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Dr. S. Aswini Kumar. MD Professor of Medicine Medical College Hospital Thiruvananthapuram 1 Management of Newly Detected Diabetes
Learning Objectives  Importance Diagnosis Diet Exercise OHAs Insulin What is new Summarize 2
importance 3
Diabetes Mellitus Pancreatic insulin deficiency state Poor cells of the body crying for more insulin 4
The Role of Insulin Insulin is the key that opens the door of the cell Without insulin glucose can not enter the cells 5
Types of Diabetes 6 IDDM <10% >90% NIDDM
Type 2 Diabetes It’s a Nightmare!      Chronic  Kidney Disease Peripheral   Occlusive  Vascular  Disease Autonomic Neuropathy  Stroke Sudden Blindness Heart Attack Peripheral  Neuropathy  7 Aswini Kumar. MD 7 Microvascular and Macrovascular Complications of Diabetes
Why control diabetes? Tight control of DM and maintaining blood sugar values within normal range has proved to prevent long term micro-vascular and macro-vascular complications of diabetes 8
Symptoms of diabetes Polyuria Polydypsia Polyphagia Weight loss in spite of adequate food Tingling and numbness in extremities Generalized pruritus Pruritus vulva, Balanoposthitis Impotency, loss of libido  Premature cataract 9
Diagnosis of Diabetes MUST  be based on blood glucose estimation NOT  urine glucose testing Fasting venous glucose > 126mg% (Normal 70-110) 2Hr PP venous glucose > 200mg% (Normal 110-140) RBS value not diagnostic To be confirmed on repeat testing with FBS PPBS In presence of symptoms of DM - diagnostic GTT is not needed in a confirmed diabetic 10
Monitoring Glycemic Control Urine sugar testing Widely used. Depends on renal threshold Of value if threshold is normal & stable What if the urine sugar is absent? What if the urine sugar is high? Blood sugar estimation: Gives prevailing blood glucose Does not assess the overall control Periodic check up necessary- monthly Diet and medicines should be continued on the day 11
Self Monitoring of Blood Glucose SMBG using test strips AcucheckActiva Use within a month Costs 30 rupees per strip Accuracy question Indications: Wide fluctuations Proneness for ketosis Need for tight control - pregnancy Acute illness: peri-operative period 12
Hb A1c Excellent test to judge overall glycemic control Gives idea of average blood sugar  Over a period of previous 120 days Because RBC Life Span is 121 days Ideally done every 3-4 months Normal < 6.5 Good <7.0 Fair <8.0 Poor<9.0 Bad >10 Disadvantages: Costly – Rs. 250 per test  Falsely high values – Renal failure Falsely low values –  RBC life span 13
What are the goals? ADA and ACE/ AACE differ from each other ADA Goals FBS - 70-130  PPBS - <180 HbA1c  - <7.0 ACE/AACE Goals FBS - <110 PPBS - <140 HbA1c  - ≤6.5 14
diet 15
Medical Nutrition Therapy      Dietprescription     Main stay of treatment Shall be  individualized, 		   realistic 		flexible & 		 suitable   to patients life style 		preferably Indian diet Patient educatedand at regular        intervals compliance  judged 16
Weight Management 17 ,[object Object]
Read against ready made charts – To get BMI
Healthy value 20-25
Above 25 – Overweight
Above 30 – Obese.
