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pathophysiology of rbc ( red blood cells)

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reb blood cells

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pathophysiology of rbc ( red blood cells)

  1. 1. content • • • • • • • History of RBC Function Shape and size Concentration Production Pathologies- polycythemia aneamia
  2. 2. RED BLOOD CELL HISTORY:- Dutch biologist Jan Swammerdam in 1658 Anton van Leeuwenhoek in 1674 In 1901, Karl Landsteiner- BLOOD GROUP The oldest intact red blood cells ever discovered were found in Ötzi the Iceman, a natural mummy of a man who died around 3255 BC. These cells were discovered in May 2012.
  3. 3. FUNCTIONS
  4. 4. Shape and Size of Red Blood Cells
  5. 5. Concentration of Red Blood Cells in the Blood Hb RBC (SI unit) USA UNIT Males 13-18g/dL (4.0-5.5)x 1012/L 4.0-5.2 x 106 /mm3 Females 11.5-16.5g/dL (3.5-5.0)x 1012/L 3.5-5.0x 106 /mm3 Neonates 17-20g/dL (6.0-7.0)x 1012/L 6.0-7.0 x 106 /mm3
  6. 6. Erythropoiesis is the process by which the origin, development and maturation of erythrocytes occur
  7. 7. PRODUCTION OF RED BLOOD CELLS IN EARLY WEEK OF EMBRYONIC LIFEDURING SECOND TRIMESTER OF GESTATIONAFTER BIRTHAFTER 20 YEARS:-
  8. 8. GENESIS of Red Blood Cells Stem cell Proerythroblast Early erythroblast Intermediate erythroblast Reticulocyte RBC
  9. 9. POLYCYTHEMIA VERA -myeloproliferative disorder -excessive proliferation of erythroid elements -RBC 6 to 12 million/cubic mm with a hemoglobin concentration of 18 to 24 g/Dl -increased blood viscosity and thrombosis -clinical picture of ruddy cyanosis is seen on the face and extremities
  10. 10. Clinical Manifestations
  11. 11. TREATMENT Myelosuppresive drugs like hydroxyurea can be used
  12. 12. SECONDARY POLYCYTHEMIA: ERYTHROCYTOSIS • increase in erythropoietin production to compensate for hypoxia • High altitudes • Chronic pulmonary disease
  13. 13. APPARENT POLYCYTHEMIA • increased hemoglobin concentration and packed-cell volume • normal RBC mass
  14. 14. ANEAMIA decrease in the normal amount of circulating hemoglobin Anemia may be defined as reduction of hemoglobin concentration per unit volume of blood below the lower limit of normal range for age & sex of the individual
  15. 15. CLASSIFICATION OF ANEAMIA
  16. 16. Common symptoms
  17. 17. 1: Clinical features:- With dry mouth
  18. 18. What can be the cause??
  19. 19. Complete blood picture • • • • • • cells are microcytic and hypochromic hemoglobin value is less low serum iron concentrations ferritin levels are markedly reduced. high serum iron-binding capacity absence of stainable iron in the bone marrow • The physician must perform a thorough search for the source of bleeding, including using radiologic surveys of the gastrointestinal tract, sigmoidoscopy, a gynecologic examination, and a complete menstrual and dietary history.
  20. 20. diagnosis
  21. 21. DAILY REQUIREMENT OF IRON
  22. 22. treatment • -ferrous sulphate 200 mg three times daily • -Alternative preparations include ferrous gluconate and ferrous fumarate. • -Iron sorbitol injection is a complex of iron, • -sorbitol and citric acid • 10-20 deep intramuscular injections are given over two to three weeks.
  23. 23. Clinical features - ATROPIC ORAL MUCOSA - ATROPIC MUCOSA OF - PHARYNX , UPPER ESOPHAGUS. SPASM IN THROAT FOOD STICKING IN THROAT DYSPHAGIA
  24. 24. • First described by Plummer and Vinson • Plummer-Vinson syndrome is potentially serious because pharyngeal and intraoral carcinoma are more common in these patients. • Patients with symptoms of this syndrome should be followed up at short intervals and checked for the development of lesions that raise the suspicion of malignancy.
  25. 25. treatment • IRON THERAPY HELPS
  26. 26. HEMOLYTIC ANEAMIA extracorpuscular intracorpuscular
