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Megaloblastic Anemia

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Megaloblastic Anemia

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Information about megaloblastic anemia and it's etiology and its classification.
Vitmain b12 deficiencies
Folic acid deficiencies
Signs and symptoms of megaloblastic anemia
Neural tube defects

Information about megaloblastic anemia and it's etiology and its classification.
Vitmain b12 deficiencies
Folic acid deficiencies
Signs and symptoms of megaloblastic anemia
Neural tube defects

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Megaloblastic Anemia

  1. 1. Megaloblastic Anemias, Etiology And Clinical Features Nishkarsh Bansal Roll No- 53
  2. 2. Megaloblastic Anemia  Group of disorders in which erythroblasts in the bone marrow, show delayed nuclear maturation relative to that of cytoplasm, due to defective DNA synthesis.  When DNA synthesis is impaired, the cell cycle cannot progress to mitosis. This leads to continuing cell growth without division, which presents as macrocytosis.
  3. 3. Morphology  The presence of red cells that are macrocytic and oval (macro-ovalocytes) is highly characteristic.  Most macrocytes lack the central pallor of normal red cells and even appear “hyperchromic”.  Anisocytosis and poikilocytosis of red cells.  Nuclear hypersegmentation of neutrophils.  Marrow is usually markedly hypercellular as a result of increased hematopoietic precursors, which often completely replace the fatty marrow.
  4. 4. Etiology 1) Vitamin B12 deficiency OR abnormalities of cobalamin metabolism. 2) Folate deficiency OR abnormalities of folate metabolism. 3) Metabolic inhibitors of DNA synthesis OR Folate metabolism.
  5. 5. Cobalamin (Vitamin B12)  Vitamin B12 is a complex organometallic compound also known as cobalamin.  It is solely synthesized by microorganisms and the only source for humans is food of animal origin like meat, fish and dairy products.  The daily requirement is 2-3 µg.
  6. 6. Absorption Of Vitamin B12 Absorption Mechanism Active (75%) Requires the presence of Intrinsic Factor (a glycoprotein produced by gastric mucosa) Passive Absorption occurs by Diffusion and works when pharmacological doses of vitamin B12 are ingested.
  7. 7. (Haptocorrins) (Cubilin)
  8. 8. Functions Of Vit B12
  9. 9. Causes Of Vit B12 Deficiency Nutritional Low intake : vegans Malabsorption Pernicious anemia Gastric causes Congenital lack of IF Total or partial gastrectomy Intestinal causes Intestinal stricture, anatomic blind loop, etc. Ileal resection and Crohn’s disease Tropical sprue Fish tapeworm
  10. 10. Pernicious Anemia  Pernicious anemia is an autoimmune disease that affects the gastric mucosa and results in gastric atrophy.  Antibodies are produced against cells of the stomach or against IF (intrinsic factor).  This leads to the destruction of parietal cells and failure to produce intrinsic factor, resulting in vitamin B12 malabsorption .
  11. 11. Morphology  The most characteristic alteration is fundic gland atrophy.  Parietal cells are virtually absent.  The glandular epithelium is replaced by mucus-secreting goblet cells that resemble those lining the large intestine, a form of metaplasia referred to as intestinalization.
  12. 12. Clinical Features
  13. 13. Pallor and mild icterus (in a patient with a haemoglobin count of 7.0g/dL)
  14. 14. Other Findings Glossitis (The tongue is beefy-red, shiny and painful) Angular Cheilosis (stomatitis)
  15. 15. Neurological Findings  Demyelination of the dorsal and lateral spinal tracts, sometimes followed by loss of axons.  These changes give rise to spastic paraparesis, sensory ataxia, and severe paresthesias in the lower limbs.  Degenerative changes in the ganglia of the posterior roots and in peripheral nerves. ( less frequent) Present in about 3/4th of all cases of pernicious anemia. Can also be seen in the absence of other hematologic findings.
  16. 16. NOTE :-  The gastric atrophy and metaplastic changes are due to autoimmunity and not of vitamin B12 deficiency.  Hence, parenteral administration of vitamin B12 corrects the megaloblastic changes in the marrow and the epithelial cells of the alimentary tract, but gastric atrophy and achlorhydria persist.  Persons with atrophy and metaplasia of the gastric mucosa associated with pernicious anemia have an increased risk of gastric carcinoma.
  17. 17. Folate  Folic acid is parent compound of large family of natural folate compounds. Its highest concentration is found in liver, yeast, spinach, other greens and nuts. Total folate in adult is ~10mg with liver containing the largest store. Daily adult requirements are ~ 50-200 µg.
  18. 18. Functions Of Folic Acid  Folic acid DHFA THFA (Active form)  THFA mediates number of one-Carbon transfer reactions :- ∞ Conversion of homocysteine to methionine ∞ Generation of thymidylate ∞ Conversion of serine to glycine ∞ Purine synthesis ∞ Histidine metabolism Folate reductase DHF reductase
  19. 19. Causes Of Folic Acid Deficiency Nutritional (old age, poverty, special diets) Malabsorption (Tropical sprue, partial gastrectomy, jejunal resection) Increased requirements Pregnancy, infancy, disseminated cancer, increased hematopoiesis Excess urinary loss (active liver disease, congestive heart failure) Drugs (anticonvulsants eg. phenytoin) Mixed (liver disease, alcoholism)
  20. 20. Clinical Features  Signs & Symptoms :  Similar to vitamin B12.  No neurologic abnormalities, unlike vitamin B12 deficiency.  Neural tube defects found.  Vascular diseases. (associated with high levels of homocysteine)

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