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Anemia is a disorder that results in a decrease in the ability of the blood to carry oxygen. Anemia by itself is not a diagnosis but merely a sign of underlying disease. The first classification of anemia is best done by examination of the blood smear. Initial clinical diagnosis of anemia is generally based upon classification of the anemia as regenerative or nonregenerative. Regenerative anemias are characterized by increased production of erythrocytes, while nonregenerative anemia show nothing of erythrocyte production. In addition, anemias are classified by certain indices that give the clinician some knowledge of cell size (microcytic, normocytic, microcytic) as well as hemoglobin content (hypochromic, normochromic, or hyperchromic). This paper will focus on microcytic anemias. The mean corpuscular volume (MCV) or average erythrocyte size is usually determined directly by automated hematology analyzers, but it can be calculated manually by the formula: (Hct x 10)/ RBC count (millions) = MCV Microcytosis is indicated by a MCV value that is below the reference interval. Furthermore, microcytosis often is accompanied by a high red blood cell distribution width (RDW) value. This value is a measure of anisocytosis or variation in erythrocyte size. Several factors influence the MCV value. Factors that associated with microcytosis include immature animals, iron lack or deficiency, portosystemic shunts,
Asian dog breeds (Akita, Shiba Inu, Chow Chow), and certain nutritional deficiencies. The primary focus of this discussion is microcytic anemia. The only way to diagnose anemia is with a blood test. Generally, a full blood count is done. Apart from reporting the amount of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells, which is an important tool in distinguishing between the causes. The most common type of anemia overall is iron deficiency anemia, which is most often microcytic. Much rarer causes are hemoglobinopathies such as sickle cell anemia and thalassemia. Iron deficiency anemia is caused when the dietary intake or absorption of iron is insufficient. Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red cells. Body iron is regulated by the rate of iron absorption rather than iron excretion. In addition, iron absorption is regulated by the amount of storage iron and rate of erythropoiesis. Ceruloplasmin, a copper containing protein, is necessary for the transfer of iron from intestinal epithelium and macrophages to plasma transferrin. Iron is transported in the plasma bound to transferrin and is measured clinically as serum iron. The total serum transferrin concentration is measured as total iron binding capacity (TBIC). Usually only 1/3 of the transferrin binding sites are occupied by iron. This is expressed as percent saturation. Iron is stored in macrophages as ferritin and hemosiderin. Ferritin is a water soluble, iron-protein complex. Small amounts of ferritin circulate in the plasma and can
be measured as an indirect indicator of the storage iron pool. However, the laboratory test to measure ferritin concentration is species-specific and only available for specimens from dogs, cats, horses, and human beings. Serum ferritin is usually decreased in iron deficiency. It is important to note that ferritin is also an acute phase protein; its concentration can be elevated in inflammation and some forms of neoplasia. Cytologically, hemosiderin can be demonstrated in the bone marrow of most healthy animals except cats by Perl’s (Prussian blue) staining. Hemosiderin is insoluble in water and will persist in processed cytologic and histologic bone marrow specimens. In iron deficiency anemia, there is a paucity or absence of stainable iron (hemosiderin) in the bone marrow. In iron deficiency, a decrease in the MCV will precede a decrease in the mean corpuscular hemoglobin concentration (MCHC). Hypochromic cells have a narrow rim of lightly stained hemoglobin and greater than normal central pallor due to decreased hemoglobin (Hg) concentration and cells being thin (leptocytes). Affected erythrocytes also may be smaller or microcytic because extra cell divisions occur before a critical hemoglobin concentration is reached to arrest mitosis. Another cause for microcytic anemia is blood loss. Blood sucking parasites (fleas, ticks, hookworms), bleeding intestinal neoplasms, transitional cell carcinoma with urogenital bleeding, gastrointestinal ulcers, thrombocytopenia, inherited hemostatic disorders, hemorrhagic colitis, chronic intravascular hemolysis with hemoglobinuria, and excessive blood draws for blood donation and diagnostic purposes can promote iron deficiency anemia.
In acute blood loss, some degree of erythrocyte regeneration (reticulocytes, except in horses) may keep the MCV within the reference interval. With chronic blood loss, iron is progressively depleted resulting in insufficient iron stores for reticulocyte production. The MCV subsequently decreases. A negative iron balance can occur with loss of as little as 3-4 ml of blood per day. A decreased serum protein concentration or panhypoproteinemia (low normal to low albumin and globulin concentrations) if the blood loss is sustained. Concurrent thrombocytosis due to an increase in erythropoietin production. Since milk does not contain much iron, dietary iron deficiency may be seen in nursing animals. In young, rapidly growing animals on an all-milk diet, transient iron deficiency may lead to mild anemia. This situation occurs within first week of life in piglets that are reared on concrete flooring without access to soil. Cautious parental or oral supplementation with iron may be necessary. Deficiencies of vitamin E, which is required for heme synthesis, also result in hypoferremia (low concentration of circulating iron). Excessive iron supplementation, in the presence of hypoferremia, may increase free iron concentration in the circulation causing peroxidation of cellular membranes and necrosis within the heart, liver, and skeletal muscle. Copper deficiency is another cause of microcytic anemia. Ceruloplasmin is a copper-containing protein that is synthesized by liver. This protein is necessary for transfer of iron from gut epithelium and macrophages to transferring (an iron transporting protein). Generally, copper deficiency is rarely encountered.
