Megaloblastic anemia

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basic info about megaloblastic anaemia and its treatment.

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Megaloblastic anemia

  1. 1. MEGALOBLASTIC ANEMIA
  2. 2. What is Megaloblastic anemia? Megaloblastic anemias are characterized by the presence of abnormally large developing red cells in the bone marrow.  The marrow is usually cellular.  Anemia is based on ineffective erythropoiesis.   These red cells are large in shape
  3. 3. Etiology Cobalamin: Deficiency / abnormal metabolism.  Folate: Deficiency / abnormal metabolism / antifolate drugs.  Drugs interfering with synthesis of DNA.  Rarely- orotic aciduria, AML, myelodysplasia.  Arsenic poisoning  Nitrous oxide inhalation. 
  4. 4. Cobalamin / Vitamin B12 Forms : 1. Ado (2-deoxyadenosyl) form; found in mitochondria; Cofactor for Methyl Malonyl CoA Mutase. 2. Methyl cobalamin; found in plasma,cytoplasm; Cofactor for Methionine synthase. 3. Hydroxocobalamin
  5. 5. Absorption Active Passive 1% • Intrinsic factor • buccal • duodenal • ileal
  6. 6. Absorption
  7. 7. Proteins ◦ ◦ ◦ ◦ ◦ involved in active absorption are, Intrinsic factor { IF=HCl }. Haptocorrins. Cubilin. Transcobalamin II. TC I – cobalamin analogues. IFs are destroyed in illeal cells Cobalamin enters portal blood after 6 hrs of oral ingestion.
  8. 8. Amount recirculated in bile 0.5 - 5µg.  Body stores 2-3mg.  Sufficient for 3-4 years without dietary intake of cobalamin.  Daily requirement: 1-3µg.  Only traces are excreted in urine; in pharmacological doses large part is excreted in urine. 
  9. 9. Causes of cobalamin defiency   Nutritional –Vegans (legumes) Abnormalities - TC II deficiency; Congenital absence of IF  Malabsorption Gastrectomy (total / partial) Tropical sprue Intestinal stagnant loop syndrome Selective malabsorption Ileal resection Crohn’s disease Pernicious anemia
  10. 10. Folate Destroyed easily by cooking especially in large amounts of water.  Storage in liver (sufficient for 3-4 months)  Total body folate around 10mg.  Daily requirements: 200-300µg.  Pregnancy: 400µg. 
  11. 11. Absorption – • Upper small intestine. Transport – • Plasma protein bound 1/3. • Considerable enterohepatic circulation occurs • Alcohol interferes with the release of methyl-THFA by hepatocytes • only traces are excreted; but in pharmacological doses 50-90% are excreted.
  12. 12. Epithelial surfaces: macrocytosis  Infertility in both men and women  CVD – IHD.  Malignancy : Acute Lymphoblastic Leukemia of childhood.  Neurologic : bilateral peripheral neuropathy and degeneration; Alzhiemer’s disease  Maternal: prematurity; abortion; neural tube defects  Children: poor brain development ; impaired intellectual development. 
  13. 13. Haematological findings Oval macrocytes  Anisocytosis (varied sizes )  Poikilocytosis ( abnormal shaped )  Hypersegmanted neutrophils  Howell – jolly bodies  Unconjugated bilirubin  Haptoglobins  Urine – urobilinogen, hemosiderin. 
  14. 14. Howell jolly bodies are the basophilic nuclear remnants in the circulating erythrocytes
  15. 15. ELISA findings Serum cobalamin normal:160-1000 ng/L severe anemia <100ng/L  Serum folate normal: 2µg/L-15µg/L  Red cell folate normal: 160 - 640µg/L. 
  16. 16. Treatment
  17. 17. Cobalamin:  Hydroxocobalamin is preferred because it is more highly protein-bound and therefore remains longer in the circulation.  Initial therapy should consist of 100–1000 mcg of vitamin B12 intramuscularly daily or every other day for 1–2 weeks to replenish body stores.  Maintenance therapy consists of 100– 1000 mcg intramuscularly once a month for life.
  18. 18. If neurologic abnormalities are present, maintenance therapy injections should be given every 1–2 weeks for 6 months before switching to monthly injections.  Oral doses of 1000 mcg of vitamin B12 daily are usually sufficient to treat patients with pernicious anemia who refuse or cannot tolerate the injections.  After pernicious anemia is in remission following parenteral vitamin B12 therapy, the vitamin can be administered intranasally as a spray or gel. 
  19. 19. Folate: 5-15mg; for 4 months  Parenteral administration of folic acid is rarely necessary, since oral folic acid is well absorbed even in patients with malabsorption syndromes.  Therapy should be continued until the underlying cause of the deficiency is removed or corrected.  Therapy may be required indefinitely for patients with malabsorption or dietary inadequacy. 
  20. 20. Folic acid supplementation to prevent folic acid deficiency should be considered in high-risk patients, including pregnant women, patients with alcohol dependence, hemolytic anemia, liver disease, or certain skin diseases, and patients on renal dialysis.  Prophylactic folic acid foods – bread, wheat, rice.  Potasssium supplements if needed.  Antiplatelets if needed. 
  21. 21. Non megaloblastic but macrocytic anemias RBC’s are round not oval  There are no hypersegmented neutrophils and howell – jolly bodies 
  22. 22. Macrocytosis without megaloblastosis

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