INTRODUCTION
Sickle cell disease (SCD) is a group of inherited disorders of the beta-hemoglobin chain. Normal hemoglobin has 3 different types of hemoglobin – hemoglobin A, A2, and F. Hemoglobin S in sickle cell disease contains an abnormal beta globin chain encoded by a substitution of valine for glutamic acid on chromosome 11 (Bunn,2007). This is an autosomal recessive disorder. Sickle cell disease refers to a specific genotype in which a person inherits one copy of the HbS gene and another gene coding for a qualitatively or quantitatively abnormal beta globin chain. Sickle cell anemia (HbSS) refers to patients who are homozygous for the HbS gene, while heterozygous forms may pair HbS with genes coding for other types of abnormal hemoglobin such as hemoglobin C, an autosomal recessive mutation which substitutes lysine for glutamic acid. In addition, persons can inherit a combination of HbS and β-thalassemia. The β-thalassemias represent an autosomal recessive disorder with reduced production or absence of β-globin chains resulting in anemia. Other genotype pairs include HbSD, HbSO-Arab and HbSE (Meremiku, 2008).
Sickle hemoglobin in these disorders cause affected red blood cells to polymerize under conditions of low oxygen tension resulting in the characteristic sickle shape. Normal red cells live about 120 days in the blood stream but sickled red cells die after about 10 – 20 days. Because they cannot be replaced fast enough, the blood is chronically short of red blood cells, a condition called anaemia. Aggregation of sickle cells in the microcirculation from inflammation, endothelial abnormalities, and thrombophilia lead to ischemia in end organs and tissues distal to the blockage (Hayes, 2004).
Terms of Use: This is an academic paper. Students should NOT copy our materials word to word, as we DO NOT encourage Plagiarism. Only use as a guide in developing your original research work. Thanks.
Disclaimer: All undertaking works, records, and reports posted on this website, eprojectguide.com are the property/copyright of their individual proprietors. They are for research reference/direction purposes and the works are publicly supported. Do not present another person’s work as your own to maintain a strategic distance from counterfeiting its results. Use it as a guide and not duplicate the work in exactly the same words (verbatim). eprojectguide.com is a vault of exploration works simply like academia.edu, researchgate.net, scribd.com, docsity.com, course hero, and numerous different stages where clients transfer works. The paid membership on eprojectguide.com is a method by which the site is kept up to help Open Education. In the event that you see your work posted here, and you need it to be eliminated/credited, it would be ideal if you call us on +2348064699975 or send us a mail along with the web address linked to the work, to eprojectguide@gmail.com. We will answer to and honor each solicitation. Kindly note notification it might take up to 24 – 48 hours to handle your solicitation.