia – predominant number of megaloblastic erythroblasts, and relatively few normoblasts, among the hyperplastic erythroid cells in the bone marrow Hemolytic anaemia – increased rate of erythrocyte destruction.
  • 79.     Sickle cell anemia – autosomal recessive anemia characterized by crescent- or sickle-shaped erythrocytes and accelerated hemolysis, due to substitution of a single amino acid - chromosome 11 Aplastic anemia – greatly decreased formation of erythrocytes and hemoglobin, usually associated with pronounced granulocytopenia and thrombocytopenia Chronic anemia Anemia of folate deficiency
  • 80.  Cooley's anemia (beta thalassemia) – syndrome of severe anemia resulting from the homozygous state of one of the thalassemia genes or one of the hemoglobin Lepore genes with onset, in infancy or childhood, of pallor, icterus, weakness, splenomegaly, cardiac enlargement, thinning of inner and outer tables of skull, microcytic hypochromic anemia with poikilocytosis, anisocytosis, stippled cells, target cells, and nucleated erythrocytes
  • 81. CAUSES     Accurate blood loss Anemia of chronic disease Bone marrow failure and Plastic anemia.
  • 82. TREATMENT    A successful treatment of anemia depends on successful diagnosis of the cause that brings about the disease. There are several causes of anemia including blood loss, cancer, a nutritional deficiency, chronic illness, bone marrow infiltration, lower response to erythropoietin and inflammation. These causes can be determined with laboratory test results and physical examination.
  • 83. Specific treatment for anemia will be determined by the physician based on:  Age, overall health, and medical history  Extent of the disease  Tolerance for specific medications, procedures, or therapies  Expectations for the course of the disease  Opinion or preference of the patient
  • 84.         Treatment of the causative disease Vitamin and mineral supplements Change in diet Medication Blood transfusion Bone marrow transplant Surgery (to remove the spleen, if related to hemolytic anemia) Antibiotics (if an infection is the causative agent)
  • 85. HEMOPHILIA     Persons with hemophilia lack the ability to stop bleeding because of the low levels, or complete absence, of specific proteins, called "factors," in their blood that are necessary for clotting. Inherited bleeding or coagulation, disorder. Proper clotting of blood helps prevent excessive bleeding. Types of hemophilias –  hemophilia A - lack of factor VIII  hemophilia B - lack of factor IX
  • 86. CAUSES     Hemophilia types A and B are inherited diseases passed on from a gene located on the X chromosome. Females carrier of hemophilia has the hemophilia gene on one of her X chromosomes, and there is a 50 percent chance that she may pass the defective gene to her male offspring. Males who inherit the defective gene will develop hemophilia. Males with hemophilia do not pass the gene to their sons; however, they do pass the gene to their daughters.
  • 87.   Females who inherit the defective gene will become carriers who may, in turn, have a 50 percent chance of passing it on to their children. Although females who inherit the gene generally have no active problems related to hemophilia, some may have other problems associated with bleeding, such as excessive menstrual bleeding, frequent or severe nosebleeds, or bleeding after dental procedures or surgery. In about 1/3rd of hemophilia cases, there is no family history of the disease. These cases are due to a new or spontaneous development of the defective gene in the female
  • 88. SYMPTOMS:       Excessive, uncontrollable bleeding Bleeding may occur even if there is no injury. Often occurs in the joints and in the head. Bruising - Occur from small accidents, which can result in a large hematoma. Bleeds easily - Tendency to bleed. Bleeding into a joint - Hemarthrosis can cause pain, immobility, and eventually deformity if not medically managed properly
  • 89.     Bleeding into the muscles - Bleeding into the muscles can cause swelling, pain, and redness. Bleeding from injury or bleeding in the brain - Bleeding from injury or spontaneously in the brain, is the most common cause of death in children with hemophilia and the most serious bleeding complication. Other sources of bleeding - Blood found in the urine or stool may also be a symptom of hemophilia. The symptoms of hemophilia may resemble other blood disorders or medical problems.
