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Diagnosis, classification and prevention of diabetes

Diagnosis, classification and prevention of diabetes. Definition of diabetes. Characterized by hyperglycaemia Defects in insulin production Autoimmune or other destruction of beta cells Insulin insensitivity Impaired action of insulin on target tissues. Definition of diabetes.

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Diagnosis, classification and prevention of diabetes

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  1. Diagnosis, classification and prevention of diabetes

  2. Definition of diabetes • Characterized by hyperglycaemia • Defects in insulin production • Autoimmune or other destruction of beta cells • Insulin insensitivity • Impaired action of insulin on target tissues Slides current until 2008

  3. Definition of diabetes Chronic hyperglycaemia associated with long-term damage to: • Eyes • Kidneys • Nerves • Heart and blood vessels Slides current until 2008

  4. The diabetes epidemic • 230 million affected in 2006 • 350 million within 20 years • Most rapid in Indian and Asian subcontinents IDF Diabetes Atlas Slides current until 2008

  5. Classification • Type 1 diabetes • autoimmune • LADA • idiopathic • Type 2 diabetes Slides current until 2008

  6. Classification Other specific types • MODY • Defects in insulin action • Diseases of the pancreas • Endocrine disorders • Drug- or chemical-induced • Infections Slides current until 2008

  7. Classification • Uncommon forms of immune-mediated diabetes • Other genetic syndromes • Gestational diabetes Slides current until 2008

  8. Insulin and glucose disposal Gluconeogenesis Glycogenolysis Glycogen synthesis Insulin Blood glucose Glycogen synthesis Glucose uptake Free fatty acid release Slides current until 2008

  9. Insulin deficiency in type 1 diabetes Glucose uptake Glycogenolysis Gluconeogenesis (amino acids) Ketone production (fatty acids) Blood glucose Glucose uptake Protein degradation  amino acids Triglyceride degradation  fatty acids Slides current until 2008

  10. Insulin insensitivity in type 2 diabetes Glucose uptake Glycolysis Gluconeogenesis (amino acids) Blood glucose Glucose uptake Protein degradation  amino acids Slides current until 2008

  11. Insensitivity to insulin in type 2 diabetes Glucose uptake Glycolysis Gluconeogenesis (amino acids) Blood glucose Glucose uptake Protein degradation  amino acids Glucose uptake Slides current until 2008

  12. Converted to triglycerides Effect of insulin resistance in type 2 diabetes Glucose uptake Glycolysis Gluconeogenesis (amino acids) Blood glucose Glucose uptake Protein degradation  amino acids Glucose uptake Slides current until 2008

  13. Pathogenesis of type 1 diabetes • Immunological activation • Progressive beta-cell destruction • Insufficient beta-cell function • Dependent on exogenous insulin • Risk of ketoacidosis Slides current until 2008

  14. Pathogenesis of type 1 diabetes • Genetic susceptibility • Immune factors • other autoimmune disease • antigen-specific antibodies • Environmental trigger • viruses • bovine serum albumin • nitrosamines: cured meats • chemicals: vacor (rat poison), streptozotin Slides current until 2008

  15. Pathogenesis of type 1 diabetes Trigger Immunological abnormalities Genetic Beta-cell mass Clinical diabetes ‘Honeymoon’ Pre-diabetes Chronic phase Time (months - years) Slides current until 2008

  16. Idiopathic type 1 diabetes Non-autoimmune type 1 diabetes • No autoimmune markers • Permanent insulinopenia • Ketoacidosis • People of African and Asian origin Slides current until 2008

  17. Epidemiology of type 1 diabetes • Increasing in recent years • Geographic variation • Relative affluence • Lack of treatment IDF Diabetes Atlas Slides current until 2008

  18. Epidemiology of type 1 diabetes • Age of onset peaks • preschool • puberty • Autumn/winter peaks Slides current until 2008

