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Case study: Diabetes mellitustype 2 - Essay Example

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The paper analyses this case by discussing the signs and symptoms that led to the diagnosis of DM 2 and the necessary tests that may have been used to confirm this diagnosis. …
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Case study: Diabetes mellitustype 2
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? Diabetes OUTLINE 0 Paper Overview……………………………………………………………………………..3 2.0 Introduction…………………………………………………………………………………3 3.0 Type versus Type 2 Diabetes……………………………………………………………...4 4.0 Signs and Symptoms…………………………………………………………………………5 5.0 Complications………………………………………………………………………………...6 6.0 Management of the Patient…………………………………………………………………...7 7.0 References…………………………………………………………………………………….8 8.0 Paper Overview A 45 year old female presented with symptoms of fatigue, hunger, increased thirst, increased urination, blurred vision and numbness in the hands and feet. Early diagnoses revealed that the patient is suffering from diabetes mellitus type 2 (DM 2) and has long term complications of diabetes mellitus type 2. The paper analyses this case by discussing the signs and symptoms that led to the diagnosis of DM 2 and the necessary tests that may have been used to confirm this diagnosis. The paper further analyses the likely course that the patient’s condition might have taken and the relevant changes in therapies that occurred with advancement of the disease. The paper will also discuss the complications that may have occurred as the disease advanced. I will discuss the case under the following headings: Introduction Diabetes mellitus (DM) is a chronic condition of enhanced blood sugars in the body in terms of millimoles of glucose in a liter of blood (mmol/l). The normal blood sugar level in a healthy individual ranges between 4 and 7 mmol/l, and in children this range is between 4 and 8 mmol/l. These figures are usually low in the morning and highest after taking meals, however, homeostatic functions of the blood usually maintain the blood glucose level within the normal limits after some time (Beaglehole 2003, p904). After taking a meal, the ideal level should not exceed 9 mmol/l for a time period of 90 minutes, and in children this should not exceed 10 mmol/l. For diabetics, the blood glucose level is outside these normal ranges unless the individuals are treated. When testing a person for diabetes, various blood glucose levels are taken after about eight hours of fasting (Fasting Blood Sugar). Blood sugar levels are then categorized into various classes. a) Normal – 4 to 5.6 mmol/l b) Pre-diabetes/ Impaired glucose tolerance 5.6 to 7 mmol/l c) Diagnosis of diabetes – greater than 7 mmol/l Glucose is the body’s source of energy for metabolism, and it is controlled and regulated by the hormone insulin that is produced by the Islets of Langerhans (Beta cells), cells found in the pancreas. Generally, insulin regulates the entry and utilization of glucose in body tissues after liver metabolism. When the amount of glucose in blood is higher than normal, insulin regulates the conversion of excess glucose into glycogen that is a storage form of glucose. When the level is lower than normal, another pancreatic hormone glucagon regulates the conversion of glycogen into blood glucose. Diabetes will develop when there is inadequate or no production of insulin by the pancreas (DM type 1/juvenile diabetes/insulin dependent diabetes) or when the body is unresponsive to the produced insulin (DM type 2/insulin resistant diabetes) (Buchanan, Xiang & Peters 2002, p2802). Type 1 versus Type 2 Diabetes DM type 1 is an autoimmune disorder that has a genetic predisposition and affects mainly children and young adults who are less than 30 years old, however, older adults may be affected. It has no sexual preponderance, with an equal incidence in the male and female sex. It affects about 15% of people with diabetes. The exact pathology behind this condition has not been understood clearly, however, environmental factors are implicated in its pathophysiology. Various hypotheses have been advanced to explain about DM type 1, but, the best hypothesis is that a virus or an environmental agent triggers the immune system of the body to attack the pancreatic beat cells. This is referred to as an autoimmune reaction, and as a result of this, the pancreatic beta cells are unable to produce sufficient insulin. Since there is no insulin/ no sufficient insulin, there is no uptake of glucose