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 …show more content…
Insulin resistance is probably the primary dysfunction. Insulin is present; however, because of other metabolic processes, it is incapable of acting on cells and tissues. The pancreas cannot increase production of insulin to compensate for the need and therefore, the insulin activity is deficient. Resistance to insulin deficiency results from a combination of genetic and environmental factors. Very often the acetyl-CoA in a type 2 patient becomes cholesterol, raising these levels and creating a high risk of coronary disease. Due to excessive blood glucose and insulin deficiency, osmotic diuresis leading to marked urinary losses of water and electrolytes is generated. Urinary excretion of ketones requires additional losses of Na and K. Although significant total body deficit of K, K initial whey is typically normal or elevated, due to the extracellular migration of K in response to acidosis. If K is not controlled and replaced, as needed, hypokalemia is potentially fatal. …show more content…
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
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 …show more content…
Insulin resistance is probably the primary dysfunction. Insulin is present; however, because of other metabolic processes, it is incapable of acting on cells and tissues. The pancreas cannot increase production of insulin to compensate for the need and therefore, the insulin activity is deficient. Resistance to insulin deficiency results from a combination of genetic and environmental factors. Very often the acetyl-CoA in a type 2 patient becomes cholesterol, raising these levels and creating a high risk of coronary disease. Due to excessive blood glucose and insulin deficiency, osmotic diuresis leading to marked urinary losses of water and electrolytes is generated. Urinary excretion of ketones requires additional losses of Na and K. Although significant total body deficit of K, K initial whey is typically normal or elevated, due to the extracellular migration of K in response to acidosis. If K is not controlled and replaced, as needed, hypokalemia is potentially fatal. …show more content…
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