Complications of Diabetes Mellitus Type II A 20 years old nursing student in her sophomore year, has been diagnosed with Diabetes Mellitus Type II (DMII). Although she has completed most of her science courses, she has not completed applied pathophysiology. She knew something was wrong due the signs and symptoms presented: polyuria, polydipsia, polyphagia, acanthosis nigricans, tingling of toes and fingers, progressive vision loss. Once she consulted her primary physician, , hyperglycemia (fasting glucose = 150 mg/dL) and increased BMI (= 30) were found, as well as increased hemoglobin A1C (= 7.9%). Her family history also played a role in diagnosing her since her mother, and grandmother presented the condition. She is currently under medication
…show more content…
This metabolic disorder is characterized mainly by chronic hyperglycemia, and decreased sensitivity to …show more content…
Under normal circumstances, as blood sugar level increases, insulin will be released from the beta cells in the pancreas in order to process glucose. More specifically, insulin will promote glucose uptake by splanchnic and peripheral tissues, and will suppress endogenous production of glucose (Boada & Martinez-Moreno, 2013). Additionally, insulin will inhibit the secretion of glucagon, which has key a role in increasing blood glucose by signaling the liver to breakdown glycogen. However, in DMII the activity of receptors found in peripheral tissues will be disrupted, allowing insulin resistance to take place. It is important to re-state that the main initial pathologic process involved in DMII is the lack of insulin sensitive receptors, and not the lack of insulin itself. Therefore, as insulin is not able to accomplish its functions, glycemic levels cannot be restored, and further glucose production will take place in the liver. As insulin resistance develops, the pancreatic beta cells will maximize the efforts to suppress glucose production, which can be translated to increased insulin secretion. This relationship is established by a feedback loop between beta cells and insulin sensitive tissues, which is aimed to maintain glucose homeostasis in the body (Khan, Cooper & Del Prato, 2014). Hence, as hyperglycemia continues to be present for long periods of time
This metabolic disorder is characterized mainly by chronic hyperglycemia, and decreased sensitivity to …show more content…
Under normal circumstances, as blood sugar level increases, insulin will be released from the beta cells in the pancreas in order to process glucose. More specifically, insulin will promote glucose uptake by splanchnic and peripheral tissues, and will suppress endogenous production of glucose (Boada & Martinez-Moreno, 2013). Additionally, insulin will inhibit the secretion of glucagon, which has key a role in increasing blood glucose by signaling the liver to breakdown glycogen. However, in DMII the activity of receptors found in peripheral tissues will be disrupted, allowing insulin resistance to take place. It is important to re-state that the main initial pathologic process involved in DMII is the lack of insulin sensitive receptors, and not the lack of insulin itself. Therefore, as insulin is not able to accomplish its functions, glycemic levels cannot be restored, and further glucose production will take place in the liver. As insulin resistance develops, the pancreatic beta cells will maximize the efforts to suppress glucose production, which can be translated to increased insulin secretion. This relationship is established by a feedback loop between beta cells and insulin sensitive tissues, which is aimed to maintain glucose homeostasis in the body (Khan, Cooper & Del Prato, 2014). Hence, as hyperglycemia continues to be present for long periods of time