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2. Question 1  What is our Global Ranking for DM ?  What is our current estimated burden?  Why is T2DM so important ?

3. Question 1  What is our Global Ranking for DM ?  What is our current estimated burden?  Why is T2DM so important ?  Numero Uno – RANK ONE Globally  About 36 million (in 2003)  DM = CAD + Its major complications !!  Shortens longevity by 10-15 years

4. Question 2  What are the TWO major defects in Type 2 Diabetes ?

5. Question 2  What are the TWO major defects in Type 2 Diabetes ?  Insulin Resistance (IR)  Insulin Deficiency (ID)

6. Question 3  What is  cell apoptosis ?   cell apoptosis occurs in how many years ?

7. Question 3  What is  cell apoptosis ?   cell apoptosis occurs in how many years ?  Progressive programmed  cell death  10 to 15 years after the onset of DM  Today’s approach is save the  cell

8. Question 4  What are the core defects of Insulin Secretion in T2DM ?

9. Question 4  What are the core defects of Insulin Secretion in T2DM ?  Loss or delay of first phase of Insulin secretion  Blunting or flattening of second phase

10. Question 5  What is Gold Standard Test to Diagnose DM ?  Should we use Plasma Sugar or Whole blood Sugar for Diagnosis ?

11. Question 5  What is Gold Standard Test to Diagnose DM ?  Should we use Plasma Sugar or Whole blood Sugar for Diagnosis ?  O-GTT – Fasting sample and 2 hours Post Glucose (75g) sample  Obviously Plasma (venous sample)

12. Question 6  What is Normal FBG & What is IFG ?  What is Normal PPBG & What is IGT ?  Is it essential two have TWO readings ?

13. Question 6  What is Normal FBG & What is IFG ?  What is Normal PPBG & What is IGT ?  Is it essential two have TWO readings ?  N =100 mg FBG; 101-125 is IFG  N =140 mg PPBG; 141-199 is IGT  YES – Two readings are a must for Dx.  FBG  126 or PPBG  200 is DM

14. Question 7  Can we use urine sugar for Dx. or F/u ?  Can we use HbA1c for Diagnosis ?  What is important in urine exam in DM ?

15. Question 7  Can we use urine sugar for Dx. or F/u ?  Can we use HbA1c for Diagnosis ?  What is important in urine exam in DM ?  No. Urine sugar is not all useful  No. HbA1c is not for Diagnosis; only F/u  Albumin, MAU, Ketones are very imp.

16. Question 8  What is the cause of Fasting Hyperglycemia ?  What is the defect that causes it ?

17. Question 8  What is the cause of Fasting Hyperglycemia ?  What is the defect that causes it ?  Increase in Hepatic Glucose Output – Called HGO  Decrease in Basal Insulin secretion

18. Question 9  What is the cause of Postprandial Hyperglycemia ?  What is the defect that causes it ?

19. Question 9  What is the cause of Postprandial Hyperglycemia ?  What is the defect that causes it ?  Decrease in peripheral utilization – removal of glucose by muscle & adipose tissue  Excess CHO meal load  Delay or absence of 1 st Phase Insulin

20. Question 10  What are the four mechanisms which contribute to ↑ plasma glucose ?

21. Question 10  What are the four mechanisms which contribute to ↑ plasma glucose ? 1.Hepatic Glucose Output (HGO) Basal In 2.Lack of peripheral utilization (IR) 3.Decrease in insulin secretion (ID) 4.Increase in absorption from GIT

22. Question 11  What is HbA1c ?  What is its normal value ?  What does it reflect ?

23. Question 11  What is HbA1c ?  What is its normal value ?  What does it reflect ?  It is a Glycated hemoglobin  Normal HbA1c is around 6%  It represents the mean plasma glucose over the previous 120 days

24. Question 12  What is the best measure to monitor glycemic control for follow up ?  What is its target value ?

25. Question 12  What is the best measure to monitor glycemic control for follow up ?  What is its target value ?  HbA1c is the measure for monitoring  It must be kept below 7, preferably 6

26. Question 13  What is IDRS ?  What are its components ?

27. Question 13  What is IDRS ?  What are its components ?  Indian Diabetic Risk Score is used to assess ones risk for DM  Age, WC, family h/o, physical activity

28. Question 14  Can we prevent Diabetes ?  If so, How ?

29. Question 14  Can we prevent Diabetes ?  If so, How ? Yes. 3 international studied confirmed it 1.Identifying people in stage 1- IR 2.Total Lifestyle Change – MNT, PA 3.If necessary Metformin, Acarbose

30. Question 15  Where can we find all info on TLC ?

31. Question 15  Where can we find all info on TLC ?  www.mypyramid.gov

32. Question 16  What is the ‘Old Paradigm’ of Diabetes management ?

33. Question 16  What is the ‘Old Paradigm’ of Diabetes management ?  It is called the ‘Step Care’ approach  It envisages Diet  OAD  Insulin

34. Question 17  What is the ‘New Paradigm’ of Diabetes management ?

35. Question 17  What is the ‘New Paradigm’ of Diabetes management ?  It is the ‘Stage Management’ approach  Stage 1 – Insulin Resistance (IR)  Stage 2 – IR + Insulin Deficiency (ID)  Stage 3 – Insulin Deficiency (ID)

