Brief Explanation Of Etiology And Pathology Of Dm Essay

Brief Explanation Of Etiology And Pathology Of Dm Essay

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A brief explanation of the etiology and pathology of DM.
In diabetes, we can find cases in which the insulin is absent, little insulin or the function of insulin is impaired or not functioning. The insulin is produced and secreted by cells in the pancreas. Insulin also stimulates gluconeogenesis is that inhibits lysis regulates glycogen and protein synthesis. Pancreatic glucagon stimulates the breakdown of glycogen and gluconeogenesis. Cortisol promotes gluconeogenesis and Epinephrine is a neurotransmitter that increases the breakdown of glycogen. The insulin stimulates the uptake and distribution of glucose from the blood into cells for energy production. Failing to provide glucose to the cells lose the glycemic balance. With the loss of this balance, the body begins to metabolize fats and proteins for energy that usually in a healthy human would get from carbohydrates. Hyperglycemia and excessive use of fats and proteins cause a high level of acetyl-CoA. The acetyl-CoA is converted to acetone, acetoacetate, and beta-hydroxybutyrate. These are known as ketones and when dissolved in bodily fluids reduce the blood pH. Increased ketones can lead to metabolic acidosis. Type 1 diabetic patients are at significant risk of ketoacidosis. Type 1 diabetes most often it occurs in childhood or young adult years. It is caused by an absolute deficiency of insulin from autoimmune destruction of pancreatic cells or degeneration of these cells. The individual has inherited a susceptibility to this autoimmune reaction and diabetes develops suddenly. Type 1 diabetics need insulin to prevent ketosis.
The cause of type 2 diabetes hyperglycemia can result from insulin resistance, insulin deficiency, or a defect in insulin secretion. Insulin resistanc...


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...e. The last one is the strongest and most prevalent acid, but the most common method of detection is nitroprusside method that only measures acetone and acetic acid. The acetic acid in an alkaline medium reacts with glycine and nitroferricyanide and as a result, of this reaction, a purplish compound is obtained. Therefore, evaluations of ketone levels in urine or serum by the method of nitroprusside is not the standard method to monitor therapy response. The acetoacetate accumulates in the blood, and a small amount becomes acetone by spontaneous decarboxylation. The method used to measure beta-hydroxybutyrate (BHB) is photometric, B-hydroxybutyrate dehydrogenase D-3-hydroxybutyrate in the presence of NAD (HBDH-B) becomes acetoacetate and NADH dehydrogenase at pH 8.5 for D-3-hydroxybutyrate. NADH is converted to a colored compound using INT and diaphorase (htt10)


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