Diabetes Mellitus Essay

Submitted By shannonbg19
Words: 2308
Pages: 10

This paper deals about the study of diabetes mellitus, the pathology, types of diabetes, further complications if not controlled and management for the prevention of this disease. Diabetes refers to a set of several different diseases. All types of diabetes result in too much sugar, or glucose, in the blood. To understand why this happens it helps to understand how the body usually works. When you eat, your body breaks down your food into simpler forms such as glucose. The glucose goes into your bloodstream, where it travels to all the cells in your body. Your cells use glucose for energy. Insulin, a hormone made by the pancreas, helps move the glucose from bloodstream to the cells. Pathophysiology of Diabetes Mellitus further explain the concept how this disease works. Pancreas plays an important role of the metabolism of glucose by means of secreting the hormones insulin and glucagon. These hormones where then secreted by Islets of Langerhans directly to the blood. Inadequate secretion of insulin results on im- paired metabolism of glucose, carbohydrates, proteins and fats which then result to hyperglycemia and glycosuria. Hyperglycemia is the most frequently observed sign of diabetes and is considered the etiologic source of diabetic complications both in the body and in the eye. On the other hand, glucagon is the hormone that opposes the act of insulin. It is secreted when blood glucose levels fall. This is also further explained in the handbook of the Disease Management of Pathophysiology of diabetes mellitus which states the following:
“Glucagon increases blood glucose concentration partly by breaking down glycogen in the liver. Following a meal, glucose is absorbed into the blood. In response to increased blood glucose levels, insulin is secreted causing rapid uptake, storage, or use of glucose by the tissues of the body. Unused glucose is stored as glycogen in the liver. Between meals, when blood glucose is at minimal levels, tissues continue to require an energy source to function properly. Stored glycogen, via glucagon, is converted to glucose by a pathway known as glycogenolysis. Gluconeogenesis is the production of glucose in the liver from noncarbohydrate precursors such as glycogenic amino acids. Elevated glucose levels result in the formation of sorbitol (a sugar alcohol) via the aldose reductase pathway. Since sorbitol cannot readily diffuse through cell membranes, cell edema and changes in function can ensue. With respect to the eye, this contributes to the evolution of premature cataractogenesis (nuclear sclerotic, senile and snowflake posterior subcapsular cataracts) and sight threatening diabetic retinopathy (compromising the pericytes that line capillary walls). An additional complication of hyperglycemia is nonenzymatic glycosylation. Nonenzymatic glycosylation is the binding of excess glucose to the amino group of proteins in the tissues. As a possible result, at the level of the capillary membranes, altered cell function may lead to the development of microaneurysms, vascular loops, and vessel dilation, allowing blood leakage. Platelet aggregation secondary to these changes initiates tissue hypoxia. These changes result in the system wide accumulation of edema and in the eye, increase the potential for retinal sequelae. Glycemic control over the course of the disease has been shown to reduce the risk of developing debilitating organ disease and retinopathy. Blood glucose levels are of even greater importance in diabetic pregnant women, as hyperglycemia during pregnancy may initiate swift and severe progression of diabetic retinopathy. Other concurrent systemic variables that may potentiate the onset of diabetic retinopathy include hypertension, nephropathy, cardiac disease, autonomic neuropathy and ocular findings such as elevated intraocular pressure and myopia.” (http://cms.revoptom.com/handbook/SECT59a.HTM).

There are two types of diabetes. Type 1 and type 2 diabetes. Type 1 diabetes…