Diet Control Principle less food –  Better insulin action No sugars sweets tubers  Otherwise eat normal food 18
Which Food To Avoid 19
Avoid all fried foods 20
What for Breakfast? 2 idli or 2 Dosa or ½ Puttu                         No Appam or Poori masala Western Style Breakfast    Tea, Milk and Eggs 21
What is for lunch? Ordinary Indian meals                      It is the ideal choice Fish 2-3 pieces everyday                     Chicken once a week 22
Which Fruit To Eat? 23
What for Evening and Dinner? 3 Arrow root biscuits                  Tea with out sugar Green Salad                                      2 Chappathi  + Veg Kuruma 24
exercise 25
26
27
28
Caloric equivalents: 29
Exercise Regular Exercise Daily at least 5 days/wk  Isotonic Exercise - Yes Isometric - No 30
What prevents one from Walking Traffic, heavy rain or  dogs on the street Choose Vellayambalam Museum or Gandhi Park 31
Precautions Correct foot wear Comfortable loose clothes Close inspection of feet every day Carry snacks as protection from hypoglycemia How it should be: Patient should be able to carry out a normal conversation while exercising without getting breathless 32
Physique Exercise Treadmill 33
DruG treatment 34
35 Causes of Hyperglycemia in DM 1	Intestine: glucose absorption 2	Muscle and adipose tissue:decreased glucose uptake 5 Insulin resistance Blood glucose 4	Liver: increased hepaticglucose output 5 Insulinresistance 3	Pancreas: impaired insulin                                             secretion
Biguanides Mode Of Action: Decreases hepatic glucose production Increases peripheral glucose uptake Increases insulin sensitivity No effect on insulin release Does not cause hypoglycemia First line choice in DM2 –  Ideal in over weight Metformin 250 to 1500mg  Phenformin no longer used 36
Sulphonylureas Stimulates Pancreatic B cells to produce MORE Second line choice after Metformin   First line in lean diabetics Most effective in Type 2 DM of recent onset Glibenglamide  2.5 to 10mg Glipizide2.5 to 10mg Glipride 1 to 4mg  Glyclazide 40 to160mg 37
Thiazolidinediones Add on druguseful for reducing PPBS Reduce insulin resistance by binding to PPAR  receptor Facilitates insulin’s effect on GLUT-4 Promote adipocyte differentiation Enhance fatty acid storage Pioglitazone 15-30mg OD  Rosiglitazone 2-4mg OD Modest weight gain  Fluid retention, edema  SGPT screening is advisable 38
 Glucosidase Inhibitors For Big Eaters who can’t stop eating MOA: inhibition of pancreatic alpha amylase in the gut lumen which hydrolyses complex starches to oligosaccharides. Delay absorption, when taken with meals  Thus reduces PPBS Do not influence insulin secretion Do not affect glucose utilization Acarbose 25-50mg BID    Voglibose 0.2 -0.3mg BID 39
Role of Incretins in Glucose Homoeostasis Blood glucose in fasting and postprandial states Glucose production by liver Ingestion of food Glucose-dependent Insulin from β cells (GLP-1 and GIP) Glucose uptake by muscles Release of gut hormones — incretins* Pancreas GI tract β cells α cells Active GLP-1 & GIP Glucose dependent  Glucagon fromα cells (GLP-1) DPP-4 enzyme InactiveGIP InactiveGLP-1 *Incretins are also released throughout the day at basal levels. 40
DPP-4 Inhibitors New class of oral agents Increase endogenous GLP-1 activity Promote insulin secretion Preferential effect on PPBS FDA approved first molecule Sitagliptin – For use with diet and exercise Or with metformin or thiozolidinediones 41
Sitagliptin in clinical practice Dose: 100mg orally once daily Reduced dose Creatinine clearance 30-50ml/min – 50mg/day Creatinine clearance <30ml/min – 25mg /day RFT done initially and repeated there after 42
Oral Hypoglycemic Agents 43
44
45 Intensifying of Oral Therapies metformin &/or glitazone sulfonylurea/repaglinide + &/or glucosidase inh sulfonylurea/repaglinide + and/or glucosidase inhibitors metformin and/or glitazone FPG < 120 mg/dl   A1C < 6.5% FPG > 120 mg/dl   A1C >6.5% Continue Add  Insulin
Insulin 46
47
48
49 Insulin secretion Years from  diagnosis 0 10 5 15 -10 -5 Onset Diagnosis Insulin resistance Postprandial glucose Fasting glucose Microvascular complications Macrovascular complications Pre-diabetes Type 2 diabetes
50
51 Hyperglycaemia (glucose toxicity) Insulin resistance b-cell (genetic background) “lipotoxicity” elevated FFA,TG Protein glycation Amyloid deposition
52
53
Insulin analogues 54
55 Short acting  Insulin Lispro and  aspart Long acting  Insulin Glargine and  Detemir Full biological activity Less tendency for self aggregation
56
57 Peak Time = 40-50 min Peak Time = 80-120 min    InsulinAspart or Lispro Subcutaneous Tissue CapillaryMembrane RegularHuman  Insulin
C14 fatty acid chain (Myristicacid) Phe Gly Phe Arg Glu Tyr Thr Gly Pro Cys Lys Val Thr Lys Cys Asn A21 B29 Leu Tyr Gly A1 Asn Tyr Ile Glu Leu Val Leu Ala Glu Glu Gln Gln Tyr Val Cys Leu Leu Cys Ser Ser Thr Cys Ile His Ser Gly Cys Leu Gln His Asn Val Phe B1 58
59
60
Guidelines 61
62 Metformin Sulfonylureas TZDs  Other oral agents  Insulin Lifestyle only 60% 45% 15% 6% 12% 15% Patients currently taking medication (%)
63 A1C < 9% A1C ≥ 9% Initiate insulin 2 oral agents 1 oral agent If not at target If not at target If not at target  Add an oral agent  ORInitiate insulin alone or in combination with an oral agent  Intensify insulin ORadd an oral agent Add insulin ORan oral agent Timely adjustments of chosen therapy shall made to attain target A1C within 6 to 12 months. Adapted from the CDA 2003 Clinical Practice Guidelines.
