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Diabetes mellitus is caused by insufficient insulin production or lack of responsiveness to insulin, resulting in hyperglycemia high blood glucose levels. There are 2 primary types of diabetes mellitus, type i insulin dependent or juvenile onset , which may be caused by an autoimmune response, and type ii non insulin dependent or adult onset. Diabetes mellitus dm is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced in the pancreas by the beta cells of the islets of langerhans. Absence, destruction, or loss of these cells causes an absolute deficiency of insulin, leading to type 1 diabetes insulin dependent diabetes mellitus iddm . Most children with diabetes have iddm and a lifetime dependence on exogenous insulin.

Type 2 diabetes non–insulin dependent diabetes mellitus niddm is a heterogeneous disorder. Patients with niddm have insulin resistance, and their beta cells lack the ability to overcome this resistance. Although this form of diabetes previously was uncommon in children, 20% or more of new patients with diabetes in childhood and adolescence now have niddm, a change associated with increased rates of obesity. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and fat cells and by stimulating the conversion of glucose to glycogen as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. Hyperglycemia results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose.

The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Without insulin, a child with iddm wastes away and eventually dies from diabetic ketoacidosis. Information on mortality rates is difficult to ascertain without complete national registers of childhood diabetes, although age specific mortality probably is double that of the general population.

Particularly at risk are children aged 1 4 years who may die with dka at the time of diagnosis. Most deaths result from delayed diagnosis or neglected treatment and subsequent cerebral edema during treatment for dka, although untreated hypoglycemia also causes some deaths. Iddm complications are comprised of 3 major categories: acute complications, long term complications, and complications caused by associated autoimmune diseases. Acute complications reflect the difficulties of maintaining a balance between insulin therapy, dietary intake, and exercise. Long term complications arise from the damaging effects of prolonged hyperglycemia and other metabolic consequences of insulin deficiency on various tissues. While long term complications are rare in childhood, maintaining good control of diabetes is important to prevent complications from developing in later life. The likelihood of developing complications appears to depend on the interaction of factors such as metabolic control, genetic susceptibility, lifestyle, pubertal status, and gender.

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Most cases of iddm are the result of environmental factors interacting with a genetically susceptible person. This interaction leads to the development of autoimmune disease directed at the insulin producing cells of the pancreatic islets of langerhans. These cells are progressively destroyed, with insulin deficiency usually developing after the destruction of 90% of islet cells. Most people with diabetes have one of the two types and can be treated with pills or insulin shots. My mother has type ii diabetes, and helping her cope with her disease gives me a wider outlook on it. I see her give herself shots every day to monitor her blood sugar levels and i also see her taking medicine to help control the amount of glucose to be present in her system.

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