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Megaloblastic Anemias

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Megaloblastic Anemias Dr. M. Waseem Ashraf PGT Pediatrics BBH, Rawalpindi Anemia Anemia is defined as a reduction of the red blood cell (RBC) volume or hemoglobin ... – PowerPoint PPT presentation

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Title: Megaloblastic Anemias


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Megaloblastic Anemias
  • Dr. M. Waseem Ashraf
  • PGT Pediatrics
  • BBH, Rawalpindi

3
Anemia
  • Anemia is defined as a reduction of the red blood
    cell (RBC) volume or hemoglobin concentration
    below the range of values occurring in healthy
    persons.

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Megaloblastic Anemias
  • Megaloblastic anemia is a subset of macrocytic
    anemias in which maturation phase of
    erythropoiesis in bone marrow is abnormal,
    resulting in erythroid precursors that are
    enlarged (MCV gt 100fL) and show failure of
    nuclear maturation (megaloblasts).

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Causes of Megaloblastic Anemias
  • Vitamin B12 Deficiency
  • Folate Deficiency
  • Other causes
  • Orotic acid uria
  • Thiamine responsive megaloblastic anemia
  • Arsenic poisoning
  • Nitrous oxide inhalation
  • Chemotherapy

7
Causes of B12 Deficiency
  • Inadequate dietary intake
  • Very rare, only in strict vegetarians (vegans)
  • Failure of absorption due to intrinsic factor
    deficiency
  • Pernicious anemia
  • Total and subtotal gastrectomy
  • Terminal ileal disease
  • Crohns disease
  • Strictures and fistulas that bypass terminal
    ileum
  • Surgical removal of terminal ileum

8
Causes of B12 Deficiency
  • Competition for vitamin B12 by intestinal
    pathogens
  • Bacterial overgrowth (blind loop Syndrome)
  • Diphyllobothrium latum infestation (fish tape
    worm)
  • Congenital deficiency of transcobalamine II

9
Causes of Folate Deficiency
  • Folate deficincy diet
  • Alcoholism
  • Poverty
  • Failure of absorption
  • Tropical sprue
  • Other malabsorptive states
  • Increased Demand
  • Pregnancy
  • Infancy
  • States of increased DNA Synthesis
  • Malignant neoplasms
  • Erythroid hyperplasia in congenital hemolytic
    anemia

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Causes of Folate Deficiency
  • Anti Folate drugs
  • Anti cancer as methotrexate
  • Anti convulsants as hydantoin

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Patho-physiology
  • Megaloblastic anemias result from conditions in
    which nucleic acid synthesis is abnormal, as in
    vitamin B12 and Folate deficiency.
  • Vitamin B12 and Folic acid play role as cofactors
    in the conversion of deoxyuridine to deoxy
    thymidine, an essential step in the synthesis of
    DNA.

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Red Cell Changes
  • When DNA synthesis is abnormal, erythropoiesis
    changes from normoblastic to megaloblastic.
  • Megaloblasts differ from normoblasts in that they
    are larger and show delayed nuclear maturation
    but normal cytoplasmic hemoglobinization,
    (nuclear cytoplasmic asynchrony).
  • The late megaloblast shows a primitive nucleus
    and a fully hemoglobinized cytoplasm in contrast
    to late normoblast which has a pyknotic nucleus.

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Red Cell Changes
  • Delayed maturation leads to accumulation of
    erythrocyte precursor cells. The bone marrow is
    hypercellular and contains large number of early
    megaloblasts.
  • As a result of intra-medullary hemolysis or
    ineffective erythropoeisis, many megaloblasts
    undergo destruction in the bone marrow before
    maturation, aggravating the anemia and producing
    mild elevation in serum bilirubin and lactate
    dehydrogenase.
  • The peripheral blood smear shows macrocytosis,
    anisocytosis and poikilocytosis. Oval forms
    (macro-ovalocytes) are prominent and Howel-Jolly
    bodies, consisting of nuclear debris are
    occasionally seen.

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Neutrophil changes
  • Neutrophil precursors in the bone marrow show
    marked enlagement,, Giant Metamyelcytes are
    characteristic.
  • On peripheral film, neutrophils show
    Hypersegmented nuclei with many cells showing
    more than 5 lobes.

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Neutrophil changes
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Changes in other cells
  • Cells having high rate of turnover are effected
    more

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Changes in other cells
  • Cells show enlargement and nuclear abnormalities.
  • Cervical smears may show changes similar to those
    of dysplasia.

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Features of Folate Deficiency
  • Mild mageloblastic anemia has been seen in very
    low birth weight infants and folate
    supplementation is advised.
  • Peak incidence in 4-7 months of age.
  • Clinical features include weakness, pallor,
    fatigue, irritbility, inadequate weight gianand
    chronic diarrhea.
  • Hemorrhages from thronbocytopenia may occur in
    advanced caess.
  • It may accompany kwashiorkor. Marasmus or sprue.

20
Lab Findings
  • Macrocytic anemia MCV gt 100fL
  • Reticulocytopenia
  • Anisocytosis and poikilocytosis
  • Nuclested RBCs with megaloblastic morphology
  • Neutropenia with thrombocytopenia
  • Large Hypersegmented neutrophils

21
Lab Findings
  • Low serum folate levels, lt3ng/dL (5-20ng/dL)
  • Low RBC folate levelRaised serum LDH
  • Hypercellular bone marrow with megaloblastic
    change nad giant metamyelocytes.

22
Treatment
  • Oral or parentral folic acid 0.5-1mg/day
  • 3-4 weeks

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Clinical Features of B12 Deficiency
  • Non specific symptoms like weakness, fatigue,
    failure to thrive, irritability, pallor,
    glossitis, vomiting, diarrhea.
  • Neurological symptoms include paresthesias,
    sensory deficits, hypotonia, seizyres,
    developmental delay, developmental regression,
    neuropsychiatric changes.
  • Neurological symptoms can occur in the absence
    ofhematological abnormalities.

24
Lab Findings
  • Hematological findings ar similar to that of
    folate deficience
  • Decreased serum folate levels
  • Raised serum methyl malonic acid and
    homocysteeine levels
  • Serum iron and folate levels are normal or raised.

25
  • Inj. Vitamin B12 mg
  • Daily for 14 days (in case of neurological
    disease)
  • Weekly for 4 weeks
  • Monthly for life long

26
Summary
  • Deficiency of folate or B12
  • Macrocytic anemias with or with out other
    cytopenias
  • Slowly developing anemia, usually well
    compensated
  • Response to therapy rapid and dramatic
  • Treatment necessary to avoid other complications
  • Anemia is secondary to other disease process
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