64
What is new 65
66
67 75 Basal   exogenous insulin is essential for regulating glycogen breakdown, gluconeogenesis lipolysis and ketogenesis For normal glucose utilization and storage Breakfast Lunch Dinner 50 Plasma insulin (µU/ml)  25 4:00 8:00 12:00 16:00 20:00   24:00 4:00 Time
68 Impressive benefits Breakfast Lunch Dinner Aspart       Aspart         Aspart or or or Personal financial cost Lispro         Lispro           Lispro Plasma insulin Detemir or Glargine 4:00 16:00 20:00   24:00 4:00 12:00 8:00 8:00 Time
69
70

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Management of a New Diabetes Patient

  • 1. Dr. S. Aswini Kumar. MD Professor of Medicine Medical College Hospital Thiruvananthapuram 1 Management of Newly Detected Diabetes
  • 2. Learning Objectives Importance Diagnosis Diet Exercise OHAs Insulin What is new Summarize 2
  • 4. Diabetes Mellitus Pancreatic insulin deficiency state Poor cells of the body crying for more insulin 4
  • 5. The Role of Insulin Insulin is the key that opens the door of the cell Without insulin glucose can not enter the cells 5
  • 6. Types of Diabetes 6 IDDM <10% >90% NIDDM
  • 7. Type 2 Diabetes It’s a Nightmare! Chronic Kidney Disease Peripheral Occlusive Vascular Disease Autonomic Neuropathy Stroke Sudden Blindness Heart Attack Peripheral Neuropathy 7 Aswini Kumar. MD 7 Microvascular and Macrovascular Complications of Diabetes
  • 8. Why control diabetes? Tight control of DM and maintaining blood sugar values within normal range has proved to prevent long term micro-vascular and macro-vascular complications of diabetes 8
  • 9. Symptoms of diabetes Polyuria Polydypsia Polyphagia Weight loss in spite of adequate food Tingling and numbness in extremities Generalized pruritus Pruritus vulva, Balanoposthitis Impotency, loss of libido Premature cataract 9
  • 10. Diagnosis of Diabetes MUST be based on blood glucose estimation NOT urine glucose testing Fasting venous glucose > 126mg% (Normal 70-110) 2Hr PP venous glucose > 200mg% (Normal 110-140) RBS value not diagnostic To be confirmed on repeat testing with FBS PPBS In presence of symptoms of DM - diagnostic GTT is not needed in a confirmed diabetic 10
  • 11. Monitoring Glycemic Control Urine sugar testing Widely used. Depends on renal threshold Of value if threshold is normal & stable What if the urine sugar is absent? What if the urine sugar is high? Blood sugar estimation: Gives prevailing blood glucose Does not assess the overall control Periodic check up necessary- monthly Diet and medicines should be continued on the day 11
  • 12. Self Monitoring of Blood Glucose SMBG using test strips AcucheckActiva Use within a month Costs 30 rupees per strip Accuracy question Indications: Wide fluctuations Proneness for ketosis Need for tight control - pregnancy Acute illness: peri-operative period 12
  • 13. Hb A1c Excellent test to judge overall glycemic control Gives idea of average blood sugar Over a period of previous 120 days Because RBC Life Span is 121 days Ideally done every 3-4 months Normal < 6.5 Good <7.0 Fair <8.0 Poor<9.0 Bad >10 Disadvantages: Costly – Rs. 250 per test Falsely high values – Renal failure Falsely low values – RBC life span 13
  • 14. What are the goals? ADA and ACE/ AACE differ from each other ADA Goals FBS - 70-130 PPBS - <180 HbA1c - <7.0 ACE/AACE Goals FBS - <110 PPBS - <140 HbA1c - ≤6.5 14
  • 16. Medical Nutrition Therapy Dietprescription Main stay of treatment Shall be individualized, realistic flexible & suitable to patients life style preferably Indian diet Patient educatedand at regular intervals compliance judged 16
  • 17.