by peripheral tissues leading to an elevated blood glucose level (hyperglycaemia). The body then turns to fat and protein reserves for energy instead of glucose. DM type 2 is the more common form of diabetes accounting for between 85 and 90% of cases. It majorly affects older adults, but incidences of younger people and children being affected by DM type 2 are increasing by the day. The condition results because adipocytes. Hepatocytes and muscle cells are unresponsive to insulin, hence the effects of insulin (stimulates increased utilization of glucose in peripheral body cells and reduced glucose synthesis/ gluconeogenesis in the liver) are not effected in the body (Goeree, Lim & Hopkins p99). As a result of this, there is hyperglycaemia in the body. Symptoms of type 2 develop slowly over time. It is also diagnosed more in overweight and obese people since increased fat in the body makes it harder for the body to utilize insulin correctly. However, it may also develop in thin people, especially in the elderly. Environmental factors and genetic factors play a large role in the pathophysiology of DM type 2. The risk factors for this condition are; poor diet rich in fats, lack of regular physical activity, positive family history for DM type 2, old age above 45 years, being overweight, high blood pressure or women who give birth to children over 4.1 kg. Signs and Symptoms Early symptoms of hyperglycaemia are constant hunger, fatigue, lethargy, frequent thirst (polydipsia), frequent urination (polyuria), frequent skin infections that heal slowly, slow healing wounds, headaches, dizziness, leg cramps and unexplained weight loss (type 1). For type 2 DM, patients gradually increase in weight. Very high levels of hyperglycaemia causes emergency symptoms such as confusion, fast breathing, loss of coordination, abdominal pain, slurred speech, nausea, vomiting, and elevated heart beat. Initially asymptomatic, complications and advanced symptoms of DM type 2 take years to manifest. Most symptoms are diagnosed as signs of aging. Complications of diabetes Short term complications are as a result of hypoglycaemia and hyperglycaemia. Hypoglycaemia results due to insulin medication, missing meals and over-exercising. Symptoms of hypoglycaemia include cold sweats, tachycardia, hunger, lightheadedness, numbness of tongue and lips, shaking, anxiety and nausea. Symptoms of hyperglycaemia are polydipsia, polyuria and blurred vision. These take time to manifest and are caused by taking too low levels of insulin, eating a lot and being stressed or being ill (Goree, Lim & Hopkins, p99). Diabetic ketoacidosis occurs mainly in people with type 1 diabetes. Long term complications are experienced mainly in patients with the type 2 form. Various organs in the body are affected forming a very large clinical picture. There are eye complications/diabetic retinopathy (glaucoma and cataracts), foot complications (neuropathies), skin infections, cardiovascular complications, mental complications, hearing abnormalities, oral disease, peripheral arterial disease, diabetic nephropathy and many more conditions. Therefore, in diagnosis of the patient, a combination of factors was considered. A complete patient history, physical examination and diagnostic tests were all used in confirming the diagnosis. Diabetes blood tests that were used to confirm the diagnosis were fasting blood glucose level, haemoglobin A1c test and oral glucose tolerance test. Fasting blood glucose levels higher than 7mmol/l; haemoglobin A1c test of 6.5% and oral glucose tolerance test of higher than 200mg/dl were all confirmatory signs of diabetes. Management of the patient DM type 2 has no cure but its symptoms can be managed; hence, management was the best alternative in dealing with complications and symptoms of the condition. Lifestyle modifications like maintenance of a healthy weight, regular physical activity, healthy eating, and management of blood pressure, coupled with medications are the ways of managing DM type 2 (Holmes et al 2000, p780). There is a wide spectrum of medications for diabetes, each with its own side effects; a) Insulin therapy b) Oral hypoglycaemic agents i) Thiazolidinediones e.g. Rosiglitazone (AVANDIA), Pioglitazone (ACTOS) ii) Sulphonylureas e.g. Tolbutamide, Tolazamide, Glipizide iii) Biguanides e.g. Metformin iv) Alpha glucosidase inhibitors v) Meglitinides e.g. Nepaglinide, Nateglinide (STARLIX) vi) DPP- IV inhibitors e.g. Incretin therapy Insulin is the most widespread, but it is used in combination with the other therapies. The patient’s health