Type 1 Diabetes Case Study Essay

Carol is a 17-year-old patient who has been admitted to hospital. She has previously been diagnosed with Type 1 diabetes, and has been suffering from this since the age of 7. Carol is 6 weeks pregnant, and is showing signs of dehydration, high blood glucose, weight loss and changes in mood. It is important to understand the underlying cause of Carol’s symptoms to eliminate any problems in both her babies and her own health. This can be done through critically analysing the pathophysiology of her overall condition and her signs and symptoms. It is also important to understand any potential effects on the developing foetus in order to help prevent any complication during her pregnancy. Understanding the pathophysiology of both her condition and her symptoms is crucial. The development of Type 1 diabetes is the consequence of an on going destruction of the beta cells (β cells). This is due to an autoimmune process that happens during an asymptomatic period. This occurs in the islets of Langerhans in the pancreas and can often be extended over many years. This results in the pancreas becoming unable to produce insulin, and the effected patient, like Carol, can no longer control their blood glucose without the aid of insulin injections. How the beta cells build up autoimmunity is still unclear in science. Some evidence shows it is a combination of genetic and environmental factors such as genetic disposition, viruses, toxins, and diet (Yoon, Jun 2005 ). Overtime this develops into an immune mediated destruction of the β cells. In the lead up to Type 1 diabetes B cells release auto-antigens that are processed by antigen-presenting cells (APC). These are presented to helper T cells (Th a type of lymphocyte). IL-12 (an interleukin) is released from APC’s and in turn activates Th1 type CD4+ T cells. This causes the immune balance between effector and regulatory cells to breakdown. Th1 cells produce IL-2, which activates B cell specific precytotoxic T cells to become cytotoxic. This also causes macrophages to become cytotoxic. CD8+ cytotoxic T cells (CTL) then recognise the antigens expressed on β cells. CTL’S release granzymes and perforin, toxic to B cells and therefore destroying them. This means that they are unable to produce insulin (including C-peptide in the proinsulin molecule) and amylin, resulting in Type 1 Diabetes. Insulin is the key to a healthy regulation of glucose in the blood. It exerts action through binding to specific receptors present on different cells such as muscle, liver and fat cells. The primary function of insulin is to stimulate glucose disappearance when concentration increases beyond </= 3.3mol/l. Insulin controls glucose levels by signalling cells of insulin sensitive peripheral tissue. This increases the uptake of glucose. It also inhibits glucagon secretion from pancreatic alpha cells, which signals the liver to stop producing glucose via glycogenesis and gluconeogenesis. C-peptide is a short 31-amino acid polypeptide that connects insulin’s A-chain to its B chain in the proinsulin molecule. In the past C-peptide was considered as a bi-product of insulin. More recent data shows that C-peptide is important for the biosynthesis of insulin (Wahren et al. 2000). Lastly, Amylin supresses’ postprandial glucagon secretion. It also slows gastric emptying and reduces food intake and body weight. These functions of insulin, C-peptide, and Amylin are all crucial in the control of glucose level within the blood. So when they do not perform to there functions, carbohydrates that are turned into glucose in the body, won’t be stimulated to disappear, and factors that usually help to regulate the glucose levels won’t occur. Therefore the glucose level in the body is uncontrolled and will keep rising. Due to a lack in blood glucose control, explained above, during her admission, Carol has experienced some acute effects. These include; excessive thirst, frequent urination, …show more content…
Hyperglycaemia is a raised serum glucose level. The main cause of hyperglycaemia in type 1 Diabetes in an insufficiency of insulin. There is also an increase in conterregulatory hormone levels; Glucagon, cortisol, catecholamines, and growth hormone. Insulin deficiency causes hyperglycaemia, as glucose can no longer be utilised in insulin-dependent tissues such as muscle and adipose tissue. This means the body has to use energy from fatty acids in adipose tissue. The fatty acids travel to the liver and are converted to ketoacids, in turn potentially causing ketoacidosis, which can be life