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Diabetes Mellitus Type II Case - Essay Example

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The author of the "Diabetes Mellitus Type II Case" paper discusses his/her experience with the patient and the interventions used to handle his diabetic condition. The paper also focuses on the normal physiology of the related body organ and pathophysiological state in the case of diabetics. …
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Diabetes Mellitus Type II Case
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Case Study Diabetes Mellitus Type II (Case Study) Introduction I am working as a health careassistant in Londons Neurological hospital in a private ward. My responsibility is to ensure proper care to the patients based on their physical and psychological needs. It is a surgical ward in which patients for brain surgeries are admitted for pre and post-operative health care. The patient referred in this text was a diabetic patient admitted for ventriculoperitoneal Shunt for treating brain stem glioma. It is a surgical procedure in which the pressure from the brain is relieved by removing excess cerebrospinal fluid from the ventricles of the brain (Campellone, 2013). The patient name has been changed to maintain the confidentiality according to the NMC code of conduct (NMC, 2014). I met the patient in the surgical ward for the first time. I took his vital signs and performed all necessary protocols required prior getting a patient admitted. I asked about his medical history and personal details. He also updated me about his family background from where I found that his mother and father were diabetics too. For around 2-3 hours, I escorted him, during that time I took all the relevant details for filling the patient related forms. The patient seemed initially nervous, but I made him relaxed and stay calm. I introduced myself and related staff to him and gave him a tour of the ward. After having some conversation about his health condition, I also offered him some tea and biscuits. He took the tea without sugar and asked for diet biscuits. Evaluating his medical condition and history, I found out that the patient has been struggling with brain glioma for a long time. He also informed that for the last few months his sugar level kept on shifting high and low. His doctor has recommended taking insulin injections prior taking meal BD. The patient was following strict diet with high fiber low calories and no sugar along with physical exercise. The patient was concerned about his information confidentiality so I made him understand that all his information will be kept extremely confidential (American Nurses Association, 2014). I have been looking after this patient for three weeks. In this report, I am going to discuss my experience with the patient and the interventions used to handle his diabetic condition. The paper also focuses on the normal physiology of the related body organ and pathophysiological state in case of diabetics. The prime objective of the paper is to focus on diabetes mellitus type II pathology and treatment with respect to the patient (see Appendix 1). Normal physiology and anatomy of pancreas Type II diabetes or non-insulin dependent diabetes is a chronic disease which impairs the glucose metabolism of the body. In this disease, the body becomes resistant to insulin action or the pancreas does not produce enough insulin to meet body requirements. Insulin is a hormone that is responsible for glucose metabolism in the cells. Glucose is used by the body as a source of energy, an impairment of glucose metabolism leads to multiple other complications (Wisse, 2013). The pancreas is around twelve inches long located in the upper abdominal cavity (Iocara, 2012) behind the stomach. It is triangular in shape where the head is on the right side connected to the curve of the duodenum through the pancreatic duct. The narrow end of the pancreas is located on the left side of the body (Gillaspy, 2014). The head part is the thick end of pancreas constituting 50% of the total mass lying towards the right side. The tail of pancreas ends at the junction of the spleen. Almost ninety-nine percent of the pancreas is composed of acini. These cells are responsible for producing exocrine enzymes, which are important in digestion (Tortora & Derrickson, 2008). The endocrine juices produced by acini secrete into small ducts and release into the duodenum via pancreatic duct. Being a part of the digestive system, it secretes chemicals which help in breaking down of food components (proteins and fats) into smaller particles (Pandol, 2010). The exocrine function of the pancreas is to secrete alkaline juices and enzymes like lipase and amylase which facilitate the digestion of fats, proteins and carbohydrates. These juices help in neutralizing the acidic pH of the stomach. The secretions are carried to the duodenum through the pancreatic duct (Thompson, 2014). Its major role is to produce insulin and glucagon, the hormones responsible for the regulation of blood glucose level. The functions of the pancreas can be easily segregated as exocrine functions and endocrine functions. The exocrine gland is involved in the synthesis and secretion of hormones, which are required in the metabolism of lipids, proteins and glucose (Martini, 2007). The set of five types of cells called as Islets of langerhans produces different types of secretions. 