Anemia occurs when the hemoglobin concentration of blood is reduced below normal levels. This condition may result from chronic blood loss, abnormal hemolysis, or nu-tritional deficiency. Many therapeutic agents can induce this change in hemoglobin as an unwanted side effect.
Different classifications of anemia are based in part on the pathophysiological factor inducing the decreased hemoglobin concentration. Anemias due to cell hy-poproliferation include aplastic anemia and iron defi-ciency anemia. Hemolytic anemia results from exces-sive destruction of red blood cells. Megaloblastic anemia, sideroblastic anemia, and iron deficiency ane-mia result from an abnormality in the maturation of red blood cells.
Iron is a constituent of hemoglobin, and iron deficiency will lead to a decrease in hemoglobin synthesis. Since iron is conserved by the body, deficiency usually results from acute or chronic loss of blood or insufficient iron intake during physiological stress. Infants, children, and premenopausal women require more iron than do men because of the increased demand that occurs during growth, pregnancy, and loss of blood during menstrua-tion. In tropical climates, bleeding due to an infestation by the hookworm parasite is a common cause of iron deficiency.
The symptoms of iron deficiency anemia include fa-tigue, weakness, shortness of breath, and soreness of the tongue. Therapeutic iron supplementation is used to treat this type of anemia. Oral administration of ferrous salts (generic ferrous sulfate, Feosol, Slo Fe) is preferred, but parenteral iron (iron dextran, InfeD) can be given if oral therapy fails. Toxic reactions occur more frequently after parenteral iron administration. Gastrointestinal disturbances are common following oral dosages.
Antacids may decrease the gastrointestinal absorp-tion of iron. Iron may chelate or decrease the gastrointestinal absorption of drugs like levodopa and tetracy-cline.
Megaloblastic anemia is characterized by the appear-ance of large cells in the bone marrow and blood due to defective maturation of hematopoietic cells. Folic acid or vitamin B12 deficiency will result in this type of ane-mia. Malabsorption, impaired use, chronic infections, and drugs can lead to folic acid or vitamin B12 deficiency.
Folic acid or folate salts (Folvite) are administered to correct folate-deficient megaloblastic anemia. Vita-min B12–deficient patients receive cyanocobalamin sup-plements. Dosage is very important, since patients with severe megaloblastic anemia may develop hypokalemia and die suddenly if treated intensively with vitamin B12. Vitamin B12 deficiency due to a lack of gastric intrinsic factor results in pernicious anemia. This type of mega-loblastic anemia causes neurological damage if it is not treated. Treatment of Vitamin B12–deficient megaloblas-tic anemia with folic acid may improve the symptoms; however, neurological damage may still occur if vitamin B12 intake is not supplemented. Parenteral injections of vitamin B12 must be given.
Sideroblastic anemia is characterized by excessive iron in the cells that cannot be incorporated into porphyrin to form heme. Although it is rare, the most common cause of sideroblastic anemia is alcoholism and pyridoxine de-ficiency. Pyridoxine is required for the formation of pyri-doxal phosphate, a coenzyme in porphyrin synthesis.
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