  • 90. DIAGNOSIS & EFFECTS        Complete medical history and physical examination Clotting factor levels Complete blood count (CBC) Assessment of bleeding times DNA testing. Most common cause of disability from hemophilia is chronic joint disease or arthropathy, which is caused by uncontrolled bleeding into the joints. Hemorrhage – severe internal or external discharge of blood, is a continuing problem.
  • 91. TREATMENT  Blood transfusions  Prophylactic (preventive) treatment with infused clotting factors
  • 92. IMMUNE THROMBOCYTOPENIC PURPURA (THROMBOCYTOPENIA)    Blood disorder characterized by an abnormal decrease in the number of blood platelets, which results in internal bleeding. Acute thrombocytopenic purpura – Most common in young children, the symptoms may follow a virus infection and disappears within a year - usually disorder does not recur. Chronic thrombocytopenic purpura – Onset of the disorder can happen at any age, and symptoms can last six months or longer. Adults have this form more often than children, and females have it 3 times more often than males.
  • 93. CAUSES      Medications - including over-the-counter Infection Pregnancy Immune disorders However, about half of all cases are classified as idiopathic.
  • 94. SYMPTOMS     Internal bleeding, which may cause: ecchymosis - bruising , petechiae - tiny red dots on skin or mucous membranes Occasionally, bleeding from the nose, gums, digestive tract, urinary tract Rarely, bleeding within the brain Symptoms may resemble other blood disorders or medical problems.
  • 95. DIAGNOSIS      Complete medical history and physical examination Additional blood and urine tests Other evaluation procedures Careful review of patient's medications Bone marrow examination
  • 96. TREATMENT      Treatment of the causative disease Discontinuation of causative drugs Treatment with corticosteroids Treatment with medications Lifestyle changes, such as: use of protective gear , avoidance of certain activity causing injuries.
  • 97. HODGKIN'S DISEASE     Type of lymphoma, a cancer in the lymphatic system. Rare disease usually occurs most often in people between the ages of 15 and 34, and in people over age 55. Hodgkin's disease causes the cells in the lymphatic system to abnormally reproduce, eventually making the body less able to fight infection. Hodgkin's disease cells can also spread to other organs.
  • 98. LYMPHADENOMA – HODGKIN'S DISEASE (PSEUDOLEUKEMIA OF GERMAN AUTHORS)
  • 99. SIGNS AND SYMPTOMS        Painless swelling of lymph nodes in neck, underarm, and groin Fever Night sweats Fatigue Weight loss Itching of the skin It may resemble other blood disorders or medical problems, such as influenza or other infections.
  • 100. DIAGNOSIS    Additional blood tests X-rays of the chest, bones, liver, and spleen Biopsy of the lymph node TREATMENT  Radiation therapy  Chemotherapy
  • 101. LEUKAEMIA   Cancer of the blood cells, usually the white blood cells. Leukemic cells look different than normal cells and do not function properly.
  • 102. LYMPHOCYTIC OR MYELOGENOUS LEUKEMIA    Cancer can occur in either the lymphoid or myeloid white blood cells. When the cancer develops in the lymphocytes (lymphoid cells), it is called lymphocytic leukemia. Cancer develops in the granulocytes or monocytes (myeloid cells) – myelogenous leukemia.
  • 103. ACUTE OR CHRONIC LEUKEMIA   Acute leukemia - The new or immature cells, called blasts, remain very immature and cannot perform their functions. The blasts increase in number rapidly, and the disease progresses quickly. Chronic leukemia - There are some blast cells present, but they are more mature and are able to perform some of their functions. The cells grow more slowly, and the number increases less quickly, so the disease progresses gradually.
  • 104. LEUKEMIA IS CLASSIFIED INTO ONE OF THE FOUR MAIN TYPES OF LEUKEMIAS     Acute myelogenous leukemia (AML) Chronic myelogenous leukemia (CML) Acute lymphocytic leukemia (ALL) Chronic lymphocytic leukemia (CL
  • 105. SIGNS AND SYMPTOMS     More frequent infections and fevers Anaemia and its symptoms: pale skin, fatigue, weakness, bleeding, bruising, fever, chills, loss of appetite, loss of weight, swollen or tender lymph nodes, liver, or spleen, petechiae (tiny red spots under the skin), swollen or bleeding gums, sweating, bone or joint pain. Acute leukaemia: headaches, vomiting, confusion, loss of muscle control, seizures, swollen testicles, sores in the eyes or on the skin. Chronic leukemia may affect the skin, central nervous system, digestive tract, kidneys, and testicles.