  • 18. Read against ready made charts – To get BMI
  • 20. Above 25 – Overweight
  • 21. Above 30 – Obese.
  • 22. Diet Control Principle less food – Better insulin action No sugars sweets tubers Otherwise eat normal food 18
  • 23. Which Food To Avoid 19
  • 24. Avoid all fried foods 20
  • 25. What for Breakfast? 2 idli or 2 Dosa or ½ Puttu No Appam or Poori masala Western Style Breakfast Tea, Milk and Eggs 21
  • 26. What is for lunch? Ordinary Indian meals It is the ideal choice Fish 2-3 pieces everyday Chicken once a week 22
  • 27. Which Fruit To Eat? 23
  • 28. What for Evening and Dinner? 3 Arrow root biscuits Tea with out sugar Green Salad 2 Chappathi + Veg Kuruma 24
  • 30. 26
  • 31. 27
  • 32. 28
  • 34. Exercise Regular Exercise Daily at least 5 days/wk Isotonic Exercise - Yes Isometric - No 30
  • 35. What prevents one from Walking Traffic, heavy rain or dogs on the street Choose Vellayambalam Museum or Gandhi Park 31
  • 36. Precautions Correct foot wear Comfortable loose clothes Close inspection of feet every day Carry snacks as protection from hypoglycemia How it should be: Patient should be able to carry out a normal conversation while exercising without getting breathless 32
  • 39. 35 Causes of Hyperglycemia in DM 1 Intestine: glucose absorption 2 Muscle and adipose tissue:decreased glucose uptake 5 Insulin resistance Blood glucose 4 Liver: increased hepaticglucose output 5 Insulinresistance 3 Pancreas: impaired insulin secretion
  • 40. Biguanides Mode Of Action: Decreases hepatic glucose production Increases peripheral glucose uptake Increases insulin sensitivity No effect on insulin release Does not cause hypoglycemia First line choice in DM2 – Ideal in over weight Metformin 250 to 1500mg Phenformin no longer used 36
  • 41. Sulphonylureas Stimulates Pancreatic B cells to produce MORE Second line choice after Metformin First line in lean diabetics Most effective in Type 2 DM of recent onset Glibenglamide 2.5 to 10mg Glipizide2.5 to 10mg Glipride 1 to 4mg Glyclazide 40 to160mg 37
  • 42. Thiazolidinediones Add on druguseful for reducing PPBS Reduce insulin resistance by binding to PPAR receptor Facilitates insulin’s effect on GLUT-4 Promote adipocyte differentiation Enhance fatty acid storage Pioglitazone 15-30mg OD Rosiglitazone 2-4mg OD Modest weight gain Fluid retention, edema SGPT screening is advisable 38
  • 43.  Glucosidase Inhibitors For Big Eaters who can’t stop eating MOA: inhibition of pancreatic alpha amylase in the gut lumen which hydrolyses complex starches to oligosaccharides. Delay absorption, when taken with meals Thus reduces PPBS Do not influence insulin secretion Do not affect glucose utilization Acarbose 25-50mg BID Voglibose 0.2 -0.3mg BID 39
  • 44. Role of Incretins in Glucose Homoeostasis Blood glucose in fasting and postprandial states Glucose production by liver Ingestion of food Glucose-dependent Insulin from β cells (GLP-1 and GIP) Glucose uptake by muscles Release of gut hormones — incretins* Pancreas GI tract β cells α cells Active GLP-1 & GIP Glucose dependent  Glucagon fromα cells (GLP-1) DPP-4 enzyme InactiveGIP InactiveGLP-1 *Incretins are also released throughout the day at basal levels. 40
