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Serum sodium concentration in sickle cell patient

 

Table Of Contents


Chapter ONE

1.1 Introduction
1.2 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 Sickle Cell Disease
2.2 Serum Sodium Concentration in Health and Disease
2.3 Relationship Between Sickle Cell Disease and Serum Sodium
2.4 Impact of Serum Sodium on Sickle Cell Patient Outcomes
2.5 Current Treatment Approaches for Managing Serum Sodium in Sickle Cell Patients
2.6 Studies on Serum Sodium Levels in Sickle Cell Disease
2.7 Challenges in Monitoring Serum Sodium in Sickle Cell Patients
2.8 Future Research Directions in Understanding Serum Sodium in Sickle Cell Disease
2.9 Global Perspectives on Sickle Cell Disease and Serum Sodium
2.10 Summary of Literature Review

Chapter THREE

3.1 Research Design and Methodology
3.2 Selection of Study Participants
3.3 Data Collection Methods
3.4 Serum Sodium Measurement Techniques
3.5 Statistical Analysis Procedures
3.6 Ethical Considerations
3.7 Limitations of the Research Methodology
3.8 Validation Methods for Study Findings

Chapter FOUR

4.1 Overview of Study Findings
4.2 Serum Sodium Levels in Sickle Cell Patients
4.3 Factors Influencing Serum Sodium Concentration
4.4 Comparison with Healthy Controls
4.5 Impact on Clinical Outcomes
4.6 Treatment Strategies and Recommendations
4.7 Discussion on Potential Mechanisms
4.8 Implications for Future Research

Chapter FIVE

5.1 Summary of Research Findings
5.2 Conclusion and Interpretation of Results
5.3 Contributions to the Field
5.4 Recommendations for Clinical Practice
5.5 Implications for Public Health
5.6 Future Research Directions
5.7 Reflection on the Research Process
5.8 Closing Remarks and Acknowledgments

Thesis 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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