Diabetes Mellitus is a group of metabolic disorders that is clarified by hyperglycemia. There are many forms of this disease and the reason for hyperglycemia may be either reduced insulin secretion, decreased glucose utilization by the tissues, and increased glucose production. Diabetes causes many secondary physiological changes in the body leading to diverse affects on different organ systems; as well as being a burden to the patient and the healthcare system as a whole. Diabetes Mellitus is the leading cause of end stage renal disease as well as the leading cause of non-traumatic limb amputation and adult blindness. In the future it will be the leading cause of morbidity and mortality in the western world in the foreseeable future (Harrison’s, 2008).
Diabetes Mellitus is classified into two major groups based on the reason for the development of hyperglycemia. Type 1 is due to a complete or near complete loss of insulin; and is thought to be due to an autoimmune disorder leading to antibodies targeting the person’s pancreatic beta cells, which are responsible for the production and release of insulin in the body (Anderson, 2008). Type 2 diabetes on the other hand is characterized by varying degrees of insulin resistance, impaired secretion of insulin, and increased glucose production. The incidence of diabetes mellitus is increasing rapidly; in 1985 the numbers of people affected was around 30 million, where as in the year 2000 the number of cases has ballooned to 177 million. While the numbers of both types of diabetes mellitus has increased; the numbers of people with type 2 diabetes mellitus has increased dramatically with the increasing number of people who are obese and the sedentary life style that many people in western civilizations lead.
Geographically there is also considerable variation in the incidence of type 1 and type 2 diabetes. In the Scandinavian countries such as, Finland, Sweden, and Norway have the highest incidence in type 1 diabetes; the countries in the Pacific Rim such as Japan and China have the lowest. The United States and Europe have an intermediate rate. The incidence rate of type 1 diabetes most likely varies due to genetic, behavioral and environmental factors. The highest numbers are seen in certain Pacific island countries, is intermediate in countries such as the United States and India, and is lowest in Russia (Zimmet, Alberti, and Shaw, 2001).
The diagnosis of Diabetes Mellitus is based on criteria issued by the National Diabetes Data Group and the World Health Organization and is based on 1. A person’s fasting blood glucose and the response to an oral glucose tolerance test; and 2. The level of glycemia where diabetes specific complications occur describes diabetes mellitus. The level of a person’s fasting blood glucose is classified into three different categories. A value of <5.6mmol/L is considered normal. A person with a fasting blood glucose level between 5.6-6.9 mmol/L is defined as having impaired fasting glucose; and a value >7.0mmol/L leads to the diagnosis of diabetes mellitus. Based on the oral glucose tolerance test, impaired fasting glucose is considered in patients with a value between 7.8-11.1 mmol/L; and diabetes is considered when glucose levels is >11.1 mmol/L. The test is done over a two-hour period with a 75g load of glucose. A person with either impaired fasting glucose and/ or impaired glucose tolerance is considered to be pre-diabetic and is at increased risk for developing type 2 diabetes.
Treatment options for patients suffering from type 1 diabetes are very simple; because these patients lack insulin they require exogenous administration of insulin. There are many different forms of insulin that can be administered depending on the convenience of the regimen. For example short acting insulin may be given right before meals while at the same time the patient will take longer acting insulin, so that there is a basal level of insulin in the patients body throughout the entire day. Type 2 diabetic patients on the other hand do not necessarily require the use of exogenous insulin. The treatment options for type 2 diabetes vary widely, for example we have glucose-lowering drugs; these include the insulin secretagogues, which result in insulin secretion. The Biguanide drugs, such as metformin, result in the reduction of hepatic glucose production. The thiazolidinediones lower insulin resistance by affecting adipose tissue. The alpha- glucosidase inhibitors reduce hyperglycemia following a meal by delaying the rate of glucose absorption in the intestine; they have no affect on glucose utilization or insulin secretion (Bolen, Feldman, Vassy, Wilson, Yeh, Marinopoulos, Wiley, Selvin, Wilson, Bass, & Brancati, 2007).
In reference to Mr. Langerhans diabetes he has many risk factors that lead to the development of this condition. Firstly, he is 60 years old, studies have shown that the prevalence is 20.9% in patients >60 years old. Secondly. Mr. Langerhans leads a sedentary lifestyle as well as an admittedly poor diet. Other risk factors that lead to the development of diabetes mellitus include a family history of diabetes, race and ethnicity, previously identified impaired glucose tolerance or impaired fasting glucose, hypertension, low HDL cholesterol levels or high triglyceride levels, and a history of vascular disease (Harrison’s, 2008).
