1. Diabetes Mellitus Type 2 DM (NIDDM) Not merely “ SUGAR DISORDER” Multi system disease – A syndrome Metabolic – endocrine – vascular – –Cardiac – cerebral – renal – Ophthalmic From blood sugar to blood vessel

2. The Fasted State Only 6 to 8 hours Insulin sensitive tissues –Muscle & adipose tissues Non insulin sensitive tissue –Brain – cannot utilize FFA, depends on glucose Liver mediated –Glycogenolysis 50% –Gluconeogenesis 50% from precursors & FFA

3. The Fed State To minimize glucose fluctuations. To restore normoglycemia. 1.Suppression of endogenous G-production. 2.Stimulation of hepatic G-uptake. 3.Acceleration of G-uptake by muscle etc.

4. The Fed State In the liver –Directly by  glucose production –Indirectly by  lipolysis –Glycogen synthesis In the muscle –Glycogen synthesis –Oxidative and non-oxidative metabolism of G In the adipose tissue –Alpha glycero phosphate – esterification of FFA to TG

5. Prandial Glucose Regulation Diet modification to reduce simple CHO Drugs modifying absorption Short action Insulin around meal Short acting insulin secretagogues Anti Glucagon (Amylin,GLP-1,Pramlnitide) Insulin sensitizers

6. Insulin Not a mere regulator of blood glucose Has profound effect on all fuels Lipid metabolism Protein metabolism CHO – metabolism –Glucose utilization – muscle & adipose tissue –Gleuconeogenesis & Glycogenolysis

7. Insulin Delivery Systems Injectable NovoPen, NovoLet. Intra nasal : conc. Preparations, nasal Infl. Intra pulmonary – good abs. Rapid than s/c. Oral insulin – Liposomal envelopes- DU. Islet cell encapsulates – underway.

8. Elliott P Joslin in 1921 “It is proper at the present time to devote time not alone to treatment but more to prevent diabetes – the results may not be so striking to us immediately, but they are sure to come and to be important.”

9. Prevention of Diabetes How we have grown ? Prevention holds the key – no users ? Diabetic care is Life long – –Nutrition – Excercise – Education on DM How about NOW – or never ? –1,49, 806 studied – 1 kg  9%  DM risk

10. Prevention of Diabetes Diets do work Yes you too can–Aerobic exercises – 20mts –50 to 70% of Max capacity x 3 times a week Diet + exercise – 6 times more than OHAs Diabetes preventable – few takers Talk is cheap – it pays Shift focus to adolescence / adult hood

11. Should we wait ? and Pay heavily on –ICUs, transplant units, amputation units –Laser therapy, physio therapy units Or pay very little now –By preventing the epidemic rise in DM Clinical diabetes – ADA – Apr/June 2001

12. Insulin Resistance Metabolic syndrome Multi system disorder Predisposes to DM & CVD Contributors to IR 1. Genetic 2. Obesity – abdominal 3. Physical inactivity 4. Advancing age

13. Insulin Resistance Atherogenic dyslipidemia –  In VLDL,  in small LDL,  in HDL Prothrombotic state –  In fibrinogen levels –  In plasminogen activator inhibitor –Various platelet abnormalities G.T. Abnormalities – IGT, hyper glycemia Hypertension

14. Evidence for Insulin Resistance Abdominal obesity B.P – High normal or Mild HT TG high normal  250 Lowered HDL  40 for men,  50 women Boarder line LDL - 130- 155 mg% IGT -- FPG – 110- 126 mg% Having Diabetes is equivalent to having IHD

15. Predictors of Worsening of GT Insulin resistance Insulin Secretory dysfunction These can be assessed by –Insulin stimulated glucose disposal (M) –Acute insulin Secretory response (AIR) –Hydrodensitometry (body composition)

16. Mandatory Examinations H/o Smoking H/o IHD Family H/o DM H/o Hypoglycemia Exam for all pulses B.P recording Foot exam Trophic Autonomic neuropathy Fundus exam for DR Fasting and PP BG GHb A1c periodically Microalbuminuria Lipid profile ACR ECG for LVH, IHD Echo for LV Dysfun. Stress test – ST Seg.

17. Risk Assessment BMI : (wt /ht 2 )  25 normal –25. To 29.9 over wt,  30 obese Waist size : males  40” (102 cm) obesity –Females  36” (88 cm) obesity –88-102 Borderline Waist/hip ratio : abnormal if –  0.8 for women –  0.9 for men

18. Detection of Clinical & Sub-clinical Cardiovascular Disease in the Diabetics Stress testing (BP & HR response blunted) Painless ST depression, lowered specificity Echo : diastolic dysfunction Tc 99 perfusion Scintigraphy Autonomic dysfunction (50% mort. In 5yrs) LVH in ECG is strong predictor of CHD Coronary calcium scoring - CT based

19. Albumin Creatinine Ratio (ACR) Early predictor of Nephropathy  in ACR occurs even with in first 5yrs Also for retinopathy First void sample of urine to test Albumin in mg% / Creatinine in m mols –Males normal up to 3.5 –Females normal up to 4.0

20. Diabetic Retinopathy Type 1 – 71% Type 2 non insulin req. – DR is 37% Type 2 insulin req. – DR is 70 % (Diabetes mellitus type 1 -10%, type 2 - 90% Risk factors –Duration  15yrs, hyperglycemia level –HT. Hyper lipidemia, nephropathy Treatment : VEGF inhibitor, Vit E. Octreotide Photocoagulation

21. Almighty Pardons and Grants me heaven Even if I don't know a single letter about –Crutz Feld Jacob’s Disease –Tsutsugamushi Fever –Criggler Nazzar Syndrome –South American equine encephalitis and –Many and much more BUT

22. Almighty Will drag me to hell and will not pardon My ignorance of even the minute details of DM My indifference to apply current knowledge My negligence in screening for DM My despondency about preventing DM My inadequacy in maintaining my patients –As normo-glycemic as possible – (This is applicable to all common diseases)

23. Do You Who I am ? I am the primary care physician On whom my patients bestow all trust

25. OUR COMMITMENT