1. 1. In the name of God 1
2. 2. Dr. Dariush Gholami 2015 2
3. 3. review History of diabetes mellitus Prevalence of Diabetes in Iran and world Types of diabetes mellitus Basic understanding of glucose metabolism and insulin action Pathophysiology of types of diabetes Risk factors & symptoms Investigation and treatment guidelines 3
4. 4. Learning Objectives At the end of this talk you should understand: What diabetes mellitus means The difference between types-1 and -2 diabetes How the different types are treated The reasons for the current epidemic of diabetes and how it can be prevented What the complications of diabetes are and how they can be prevented 4
5. 5. History 5
6. 6. History The term diabetes" or "to pass through" was first used in 230 BCE by the Greek Appollonius of Memphis Type 1 and type 2 diabetes were identified by the Indian physicians Sushruta and Charaka in 400 CE The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 This was followed by the development of the long-acting insulin NPH in the 1940s 6
7. 7. Prevalence (%) of people with diabetes by age and sex, 2013
8. 8. Prevalence (%) of people with diabetes by age and sex, 2013 8
9. 9. Almost half of all people with diabetes live in just three countries China India USA
10. 10. Diabetes in Iran There were over 4.3 million cases of diabetes in Iran in 2013. The majority of people with diabetes (>90%) have Type 2 diabetes (T2DM). 10
11. 11. 11
12. 12. 12
13. 13. Types of diabetes Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Gestational Diabetes Mellitus Type 4 Diabetes Mellitus 13
14. 14. Pathophysiology of Type1 Type 1 diabetes is characterized by destruction of the pancreatic beta cells. Most likely cause of these conditions is combined genetic, immunologic and possibly environmental (e.g. viral) factors contribute to cell destruction. specific area of the pancreas that produce insulin, reducing the production of insulin or totally no production of insulin. 14
15. 15. Pathophysiology of Type2 15
16. 16. Pathophysiology of type2 Type 2 Diabetes Mellitus is a adult onset non-insulin dependent insulin resistance (insulin do not bind with the special receptor on cell surface) impaired insulin secretion (insulin secreting glands release irregular amount of insulin). 16
17. 17. 17
18. 18. Pathophysiology of Gestational Diabetes Diabetes diagnosed during pregnancy Gestational diabetes is caused when the insulin receptors do not function properly human placental lactogenic Increased health risk to mother and baby Goes away after birth, but increased risk of developing Type 2 DM for mother and child 18
19. 19. Type 4 Diabetes Mellitus 1. Pancreatic Diseases 2. Cystic Fibrosis 3. Hemochromatosis 4. Pancreatic Cancer 5. Hormonal Disorders 6. Genetic defects of beta cell function 7. Genetic defects in insulin action 8. Infections 9. Drugs 19
20. 20. Differences between type-1 and type-2 Diabetes Mellitus Type 1 Young age not obese No immediate family history Short duration of symptoms (weeks) Can present with diabetic coma (diabetic ketoacidosis) Insulin required Type 2 Middle aged, elderly Usually overweight/obese Family history usual Symptoms may be present for months/years Do not present with diabetic coma Insulin not necessarily required 20
21. 21. 21
22. 22. RISK FACTORS &SYMPTOMS 22
23. 23. 23 RISK FACTORS
24. 24. Polyurea Polydipsia Polyphagia Weight loss Fatigue 24
25. 25. Symptoms Hypoglycemia Hyperglycemia Tremor Headache Pallor Dizziness Loss of coordination Anxiety Polyurea Polydipsia Dry mouth Ketoacidosis 25
26. 26. Investigation Fasting blood sugar Postprandial blood sugar HbA1C Lipid Profile To diagnose dyslipidaemia 26
27. 27. Fasting Serum Glucose (mg/dl) Diagnosis Below 110 Normal Between 110 and 126 Pre-diabetes Above 126 Diabetes (Must be confirmed with a second fasting test) Fasting Blood Sugar 27
28. 28. Postprandial blood sugar 28 Postprandial blood sugar Diagnosis < 140 mg/dl Normal 140-200 mg/dl Pre -diabetic >200 mg/dl Diabetic
29. 29. HbA1C 29 HbA1C Levels (%DCCT) Diagnosis 4 - 6 Normal for those without diabetes 6.1-7 Target range for diabetics >7 Poor control
30. 30. Treatment 30
31. 31. Treatment Guidelines Major Risk Factors (Exclusive of LDL Cholesterol) Cigarette smoking Hypertension (BP >140/90 mmHg) Low HDL cholesterol (45 years; women >55 years) 31