  19. Type 2 diabetes • 90%-95% of people with diabetes • Insulin insensitivity and relative insulin deficiency • Obesity or overweight • Complications often present at diagnosis Slides current until 2008

  20. Pathogenesis of type 2 diabetes • Multiple genes involved • Hyperinsulinaemia • Poor fetal nutrition   beta-cell formation • Low birth weight/weight change • “Thrifty gene” • 7%beta-cell loss Slides current until 2008

  21. Primary failure The natural history of type 2 diabetes Beta-cell loss  Insulin requirements with age Insulin requirements Endogenous insulin Age (years) Slides current until 2008

  22. The natural history of type 2 diabetes Beta-cell loss  Insulin requirements with age Hyper- insulinaemia Insulin requirements Insulin insensitivity Endogenous insulin Age (years) Slides current until 2008

  23. The natural history of type 2 diabetes Secondary failure Beta-cell loss  Insulin requirements with age Hyper- insulinaemia Effect of oral drugs Insulin requirements Insulin insensitivity Endogenous insulin Age (years) Slides current until 2008

  24. Epidemiology of type 2 diabetes • Dramatic increase • Aging population • Disturbing trends parallel obesity epidemic • Especially in adolescents and minority groups • Increasing in young people Slides current until 2008

  25. What are the most common risk factors for type 2 diabetes for people in your country? • Are any of these risk factors modifiable? Slides current until 2008

  26. Risk factors for type 2 diabetes • Age > 40 years • First-degree relative with diabetes • Member of high risk population • History of impaired glucose tolerance, impaired fasting glucose • Vascular disease • History of gestational diabetes • History of delivery of macrosomic baby CDA 2003 Slides current until 2008

  27. Risk factors for type 2 diabetes • Hypertension • Dyslipidaemia • Abdominal obesity • Overweight • Polycystic ovary disease • Acanthosis nigricans • Schizophrenia Slides current until 2008

  28. Polydipsia Polyuria Nocturia Visual disturbance Fatigue Weight loss Infections Signs and symptoms Slides current until 2008

  29. Diagnosing diabetes CDA 2003, ADA 2004, WHO 2002 Slides current until 2008

  30. Table 2—Criteria for the diagnosis of diabetes1. A1C 6.5%. The test should be performed in a laboratory using a methodthat is NGSP certified and standardized to the DCCT assay.*OR2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.OR3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT.The test should be performed as described by the World HealthOrganization, using a glucose load containing the equivalent of 75 ganhydrous glucose dissolved in water.*OR4. In a patient with classic symptoms of hyperglycemia or hyperglycemiccrisis, a random plasma glucose 200 mg/dl (11.1 mmol/l).*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing.ADA 2010 Guideline

  31. Impaired glucose toleranceImpaired fasting glucose • Intermediate states • Increased risk of developing diabetes • Prevention strategies to prevent or delay progression • Increased risk of cardiovascular disease Slides current until 2008

  32. Uncertain diagnosis:Oral glucose tolerance test • 75 g glucose load after 8 hours fasting • Readings taken in fasting state and at 1 and 2 hours • Possible problems Slides current until 2008

  33. Tests for differential diagnosis • Urinary ketones • Antibodies • C-peptide Slides current until 2008

  34. Metabolic syndrome • Cluster of risk factors or syndrome • Type 2 diabetes • Different criteria • Three-fold increase in heart disease and stroke • Two-fold increase in cardiovascular disease deaths Slides current until 2008

  35. Prevention of type 1 diabetes • Early exposure to cows milk protein • Nicotinamide Slides current until 2008

  36. Prevention of type 1 diabetes • Insulin • Diabetes Prevention Trial • Diabetes Prediction and Prevention Project Slides current until 2008

  37. Prevention of type 2 diabetes • Lifestyle modification • Da Qing Study • Finnish Diabetes Prevention Study Slides current until 2008

  38. Prevention of type 2 diabetes • Lifestyle vs medication • Diabetes Prevention Program • STOP-NIDDM Slides current until 2008

