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    Megaloblastic Anaemia

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    Jesmin_36
    1. Megaloblastic anemia can be caused by vitamin B12 or folate deficiency, abnormalities in their metabolism, or defects in DNA synthesis. 2. In Western countries, the most common cause is pernicious anemia, an autoimmune disease where the stomach cannot produce intrinsic factor needed for B12 absorption. 3. Symptoms include fatigue, pale skin, sore tongue, neurological problems, and bleeding due to low platelets. Laboratory tests show large red blood cells and low B12 levels.

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    Megaloblastic Anaemia

    Uploaded by

    Jesmin_36
    298 views11 pages
    1. Megaloblastic anemia can be caused by vitamin B12 or folate deficiency, abnormalities in their metabolism, or defects in DNA synthesis. 2. In Western countries, the most common cause is pernicious anemia, an autoimmune disease where the stomach cannot produce intrinsic factor needed for B12 absorption. 3. Symptoms include fatigue, pale skin, sore tongue, neurological problems, and bleeding due to low platelets. Laboratory tests show large red blood cells and low B12 levels.

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    1. Megaloblastic anemia can be caused by vitamin B12 or folate deficiency, abnormalities in their metabolism, or defects in DNA synthesis. 2. In Western countries, the most common cause is pernicious anemia, an autoimmune disease where the stomach cannot produce intrinsic factor needed for B12 absorption. 3. Symptoms include fatigue, pale skin, sore tongue, neurological problems, and bleeding due to low platelets. Laboratory tests show large red blood cells and low B12 levels.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    298 views11 pages

    Megaloblastic Anaemia

    Uploaded by

    Jesmin_36
    1. Megaloblastic anemia can be caused by vitamin B12 or folate deficiency, abnormalities in their metabolism, or defects in DNA synthesis. 2. In Western countries, the most common cause is pernicious anemia, an autoimmune disease where the stomach cannot produce intrinsic factor needed for B12 absorption. 3. Symptoms include fatigue, pale skin, sore tongue, neurological problems, and bleeding due to low platelets. Laboratory tests show large red blood cells and low B12 levels.

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    Download as PPT, PDF, TXT or read online from Scribd
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    of 11

    MEGALOBLASTIC

    ANAEMIA
    VIT B12 DEFICIENCY
    CAUSES OF MEGALOBLASTIC
    ANAEMIA
    VIT B12 DEFICIENCY
    FOLATE DEFICIENCY
    ABNORMALITIES OF VIT B12 OR
    FOLATE METABOLISM
    DEFECTS OF DNA SYNTHESIS:
     Congenital enzyme deficiencies
     Acquired enzyme defienciencies
    In Western countries, severe deficiency is
    usually by pernicious anaemia.
    Less commonly, it may caused by
    veganism in which the diet lacks B12,
    gastrectomy or small intestinal lesions.
    The deficiency takes at least 2 years to
    develop when there is severe
    malabsorption of B12 from diet.
    Nitrous oxide, however, may rapidly
    inactivate body B12
    VIT B12 DEFICIENCY
    Low dietary intake (strict vegetarian)
    Absorption:
     Pernicious A / Gastrectomy- malabsorption
    syndromes- terminal ileal disorder
     Congenital deficiency of intrinsic factor (IF)/
    transcobalamin II
    In small gut: Vit B12 binds IF which is synthesized by the gastric
    parietal cells

    The IF-B12 complex can then bind to a specific surface receptor


    for IF, cubilin, which then binds to a second protein, amnionless which
    directs endocytosis of the cubilin IF-B12 complex in the distal ileum

    Vit B12 is then absorbed & IF is destroyed

    Vit B12- absorbed in portal blood = becomes attached to the plasma-


    binding protein- transcobalamic---which delivers B12 to bone marrow (BM)
    and other tissues
    PERNIOUS ANAEMIA
    AUTOIMMUNE
    DISEASE
    CHARACTERIZED BY
    ATROPHY OF THE
    GASTRIC MUCOSA
    RESULTING = failure
    of the IF production &
    hence failure of B12
    absorption
    CLINICAL FEATURES OF VIT B12
    DEFICIENCY
    • FATIGUE, HEADACHE, PALPITATION, ANGINA, PALLOR,
    TACHYCARDIA

    3. SKIN HAS A LEMON YELLOW (MILD JAUNDICED) = excess


    breakdown of haemoglobin resulting from increased ineffective
    erythropoiesis in BM

    5. GLOSSITIS (a beefy-red sore tongue) & ANGULAR STOMATITIS

    7. PURPURA & BLEEDING TENDENCY DUE TO


    THROMBOCYTOPENIA

    9. SEVERE VIT B12 DEFICIENCY ANAEMIA= Progressive


    neuropathy affecting the sensory nerves & posterior & lateral
    columns
    LAB FINDINGS
    Serum B12 low
    MCV>95 fl (severe 120-140 fl)
    Macrocytes- typically oval in shape
    Reticulocyte count decreased
    Total WC & platelet count may moderately
    reduced
    Neutrophils show hypersegmented nuclei( with
    6/> lobes)
    BM= hypercellularity & erythroblasts are large
    Serum unconjugated bilirubin & LDH raised as
    result of marrow cell breakdown
    Hypersegmented Neutrophils

    Multilobed polymorphonuclear
    neutrophils are
    characteristically found in
    megaloblastic anaemia which
    is usually consequent on
    deficiency of either vitamin
    B12 or folic acid. In normal
    people, not more than 3% of
    neutrophils have more than
    five lobes; in megaloblastic
    anaemia the average lobe
    count is increased and
    neutrophils with 6, 7, or 8
    lobes may be seen. This film
    also shows macrocytosis,
    anisocytosis and poikilocytosis
    Schiling Test – used to distinguish malabsorption from
    inadequate diet.
    A Schilling 24-hour urine test is done to evaluate whether
    vitamin B12 is being absorbed by the body. It is usually
    done when the results of a vitamin B12 blood test are
    low.
    A Schilling test may be given in two parts. Part one
    measures the amount of vitamin B12 passed in urine
    after a known amount of the vitamin tagged with a
    radioactive substance is swallowed. If the intestines
    absorb vitamin B12 normally, a certain amount of the
    vitamin (up to 25% of the amount swallowed) will be
    passed in the urine. If the intestines cannot absorb the
    vitamin normally, very little or no vitamin B12 will be
    present in the urine.
    TREATMENT
    Hydroxylocobalamine

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