Diabetes mellitus: balancing blood glucose

01 July 2013
Volume 5 · Issue 7

Abstract

This case study seeks to explore the pathophysiology of diabetes mellitus and the effects that this condition has upon the individual. The aetiology of diabetes mellitus will be discussed, in conjunction with an analysis of clinical signs and symptoms presented by the disease reflecting the underlying pathophysiological processes. Clinical treatment options will also be discussed, in relation to their influence on the management of disturbances in the underlying disease process. In line with patient confidentiality guidelines (Department of Health (DH), 1997), patient-identifiable information will be omitted.

Diabetes mellitus is a metabolic disorder of the endocrine system, defined by chronic hyperglycaemia (Guyton and Hall, 2010). It is characterised by an acquired and/or idiopathic inability to produce insulin or increased insulin resistance, causing an imbalance between supply and demand of insulin. Insulin is a pancreatic hormone secreted by beta cells of the islets of Langerhans, essential for the metabolism of glucose. Insulin regulates blood glucose by facilitating the transport of glucose into the cell membrane. If these deficiencies are left unmanaged, or are managed incorrectly, this results in glucose homoeostatic imbalances known as hypoglycaemia or hyperglycaemia (Tortora and Derrickson, 2012).

Body cells need energy to function; glucose (sugar obtained from digestion and metabolism of carbohydrates) is the body's main energy source. The glucose in digested food is absorbed in the small intestine via glucose co-transporters located on the intestinal epithelial cells, and subsequently into the bloodstream (Marieb, 2012). The hormone insulin facilitates the uptake of glucose into muscle, fat and liver cells, where it is stored as the rapidly accessible energy source glycogen. In the absence of insulin, these cells are unable to uptake glucose as the receptors that transport glucose (GLUT4) are inactive. Insulin bonds to GLUT4 receptor sites on the outside of cells, acting like a key unlocking the doorway allowing access to the cell. Glucose can then enter the cell through this channel. The inability of glucose to enter these cells in the absence of insulin means it remains circulating in the bloodstream, resulting in hyperglycaemia (Zhu et al, 2013).

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