  • 106. DIAGNOSIS        Physician examination for swelling in the: liver, spleen, lymph nodes under the arms, in the groin, and in the neck Blood tests and laboratory tests Blood tests to examine the blast (immature) blood cells Bone marrow aspiration and biopsy Lymph node biopsy Spinal tap Imaging procedures, such as x-ray, ultrasound, and computed tomography (CT)
  • 107. TREATMENT        Chemotherapy Radiation therapy Bone marrow stem cell transplantation Biological therapy Platelet transfusion Red blood cell transfusion Medications to prevent or treat damage to other systems of the body caused by leukemia treatment
  • 108. NON-HODGKIN'S LYMPHOMA    Type of lymphoma, which is a cancer in the lymphatic system. Non-Hodgkin's disease causes the cells in the lymphatic system to abnormally reproduce eventually causing tumors to grow and can also spread to other organs. Etiology is idiopathic
  • 109. SYMPTOMS        Painless swelling of underarm, and groin Fever Night sweats Fatigue Weight loss Itching of the skin Recurring infections lymph nodes in neck,
  • 110. DIAGNOSIS       Blood tests X-rays of the chest, bones, liver, and spleen Biopsy of the lymph nodes, bone marrow, and other sites Lymphangiograms - lymphatic system x-rays CT scan Ultrasonography scan TREATMENT  Radiation therapy  Chemotherapy
  • 111. THROMBOCYTHEMIA     It is a myeloproliferative blood disorder. It is characterized by the production of too many platelets in the bone marrow. Too many platelets make normal clotting of blood difficult Etiology is idiopathic
  • 112. SYMPTOMS         Increased blood clots in arteries and veins Bleeding Bruising easily Bleeding from the nose, gums, gastrointestinal tract Bloody stools Hemorrhaging after injury or surgery Weakness Enlarged lymph nodes
  • 113. DIAGNOSIS    Complete medical history and physical examination Blood counts and elevated platelet levels Bone-marrow biopsy TREATMENT   Chemotherapy Plateletpheresis - a procedure to remove extra platelets from the blood
  • 114. BONE MARROW TRANSPLANTATION [BMT]    BMT is a special therapy for patients with cancer or other diseases which affect the bone marrow. A bone marrow transplant involves taking cells that are normally found in the bone marrow (stem cells), filtering those cells, and giving them back either to the patient or to another person. The goal of BMT is to transfuse healthy bone marrow cells into a person after their own unhealthy bone marrow has been eliminated
  • 115. NORMAL ANATOMY
  • 116. INDICATION
  • 117. PROCEDURE
  • 118. A BONE MARROW TRANSPLANT CAN BE USED TO    Replace diseased, non-functioning bone marrow with healthy functioning bone marrow Replace the bone marrow and restore its normal function after high doses of chemotherapy or radiation are given to treat a malignancy – process called "rescue". Replace bone marrow with genetically healthy functioning bone marrow to prevent further damage from a genetic disease process
  • 119. CONCLUSION : Human body is an intricate system of various tissues and organs  Blood and lymphatic system forms an integral part of life’s sustainance.  As a public health dentist ,it is essential to have a proper understanding of blood and its components and blood related diseases so as to be well prepared for their diagnosis and appropriate treatment 
  • 120. REFERENCES: Guyton C Arthur , Hall E John .Textbook of medical physiology. 9th ed . Singapore : W B Saunders; 2000.  Textbook of Physiology: A. K. Jain , 3rd edition page no. 45 -110  Essentials of Medicine: Davidson  Essentials of Medicine :K. Sembulingam, Prema Sembulingam , 4th edition, page no. 53-87  Textbook of Pathology: Harsh Mohan Malik A Neelima. Textbook of oral and maxillofacial surgery.2nd ed:jaypee;new delhi:2010;p.205-225 