Diabetes mellitus is a metabolic disorder that is chronic and is characteristic of a hyperglycemia that is persistent. This can be caused by an impairment of the secretion of insulin hormone, resistance to insulin activity or even both. A chronic hyperglycemia in collaboration with other metabolic issues in individuals suffering from type two diabetes can cause harm to some body organs and lead to disability, elevated risk of developing cardiovascular disorders and other complications (Campbell & Lebovitz, 2001). In this paper, the diagnosis, pathophysiology, laboratory tests/radiologic exams, treatment, prognosis, and nursing care for the primary disease process for this patient.
Pathophysiology
Type two diabetes is an insulin resistance disorder that is related to beta cell dysfunction (Alberti & Zimmet, 2011). At the onset, more insulin is secreted in order to maintain the elevated glucose at normal levels. In addition, it causes a reduction in the transport of glucose in body parts such as the liver. The decrease also impacts the muscle and fat cells. In hyperglycemia, more fat is broken down. As the problem continues, the beta cells change. The insulin secreted is no longer able to ensure glucose homeostasis. This in turn leads to hyperglycemia. Most people suffering from diabetes mellitus are obese or increased body fat around the abdomen. This fat encourages insulin resistance by causing a number of inflammatory activities. Although the most common theory that explains this association is the visceral hypothesis that gives a major role in increased non-esterified fatty acids levels, there is another theory which is the ectopic fat storage syndrome (Yki-Järvinen, 2011).
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In addition, lack of or inadequate physical activity elevates the risk of developing type two diabetes. The impairment of alpha-cell function has also been identified as a contributor in the pathophysiology of diabetes mellitus (Campbell & Lebovitz, 2001). In addition, it causes a reduction in the transport of glucose in body parts such as the liver. The decrease also impacts the muscle and fat cells. In hyperglycemia, more fat is broken down. Due to this dysfunction, glucagon levels which become elevated during the fasting period are not reduced by a meal. In addition, hepatic glucose amounts that increase during fasting are also not suppressed by a meal.
Diagnosis
The symptoms of type 2 diabetes in most cases appear immediately and are in most cases the reason for having a checkup for blood sugar. There are several tests that can be carried out in the diagnosis of diabetes. One of them is glycated hemoglobin (A1C) test. During this test, one does not need to fast. It shows the average blood glucose level for the past two to three months. The test assess the amount of blood glucose that is bound to hemoglobin. More glucose on hemoglobin indicate increased blood glucose levels. A 6.5% or more of A1C levels on two different instances shows that the patient is suffering from diabetes(Campbell & Lebovitz, 2001). When the A1C is between 5.7% and 6.4%, it shows that the patient is pre-diabetes. However, an A1C of 5.7% shows that the patient’s glucose levels are normal. In cases when the AIC tests outcomes are not consistent, it indicates that the test is not available. In addition, it may show that the patient is having some issues that can make the test incorrect. Such issues include pregnancy or a type of hemoglobin that is commonly referred to as hemoglobin variant.in such instances, other tests can be used (Sukhareva, 2009).
Another test that can be used in diagnosis is random blood sugar test. In this test, a blood sample from the patient is obtained at random periods. Regardless of the time for the last meal, a random blood glucose of 200mg/dl to 11.1mmol/L or more indicate that the patient is suffering from diabetes (Campbell & Lebovitz, 2001). In fasting blood sugar test, a sample of the patient’s blood is obtained after the patient has had a fast throughout the night. A blood glucose level that is below 100mg/dl after an overnight fast is considered normal. A level that is between 100mg/dl and 125mg/dl is diagnosed as pre-diabetes. In cases where the levels are 126mg/dl or more on two different occasions is considered diabetes.
