Diabetes mellitus

Diabetes Mellitus Diabetes Mellitus (DM) — “ a chronic, progressive disease characterized by the body’s inability to metabolize carbohydrates, fats, and proteins, leading to hyperglycaemia (high blood glucose level)” (Black & Hawks, 2009, p. 1062) Epidemiology: Pathophysiology Overview According to Canadian Chronic Disease Surveillance System, “[i]n 2008/09, close to 2. 4 million Canadians aged 1 yr and older were living w/ diagnosed diabetes (either type 1 or type 2)” making diabetes as one of the most common chronic diseases in Canada (Public Health Agency of Canada, 2011). most common chronic disease among children and youth, particularly Type 2 since it has been on the rise globally for the last two decades (Public Health Agency of Canada, 2011) In a decade (1998/99-2008/09), diabetes’ prevalence in Canada increased by 70% (Public Health Agency of Canada, 2011) More prevalent in males (5. 4%) than females (4. 4%) (Sanmartin & Gilmore, 2008) Prevalence of Type 2 diabetes in lowest income group is 4. 14X higher than in the highest income group in Canada (Dinca-Panaitescu et al., 2011) Prevalence of diabetes were more than 4X higher among First Nations than among non-First nations people (Dyck et al., 2010) Those w/ diabetes are over 3X more likely to be hospitalized w/ cardiovascular disease than individuals without diabetes (Public Health Agency of Canada, 2011) 11% of Canadian adults w/ diabetes were reported to have 2 or more other serious chronic conditions besides diabetes (Canadian Diabetes Association, 2008) Glucose-regulating hormones (secreted by the pancreas’ Islets of Langerhans): Alpha cells = secrete glucagon (↑ glucose) β —cells = secrete INSULIN (↓ glucose) delta cells = secrete somatostatin (inhibit release of glucagon + insulin to extend time of nutrient absorption by tissues) Incretin — GI hormone that ↑ insulin release of β-cells Glucose transporters = “ special carriers” that help move glucose from blood into the cell Glucogenesis — breakdown of glycogen to form glucose Gluconeogenesis — breakdown of non-carbohydrate sources to form glucose Diabetes Overview TARGET CELLS Summary of comparisons between Type 1 & Type 2 diabetes: | Type 1 | Type 2 | Also known as: | “ juvenile-onset” or “ insulin-dependent diabetes mellitus” (IDDM) | “ adult-onset” or “ non-insulin-dependent diabetes mellitus” (NIDDM) | Description: | Destruction of pancreatic β-cells by Islet cell antibodies leading to insulin deficiencyType1A = “ autoimmune” — genetic predisposition or environmental factorsType1B = idiopathic | Insulin resistance — “ resistance to biological activity of insulin in both the liver and peripheral tissues” (Black & Hawks, 2009, p. 1066) ex. due to defective insulin receptors Insulin production of inactive insulin, or impaired release of insulin d/t exhausted β-cells etc. | Age of Onset | Typically < 30 years of age | < 40 years of age | Pancreatic Function | Little to none | Insulin may be in low, normal, or high amounts | Clinical Presentation | Acute or rapidly progressive hyperglycemia w/ symptoms of polyuria, polydipsia, fatigue, sudden weight loss, slow wound healing, ↑ appetite, blurred vision, thrush or genital infections, neuropathy, and ketoacidosis | Similar to Type 1 except more chronic and progressive symptoms | Genetic Predisposition | Yes | Yes, heredity applies | Environmental factors: | Virus infection (triggers autoimmune process) | ↓ physical activity, obesity (particularly central obesity) — “ adipokines" (adipose tissue cells release these cytokines that have shown to cause cellular resistance to insulin) | (Porth, 2007; Black & Hawks, 2009; Thevenod, 2008) References Black, J. M., & Hawks, J. H. (2009). Medical-surgical nursing: Clinical management for positive outcomes (8th ed.). Philadelphia, PA: Saunders Elsevier. Canadian Diabetes Association (2008). Canadian journal of diabetes: Canadian diabetes association 2008 clinical practice guidelines for the prevention and management of diabetes. Retrieved from: http://www. diabetes. ca/files/cpg2008/cpg-2008. pdf Dinca-Panaitescu, M., Dinca-Panaitescu, S., Bryant, T., Daiski, I., Pilkington, B., & Raphael, D. (2011). Diabetes prevalence and income: Results of the Canadian community health survey. Health Policy, 99(2), 116-123. doi: 10. 1016/j. healthpol. 2010. 07. 018 Dyck, R., Osgood, N., Lin, T. H., Gao, A., & Stang, M. R. (2010). Epidemiology of diabetes mellitus among first nations and non-first nations adults. CMAJ : Canadian Medical Association Journal = Journal De l'Association Medicale Canadienne, 182(3), 249-256. doi: 10. 1503/cmaj. 090846 Thevenod, F. (2008). Pathophysiology of diabetes mellitus type 2: roles of obesity, insulin resistance and β-cell dysfunction. Retrieved from: http://content. karger. com/ProdukteDB/Katalogteile/isbn3_8055/_86/_40/fdiab19_02. pdf Porth, C. M. (2007). Essentials of Pathophysiology: Concepts of Altered Health States. (2nd Edition). Philadelphia, PA: Lippincott Williams & Wilkins. Public Health Agency of Canada (2011). Diabetes in Canada: facts and figures from a public health perspective. Retrieved from: http://www. phac-aspc. gc. ca/cd-mc/publications/diabetes-diabete/facts-figures-faits-chiffres-2011/pdf/facts-figures-faits-chiffres-eng. pdf Sanmartin, C., & Gilmore, J. (2008). Diabetes-prevalence and care practices. Health Reports / Statistics Canada, Canadian Centre for Health Information = Rapports Sur La Santé / Statistique Canada, Centre Canadien d'Information Sur La Santé, 19(3), 59.