1. DIABETES Presentation by DR.VIOLET (de Sa) PINTO Lecturer, Department of PSM

2. Objectives At the end of the session the student shall have knowledge of : Diabetes - definition, types and problem statement Factors involved in causation Screening for diabetes- Types and choice of tests Prevention – Primary, secondary and tertiary levels.

3. A heterogeneous group of diseases, characterized by chronic hyperglycemia, resulting from a diversity of etiologies, environmental and genetic, acting jointly.

4. PROBLEM STATEMENT ICEBERG phenomenon of disease Expected no. of cases will double in 2025, with greatest expected in India & China. Now in younger age group also (including adolescents). Most productive period of life.

5. Major determinants for projected increase (developing countries) Population growth Age structure Urbanization Ethnic Amongst 5 major causes of cardiovascular disease epidemic in Asia. Lack of awareness about disease Lack of awareness about existing interventions for preventing disease & management Inadequacy in primary health care systems to cope.

6. Diabetes mellitus (D.M.) 1.Insulin dep. D.M. [I.D.D.M. type 1] ( abrupt inset, <30 years) 2.Non Insulin dep.D.M. [N.I.D.D.M. type 2] ( middle age, elderly) 3.Malnutrition related D.M.[M.R.D.M.] 4.Other (secondary to pancreatic,hormonal, drug induced, genetic & other Abnormal) Impaired Glucose tolerance (I.G.T.) Gestational D.M. CLASSIFICATION

7. Underlying cause is insulin deficiency- absolute in IDDM & partial in NIDDM 1.Pancreatic disorder- inflammatory or neoplastic 2.Defects in insulin formation 3.Destruction of β cells- viral infection, chemical agents 4.Decreased insulin sensitivity 5.Genetic defects- mutation of insulin gene 6.Auto immunity AGENT

8. 1.Age: NIDDM,chance> with age Malnutrition related D.M. affects large no. of young people. 2.Sex: SEAR, > in males, open to question 3. Genetic factors: NIDDM - strong genetic component IDDM – not totally a genetic entity 4.Genetic markers: IDDM has > risk with HLA-DR 3 & DR4 NIDDM not HLA associated

9. 5.Immune mechanisms- Some evidence of activity against islet cells. Defects mechanism- environmental trigger – destroy cells 6.Obesity- central obesity – waist to hip ratio to NIDDM < insulin receptors on target cells 7.Maternal diabetes – babies large at birth, obesity childhood, type 2 diabetes early age.

10. 1.Sedentary lifestyle- alters the interaction between insulin & receptors- NIDDM 2.Diet – > saturated fat intake along with total fat intake 3.Dietary fibre- minimum of 20gm recommended 4. Malnutrition- damage to β cells 5. Alcohol – damage liver and pancreas & promote obesity

11. 6. Viral Infections- Rubella, mumps, human coxsakie virus B4 may trigger immunogenecity- β cell destruction. 7. Chemical Agents- Alloxan, Streptozocin, Rodenticide VALCOR, ( Cassava, certain beans, cyanide producing foods.) 8. Stress- Surgery, Trauma & Stress of situations, bring out disease. 9. Other – Now even seen in low SE class – change in lifestyle.

12. SCREENING FOR DIABETES 1.Urine Examination Urine examination for glucose 2 hours after meal. Lack of sensitivity – only 10-50 % of diseased patients have a positive test. Yield many false negatives. Specificity – 90%, therefore 10% may have a false positive.

13. SCREENING FOR DIABETES 2.Blood sugar testing Standard oral glucose tolerance test + fasting test Target population: Age group 40 and > Those with family h/o of diabetes The obese Women who had baby >4.5kg( 3.5kg in constitutionally small population) Women who show excess wt. gain in pregnancy. Patients with premature atherosclerosis.

14. VALUES Glucose (mg/dl) Whole bloodCapillary VenouscapillaryVenouscapillary Diabetes mellitis Fasting120 140 2hrs after glu.180200 Impaired glu. tolerance Fasting<120 <140 2hrs after glu.120-180140-200 160-220

15. PREVENTION & CARE T Se c Primar y Primordial

16. PRIMARY PREVENTION 1)POPULATION STRATEGY 2) HIGH RISK STRATEGY (Mainly for NIDDM) Avoid sedentry lifestyle, PRIMORDIAL PREVENTION Avoid over nutrition, obesity Normal body wt.maintenance Avoid alcohol Nutrition, physical exercise Avoid oral contraceptives Adequate protein intake Decrease smoking, B.P., Intake of dietary fibre cholesterol, TG levels. Avoid sweet foods Avoid toxins

17. SECONDARY PREVENTION Treatment based on: 1)Diet alone- small balanced, more frequently 2)Diet and oral drugs 3)Diet and insulin 1)Maintain blood glucose level as close to normal as practical 2)Maintain ideal body weight

18. DIET Diabetics…. 1) Diet did not differ except in quality 2) Ate on an average 1000 kcal > than non diabetics Glycemic Index The blood glucose and insulin response to various CHO is not similar. Some increase blood glucose levels significantly.

19. Glycemic index of some foods: 100%- glucose 80-90%- cornflakes, carrots, potatoes, honey,idli 70-79%- bread(whole meal), millets, rice(white), upma 60-69%- bread(white), paratha(wheat), rice briwn,sprout, beetroot, 50- 59%- buck wheat, noodles, peas, pongal, sweet corn 40-49%- noodles (whole meal), porridge oats dhalia, bengal gram, 30-39%- black eyed peas, chick peas, apple, tomato soup 20-29%- kidney beans, lentils, rajmaah 10-19%- soya beans, groundnuts

20. PROPER MANAGEMENT 1)Routine checking of blood sugar- (glycosylated HB ½ yearly, levels 2-3 months, home glucose monitoring- direct, haemoglucotest strip) 2)Urine for proteins,& ketones 3)Visual acuity 4)Weight 5)Feet examined for defective blood circulation * PRIMARY HEALTH CARE

21. SELF CARE Adherence to diet and drug regimen Abstinence from alcohol Examination of his own urine and self blood glucose testing Self administration of insulin Maintenance of optimum weight Attending periodic checkups Recognizing of symptoms of hypoglycemia etc. Identification Card.

22. TERTIARY PREVENTION Blindness, kidney failure, coronary thrombosis, gangrene of lower extremities. Organize specialized clinics Diagnostic & management skills of a high order Basic, clinical & epidemiological research Need for national & local registries for diabetes.