Download Anemias and Abnormal Red Cell Morphology

 Low
hemoglobin concentration
and/or hemoglobin abnormality
 Reduction in RBC count
 Reduction in hematocrit
 Immature reticulocytes
 Abnormal RBC morphology
Inherited
 Reduced red cell survival as in hemolytic anemias
 Hemoglobin defects e.g. sickle cell hemoglobin
 Acquired
 Reduced RBC production e.g. iron, B12, and folic acid;
marrow replacement by tumor cells, or marrow aplasia
 Increased RBC destruction (hemolytic anemia) e.g.
immune destruction, chemicals, and infections.
 Systemic illnesses e.g. anemia of chronic disease, renal
failure, liver disease, and cardiac disease
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Iron is absorbed by the lining of the gastrointestinal
tract.
The body only absorbs a small fraction of the iron
ingested.
The iron absorbed is released into the blood stream,
where a protein called transferrin attaches to it and
delivers the iron to the liver.
Iron is stored in the liver as ferritin and released as
needed to make new red blood cells in the bone
marrow.
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Chronic Blood Loss from:
 Menorrhagia or postmenopausal bleeding
 Gastrointestinal bleeding from esophageal varices, hiatal
hernia, peptic ulcer, Helicobacter infection, aspirin ingestion
(or other anti-inflammatory drugs), gastrectomy, carcinoma,
hookworm, colitis, diverticulitis, or hemorrhoids.
Increased Demands from:
 Growth or pregnancy associated with a poor diets
Malabsorption from:
 Postgrastrectomy, any disease of the digestive system such
as gluten-induced gastroenteropathy
Poor Diet
 Rarely the only cause in developed countries
Occurs because iron is needed to form heme to make
hemoglobin. When not enough iron is available, the resulting
cells are small with low amounts of hemoglobin.
 Iron Deficiency anemia is a microcytic, hypochromic anemia.
 Blood Smear shows anisocytosis (varying size of cells),
poikilocytosis (varying shape of cells), including target cells,
and “pencil” cells.
 Serum iron levels low, serum ferritin reduced, raised
transferrin, with a raised unsaturated iron-binding capacity.
 Bone marrow is not needed to diagnose - erythroblasts have a
ragged cytoplasm and iron stores are absent.
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General features of anemia
 A minority of patients have koilonychia
(ridged, brittle nails), angular cheilosis
(sore corners of mouth), pica (abnormal
appetite), and hair thinning.
 Iron deficiency anemia is the most
common cause of anemia in all countries
of the world.
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In megaloblastic anemia the nuclear
development is delayed because of a
deficiency of vitamin B12 or folic acid (folate).
 Hemoglobin continues to be made while the
cells is waiting for the feedback from a mature
nucleus to expel itself.
 The result is a very large RBC before the
nucleus is finally mature enough to be
expelled.
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In order to absorb vitamin B12, it must bind to
intrinsic factor which is produced by cells lining the
stomach (parietal cells).
The B12 intrinsic factor complex attaches to receptors
in the ileum where it is absorbed.
Normal body stores of B12 (mostly in the liver), are
sufficient to last 2 to 4 years.
Inadequate Diet in:
 Vegans (takes several years)
 Infants born of B12 deficient mothers and breast fed by them
 Malabsorption
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 Autoimmune gastritis and other autoimmune diseases
 Reduced production of intrinsic factor (IF)
 Gastrectomy
 Rarely – congenital IF deficiency or abnormality
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Treatment
 Intramuscular injections of hydroxocolbalamin (B12 made by bacteria
for commercial use). Every 2-3 days for 6 injections, then continued
every 3 months for life.
Folate (Folic Acid) occurs in many foods,
especially green vegetables and liver.
 Normal diet contains about 200-250 µg.
About 50% of ingested folic acid is absorbed.
Daily adult requirement is 100 µg.
 Body stores are sufficient for 4 months.
 Folate is absorbed through the upper small
intestine with the help of a specific protein.
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Poor dietary intake
 Increased utilization (e.g. pregnancy or
hemolytic anemia). Folate supplements are given
to women of childbearing age to help prevent
neural tube defects of the fetus.
 Malabsorption (in gluten-induced
gastroenteropathy or tropical sprue)
 Increased cell turnover and DNA synthesis
 Dialysis can easily remove folate from the blood
as it is loosely bound to protein in plasma
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The treatment for folate deficiency is basic:
 5 mg of folic acid orally daily for 4 months, then
determine amount of folate supplements needed by
the patient.