Diabetes Mellitus Type 2 DM NIDDM Not merely

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

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

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.

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

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

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

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

“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. ” Elliott P Joslin in 1921

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

Prevention of Diabetes • Diets do work • Yes you too can–Aerobic exercises – 20 mts – 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

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

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

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

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

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)

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 A 1 c periodically Microalbuminuria Lipid profile ACR ECG for LVH, IHD Echo for LV Dysfun. Stress test – ST Seg.

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

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 5 yrs) LVH in ECG is strong predictor of CHD Coronary calcium scoring - CT based

Albumin Creatinine Ratio (ACR) • • • Early predictor of Nephropathy in ACR occurs even with in first 5 yrs 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

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 15 yrs, hyperglycemia level – HT. Hyper lipidemia, nephropathy • Treatment : VEGF inhibitor, Vit E. Octreotide • Photocoagulation

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

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)

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

OUR COMMITMENT