In oral glucose tolerance test, the patient has to fast for a whole night after which the blood glucose levels are measured. Afterwards, the patient is given a sugary drink to consume after which the glucose levels are assessed on periodic basis for two hours. A blood glucose level that is below 140mg/dl is considered normal. A level that is above 200mg/dl after a period of two hours shows that the patient is diabetic (Alberti & Zimmet, 2011). However, a level between 140mm/dl and 199mg/dl shows that the patient is pre-diabetic. In cases where there are suspicions for type 1 diabetes, the patient’s urine is tested to establish if there are ketones. Ketones are produced as a byproduct in cases when fats and muscle are used in the production of energy when the body does not adequate insulin to act on the present glucose(Campbell & Lebovitz, 2001). In this case also, a test to establish if the cells involved in the destruction of the immune system that are linked to type 1 diabetes is also done. These cells are known as autoantibodies.
Treatment and Management
Metformin is the first line of treatment in type 2 diabetes in cases where there are no contraindications. Metformin’s mechanism of action involves changing the components of the gut micro biota. It also activates the mucosal AMP. The mucosal AMP ensures the integrity of the intestinal protection. The impacts put together with the activated AMP located in the hepatocytes seem to be the way in which metformin reduce the levels of lipopolysaccharide circulating in the blood and the ones found in the liver. After getting to the liver, metformin prevents gluconeogenesis in four different ways. The mechanisms include the stimulation of hepatic AMPK by liver kinase, preventing the production of Camp that is caused by glucagon by stopping adenylcyclase, prevent the production of NADH coenzyme in the mitochondria and the prevention of mitochondrial glycerol phosphate dehydrogenase (Yki-Järvinen, 2011).
In addition, insulin secretagogues are used in the treatment of diabetes. They include meglitinides and sulfonylureas. The two drugs have the same mechanism of action. They activate beta cells in order to produce insulin. The drugs are a first or second line treatment the diabetic patient. They are mostly used as a reference in comparing the efficiency and safety of other drugs apart from insulin (Campbell & Lebovitz, 2001). On the other hand, meglitinides activate the production of insulin in a similar way. They have a different site for binding that has an increased absorption and stimulus to the production of insulin. However, the patient requires frequent dosing with the drug.
In addition, both drugs act by promoting the secretion of insulin. It is controlled by ATP sensitive potassium channels that are found in the beta cells. Despite the fact that the binding sites for both drugs are different, they both cause a closure of the channels. In addition, they depolarize cells thereby causing an elevation in the levels of calcium in the cytoplasm and as a result the release of insulin. Both Sulfonylureas and meglitinides are efficient when used as a monotherapy or when used together with other oral hypoglycemic medicines or insulin (Sukhareva, 2009). Sulfonylureas are cost effective in the managing glucose levels in a patient. They are commonly used because of their efficiency in the long time and safety.
In cases where metformin cause contradictions or the patient’s body cannot tolerate it, meglitinides and sulfonylureas are usually used as an alternative. They can be used as an alternative treatment choice both in triple and double treatment. However, the use of these drugs can lead to decrease of blood sugar below normal levels and increase in weight(Yki-Järvinen, 2011). With time, the secretagogues of insulin become ineffective. This is caused by the continued failure of beta cells. Therefore, the patient’s ability to keep an adequate control of blood glucose decreases. Despite the fact that this impact can be associated with the progression of the disease, it has been identified to cause an elevation of secondary failure as compared to other drugs (Sukhareva, 2009). A number of studies have confirmed that weight gain can occur because of the insulin therapy.
Besides pharmacotherapy, diet is vital in the treatment and management of type 2 diabetes. Weight loss is one of the main objectives in individuals suffering from type 2 diabetes. Weight loss can assist in promoting the sensitivity of insulin. This can make the management of diabetes easy. To ensure that weight loss is achieved, a patient’s diet ought to be low in calories(Campbell & Lebovitz, 2001). Due to the fact that type 2 diabetes is a chronic disorder, a healthy diet is vital for the patient. A low glycemic diet can assist type 2 diabetes patients maintain a normal blood sugar level, facilitate in weight loss and decrease the dependency on drugs.
