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 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.

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.”

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 – 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

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 A1c periodically• Microalbuminuria• Lipid profile • ACR• ECG for LVH, IHD• Echo for LV Dysfun.• Stress test – ST Seg.

Risk Assessment

• BMI : (wt /ht2) 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 5yrs)

• 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 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

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

Almighty

Pardons and Grants me heavenEven 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

AlmightyWill 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