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University of Basrah

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anemia blood disorders red blood cells medical conditions

Summary

This document provides information on different types of anemia, including aplastic, hemolytic, and megaloblastic anemias. It describes the causes and effects of these conditions and highlights the role of red blood cells. The document is suitable for undergraduate-level study.

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APLASTIC ANEMIA It is anemia caused by the loss of function of the bone marrow. Poisons such as lead, benzene, or arsenic can be caused by gamma ray exposure, X-ray exposure, some industrial poisons, and even some drugs. As a result of these effects, the number...

APLASTIC ANEMIA It is anemia caused by the loss of function of the bone marrow. Poisons such as lead, benzene, or arsenic can be caused by gamma ray exposure, X-ray exposure, some industrial poisons, and even some drugs. As a result of these effects, the number of erythrocytes and leukocytes drops too low, and death may occur within a few weeks. HEMOLYTIC ANEMIA Various erythrocyte abnormalities, many of which are hereditary, make the cells fragile. Such erythrocytes break down easily and cause hemolysis, especially when passing through capillaries. HEMOLYTIC ANEMIA Another example of hemolytic anemias is thalassemias. Hb mutants that occur in thalesemia have abnormalities resulting from the construction of the polypeptide chain that makes up hemoglobin. It is also called Mediterranean anemia because it is usually seen in Mediterranean countries. Megaloblastic and pernicious anemia As a result of the reduction of B9 (folic acid) and B12 (cyanocobolamine) and any of the intrinsic factors released from the gastric mucosa, erythroblasts are slowed down in the bone marrow, resulting in oddly shaped, large megaloblasts. Both B9 and B12 vitamins are required for DNA construction. Because erythroblasts cannot divide quickly enough to form a normal number of erythrocytes, large oddly shaped and fragile membrane cells emerge. Megaloblastic anemia arises from folic acid deficiency Pernicious anemia develops in the deficiency of a glycolipid, one of the intrinsic factors that enable vitamin B12 absorption from the gastric mucosa.

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