Diabetes/Hyperglycemia
NRS 339L: Hyperglycemia
Cindy Clair & Sara Scaggs
Northern Kentucky University
1. Type 1 Diabetes: Formerly known as juvenile onset diabetes or insulin-dependent diabetes. Type 1 diabetes is an immune-mediated disease. The body’s own T cells attack and destroy pancreatic beta (B) cells, which are the source of insulin. In addition, autoantibodies to the islet cells cause a reduction of 80-90% of normal B cell function before hyperglycemia and other manifestations occur. (Mosby, 2011)
Risk Factors: Genetic predisposition & exposure to a virus may contribute to the pathogenesis of Type 1 DM. Type 2 Diabetes: Formerly known as adult-onset diabetes & non-insulin dependent diabetes. Type 2 DM accounts for 90% of diabetic patients and is also being seen in children with the increased rate of obesity. In Type 2 diabetes, the pancreas usually continues to produce some endogenous (self-made) insulin. The insulin that is produced is either insufficient for the needs of the body or is poorly utilized by the tissues, or both. The presence of insulin is used as the differentiating factor of Type 1 and Type 2 DM. (Mosby, 2011)
Risk Factors: Obesity (specifically abdominal and visceral adiposity) and genetic mutations that lead to insulin resistance.
Insulin Use: Rapid-acting insulin begins working approximately 5 minutes after injection, peaks at about 1 hour, and continues to work for another 2-4 hours. Rapid-acting insulins include lispro, aspart, and glulisine. Rapid-acting insulin is used when. Regular of short-acting insulin (human insulin) usually reaches the bloodstream within 30 minutes after injection, it peaks from 2-3 hours after injection, and works on the body for another 3-6 hours. Regular insulin is used when. Intermediate-acting insulin (human insulin) usually reaches the bloodstream 6-20 hours after the injection; it is effective for 20-24 hours. Glargine and detemir are long-acting insulins and tend to lower glucose levels
Cindy Clair & Sara Scaggs
Northern Kentucky University
1. Type 1 Diabetes: Formerly known as juvenile onset diabetes or insulin-dependent diabetes. Type 1 diabetes is an immune-mediated disease. The body’s own T cells attack and destroy pancreatic beta (B) cells, which are the source of insulin. In addition, autoantibodies to the islet cells cause a reduction of 80-90% of normal B cell function before hyperglycemia and other manifestations occur. (Mosby, 2011)
Risk Factors: Genetic predisposition & exposure to a virus may contribute to the pathogenesis of Type 1 DM. Type 2 Diabetes: Formerly known as adult-onset diabetes & non-insulin dependent diabetes. Type 2 DM accounts for 90% of diabetic patients and is also being seen in children with the increased rate of obesity. In Type 2 diabetes, the pancreas usually continues to produce some endogenous (self-made) insulin. The insulin that is produced is either insufficient for the needs of the body or is poorly utilized by the tissues, or both. The presence of insulin is used as the differentiating factor of Type 1 and Type 2 DM. (Mosby, 2011)
Risk Factors: Obesity (specifically abdominal and visceral adiposity) and genetic mutations that lead to insulin resistance.
Insulin Use: Rapid-acting insulin begins working approximately 5 minutes after injection, peaks at about 1 hour, and continues to work for another 2-4 hours. Rapid-acting insulins include lispro, aspart, and glulisine. Rapid-acting insulin is used when. Regular of short-acting insulin (human insulin) usually reaches the bloodstream within 30 minutes after injection, it peaks from 2-3 hours after injection, and works on the body for another 3-6 hours. Regular insulin is used when. Intermediate-acting insulin (human insulin) usually reaches the bloodstream 6-20 hours after the injection; it is effective for 20-24 hours. Glargine and detemir are long-acting insulins and tend to lower glucose levels
Bibliography: Defeat Diabetes Foundation, Inc. (2013, March 24). Self-Management. Retrieved April 4, 2013, from Defeat Diabetes Foundation, Inc.: http://www.defeatdiabetes.org/self_management/text.asp?id=kentucky_supp_grps (2011). Diabetes Mellitus. In S. Lewis, S. Dirksen, M. Heitkemper, L. Bucher, & I. Camera, Medical Surgical Nursing Assessment and Management of Clinical Problems (pp. 1221-1243). St. Louis: Elsevier Mosby. 2011. Gilhul, Kathryn. How Does Protein Affect Blood Sugar in Diabetics? Retrieved from: http://www.livestrong.com/article/458239-how-does-protein-affect-blood-sugar-in-diabetics/ (2010) Insulin basics. American Diabetes Association. Retrieved from: http://www.diabetes.org/living-with-diabetes/treatment-and-care/medication/insulin/insulin-basics.html. (2012). Pharmacotherapy of Diabetes Mellitus. In P. Adams, & C. Urban, Pharmacology Connections to Nursing Practice (pp. 1183-1209). New York: Pearson.