Hemolytic anaemia
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The cause is the breakdown of erythrocytes (hemolysis – intra- or extravascular). characters:
- general signs Hemolysis,
- noticeable hypercellularity of bone marrow (it fills all the marrow spaces - even places where the marrow is fatty in an adult),
- change normal ratio of granulo- and erythropoiesis (3:1) in favor of erythropoiesis,
- sometimes we also encounter extramedullary hematopoiesis (liver, spleen) - erythrocyte production increases up to eight times (there are numerous reticulocytes in the blood, but the lifespan of such erythrocytes is significantly reduced - only for 15 days) - compensated anemia, the number of erythrocytes is, however, very sensitive to the reduction of erythrocyte production (e.g. by a common infectious disease) - then a so-called aplastic crisis occurs,
- extravascular hemolysis is characterized by a hemosiderosis of macrophages, some of which accumulate lipids from disintegrated erythrocytes and thus resemble lipophages in Gaucher's disease - the so-called gaucheroid cells.[1]
Division
- mostly congenital
- erythrocyte membrane disorders: hereditary spherocytosis, elliptocytosis, paroxysmal nocturnal hemoglobinuria (acquired disease);
- erythrocyte metabolism disorders: enzyme defects pentose cycle (glucose-6-phosphate dehydrogenase deficiency, glutathione reductase), enzyme defects Embden -Meyerhof cycle (hexokinase defect, pyruvate kinase deficiency);
- hemoglobinopathy: thalassemia, sickle cell anemia.
- damage by physical and toxic influences (mechanical, thermal, bacterial toxins, malaria);
- antibody damage: autoantibodies, anti-Rh-factor antibodies (fetal erythroblastosis), isoagglutinins (post-transfusion hemolytic reactions).[2]
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Reference[edit | edit source]
- ↑ PASTOR, Jan. Langenbeck’s medical web page [online]. [cit. 12.4.2010]. <http://langenbeck.webs.com>.
- ↑ LEBL, J – JANDA, J – POHUNEK, P, et al. Clinical pediatrics. 1. edition. Galén, 2012. 698 pp. pp. 543. ISBN 978-80-7262-772-1.