Physical activity is also an important component in the management of type 2 diabetes. When muscles are involved in physical activity, they use the glucose in the body to produce the required energy. After the physical activity, the body begins to replenish its glucose stores by rapidly absorbing the glucose present in the blood. In addition, besides assisting in reducing blood glucose levels, physical activity uses the energy produced from food (Sukhareva, 2009). Therefore, if there is more physical activity and limit the amount of calories consumed, diabetic patients are able to lose weight. Besides exercise and diet modifications, other lifestyle changes such as avoiding or significantly reducing the amount of alcohol consumed and smoking cessation can assist in improving the diabetes condition and the overall health.
Prognosis
Diabetes mellitus is a progressive disorder in which the involved risks of microvascular disorder and death are firmly related to high levels of blood glucose. The course of type 2 diabetes is characteristic of a decrease in the function of beta cells. In addition, the continued resistance of insulin is evident. This is because the cells located in the muscles and the fats are not able to adequately react to insulin and cannot absorb the glucose in the blood. This process includes the degeneration of a number of vital parameters which include HbA1c, fasting blood sugar and postprandial sugar levels (Campbell & Lebovitz, 2001).
In the development of type 2 diabetes, beta cells that are located in the pancreas are unable to cope with the impaired blood sugar tolerance. This causes a reduction in their activity. Continued inability of the beta cells to function and to a smaller extent decline in beta cell mass cause a deterioration in blood sugar regulation and the onset of complications. Most of the therapies that are used are not able to inhibit the continued loss of the function of beta cells completely. They only decrease blood sugar levels. Unfortunately, they can also lead to increase in weight and hypoglycemia with continued use.
For most people, by the time a diagnosis is made, half of the patients suffering from type 2 diabetes manifest the complications of the disease. The onset of the complications is usually 5-6 years prior diagnosis (Sukhareva, 2009). Diabetes may begin ten or more year’s prior diagnosis. Cardiovascular disorders are a main cause of mortality in diabetic people. It accounts for approximately 52% of deaths in diabetic patients. Individuals suffering from diabetes mellitus have a double risk of suffering from stroke in the first five years after a diagnosis is made when compared to the rest of the population that are not diabetic(Campbell & Lebovitz, 2001). Other complications associated include kidney disease, depression, damage to the nerves and limb amputation. Diabetes is the major cause of end stage kidney failure. One out of every three diabetic patients suffers from kidney disease. In addition, the rates of depression in individuals suffering from diabetes is double that of the general population.
Neuropathy is another complication that arises from diabetes. Approximately half of the people suffering from diabetes experience damage to their nerves (Yki-Järvinen, 2011). The verves are involved in the transmission and relaying of information to and from the brain and other body parts. It can also lead to chronic pain and other health related complications. Finally, type 2 diabetes is the major cause of limb amputation. Approximately one out of every 20 individuals suffering from diabetes may experience foot cancer (Campbell & Lebovitz, 2001). In addition, approximately 70% of the amputated diabetic patients die within a period of five years after having an amputation.
References
Alberti, K. G., & Zimmet, P. (2011). Classification and diagnosis of diabetes mellitus. Oxford Textbook of Endocrinology and Diabetes,1703-1711. doi:10.1093/med/9780199235292.003.1304
Campbell, I. W., & Lebovitz, H. E. (2001). Diabetes mellitus. Oxford, England: Health Press.
Diabetes mellitus. (2011). New Delhi: Central Council for Research in Homoeopathy.
Sukhareva, O. Y. (2009). American Diabetes Association proposes to use HbA1c level for diagnosis of diabetes mellitus. Diabetes Mellitus,12(4), 126. doi:10.14341/2072-0351-5722
Yki-Järvinen, H. (2011). Pathophysiology of type 2 diabetes mellitus. Oxford Textbook of Endocrinology and Diabetes, 1740-1748. doi:10.1093/med/9780199235292.003.1336
