Chronic Conditions Prevention and Management - Essay Example

Chronic Conditions Prevention and Management In 1970, both the WHO and the national diabetes data group released new classification methods for diabetes mellitus. The classification method that was introduced brought a new order to the chaotic situation that existed in which the nomenclature, as well as the diagnostic criteria widely varied. Diabetes mellitus is a metabolic disease that is characterised by an elevated blood glucose level as a result from the problem in insulin secretion, and action of insulin or both (Drouin et al., 2013). The chronicity of hyperglycaemia in diabetes is associated with prolonged destruction of several organs especially the nerves, eyes, kidneys and cardiovascular organs. There are myriad pathogenic processes that are involved in the development of the disease. These processes range from destruction of the β-cells of pancreas, which is an autoimmune process, with concurrent deficiency of insulin to different abnormalities that leads to the resistance to insulin action. The underlying factor of the abnormalities in protein, fat and carbohydrates metabolism in diabetes disease is as a result of reduced insulin action on target tissues. Studies have shown that insulin secretion impairment, as well as the defect in insulin action, often coexists in one patient but it is not clear which abnormality is usually the primary cause of the elevated blood sugars (American Diabetes Association, 2011). Burden and prevalence of diabetes mellitus in Australia Diabetes causes substantial morbidity and mortality in Australia and the estimates of diabetes prevalence provide stakeholders to plan and allocate enough funds for health services. Therefore, the continuous availability of data on the prevalence of diabetes in Australia is significant for disease monitoring, planning, identifying the population at risk, providing services for people and developing an effective preventive strategies (Shaw & Tanamas, 2012). It is approximated that one million Australians are diagnosed with diabetes mellitus and the prevalence increases with age, which is noted to be higher in male gender (4.9%) than in female gender (3.8%). In addition, the prevalence is high in the northern part of Australia (10.6%) and lowest in the Central part of Australia (3.0%). The disease has been noted to have an onset at childhood in several cases. A report issued by an Australian Institute of health showed that 0.3% of Australians aged below 35 years were diagnosed with diabetes as compared to 16% of Australians aged above 65 years. Australia is ranked the seventh globally for the prevalence of diabetes type one among children aged below 14 years and the sixth in the incidence. Moreover, studies have shown that there are increased number of adolescents and young children who are currently affected by diabetes type two (Shaw & Tanamas, 2012). The impact of diabetes in Australia is enormous since it is associated with chronic complication in individuals that ultimately increases morbidity in the population. Diabetes is among the leading diseases in causing non-traumatic limb amputation in Australia. The disease majorly affects the feet, kidney, eyes and cardiovascular system. Approximately 13% of Australians with diabetes have nerve damage as well as limbs damage, in addition, retinopathies related to diabetes occurs in approximately fifteen percent of the total people suffering from diabetes (Committee & Classification, 2010). Cardiovascular disease leads in causing death among individuals suffering from diabetes. Furthermore, approximately 41% of individuals with diabetes have poor psychological problems such as anxiety, depression, stress as well as burnout in coping with diabetes care. Diabetes is a disease that is listed among the top ten leading cause of mortality in Australia. The total yearly expenditure of individuals with type one diabetes mellitus in Australia is approximated to be six billion U.S dollars and $570 million for individuals with diabetes type 2. In addition, it is approximated that the annual cost per an individual with type two diabetes increases significantly due to complications related to the disease, ranging from $ 9, 645 per head to $16, 698 per person. In essence, type two diabetes mellitus has been seen to pose the highest burden in the healthcare system as compared to type one diabetes mellitus as shown in the table 1 below. These figures are high thus call for a quick solution to curb the exponential rise of diabetes in the population (Shaw & Tanamas, 2012). Table One: Average annual health care expenditure of diabetes per an individual in Australia Type one diabetes mellitus Type two diabetes mellitus No complications related to diabetes $3, 468 $4,025 Complications related to microvascular structures $8, 122 $7,025 Complications related to macrovascular structures $12, 105 $9, 055 Combined micro and Macrovascular complications $16, 698 $9, 645 Classification of diabetes mellitus It is imperative to note that stating a given type of diabetes to a person usually depend on the circumstance that is current at diagnosis time, and several people do not often fit in one category. For example, an individual diagnosed of gestational diabetes mellitus may still have high blood glucose after giving birth and may be diagnosed later to have type 2 diabetes. Similarly, a person who develop diabetes due to injudicious use of steroids may have normal sugar levels once glucocorticoid is discontinued but may develop type two diabetes later in the years after a reoccurrence of pancreatitis. Therefore, it is for these reasons that it is less important to label a particular type of diabetes but it is wise to understand the pathogenesis and manage the disease accordingly. For understanding the pathogenesis and management of different type of diabetes, this article shall discuss them differently (Olson et al., 2010). Type 1 diabetes mellitus Diabetes mellitus type one account for 5-10% of total people having diabetes. The disease results from the destruction of the β-cells of pancreas, which is an autoimmune process. The primary markers of the beta cells that are destroyed include the