Although copper deficiency is rare, some Bedlington Terriers are genetically predisposed to the development of copper storage disease. Affected individuals may become copper deficient as a result of long term dietary copper restriction and administration of copper chelating drugs. Microcytic, hypochromic anemia has been documented with long-term copper restriction and chelation therapy. This condition may be due to chelation of copper and other bivalent cations including iron. Lastly, Pyridoxine or vitamin B6 is a cofactor for heme synthesis. Deficiency of this vitamin is rare but may leads to failure of iron utilization.
http://www.gomcl.com/hema/anemia/
http://www.copacabanarunners.net/i-anemia.html
http://www.vet.uga.edu/vpp/clerk/mwoods/
Asian dog breeds (Akita, Shiba Inu, Chow Chow), and certain nutritional deficiencies. The primary focus of this discussion is microcytic anemia. The only way to diagnose anemia is with a blood test. Generally, a full blood count is done. Apart from reporting the amount of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells, which is an important tool in distinguishing between the causes. The most common type of anemia overall is iron deficiency anemia, which is most often microcytic. Much rarer causes are hemoglobinopathies such as sickle cell anemia and thalassemia. Iron deficiency anemia is caused when the dietary intake or absorption of iron is insufficient. Iron is an essential part of hemoglobin, and low iron levels result in decreased incorporation of hemoglobin into red cells. Body iron is regulated by the rate of iron absorption rather than iron excretion. In addition, iron absorption is regulated by the amount of storage iron and rate of erythropoiesis. Ceruloplasmin, a copper containing protein, is necessary for the transfer of iron from intestinal epithelium and macrophages to plasma transferrin. Iron is transported in the plasma bound to transferrin and is measured clinically as serum iron. The total serum transferrin concentration is measured as total iron binding capacity (TBIC). Usually only 1/3 of the transferrin binding sites are occupied by iron. This is expressed as percent saturation. Iron is stored in macrophages as ferritin and hemosiderin. Ferritin is a water soluble, iron-protein complex. Small amounts of ferritin circulate in the plasma and can
be measured as an indirect indicator of the storage iron pool. However, the laboratory test to measure ferritin concentration is species-specific and only available for specimens from dogs, cats, horses, and human beings. Serum ferritin is usually decreased in iron deficiency. It is important to note that ferritin is also an acute phase protein; its concentration can be elevated in inflammation and some forms of neoplasia. Cytologically, hemosiderin can be demonstrated in the bone marrow of most healthy animals except cats by Perl’s (Prussian blue) staining. Hemosiderin is insoluble in water and will persist in processed cytologic and histologic bone marrow specimens. In iron deficiency anemia, there is a paucity or absence of stainable iron (hemosiderin) in the bone marrow. In iron deficiency, a decrease in the MCV will precede a decrease in the mean corpuscular hemoglobin concentration (MCHC). Hypochromic cells have a narrow rim of lightly stained hemoglobin and greater than normal central pallor due to decreased hemoglobin (Hg) concentration and cells being thin (leptocytes). Affected erythrocytes also may be smaller or microcytic because extra cell divisions occur before a critical hemoglobin concentration is reached to arrest mitosis. Another cause for microcytic anemia is blood loss. Blood sucking parasites (fleas, ticks, hookworms), bleeding intestinal neoplasms, transitional cell carcinoma with urogenital bleeding, gastrointestinal ulcers, thrombocytopenia, inherited hemostatic disorders, hemorrhagic colitis, chronic intravascular hemolysis with hemoglobinuria, and excessive blood draws for blood donation and diagnostic purposes can promote iron deficiency anemia.
In acute blood loss, some degree of erythrocyte regeneration (reticulocytes, except in horses) may keep the MCV within the reference interval. With chronic blood loss, iron is progressively depleted resulting in insufficient iron stores for reticulocyte production. The MCV subsequently decreases. A negative iron balance can occur with loss of as little as 3-4 ml of blood per day. A decreased serum protein concentration or panhypoproteinemia (low normal to low albumin and globulin concentrations) if the blood loss is sustained. Concurrent thrombocytosis due to an increase in erythropoietin production. Since milk does not contain much iron, dietary iron deficiency may be seen in nursing animals. In young, rapidly growing animals on an all-milk diet, transient iron deficiency may lead to mild anemia. This situation occurs within first week of life in piglets that are reared on concrete flooring without access to soil. Cautious parental or oral supplementation with iron may be necessary. Deficiencies of vitamin E, which is required for heme synthesis, also result in hypoferremia (low concentration of circulating iron). Excessive iron supplementation, in the presence of hypoferremia, may increase free iron concentration in the circulation causing peroxidation of cellular membranes and necrosis within the heart, liver, and skeletal muscle. Copper deficiency is another cause of microcytic anemia. Ceruloplasmin is a copper-containing protein that is synthesized by liver. This protein is necessary for transfer of iron from gut epithelium and macrophages to transferring (an iron transporting protein). Generally, copper deficiency is rarely encountered.
Although copper deficiency is rare, some Bedlington Terriers are genetically predisposed to the development of copper storage disease. Affected individuals may become copper deficient as a result of long term dietary copper restriction and administration of copper chelating drugs. Microcytic, hypochromic anemia has been documented with long-term copper restriction and chelation therapy. This condition may be due to chelation of copper and other bivalent cations including iron. Lastly, Pyridoxine or vitamin B6 is a cofactor for heme synthesis. Deficiency of this vitamin is rare but may leads to failure of iron utilization.
http://www.gomcl.com/hema/anemia/
http://www.copacabanarunners.net/i-anemia.html
http://www.vet.uga.edu/vpp/clerk/mwoods/
