Megaloblastic Anemia free essay sample

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 b one 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. We will write a custom essay sample on Megaloblastic Anemia or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page ?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 ? g 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 cells of the stomach, the same cells that secrete chlorhidric acid. ?Transcobalamin II is responsible for transporting vit. B12. Causes of deficiency I. Dietary deficiency (true vegetarians) II. Malabsorption: 1. Lack of intrinsic factor: pernicious anemia, ga strectomy, congenital defect of IF 2. Diseases of the terminal ileonum: tropical sprue, celiac diseases, Crohn disease, Resections, cancer, selective malabsorption of vit. B12 (Immerslund sdr. ) 3. Intestinal consumption of Vit. B12: PARAZITES (Botriocefal), bacteria 4. Drugs: colchicine, neomicine III. Transport and usage defects: congenital deficiency of TC II, excess of TC I and TC III with high affinity for vit. B12 (chronic myeloproliferative diseases), long exposure to NO, enzymathic defects (meilmalonuria, homocistinuria) Pernicious anemia- Addison Biermer disease ?Autoimmune disease characterized by the presence of auto-antibodies against parietal cells and against IF, resulting in atrophic gastritis and malabsorption of B12 due to IF deficiency. For the autoimmune mechanism plede the presence of anti IF antibodies in 70% of the patients, the association with other autoimmune diseases ( Basedow disease) ? Onset after 40 years, higher incidence in nordic countries ? Patients present anemia, pallor, jaundice, glossitis, mild splenomegaly, neurological and psychiatric manifestations: paresthesias, weakness, dementia, incontinence, paraplegia. Labo ratory evaluation: macrocytic anemia (MCV100 fl) leucopenia, trombocytopenia blood smear: macrocytes, hypersegmented neutrophils reticulocytes-low BM: megaloblastic changes LDH ^, low serum cobalamine (