islet cells autoantibodies, the body related autoantibodies to GAD65 as well as autoantibodies to tyrosine phosphates (IA-2 and IA-2B). In type one diabetes, the rate of destruction of the cells vary, which is being fast in early childhood and slow in adults (Canivell & Gomis, 2014). This type of diabetes is usually seen in children and adolescents but it can occur at all age groups. Destruction of the beta cells has been linked to multiple genetic predispositions as well as being associated with some environmental factors such as infections (Reddy, Ford, & Dunbar, 2010). The pathogenesis of diabetes type one in relation to β-cell damage within the islet may be difficult to follow due to increased heterogeneity of the pancreatic lesions. However, some scholars have argued that at the beginning of the overt hyperglycaemia, a conglomeration of pseudo atrophic islets with glycogen producing cells, pancreatic polypeptide, lymphocytes and somatostatin may be seen. The lymphocytic infiltration is only seen in the islets cells that contain residual β-cell and is the likely explanation of the chronicity of diabetes type 1. The symptoms developed include elevated blood glucose level, increased urination, polydipsia, polyphagia and failure to grow normally as seen in children, in addition, a life-threatening ketoacidosis may ensue(Selvin et al., 2011) . Type 2 diabetes mellitus This form of diabetes accounts for the larger group in the affected population (90-95%) with diabetes mellitus. Type 2 diabetes mellitus involves individuals who are having insulin resistance and occasionally have relative insulin deficiency, at least at the onset of the disease or throughout their lifetime (McKenney & Short, 2011). There are several causes of type 2 diabetes although there is no precise aetiology that is known. This form of diabetes usually goes undiagnosed since hyperglycaemia develops gradually that is not severe enough bring any symptoms for the patient to realise. This put the patients at increased risk of developing microvascular complications. Even though patients with diabetes type 2 may have normal or high insulin levels, hyperglycaemia in these patients will be expected to, result in much higher levels of insulin had beta cells functions been normal. Therefore, insulin secretion is defective in these people and low to compensate for the insulin resistance. The risk of developing type 2 diabetes mellitus is associated with an increase in age, hypertension, obesity and in women who had previously developed gestational diabetes mellitus (Stumvoll, Goldstein, & van Haeften, 2010). This form of diabetes is characterised by a mixture of peripheral insulin resistance as well as inadequate secretion of insulin by the β- cells of pancreatic cells. The elevation of free fatty acids and increased proinflammatory levels of cytokines in the plasma has been attributed to insulin resistance. This ultimately results to a reduction in glucose transport into the muscles, elevated breakdown of fats and increased hepatic glucose secretion. Glucagon role cannot be underestimated in this form of diabetes; indeed, this form of diabetes can be termed as an islet paracrinopathy. Whereby the reciprocal in relation to the glucagon secreting α-cells and the insulin-secreting β-cells are lost, which results into hyperglucagonemia that consequently lead to hyperglycaemia (Reinehr, 2013). In essence, for this form of diabetes to occur, there must be a coexistence of insulin resistance and inadequate secretion of insulin. For example, overweight people have insulin resistance, but diabetes shall only develop to those individuals who cannot increase the level of insulin secretion to compensate sufficiently for their insulin resistance. The insulin concentration in these individuals may be high yet inappropriate for the level of their glycaemia (Imam, 2012). Diagnosis criteria for diabetes mellitus The sign and symptoms such as polydipsia, polyuria, recurrent infections, drowsiness and unexplained weight often bring about the clinical diagnosis of diabetes mellitus (Donath & Shoelson, 2011). A triple step screening and diagnosis procedure is often recommended for detecting diabetes in undiagnosed individuals. The three steps include; an initial assessment of risk factors of an individual, measurement of fasting blood glucose and analysis of oral glucose tolerance test. In addition, diagnosis must be verified on subsequent days not at all unequivocal hyperglycaemia with metabolic decomposition is present. The following groups of individuals should be tested for undiagnosed diabetes; individuals with impaired glucose tolerance, people aged 40 years and are obese or hypertensive, all individuals with cardiovascular diseases, women with polycystic ovarian disease and individuals on antipsychotic drugs (WHO, 2006). Diagnosis for patient complaining of symptoms suggesting diabetes shall include; testing glucosuria, ketones and measuring random or fasting blood glucose level. The following parameters should be taken into consideration during diagnosis (fasting plasma glucose ≥ 7.0mmol/L and random plasma glucose ≥ 11.1 mmol/L). The indication for OGTT test shall be done when fasting blood glucose levels ranges between 6.1-7.0 mmol/L while random plasma glucose ranges between 7.8-11.0 mmol/L. The oral glucose tolerance test is performed in the following manner: unrestricted carbohydrate diet is given to the patient 3 days before the test, the client is fasted overnight for eight hours, the patient is counselled to have a rest of thirty minutes before the test and he/she should not smoke. Then the plasma glucose level is measured prior and two hours after administration of 75 grams of glucose load (Sacks et al., 2011). The results obtained shall be interpreted based on the WHO recommendations as shown in Table 2. Table 2: glucose tolerance test: WHO diagnostic criteria Venous plasma measured in (mmol/L) Venous whole blood measured in (mmol/L) Capillary plasma measured in (mmol/L) Capillary whole blood (mmol/L) Diabetes mellitus Fasting 2 hours post glucose load ≥7.0 ≥11.1 ≥ 6.1 ≥10.0 ≥7.0 ≥12.2 ≥6.1 ≥11.1 Impaired glucose tolerance Fasting 2 hours post glucose load < 7.0 7.8-11.0 Read More