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Megaloblastic Anemia

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Megaloblastic Anemia
Megaloblastic anemias
Definition: groups of anemias characterized by macrocytosis (in the peripheral blood) and megaloblastic changes in the bone marrow.
The megaloblasts are large blasts – bone marrow.
In periphery= macrocytosis= macrocytic anemia
Cause: IMPAIRED DNA SYNTHESIS due to folate/ B12 deficiency
Vitamin B12 is involved in the synthesis of methionine from homocysteine;methionine is necessary for the synthesis of myeline; B12 deficiency will explain the neurological manifestation, because of demyelination.
Also B12 is involved in the reaction that transforms folic acid from inactive form (methyl TH4) in the active form (TH4).
Folic acid is involved in biosynthesis of nucleic acids (DNA)
DNA synthesis impairment:
 Affects tissues with rapid turnover: hematopoietic precursors, gastrointestinal epithelial cell
 Takes longer for nucleus to mature, but cytoplamic synthesis is not affected => Larger cells => megaloblastic haematopoiesis
Megaloblastic changes in the bone marrow (BM):
 On the erythroid line: abnormal precursors of erythrocytes called megaloblasts (large cells)
 On the granulocytic line: gigantic metamyelocytes
 On the megacariocytic line: large megacariocytes, with polilobulated nucleus.
Because of the destruction of the abnormal precursors in the BM (ineffective erythropoiesis, granulopoiesis, megacariopoiesis) on the hemogram we have macrocytic anemia/ leucopenia/trombocytopenia.
On the peripheral blood smear: macrocytes, hypersegmented neutrophils.
Source for both B12 and folate: exogenous.
B12:
Source: animal (meat, dairy products); usually dietary intake far exceeds needs => a deficiency is almost always due to malabsorbtion (exception: true vegetarians and their breast-fed infants).
1 μg is necessary every day.
Liver deposits last about 3-5 years.
Serum level: 200-600pg/ml.
Absorption takes place in the terminal ileonum and is dependant of intrinsic factor (IF, Castle’s) secreted by parietal

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