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DIABETES
Presentation by
DR.VIOLET (de Sa) PINTO
Lecturer, Department of PSM
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.
A heterogeneous group of diseases,
characterized by chronic hyperglycemia,
resulting from a diversity of etiologies,
environmental and genetic, acting jointly.
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.
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.
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
Underlying cause is insulin deficiency- absolute in IDDM & partial in NIDDM
1. Pancreatic disorder- inflammatory or neoplastic2. Defects in insulin formation3. Destruction of β cells- viral infection, chemical
agents4. Decreased insulin sensitivity5. Genetic defects- mutation of insulin gene6. Auto immunity
AGENT
1. Age: NIDDM ,chance> with age Malnutrition related D.M. affects large no. of young people.2. Sex:SEAR, > in males , open to question3. Genetic factors: NIDDM - strong genetic componentIDDM – not totally a genetic entity4. Genetic markers:IDDM has > risk with HLA-DR 3 & DR4NIDDM not HLA associated
5. Immune mechanisms- Some evidence of activity against islet cells. Defects mechanism- environmental trigger – destroy
cells6. Obesity- central obesity – waist to hip ratio to NIDDM< insulin receptors on target cells7. Maternal diabetes – babies large at birth, obesity childhood, type 2diabetes early age.
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
6. Viral Infections- Rubella, mumps, human coxsakie virus B4may 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.
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.
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 obeseWomen who had baby >4.5kg( 3.5kg inconstitutionally small population) Women who show excess wt. gain in pregnancy.Patients with premature atherosclerosis.
VALUES
Glucose (mg/dl)
Whole blood CapillaryVenous capillary Venous capillary
Diabetes mellitisFasting ≥120 ≥120 ≥140 ≥140
2hrs after glu. ≥180 ≥200 ≥200 ≥200
Impaired glu. toleranceFasting <120 <120 <140 <140
2hrs after glu. 120-180 140-200 140-200 160-220
PREVENTION & CARE
TSec
Primary
Primordial
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 contraceptivesAdequate protein intake Decrease smoking, B.P., Intake of dietary fibre cholesterol, TG levels.Avoid sweet foodsAvoid toxins
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
practical2)Maintain ideal body weight
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.
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
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
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.
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.
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