15% of the endocrine cells are composed of alpha cells. They are located along the periphery of the islets and are responsible for the production of glucagon, a hormone that regulates gluconeogenesis the release of glucose in the blood. The beta cells, which are responsible to produce insulin. Insulin is a peptide hormone consisting of 51 amino acids which are synthesized by the pancreatic beta cells. The pancreatic beta cells are located in the islets of Langerhans that are composed of hundreds to thousands of endocrine cells. The islets are present separately and also function individually from exocrine tissues that secrete pancreatic enzymes that help in digestion. Normal people have one million islets constituting 1 to 2 percent of the total mass of the pancreas. The size of islets may vary from 50 to 300 micrometers in diameter. 80% of the islet cells are beta cells, which are found in the core of the islets. An increased level of glucose in the blood triggers beta cells to release insulin. These cells are equipped with channels in the plasma membrane which act as glucose detectors. When these detectors sense an increased level of plasma glucose, they initiate the release of insulin. These beta cells are surrounded by various other cells, which secrete different chemicals like somatostatin by delta cells and pancreatic polypeptide by PP cells (Quesada et al., 2008). The somatostatin is responsible for glucagon secretion and inhibition of insulin forming 5% of the endocrine cells. The secretion of PP gamma cellshelps in self-regulation of endocrine and exocrine pancreatic secretions (Robson, 2012). All these cells work in interaction with each other where the releases of one type of cellular products influence the function of another type of secretions. Three types of mechanisms are followed for communication between these cells: paracrine and autocrine messaging, GAP junctions and adhesion molecules on the cell surface. Through the central core of the beta cells, a neurovascular bundle of arterioles and nerves enters into the islets. The arteries further branched into capillaries passing through the periphery of the islets enters into portal venous circulation (Robertson, 2013). Regulation of hormones The endocrine secretions are governed by autonomic nervous system and hormones. The capillaries are present in the pancreatic cells such that the cells remain in direct contact with the blood vessels. This aids in autocrine and paracrine signaling between the cells. This positive or negative signal activity determines the release and inhibition of endocrine secretions. The alpha cells are stimulated by low levels of glucose, glucagon and fatty acid level. The beta cells are stimulated by high glucose level, glucagon and insulin (Bowen, 2002). The delta cells are stimulated by glucagon. The release of somatostatin inhibits the release of CCK, glucagon, insulin and secretin. The autonomic nerve innervations also help in regulating endocrine secretions. Parasympathetic innervations stimulate glucagon and insulin secretions and sympathetic innervations stimulate glucagon release and inhibit insulin release. Altered physiology An alteration in normal physiology of the pancreas may result in various disorders. Keeping in view the patient, the two most-common diseases are Diabetes Mellitus (Type I & Type II). Diabetes mellitus occurs due to absence or shortage of insulin in the blood. It could be of two types: in type I diabetes the production of insulin suffers due to destruction of pancreatic beta cells, whereas type II diabetes is characterized by insulin resistance or low secretion of insulin (Barron, 2010). The patient under discussion had type II diabetes. The patient history tells us that the contributing factors in developing diabetes II in his case were obesity, lack of physical exercise and poor diet pattern. In order to understand the alteration in physiology, it is important to overview the normal glucose regulation of the body. Glucose is obtained mainly from the metabolism of carbohydrates. Different body cells are capable of transforming different carbohydrates into glucose. The liver also converts glycogen into glucose. In healthy individuals the increase in blood glucose level triggers the release of insulin from beta pancreatic cells, which takes up blood glucose leaving a decline in glucose level of the blood. Insulin not only regulated glucose uptake it also induces glycolysis, which converts glucose into pyruvate releasing free energy. IT also converts the extra glucose into glycogen by the process of glycogenesis in liver. Insulin also governs the synthesis and uptake of proteins and fats (Yki-Järvinen, 2011). Hypothetically every cell in the body lives by converting glucose into energy, where skeletal muscles act as a ‘sink’ for converting excess glucose into glycogen. In type II diabetes, this ability of the skeletal muscles