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| ==Overview== | | ==Overview== |
| | [[Erythropoietin]] produced in the [[kidneys]] are the major stimulant of [[red blood cell]] (RBC) production as a response to anemia. Erythropoietin is stimulated by tissue hypoxia, that in turn stimulates erythroid progenitor cells to proliferate. The EPO levels follow a reverse relationship with the [[hemoglobin]] levels. Thus, in normal hosts, low levels of hemoglobin are associated with high levels of EPO. However, in patients with [[chronic kidney disease]] and [[anemia of chronic disease]]s the response may not be as strong as seen in patients without these comorbidities. |
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| ==Specific anemias== | | ==Pathophysiology== |
| * [[Anemia of prematurity]] occurs in premature infants at 2 to 6 weeks of age and results from diminished erythropoietin response to declining hematocrit levels
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| * [[Fanconi anemia]] is an hereditary disorder or defect featuring [[aplastic anemia]] and various other abnormalities
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| * [[Hemolytic anemia]] causes a separate constellation of symptoms (also featuring [[jaundice]] and elevated [[lactate dehydrogenase|LDH]] levels) with numerous potential causes. It can be [[autoimmune]], [[immune]], [[genetic disorder|hereditary]] or mechanical (e.g. [[heart surgery]]). It can result (because of cell fragmentation) in a microcytic anemia, a normochromic anemia, or (because of premature release of immature red blood cells from the bone marrow), a macrocytic anemia.
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| * [[Hereditary spherocytosis]] is a hereditary defect that results in defects in the RBC cell membrane, causing the erythrocytes to be sequestered and destroyed by the spleen. This leads to a decrease in the number of circulating RBCs and, hence, anemia.
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| * [[sickle-cell disease|Sickle-cell anemia]], a hereditary disorder, is due to [[Zygosity|homozygous]] hemoglobin S genes.
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| * [[Warm autoimmune hemolytic anemia]] is an anemia caused by autoimmune attack against red blood cells, primarily by IgG
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| * [[Cold agglutinin hemolytic anemia]] is primarily mediated by IgM
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| * [[Pernicious anemia]] is a form of [[megaloblastic anaemia]] due to [[vitamin B12]] deficiency dependent on impaired absorption of vitamin B12.
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| * [[Myelophthisic anemia]] or [[Myelophthisis]] is a severe type of anemia resulting from the replacement of bone marrow by other materials, such as malignant tumors or granulomas.
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| == Anemia during pregnancy==
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| Anemia affects 20% of all females of childbearing age in the United States. Because of the subtlety of the symptoms, women are often unaware that they have this disorder, as they attribute the symptoms to the stresses of their daily lives. Possible problems for the fetus include increased risk of growth retardation, [[prematurity]], [[stillbirth|intrauterine death]], rupture of the [[amnion]] and infection.
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| During pregnancy, women should be especially aware of the symptoms of anemia, as an adult female loses an average of two milligrams of iron daily. Therefore, she must intake a similar quantity of iron in order to make up for this loss. Additionally, a woman loses approximately 500 milligrams of iron with each pregnancy, compared to a loss of 4-100 milligrams of iron with each [[menstrual period|period]]. Possible consequences for the mother include cardiovascular symptoms, reduced physical and mental performance, reduced immune function, tiredness, reduced peripartal blood reserves and increased need for blood transfusion in the postpartum period.
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| ==References== | | ==References== |
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| {{Reflist|2}} | | {{Reflist|2}} |
| | {{WikiDoc Help Menu}} |
| | {{WikiDoc Sources}} |
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| [[Category:Needs content]] | | [[Category:Disease]] |
| | [[Category:Hematology]] |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Erythropoietin produced in the kidneys are the major stimulant of red blood cell (RBC) production as a response to anemia. Erythropoietin is stimulated by tissue hypoxia, that in turn stimulates erythroid progenitor cells to proliferate. The EPO levels follow a reverse relationship with the hemoglobin levels. Thus, in normal hosts, low levels of hemoglobin are associated with high levels of EPO. However, in patients with chronic kidney disease and anemia of chronic diseases the response may not be as strong as seen in patients without these comorbidities.
Pathophysiology
References
Template:WikiDoc Sources