The HbA1c level of Mr. Langerhans is disturbing. This test is used to determine how well a person’s diabetes is controlled. Its value tells the clinician how well a person has controlled his/ her blood sugar over a period of 6-12 weeks. Hemoglobin is what carries oxygen in our bodies. When diabetes is poorly controlled and sugar builds up in the body, it combines with hemoglobin, becoming glycated. In healthy individuals a HbA1c level of 3.5-5.5% is considered normal; while in patients with diabetes mellitus a HbA1c level of 6.5% is considered to be good and controlled. There are some limitations to the use of HbA1c measurements. Firstly, it cannot be used to monitor daily fluctuations in blood glucose concentration because it is not influenced by the daily changes in a persons glucose levels. Secondly, it may be increased in the presence of other medical problems such as uremia and chronic alcohol abuse. The levels may be decreased in medical conditions, such as acute or chronic blood loss; pregnancy can lead to either increases or decreases of the HbA1c levels.
Proteinuria is where there is an abnormal amount of protein, specifically albumin, in the urine. Albumin in a normal healthy person is too large of a molecule to be filtered by the kidney and be present in the urine. However, when the glomeruli of the kidneys are damaged protein can end up being filtered into the urine of an individual. Proteinuria is a sign of chronic kidney disease that may be seen as a result of diabetes, high blood pressure, or any other disease that damages the kidney. When albumin is present in a patients urine, this is the first sign of a serious deterioration of kidney function, and as the kidney continues to loose function, the amount of protein in the urine increases (Gross, de Azevedo, Silveiro, Canani, Caramori, and Zelmanovitz, 2005).
As said previously, diabetes mellitus is the leading cause of blindness worldwide. Blindness results from diabetic retinopathy and macular edema. Diabetic retinopathy itself is broken up into two phases, a proliferative and a non – proliferative phase. The non – proliferative phase due to the development of vascular microaneurysms, blot hemorrhages, and cotton wool spots. The pathophysiology of this stage is due to increased vascular permeability of the retina and abnormal microvasculature leading to the development of retinal ischemia. The proliferative phase is characterized by the development of neovascularization due to the hypoxia resulting from the non-proliferative phase. The new vessels that form around the optic nerve and macula are very fragile and tend to rupture very easily leading to the consequences of hemorrhage into the vitreous humor, fibrosis, and retinal detachment (Saudek, Derr, & Kalyani, 2006).
Besides the retinal and renal problems that are prominent in patients suffering from diabetes, this disease affects other systems in the body. In approximately 50% of patients, diabetic neuropathy develops. The neuropathy may manifest as a poly-, mono-, or autonomic neuropathy. Its development depends on the duration of a person’s diabetes as well as how well they have controlled there blood glucose levels. Both myelinated and unmyelinated nerves are affected and therefore other reasons for neuropathy must be ruled out. By far the most common type of neuropathy that develops is a distal polyneuropathy and symptoms include numbness, tingling, or burning. The development of mononeuropathy is less common and presents with pain and weakness in the single in nerves distribution pattern. Other systemic problems that occur in these patients include gastrointestinal and genitourinary dysfunction. The most common GI dysfunction that occurs is delayed gastric emptying and differences in motility leading to fluctuating diarrhea and constipation. Genitourinary dysfunction is the result of autonomic dysfunction as a result of autonomic neuropathy. The last major organ system affected by diabetes is the cardiovascular system. The combination of already existing cardiovascular problems and diabetes leads to increased morbidity and mortality in these patients. Besides the major organ systems affected, other complications of patients that suffer from diabetes include, increases in infection rates due to impaired response to infection as well as dermatologic conditions that may be associated with the decreased clearance of infection.
Diabetes is a serious condition that affects every system in the body. With proper control of the person’s blood glucose levels the major causes of morbidity and mortality can be decreased and the diabetes is just something the person has to live with. However, when the level of blood glucose is not properly controlled thee effects on the body and the systems can be disastrous to the patient and their family.
Work Cited
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Anderson, M. (2008) Update in Endocrine Autoimmunity. Journal of Clinical Endocrinology Metabolism. 93(10) 3663-3670 doi: 10.1210/jc.2008-1251
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