32. 32. Management of DM The major components of the treatment of diabetes are: 32 Diet and ExerciseA Oral hypoglycaemic therapyB Insulin TherapyC
33. 33. 33
34. 34. Management o type 1 diabetes 34
35. 35. 35
36. 36. Stepwise Management of Type 2 Diabetes 36 Insulin oral agents Oral combination Oral monotherapy Diet & exercise
37. 37. Oral Hypoglycaemic Medications 37
38. 38. Modern methods of treatment Pancreas Transplantation Pancreatic islet transplantation The use of stem cells 38
39. 39. 39
40. 40. GENERAL TIPS Steps to lower risk of diabetes complications: A1C < 7, which is an estimated average glucose of 154 mg/dl Blood pressure < 130/80 Cholesterol (LDL) < 100 Cholesterol (HDL) > 40 (men) and > 50 (women) Triglycerides < 150 Quitting smoking Active life style Healthy food choices 40
41. 41. foot care Patient should check feet daily Wash feet daily Keep toenails short Protect feet Always wear shoes Look inside shoes before putting them on Always wear socks Break in new shoes gradually 41
42. 42. Quarterly review Weight/waist Height (children and adolescents) Blood pressure Feet examination without shoes, if new symptoms or at risk 42
43. 43. Annual review Weight/waist Height (children and adolescents) Blood pressure Feet examination Blood glucose at examination Urinalysis Visual acuity 43
44. 44. Cornerstones of Diabetes Management Healthy eating Exercise Monitoring Medication/Insulin Health Care Team 44
45. 45. References "About diabetes". World Health Organization. Retrieved 4 April 2014 Kitabchi, AE; Umpierrez, GE; Miles, JM; Fisher, JN (Jul 2009). "Hyperglycemic crises in adult patients with diabetes."Diabetes Care 32 (7): 133543 Shoback, edited by David G. Gardner, Dolores (2011). "Chapter 17". Greenspan's basic & clinical endocrinology (9th ed.). New York: McGraw-Hill Medical Cash, Jill (2014). Family Practice Guidelines (3rd ed.). Springer. p. 396 IDF DIABETES ATLAS (6th ed.). International Diabetes Federation. 2013. p. 7 Rother KI (April 2007). "Diabetes treatmentbridging the divide". The New England Journal of Medicine 356 (15): 1499501 "Diabetes Mellitus (DM): Diabetes Mellitus and Disorders of Carbohydrate Metabolism: Merck Manual Professional". Merck Publishing. April 2010. Retrieved 2010-07-30 Hu EA, Pan A, Malik V, Sun Q (2012-03-15). "White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review". BMJ (Clinical research ed.) 344: e1454 45
46. 46. THANK YOU 46
47. 47. 47 Mechanism of glucose dependent insuline release
48. 48. Mechanism of insulin release in normal pancreatic beta cells insulin production is more or less constant within the beta cells. Its release is triggered by food, chiefly food containing absorbable glucose 48
49. 49. 49
50. 50. PHYSICAL EXAMINATION 50
51. 51. Complete physical examination Examination Weight/waist: Body Mass Index (BMI) Waist circumference Cardiovascular system: Blood pressure, ideally lying and standing Peripheral, neck and abdominal vessels Eyes: Visual acuity (with correction) Cataracts Retinopathy (examine with pupil dilation) 51
52. 52. 52 Feet: Sensation and circulation Skin condition Pressure areas Interdigital problems Abnormal bone architecture Peripheral nerves: Tendon reflexes Sensation: touch -vibration Urinalysis: Albumin Ketones Nitrites and/or leucocytes
53. 53. 53
54. 54. 54
55. 55. 55
56. 56. It works in the following way: During and immediately after a meal, digestion breaks carbohydrates down into sugar molecules (of which glucose is one) and proteins into amino acids. Right after the meal, glucose and amino acids are absorbed directly into the bloodstream, and blood glucose levels rise sharply. (Glucose levels after a meal are called postprandial levels.) Action of insulin 56
57. 57. 57 The rise in blood glucose levels signals important cells in the pancreas, called beta cells, to secrete insulin, which pours into the bloodstream. Within 20 minutes after a meal insulin rises to its peak level. Insulin enables glucose to enter cells in the body, particularly muscle and liver cells. Here, insulin and other hormones direct whether glucose will be burned for energy or stored for future use. When insulin levels are high, the liver stops producing glucose and stores it in other forms until the body needs it again.