Serum sodium concentration in sickle cell patient
Table Of Contents
Chapter ONE
1.1 Introduction1.2 Background of Study
1.3 Problem Statement
1.4 Objective of Study
1.5 Limitation of Study
1.6 Scope of Study
1.7 Significance of Study
1.8 Structure of the Research
1.9 Definition of Terms
Chapter TWO
2.1 Overview of Serum Sodium Concentration2.2 Sickle Cell Disease: An Introduction
2.3 Relationship Between Sickle Cell Disease and Serum Sodium Concentration
2.4 Previous Studies on Serum Sodium Concentration in Sickle Cell Patients
2.5 Factors Affecting Serum Sodium Concentration
2.6 Importance of Monitoring Serum Sodium Concentration in Sickle Cell Patients
2.7 Effects of Abnormal Serum Sodium Levels in Sickle Cell Patients
2.8 Treatment and Management of Abnormal Serum Sodium Levels in Sickle Cell Patients
2.9 Technologies for Measuring Serum Sodium Concentration
2.10 Future Research Directions in Studying Serum Sodium Concentration in Sickle Cell Patients
Chapter THREE
3.1 Research Methodology Overview3.2 Research Design
3.3 Sampling Techniques
3.4 Data Collection Methods
3.5 Data Analysis Procedures
3.6 Ethical Considerations
3.7 Validity and Reliability
3.8 Limitations of the Research Methodology
Chapter FOUR
4.1 Overview of Findings4.2 Analysis of Serum Sodium Concentration Levels in Sickle Cell Patients
4.3 Relationship Between Serum Sodium Concentration and Disease Severity
4.4 Comparison of Serum Sodium Levels in Different Sickle Cell Genotypes
4.5 Impact of Treatment on Serum Sodium Concentration
4.6 Factors Influencing Variability in Serum Sodium Levels
4.7 Discussion on Clinical Implications of Findings
4.8 Future Research Directions Based on Findings
Chapter FIVE
5.1 Summary of Findings5.2 Conclusion
5.3 Recommendations for Clinical Practice
5.4 Contributions to the Field
5.5 Implications for Future Research
Project Abstract
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).
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