Preventing Medication Errors Essay

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Diabetes Mellitus The pathophysiology of Diabetes Mellitus rests upon knowledge of the basics of carbohydrate metabolism and insulin action. The consumption of food, carbohydrates are broken down into glucose molecules in the stomach. Glucose is absorbed into the bloodstream increasing blood glucose levels. This rise in glycemia stimulates the secretion of insulin from the beta cells of the pancreas. Insulin is needed from most cells to allow glucose entry. Insulin binds to specific cellular receptors and facilitates entry of glucose into the cell, which uses the glucose for energy. The increased insulin secretion from the pancreas and the subsequent cellular use of glucose results in lowered of blood glucose levels. Lower glucose levels then result in decreased insulin secretion. If insulin production and secretion are reformed by disease, blood glucose dynamics will also change. If insulin production is decreased, glucose entry into cells will be withdrawn, resulting in hyperglycemia. If insulin secretion is increased, blood glucose levels may become very low as large amounts of glucose enter tissue cells and little remains in the bloodstream. After meals, the amount of glucose available from carbohydrate breakdown often exceeds the cellular need for glucose. Excess glucose is stored in the liver in the form of glycogen, which serves as a ready reservoir for future use. When energy is required, glycogen stores in the liver are converted into glucose through glycogenolysis, elevating blood glucose levels and providing the needed cellular energy source. The liver also produces glucose from fats and proteins through the process of gluconeogenesis. Glycogenolysis and gluconeogenesis both serve to increase blood glucose levels. Glycemia is controlled by a complex interaction between the gastrointestinal tract, the pancreas, and the liver. Multiple hormones may

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