Bachelor of Nursing for Carbohydrates and Proteins- myassignmenthelp

Question: Discuss about theBachelor of Nursing for Carbohydrates and Proteins. Answer: Insulinis apeptide hormone, produced by -cellsof theislets of langerhans, and regulates the carbohydrates,proteins and fatsmetabolismby promoting the glucose absorption from blood. Its effects are initiated by binding to a receptor containing - and subunits. This binding triggers tyrosine kinase activity that promotes subunits autophosphorylation. This activates a signal transduction cascade that aids in glucose absorption. In the patient with type2 diabetes, there is insufficient insulin production fromthe -cells (American Diabetes Association, 2014). This leads to insulin resistance. There occurs inappropriate release of glucose from the liver cells into the bloodstream. The signal pathway gets inactivated which leads to this resistance. Thus, the cells are unable to use insulin effectively, leading toincreased blood sugar. There is a high risk for angina pectoris in the patient because high blood glucose affects the artery walls and increase the likelihood to degenerate the walls. Moreover, type 2 diabetes increases risk of hypertension, high triglyceride levels and low levels of HDL cholesterol. Thus, the risk of atheroma will increase (Shah et al., 2015). The heart muscles will become less efficient to pump blood. Family history of diabetes, smoking and obesity will also make the patient vulnerable to angina pectoris. The patient is also at a risk of diabetic retinopathy due to chronically high blood glucose levels. Light rays are detected by the retina and converted to signals, which are sent to the CNS through the optic nerve. Type 2 diabetes will damage the blood vessels in the retina, and may lead to diabetic retinopathy. The blood vessels may bleed (hemorrhage) or leak fluid, thereby distorting the vision (Ruta et al., 2013). In advanced stage, there may be abnormal proliferation of the blood vessels on the retina surface, which in turn can lead to cell loss and scarring. Metformin can be considered as an effective drug for the patient. It works principally by reducing or lowering the amount of glucose production from the liver.Metformin plays a role in influencing peripheral glucose uptake and insulin sensitivity in the cells. It decreaseselevated blood sugar by the process of hepaticgluconeogenesis. Gluconeogenesis occurs three times the normal rate in an average patient suffering from type 2 diabetes. Administration of metformin reduces this amount by more than one-third. The potential action mechanisms include: AMP-activated protein kinase(AMPK) activation, inhibition or suppression of mitochondrial respiratory chain complex I and elevated cyclic adenosine monophosphate(cAMP) induced by glucose, reduction of protein kinase A(PKA) and on gut microbiota effects (Pernicova Korbonits, 2014). Inhibition of liver glucose production primarily depends on AMPK activation. The enzyme plays an essential role in maintaining energy balance, glucose metabolism and insulin signaling. The drug also increases peripheralglucose uptake by GLUT4 phosphorylation and enhances insulin sensitivity. However, it can lead to some gastrointestinal side effects in the patient. Insulin resistance often is among patients with visceral adiposity. These people have an increased amount of fatty tissue within their abdomen. This is distinct from any subcutaneous adiposity. There are several evidences that suggest correlation between insulin resistance and abdominal adiposity. Unlike subcutaneous adipose tissue, the visceral adipose cells produce increased amount of pro-inflammatorycytokines(Interleukins-1 and 6 and tumor necrosis factor-alpha/TNF-). Normal insulin function gets disrupted by these pro-inflammatory cytokines in muscle and fat cells. This acts as the major contributor of development of insulin resistance in patients with visceral adiposity. The NF-kappa-B/IKK-pathway is a protein network, which enhances transcription of inflammatory mediators and marker that are responsible for insulin resistance (Hocking et al., 2013). Moreover, abdominal adiposity is associated with an accumulation of fat in liver cells. This leads to a condition callednon-alcoho lic fatty liver disease (NAFLD). Thus, free fatty acids get released into the bloodstream in excess amounts due to increased lipolysis, followed by hepatic glycogenolysis increase. This exacerbates peripheral insulin resistance and increases the likelihood ofdeveloping type 2 diabetes mellitus (Nolan et al., 2015). HbA1crefers to glycatedhaemoglobin. It develops when haemoglobin joins with blood glucose. The amount of glycated hemoglobin is directly proportional to total amount of blood sugar level. Owing to the property of RBCs surviving for 8-12 weeks before they get renewed, a measurement of HbA1c will reflect the average blood glucose level for the timespan (Sjaarda et al., 2012). This measurement will provide a long-term gauge of the patients blood glucose control. If her HbA1c levels are found to be more than 6.5%, it will indicate that her blood sugar levels have been elevated in the past few weeks. This will prove effective in administering medications. Annotated bibliography American Diabetes Association. (2014). Diagnosis and classification of diabetes mellitus.Diabetes care,37(Supplement 1), S81-S90. I used this journal to understand the basic classification of diabetes and the changes in insulin hormone production associated with it. It is a reliable source as it is peer-reviewed. Hocking, S., Samocha-Bonet, D., Milner, K. L., Greenfield, J. R., Chisholm, D. J. (2013). Adiposity and insulin resistance in humans: the role of the different tissue and cellular lipid depots.Endocrine reviews,34(4), 463-500. I used this journal to examine the relative link between abdominal adiposity, hyperglycemia and insulin resistance. It is a reliable source as it is peer-reviewed. Nolan, C. J., Ruderman, N. B., Kahn, S. E., Pedersen, O., Prentki, M. (2015). Insulin resistance as a physiological defense against metabolic stress: implications for the management of subsets of type 2 diabetes.Diabetes,64(3), 673-686. I used this journal to examine the effects of insulin resistance on obese patients with type 2 diabetes. It is a reliable source as it is peer-reviewed. Pernicova, I., Korbonits, M. (2014). Metformin [mdash] mode of action and clinical implications for diabetes and cancer.Nature Reviews Endocrinology,10(3), 143-156. I used this article to understand the action of metformin in liver and its implications in discovering metformin targets for diabetes mellitus and cancer treatment. It is a reliable source as it is peer-reviewed. Ruta, L. M., Magliano, D. J., Lemesurier, R., Taylor, H. R., Zimmet, P. Z., Shaw, J. E. (2013). Prevalence of diabetic retinopathy in Type 2 diabetes in developing and developed countries.Diabetic medicine,30(4), 387-398. I used this journal to study the association between type 2 diabetes and prevalence of diabetic retinopathy among people belonging to developing and developed countries. It is a reliable source as it is peer-reviewed. Shah, A. D., Langenberg, C., Rapsomaniki, E., Denaxas, S., Pujades-Rodriguez, M., Gale, C. P., ... Hemingway, H. (2015). Type 2 diabetes and incidence of cardiovascular diseases: a cohort study in 1 9 million people.The lancet Diabetes endocrinology,3(2), 105-113. I used this journal to study the association between type 2 diabetes and cardiovascular diseases. It is a reliable source as it is peer-reviewed. Sjaarda, L. A., Michaliszyn, S. F., Lee, S., Tfayli, H., Bacha, F., Farchoukh, L., Arslanian, S. A. (2012). HbA1c diagnostic categories and -cell function relative to insulin sensitivity in overweight/obese adolescents.Diabetes Care,35(12), 2559-2563. I used this article to understand the relationship between HbA1c diagnosis and the pathophysiologic mechanism of type 2 diabetes. It is a reliable source as it is peer-reviewed.