is reduced to 20% than the normal. Increase physical activity help in transporting glucose across the membrane and therefore decreasing the impact of insulin resistance. Research proves that people with sedentary lifestyles are more likely to develop diabetes II (Guthrie & Guthrie, 2004). Same implies to our patient, when inquired about his routine and physical exercise it was informed that most of his time is utilized in sitting on the job, and his daily routine did not include regular exercise. The clinical indications of Type II diabetes mellitus are hyperglycemia, relative impairment in insulin secretion and insulin resistance. The pathophysiology of diabetes mellitus II is influenced by various factors. Patients with a tendency to develop insulin resistance and comparative insulin deficiency lead contribute in diabetes mellitus (McCulloch & Robertson, 2014). Insulin resistance causes improper insulin-mediated glucose uptake by muscles and fats, impaired triglyceride uptake and incomplete suppression of glucose produced by liver the action of glycogen. In order to overcome the insulin resistance the beta cells of islets will increase the production of insulin. This condition remains for many years. The uncoordinated and abnormal metabolism of fats and glucose occurs when the insulin requirements do not match with insulin production by the beta cells. Hence, for developing Diabetes mellitus type II the patient would have impaired insulin production and insulin resistance (Pittas, 2014). In type II diabetes mellitus either there is a decreased amount of insulin as compared to the body requirement, or there is insulin resistance. Insulin resistance means that the body muscles become unresponsive to insulin (Thévenod, 2008). In fat tissues, triglycerides are broken down into free fatty acids for energy, and the muscles do not have any source of energy and the hepatocytes show impaired glycogenesis. This series of events lead to increased blood glucose level. Glycogen stores are depleted, and body has no reservoirs of energy when required by the body (Mandal, 2013). Effects of Diabetes type II on patient health The progression of normal glucose metabolism into type II diabetes entails number of complicated metabolic alterations. The early state is termed as prediabetes, which is characterized by hyperglycemia, increased risk to nephropathies, neuropathies and retinopathies. In the progressive stages, there will be an accumulation of Amylin fibers in the Langerhans cells from amyloid peptide (IAPP). This occurs due to excessive workload because of biosysthesisoverproduction of insulin and IAPP leading to alpha cell apoptosis. Along with these alterations there is also change in incretin profile GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic polypeptide) which are linked directly to maintaining glucose homeostasis (Quesada et al., 2008). There are multiple risk factors which predispose a normal person to Diabetes, type II, but the most prevalent is obesity. BMI Body mass index is used as a major tool to studying risks to DM II (Boada & Moreno, 2013). Apart from obesity, lack of physical activity has been considered as a dominant factor which contributes in developing diabetes mellitus II. Different treatment options have been used for the treatment of diabetes mellitus type II. The first-line therapy for diabetes mellitus type II is to take lifestyle measures. On inquiring about the dietary pattern, he told me that his diabetitian has given him a complete chart to follow for diet. He only takes particular fruits like apple, plums, watermelon, etc. Fruits like banana and mangoes are completely restricted in his diet. Similarly, instead of taking white flour stuff like pasta noodles, etc. he has been advised to take brown rice and brown wheat. The patient did not have much-physical activity in his routine therefore he was advised to do one-hour jogging daily (Kenny & Tidy, 2013). The patient reached the hospital for admission one day prior to his surgery. His BM at the time of admission was 14mmol/l which was very high as compared to the normal target for a diabetic patient that is 8.5 mmol/l. This was a random glucose level check and seemed exceeding the high range. For the patients of diabetes, the normal range is 4 to seven mmol/l before meal and below 8.5 mmol/l after two hours of taking meal (Diabetes.co.uk, 2014). The patient was not given any food from last night before the day the surgery has to be performed. In the morning at 6 am, I took his BM was 9mmol/l. This reading was again higher than the normal range. After having the surgery, the patient came back in the ward and was prescribed with Human Actrapid insulin on a sliding scale. The sliding scale therapy means a gradual increase in the insulin dose before taking meal or bedtime, depending upon the blood glucose level of the patient. As the glucose level of the patient was raised, each time it was checked, and insulin is prescribed to keep the glucose level normal. In the insulin sliding scale, the rate of insulin infusion is titrated based on the sugar level and is monitored strictly after every 1 to two hours (Strachan & Jankins, 2005).The