  27. 27. diagnosis • -decreased hemoglobin, increased reticulocytes. • Coombs test directLooks for immunoglobulin &/or complement of • • • • • • • surface of red blood cell (normally neither found on RBC surface) Coombs reagent - combination of anti-human immunoglobulin & anti-human complement Mixed with patient’s red cells; if immunoglobulin or complement are on surface, Coombs reagent will link cells together and cause agglutination of RBCs INDIRECT coomb Looks for anti-red blood cell antibodies in the patient’s serum, using a panel of red cells with known surface antigens Combine patient’s serum with cells from a panel of RBC’s with known antigens Add Coombs’ reagent to this mixture If anti-RBC antigens are in serum, agglutination occurs
  28. 28. Clinical features • pallor of nails bed, sclera , skin , soft palate , tongue . • Produces jaundice due to hyperbilirubineamia
  29. 29. Hemolysis due to:Paroxysmal nocturnal hemoglobinuria defect is an acquired clonal stem cell disorder that results in abnormal sensitivity of the RBC membrane to lysis by complement. Glucose 6 phosphate dehydrogenase deficiency Lack of G6PD leads to hemolysis during oxidative stress
  30. 30. • Due to hemolysis hb can be reduced by 34g/dl • Drugs that induce hemolysis should be avoided such as dapsone,phenacetin.
  31. 31. c/f Glossitis , Glossodynia red beefy tongue Dysphagia and taste change Burning mouth Dysphagia , taste aberrations
  32. 32. c/f
  33. 33. cause
  34. 34. Lab finding macrocytic normochromic red cells MCV increased MCH increased shape of the red cells varies presence of megaloblastic marrow changes Schilling test is used
  35. 35. Causes of B12 deficiency Inadequate intake Increased need Malabsorption B12 deficiency Impaired absorption Gastrectomy Lack of IF Pernicious anaemia 42
  36. 36. treatment administration of parenteral cyanocobalamin 1000 μg/day for 1 week, then 1000 μg/week for 1 month, followed by 1000 μg/month for life
  37. 37. Clinical feature
  38. 38. Lab findings • • • • • • low serum assays of folic acid macrocytic normochromic red cells MCV increased MCH increased shape of the red cells varies presence of megaloblastic marrow changes
  39. 39. Treatment 5mg per day for 3 weeks sufficient
  40. 40. c/f Absent or hypoplastic thumb Mental and sexual retardation
  41. 41. Causes of aplastic
  42. 42. Aplastic aneamia • Caused by bone marrow failure. • Fanconi aneamia:IS INHERITED APLASTIC ANEAMIA
  43. 43. Lab findings • Sickle shaped cell • Hemoglobin electrophoresis is less expensive, more accurate, and more definitive in the diagnosis of sickle cell disease as it detects hemoglobin S.
  44. 44. • chipmunk facies.” • Frontal bossing, maxillary hypertrophy, depression of nasal bridge , Malocclusion of teeth
  45. 45. PARAVERTEBRAL MASSES: • Broad expansion of ribs at vertebral attachment PATHOLOGICAL FRACTURES: • Cortical thinning • Increased porosity of long bones DELAYED PNEUMATISATION OF SINUSES
  46. 46. X ray skull: “ hair on end” appearance or “crew-cut” appearance
  47. 47. • The skin color becomes ashen-gray due to the combination of pallor, jaundice, and hemosiderosis. • Patients also present with cardiomegaly, hepatomegaly, and splenomegaly
  48. 48. Lab findings • Hemolytic anemia with hypochromic microcytic • red blood cells that vary in size and shape • increased amounts of fetal hemoglobin • Prenatal diagnosis of thalassemia is facilitated by deoxyribonucleic acid(DNA) analysis of amniotic fluid cells, and it plays an important role in genetic counseling.
  49. 49. References:-DAVIDSONS- GENERAL MEDICINE 20TH EDITION -ABC OF CLINICAL HAEMATOLOGY2ND EDITION -GUYTON – TEXT BOOK OF MEDICAL PHYSIOLOGY 11TH EDITION -WILLIAMS HEAMATOLOGY- 7TH EDITION -BURKETS – TEXT BOOK OF ORAL MEDICINE – 7TH EDITION
  50. 50. NEXT SEMINAR • BY DR.CHINTAN SAVANI PATHOPHYSIOLOGY OF WHITE BLOOD CELLS

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