  39. Type 2 diabetes can be delayed in people with IGT Lifestyle modification is most effective What do you think could be done at community level to prevent or delay diabetes? Slides current until 2008

  40. Summary Type 1 diabetes • Results from progressive beta-cell destruction • People with type 1 diabetes need insulin therapy to live Slides current until 2008

  41. Summary Type 2 diabetes • Often characterized by insulin insensitivity and relative rather than absolute insulin deficiency • A progressive condition • Most people with type 2 diabetes will need insulin within 5 to 10 years of diagnosis Slides current until 2008

  42. Review question 1. The pathogenesis for type 2 diabetes includes: • a. Insulin deficiency and insulin insensitivity • b. Insensitivity to insulin and autoimmune beta-cell destruction • c. Autoimmune beta-cell destruction and glucagon deficiency • d. Insulin deficiency and glucagon deficiency Slides current until 2008

  43. Review question 2. A person with type 2 diabetes, recently started on insulin, asks if there is a way to measure if he/she is still producing any insulin. The correct response would be: a. Islet cell antibody tests b. C-peptide test c. HbA1c test d. Serum insulin test Slides current until 2008

  44. Review question 3. The Diabetes Prevention Program (DPP): a. Included people with type 1 diabetes b. Included only people with IGT c. Tested the value of exercise d. Included people with type 2 diabetes Slides current until 2008

  45. Review question 4. Type 1 diabetes is usually caused by: a. Injury to the pancreas b. An autoimmune reaction c. Insulin insensitivity in the cells d. Hypersensitivity to insulin Slides current until 2008

  46. Answers • a • b • b • b Slides current until 2008

  47. References • American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2004; 27(suppl 1): S5-S10. • Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2003 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diab 2003; 27(suppl 2). • Chiasson JL, Josse RG, Gomis R, et al. Acarbose for prevention of type 2 diabetes mellitus: The STOP-NIDDM randomized trial. Lancet 2002; 346: 393-403. • Delahanty LM and Halford BN. The role of Diet Behaviours in Achieving improved glycaemic control in intensively treated patients in the Diabetes Control and Complications Trial. Diabetes Care 1993; 16(11): 1453-58. • Diabetes Control and Complications Trial Research Group. Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin dependent diabetes mellitus: Diabetes Control and Complications Trial. The Journal of Paediatrics 1994; 125(2): 177-88. • Diabetes Control and Complications Trial/epidemiology of diabetes interventions and complications research group intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. New Engl J Med 2003; 348: 2294-303. • Diabetes Control and Complications Trial: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993; 329: 977-86. Slides current until 2008

  48. References • Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA2002; 297: 356-59. • Diabetes Atlas 2006. Brussels: International Diabetes Federation, 2006. • Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 2001; 24(4): 683-9. • Pan X, Li G, Hu Y, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: The Da Qing IGT and Diabetes Study. Diabetes Care 1997; 20(4): 537-44. • Report of a WHO Consultation. Laboratory Diagnosis and monitoring of Diabetes Mellitus. World Health Organisation 2002. http://whqlibdoc.who.int/hq/2002/9241590483.pdf cited April 30, 2005. • Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Eng J Med 2001; 344: 1343-50. • The Diabetes Prevention Program Research Group. The diabetes prevention Program (DPP). Diabetes Care 2002; 23(12): 2165-71. • UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulpfonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. Lancet 1998; 352: 837-53. Slides current until 2008

  49. References • UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes UKPDS 38. BMJ1998; 317: 703-13. • IDF Clinical Guidelines Task Force. Global Guideline for Type 2 Diabetes. Brussels: International Diabetes Federation, 2005. • Harris SB, Ekoe JM, Zdanowicz Y, Webster-Bogaert S. Glycemic Control and morbidity in the Canadian primary care setting (results of the diabetes in Canada evaluation study). Diab Research and Clin Pract 2005; 70: 90-7. Slides current until 2008

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