  • 45. DPP-4 Inhibitors New class of oral agents Increase endogenous GLP-1 activity Promote insulin secretion Preferential effect on PPBS FDA approved first molecule Sitagliptin – For use with diet and exercise Or with metformin or thiozolidinediones 41
  • 46. Sitagliptin in clinical practice Dose: 100mg orally once daily Reduced dose Creatinine clearance 30-50ml/min – 50mg/day Creatinine clearance <30ml/min – 25mg /day RFT done initially and repeated there after 42
  • 48. 44
  • 49. 45 Intensifying of Oral Therapies metformin &/or glitazone sulfonylurea/repaglinide + &/or glucosidase inh sulfonylurea/repaglinide + and/or glucosidase inhibitors metformin and/or glitazone FPG < 120 mg/dl A1C < 6.5% FPG > 120 mg/dl A1C >6.5% Continue Add Insulin
  • 51. 47
  • 52. 48
  • 53. 49 Insulin secretion Years from diagnosis 0 10 5 15 -10 -5 Onset Diagnosis Insulin resistance Postprandial glucose Fasting glucose Microvascular complications Macrovascular complications Pre-diabetes Type 2 diabetes
  • 54. 50
  • 55. 51 Hyperglycaemia (glucose toxicity) Insulin resistance b-cell (genetic background) “lipotoxicity” elevated FFA,TG Protein glycation Amyloid deposition
  • 56. 52
  • 57. 53
  • 59. 55 Short acting Insulin Lispro and aspart Long acting Insulin Glargine and Detemir Full biological activity Less tendency for self aggregation
  • 60. 56
  • 61. 57 Peak Time = 40-50 min Peak Time = 80-120 min InsulinAspart or Lispro Subcutaneous Tissue CapillaryMembrane RegularHuman Insulin
  • 62. C14 fatty acid chain (Myristicacid) Phe Gly Phe Arg Glu Tyr Thr Gly Pro Cys Lys Val Thr Lys Cys Asn A21 B29 Leu Tyr Gly A1 Asn Tyr Ile Glu Leu Val Leu Ala Glu Glu Gln Gln Tyr Val Cys Leu Leu Cys Ser Ser Thr Cys Ile His Ser Gly Cys Leu Gln His Asn Val Phe B1 58
  • 63. 59
  • 64. 60
  • 66. 62 Metformin Sulfonylureas TZDs Other oral agents Insulin Lifestyle only 60% 45% 15% 6% 12% 15% Patients currently taking medication (%)
  • 67. 63 A1C < 9% A1C ≥ 9% Initiate insulin 2 oral agents 1 oral agent If not at target If not at target If not at target Add an oral agent ORInitiate insulin alone or in combination with an oral agent Intensify insulin ORadd an oral agent Add insulin ORan oral agent Timely adjustments of chosen therapy shall made to attain target A1C within 6 to 12 months. Adapted from the CDA 2003 Clinical Practice Guidelines.
  • 68. 64
  • 70. 66
  • 71. 67 75 Basal exogenous insulin is essential for regulating glycogen breakdown, gluconeogenesis lipolysis and ketogenesis For normal glucose utilization and storage Breakfast Lunch Dinner 50 Plasma insulin (µU/ml) 25 4:00 8:00 12:00 16:00 20:00 24:00 4:00 Time
  • 72. 68 Impressive benefits Breakfast Lunch Dinner Aspart Aspart Aspart or or or Personal financial cost Lispro Lispro Lispro Plasma insulin Detemir or Glargine 4:00 16:00 20:00 24:00 4:00 12:00 8:00 8:00 Time
  • 73. 69
  • 74. 70
  • 75. 71
  • 76. 72
  • 77. 73
  • 78. Thank You For The Patient Listening 74