36. Question 18  What is total metabolic control ?

37. Question 18  What is total metabolic control ?  Glycemic control is essential but we also need to control all components  We must maintain the B.P <130/80  The lipids under target values  See that pt. avoids smoking  Reduce his weight and waist  This is total METABOLIC CONTROL

38. Question 19  List the microvascular complications

39. Question 19  List the microvascular complications 1.Diabetic Retinopathy (DR) 2.Diabetic Kidney Disease (DKD) – Nephropathy 3.Diabetic Neuropathy – DPN, DAN These start right at the onset of ↑ BG We must screen for and prevent them

40. Question 20  List the macrovascular complications

41. Question 20  List the macrovascular complications 1.Coronary Artery Disease - CAD 2.Cerebro Vascular Disease, TIA 3.Peripheral Vascular Disease PVD These start right at the onset of IR We must screen for and prevent them

42. Question 21  How do we identify persons with IR ?

43. Question 21  How do we identify persons with IR ? 1.IGT or IFG 2.WC > 36 (32) BMI > 23 3.B.P > 140/90 4.Dyslipidemia –TG>150, HDL<40(50) 5.Acanthosis Nigricans 6.Fasting C-Peptide levels increased

44. Question 22  What is C-Peptide ?

45. Question 22  What is C-Peptide ? 1.When proinsulin is cleaved into active Insulin, C-peptide is formed 2.It is measured in the fasting serum 3.It reflects the endogenous insulin secretion by  cells 4.It is used in HOMA IR model

46. Question 23  What are the ABC of Diabetes ?

47. Question 23  What are the ABC of Diabetes ? 1.A1c target of < 7% 2.B.P  130/80 3.Cholesterols  TG 40(50), Lp(a) <25

48. Question 24  What are the 4 major classes of OAD ?

49. Question 24  What are the 4 major classes of OAD ? Those  That decrease HGO - Metformin  Improve insulin Resistance - Met, TZD  Stimulate  cell – SU, Repaglinide  Slow absorption of CHO - Acarbose

50. Question 25  Which OAD is the sheet anchor of Diabetes treatment ?

51. Question 25  Which OAD is the sheet anchor of Diabetes treatment ?  Metformin in all 3 stages  Not SU – it is only in stage 2 (IR+ID)  Not Glitazone – It is not 1 st line drug

52. Question 26  What is the relative efficacy of OAD in terms of the glucose lowering potency ?

53. Question 26  What is the relative efficacy of OAD in terms of the glucose lowering potency ? 1.Metformin and SU –HbA1c ↓ 1.5% 2.Pio and Rosi – HbA1c ↓ 1.0% 3.Acarbose – HbA1c ↓ 0.5%

54. Question 27  What are the cut-off levels of HbA1c to make treatment decisions ?

55. Question 27  What are the cut-off levels of HbA1c to make treatment decisions ? 1.HbA1c of 9 or above straight away consider Insulin 2.HbA1c of < 9 to 7 consider OAD 3.HbA1c of < 7 – TLC only + Follow up

56. Question 28  What are the key contraindications of OAD ?

57. Question 28  What are the key contraindications of OAD ? 1.ALD – Met, SU, TZD 2.Renal Insufficiency – Met, SU 3.CHF, edema – TZD, Metformin 4.IBD, ALD – Acarbose 5.Pregnancy – All OADs 6.Age > 80 – Metformin, Glibenclamide

58. Question 29  What are the key side effects of Rx. ?

59. Question 29  What are the key side effects of Rx. ? 1.Metformin – GI side effects, Lactic Acidosis 2.SU – Hypoglycemia, allergy, weight gain 3.TZD – Weight gain, edema, abn. LFT 4.Acarbose – Flatulence, GI side effects 5.Insulin – Weight gain, Hypoglycemia

60. Question 30  Which are the best SU ?

61. Question 30  Which are the best SU ? In the order of superiority  Glimepiride  Gliclazide  Glipizide  Not Glibenclamide

62. Question 31  Which Glitazone is preferable ? Why ?

63. Question 31  Which Glitazone is preferable ? Why ?  Both Rosi and Pio are equally good  Slight differences in their lipid effects  Choice is individualized

64. Question 31  Which Glitazone is preferable ? Why ?  Pioglitazone – because it is 1.Lipid favourable 2.Comparatively less costlier 3.Of once daily dosage

65. Question 32  What is the difference between Analog insulins and conventional insulins ?

66. Question 32  What is the difference between Analog insulins and conventional insulins ? 1.Precise onset of action 2.No need to give 30’ before a meal 3.Highly predictable duration 4.Predictable absorption kinetics 5.Smaller dose sufficient (70%) 6.But costly 2 to 3 times

67. Question 33  What medicines are must for all Diabetics to prevent CAD ?

68. Question 33  What medicines are must for all Diabetics to prevent CAD ? 1.Aspirin daily 100 mg o.d. 2.Atorvastatin – min of 10 mg or equivalent 3.ACEi or ARB to protect kidney and heart 4.Adequate control of B.P and Lipids

69. Question 34  What is the take home message ?

70. Question 34  What is the take home message ? 1.Diabetes is mainly asymptomatic (80%) 2.Not screening for DM is a Deadly SIN 3.Only 70 % of diabetics are detected 4.Less than 20% are under < 7% HbA1c 5.The A, B, C, D, E must be kept in mind always and targets must be achieved 6.Early use of insulin is essential for this

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