condition determines the therapy to be used. For instance, Thiazolidinediones are efficient even in patients with renal insufficiency and hepatic complications. Sulfonylureas on the other hand are contraindicated in patients with hepatic and renal insufficiencies (Knowler, Connor & Fowler 2002). Hence, the patient’s condition determined the therapy applied. References Anderson R, Freedland K, douse RE, Lustman P 2001, “The prevalence of comorbid depression in adults with diabetes.” Diabetes Care; 24:1069-1078. Beaglehole, R., Yach, D 2003, “Globalization and the prevention and control of non-communicable disease: the neglected chronic diseases of adults”, Lancet, vol. 362, pp. 903-908. Buchanan, T., A., Xiang, A., H., Peters, R 2002,“Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk Hispanic women”, Diabetes, vol. 51, pp. 2796-2803. Cameron, A., J., Welborn, T., A., Zimmet, P 2003, “Overweight and obesity in Australia: the 1999-2000 Australian Diabetes, Obesity and Lifestyle Study (AusDiab)”, Med J Aus. Vol.178, pp. 427-432 Colagiuri S, Colagiuri R, Conway B, Grainger D, Davey P. DiabCost Australia: Assessing the Burden of Type 2 Diabetes in Australia. Canberra, Australian Capital Territory, Australia: Diabetes Australia; 2003. Colagiuri, R., Colagiuri, S., Yach, D & Pramming, S 2006, "The Answer to Diabetes Prevention: Science, Surgery, Service Delivery, or Social Policy?", American Journal of Public Health, vol. 96, no. 9, pp. 1562-9 Colagiuri, S. & Walker, A 2008, "Using An Economic Model Of Diabetes To Evaluate Prevention And Care Strategies In Australia", Health affairs, vol. 27, no. 1, pp. 256-68. Eriksson KF, Lindgarde F 1998, “No excess 12-year mortality in men with impaired glucose tolerance who participated in the Malmo Preventative Trial with diet and exercise”, Diabetologia; 41:1010-1016. Federal Bureau of Prisons, November 2009. Management of Diabetes, Clinical practice guidelines, retrieved from http://www.bop.gov/news/PDFs/diabetes.pdf Accessed on Nov 23, 2011. Goeree, R., Lim, M., E., Hopkins, R 2009, “Excess risk of mortality and complications associated with newly diagnosed cases of diabetes in Ontario, Canada”, Can J Diabetes, vol. 33, no. 1, pp. 93-104. Holmes J, McGill S, Kind P, Bottomley J, Gillam S, Murphy M 2000, “Health-related quality of life in type 2 diabetes (T^sup 2^ARDIS-2)”, Value Health; 3(suppl 1): S47-S51. Hu, F., B., Li, T.,Y., Colditz, G.,A., Willett, W.,C., Manson, J 2003, “ Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women”, JAMA, vol. 289, pp. 1785-1791 International Diabetes Federation, 2009, Diabetes atlas. 3rd ed. Brussels: International Diabetes Federation, Retrieved from http://www.diabetesatlas.org/content/diabetes Accessed on Nov 23, 2011. Knowler WC, Barrett-Connor E, Fowler SE, et al. 2002, “Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin”, N Engl J Med; 346:393-403. Koopmanschap M. 2002, “Coping with type II diabetes: the patient's perspective”, Diabetologia; 45:S18-S22 Kruse J, Schmitz N, Thefeld W.2003, “On the association between diabetes and mental disorders in a community sample: results from the German National Health Interview and Examination Survey”, Diabetes Care; 26:1841-1846. Lustman P, J, Anderson R, J, Freedland K de Groot M, Carney R, M, Clouse R, E. 2000, “Depression and poor glycemic control: a meta-analytic review of the literature”. Diabetes Care; 23:934-942. Padwal R, Majumbar SR, Johnson JA, Varney J, McAlister FA. 2005, “A systematic review of drug therapy to delay or prevent type 2 diabetes”, Diabetes: 28:736-744. Pan XR, Li GW, Hu YH, et al. 1997, “Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: the Da Qing IGT and Diabetes Study”, Diabetes Can; 20:537-544. Paton, N. 2008, "Charity warns the UK is on track for a diabetes explosion by 2025", Occupational Health, vol. 60, no. 7, pp. 7-7. Tarride, J., Hopkins, R., Blackhouse, G., Bowen, J., Bischof, M., Von Keyserlingk, C., O'Reilly, D., Xie, F. & Goeree, R. 2010, "A Review of Methods Used in Long-Term Cost-Effectiveness Models of Diabetes Mellitus Treatment", PharmacoEconomics, vol. 28, no. 4, pp. 255-77. Torgerson J, Hauptman J, Boldrin MN, Sjostrom L. Xenical, 2004. Prevention of Diabetes in Obese Subjects (XENDOS) Study. Diabetes Can. 27:155-161. Tuomilehto J, Lindstrom J, Eriksson JG, et al. 2001, “Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance”, N Engl J Med ;344:1343-1350. Wald N, J., Law M, R., 2003, “A strategy to reduce cardiovascular disease by more than 80%”, BMJ, vol. 326, pp. 1-6. Read More
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