nurse prepared the insulin infusion by adding 50 units of Actrapid into normal saline to make up the volume up to 50 ml. So, each ml of the solution contained 1 unit of insulin (Strachan & Jankins, 2005). The dose adjustment was then made according to the varying blood glucose level during the course. The blood sugar of the patient was rechecked after surgery that came up 7mmol/l. After the induction of insulin on sliding scale at the rate of 1ml/hr, after each hour his glucose level was checked. After five checks, the reading was 16mmol/mol. As the glucose level was exceeding the infusion rate was adjusted and increased up to4ml/hr. The patient was continuously monitored for his glucose level on that day. The next day his condition got stabilized. His blood glucose reading was 8mmol/l after meal and 5mmol/l before meal. The patient was not allowed to move for around 48 hours. I was assisting him in performing urination and defecation on the bed. The patient was continually complaining of severe headache. I asked the nurse to prepare an analgesic dose for him to relieve him from the pain. Headaches are usually associated with high glucose level, but on the second day the glucose level of the patient was stable. So, I checked his blood pressure it was low and for managing it he was taking Amlodipine. I was concerned about my patient’s physical and mental health. I kept on checking his glucose level and vital signs with regular intervals. I also tried to make his relax more and should not worry about his health by having general conversation with him. Till two days, he was restricted on his bed that was making him irritated. So, I tried to divert his mind by engaging him in dialogue about different general topics so that he would not feel low. After two days, he was able to move slowly and go to the toilet himself. I used to give him a hand while moving in the room or going to the restroom. I also requested him to avoid unnecessary movement in the room otherwise he may get into trouble by developing pain. The patient was very cooperative, and he followed the directions exactly. I used to visit the patient very frequently and ask him how he was feeling. The patient has become much weaker therefore I gave him extra care and took good care about his dietary pattern in the ward. I found that most of the time he is drowsy, so I checked his blood glucose level. The sleepiness was due to the side effect of anti-emetic medicine that was given to him in order to prevent the post-surgical nausea and vomiting. I made him understand that he should not worry about getting sleepy as his health condition has become much more stable. I observed that he used to wait for his family members very anxiously every day. His family used to visit with him every afternoon, which made him very happy. From the morning till afternoon he seemed very active waiting for his family and talking about his kids and wife. But after the visiting hours he became very dull and lethargic. His attitude showed that he was very attached to his family. Most often he used to show me the pictures of his pet dogs that he used to miss a lot. Considering the condition of the patient I made an effort to talk to his family in isolation. I instructed them to increase their visits in the hospital and take good care of the patient when he will get discharged. Because along with therapy the moral and emotional support of the family would be very necessary for his further progress (Davidson et al., 2007). So, as many times as they could spend with him it will make him recover faster. Conclusion From the experience with a patient, I learned a lot of things. Management of the diabetic patient is more complicated than any other disease. It needs continuous monitoring, and the interventions are highly dependent on the monitoring. I also found that apart from treatment emotional support from family is very important for the patient. Bringing modification in the living style is the first step towards betterment for diabetic patients. As, it is also seen in the case of my patient he has been taken strict low-calorie diet without sugar. The patient had a history of diabetes that also seems inherited as it was running in his family; both his mother and father were diabetic patients. I also observed that close monitoring of blood glucose level, as well as other vital signs, is integral in taking care of a diabetic patient. I also used to take care that he must not get any cut or wound because the healing process in diabetic patients becomes very disturbed. The sliding mechanism of insulin administration was another new learning for me. I got to know how dose calculation and tapering is carried out with the blood glucose level. As, diabetes is the most-common disease these days and mostly patients who come for surgery have this disease. The learning and experience I had will be very useful for me in handling patients with diabetes in the future also. There are huge chances of further learning in this subject that I am keen to have in the future. List of Reference American Nurses Association, 2014. Privacy and Confidentiality. [Online] Available at: http://www.nursingworld.org/MainMenuCategories/EthicsStandards/Ethics-Position-Statements/PrivacyandConfidentiality.html [Accessed 11 August 2014]. Barron, J., 2010. The Endocrine System: The Pancreas & Diabetes. [Online] Available at: http://jonbarron.org/article/endocrine-system-pancreas-diabetes#.U-h5v-OSyVJ [Accessed 11 August 2014]. Boada, C. & Moreno, M., 2013. Pathophysiology of diabetes mellitus type 2: beyond the duo "insulin resistance-secretion deficit". Nutrición hospitalaria., 2(1), pp.78-87. Bowen, R., 2002. The Endocrine Pancreas: Introduction and Index. [Online] Available at: http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/ [Accessed 12 August 2014]. Campellone, J., 2013. Ventriculoperitoneal shunting. [Online] Available at: http://www.nlm.nih.gov/medlineplus/ency/article/003019.htm [Accessed 11 August 2014]. Davidson, J. et al., 2007. Clinical practice guidelines for support of the family in the patient- centered intensive care unit: American College of Critical Care Medicine Task Force 2004 –2005. Critical Care Medicine, 35(2), pp.605-22. Diabetes.co.uk, 2014. Blood Sugar Level Ranges. [Online] Available at: http://www.diabetes.co.uk/diabetes_care/blood-sugar-level-ranges.html [Accessed 12 August 2014]. Gillaspy, R., 2014. Pancreas: Functions, Anatomy & Insulin Production. [Online] Available at: http://education-portal.com/academy/lesson/pancreas-function-and-anatomical-features.html#lesson [Accessed 11 August 2014]. Guthrie, A. & Guthrie, W., 2004. Pathophysiology of diabetes mellitus. Critical care nursing quaterly, 27(2), pp.113-25. Iocara, S., 2012. Normal anatomy and physiology. [Online] Available at: http://www.educationdiabetes.com/for-doctors/diabetes-textbook/normal-anatomy-and-physiology [Accessed 11 August 2014]. Kenny, T. & Tidy, C., 2013. Treatments for Type 2 Diabetes. [Online] Available at: http://www.patient.co.uk/health/treatments-for-type-2-diabetes [Accessed 12 August 2014]. Mandal, A., 2013. Diabetes Mellitus Type 2 Pathophysiology. [Online] Available at: http://www.news-medical.net/health/Diabetes-Mellitus-Type-2-Pathophysiology.aspx [Accessed 11 August 2014]. Martini, F., 2007. Anatomy and Physiology. Quezon City: Rex Bookstore. McCulloch, D. & Robertson, P., 2014. Pathogenesis of type 2 diabetes mellitus. [Online] Available at: http://www.uptodate.com/contents/pathogenesis-of-type-2-diabetes-mellitus [Accessed 11 August 2014].NMC, 2014. Confidentiality. [Online] Available at: http://www.nmc-uk.org/nurses-and-midwives/advice-by-topic/a/advice/confidentiality/ [Accessed 12 August 2014]. Pandol, S., 2010. The exocrine Pancreas. California: Morgan and Claypool Life sciences. Pittas, A., 2014. Diabetes Mellitus: Diagnosis and Pathophysiology. [Online] Available at: http://ocw.tufts.edu/Content/14/lecturenotes/265878 [Accessed 11 August 2014]. Quesada, I., Tudurí, E., Ripoll, C. & Nadal, Á., 2008. Physiology of the pancreatic α-cell and glucagon secretion: role in glucose homeostasis and diabetes. Journal of Endocrinology, 1(2), pp.1995-99. Robertson, P., 2013. Insulin secretion and pancreatic beta-cell function. [Online] Available at: http://www.uptodate.com/contents/insulin-secretion-and-pancreatic-beta-cell-function [Accessed 11 August 2014]. Robson, R., 2012. The Pancreas. [Online] Available at: http://www.patient.co.uk/health/the- pancreas [Accessed 12 August 2014]. Strachan, M. & Jankins, J., 2005. Management of people with diabetes on the surgical wards. [Online] Available at: http://www.nhslothian.scot.nhs.uk/Services/A-Z/DiabetesService/InformationHealthProfessionals/MUHDiabetesProtocols/002_diabetes.pdf [Accessed 12 August 2014]. Thévenod, F., 2008. Pathophysiology of Diabetes Mellitus Type 2: Roles of Obesity Insulin Resistance and Beta Cell Dysfunction. Diabetes and Cancer, 19(1), pp.1-18. Thompson, L., 2014. Physiology of the Pancreas. [Online] Available at: http://teachmeanatomy.info/abdomen/physiology/pancreas/ [Accessed 11 August 2014]. Tortora, G. & Derrickson, B., 2008. Principles of Anatomy and Physiology. London: John Wiley & Sons. Wisse, B., 2013. Type 2 Diabetes. [Online] Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000313.htm [Accessed 12 August 2014]. Yki-Järvinen, H., 2011. Oxford Textbook of Endocrinology and Diabetes. 2nd ed. Oxford: Oxford University Press. Appendix 1 Patient profile Age 45 General - No smoking - Drinking occasionally - Family- mother died of heart attack at 60 yr. - GCS 15/15 - Pupils- equal on both sides reactionstolights - Patient admitted for brain steam gliome for VPS Current medical history - Presented with balance problem and nausea - vomiting twice per week - headache (7/10 score) top of head pain - dizziness -no visual disturbance -no weakness in limbs -no urinary and bowel problems - hypotension on med: Amlodipine - diabetic type 2 - blood sugar on admission 14 mmol -med: insulin Previous relevant medical history ⦁ Endoscopic 3 rd ventriculostomy in March 2011 ⦁ 21/03/12 Astrocytoma with early progression to grade III ⦁ Chemo radiation completed 14/06/2012 ⦁ history of diabetece in familly- father and mother Relevant social history Patient lives with wife and 2 kids. Happy Social live. Read More

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