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Diabetes mellitus



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  • Many patients are asymptomatic at diagnosis (Hyperglycemia is an incidental detection)


  • 1. Diabetes MellitusEpidemiology, Definition, Pathophysiology,Diagnosis and PresentationSharat S. KolkeMD, DNB, MNAMS Asian Heart Institute and Research Center Fauziya Hospital 1
  • 2. Epidemiology(1)In most countries, diabetes is now one of the leading causes of death through its effects on cardiovascular disease: 70-80% of people with diabetes die of cardiovascular disease.(2)Diabetes is ranked among the leading causes of blindness, renal failure and lower limb amputation with type 2 diabetes accounting for 85-95% of cases of diabetes.(3)The total cost of caring for people with diabetes in Europe is estimated between 28 billion and 53 billion Euros per year 2
  • 3. The global prevalence of type 2 diabetes isprojected to increase to >330 million by 2025 3
  • 4. ….and in India• There were 32 million diabetics in 2000• Expected to grow up to 80 million in 2030• Prevalence increased in urban areas from 2% in 1973 to 12% in 2000• Beginning to increase in rural areas too!! ICMR guidelines for management of Diabetes 2005 4
  • 5. Epidemiology• Ethnicity• Sex ratios• Genetic and environmental factors – The thrifty gene hypothesis – The fetal origins hypothesis• Age related prevelance• Clinical and metabolic characteristics – Association with obesity – Other diabetogenic factors 5
  • 6. Ethnicity• Lowest prevalence are seen in less developed countries• High prevalence is seen in populations that have adopted a ‘westernized’ lifestyle• Social and behavioral changes• Different ethnic groups have different lipid patterns. 6
  • 7. Sex ratios• Type 2 Diabetes is more common in men than women 7
  • 8. Genetic and environmental factors• Thrifty genotype hypothesis• Fetal origins hypothesis (Barker and Hales)• Other genetic factors – Family history of T2DM is common – Life time risk associated with one T2DM parent is 40% 8
  • 9. Age related prevalence• Prevalence of Diabetes increases with age – Glucose tolerance decreases with age – Weight gain between 40s and 70s, particularly central obesity creates Insulin resistance ..…..but recent years have witnessed the emergence of T2DM in younger groups including children and adolescents 9
  • 10. Clinical and metabolic characteristics• Association with obesity – Obesity is directly correlated with an increased risk of type 2 diabetes• Dietary composition – Increased proportion of saturated fat is linearly associated with diabetes prevalence – Fish diets of Eskimos and Japanese which are rich in δ-3- poly unsaturates improve insulin sensitivity 10
  • 11. 11
  • 12. DefinitionDiabetes Mellitus is a group of metabolicdisorders characterized by chronichyperglycemia resulting from defects of insulinaction (Insulin resistance) , insulin secretion(β cell dysfunction/destruction) or both 12
  • 13. Pathogenesis ofDiabetes Mellitus 13
  • 14. Insulin ResistanceWhat, Why and What? 14
  • 15. What is Insulin Resistance?• Insulin resistance plays a major role in development of T2DM.• A reduced biological response to a physiological amount of insulin• Fasting hyperinsulinemia in the presence of normal or elevated plasma glucose level implies Insulin resistance 15
  • 16. Insulin Resistance• Insulin resistance per se is asymptomatic• IR precedes the onset of T2DM by 10 – 20 years• But an additional defect in insulin secretion is required for the development of frank T2DM 16
  • 17. EnvironmentGenetic Obesity INSULIN RESISTANCE` 17
  • 18. Insulin Resistance Effect of Insulin Resistance on Body Tissues Skeletal muscle It accounts for about 80% of glucose disposal afterglucose infusion or ingestion. Thus in an IR state, inability to stimulate glucosedisposal by the muscles alters glucose homeostasis 18
  • 19. Insulin ResistanceEffect of Insulin Resistance on Body Tissues Adipose tissues IR decreases suppression of lipolysis by adipose tissues causing increase in the levels of FFAs 19
  • 20. Insulin ResistanceEffect of Insulin Resistance on Body TissuesLiverInsulin suppresses hepatic gluconeogenesis partlyby reducing the flux of amino acids and FFAs fromthe muscle and adipose tissue into the liver andalso by its direct effects.In T2DM, the IR state causes excessive hepaticglucose production due to inadequate suppressionof gluconeogenesis. 20
  • 21. Liver Lipolysis Triglycerides Fatty Acid Fatty Acid B oxidation +ve -ve Acetyl Co A Glucose Triglyceride Ketone bodies Re - esterification Adipose Tissue Ketogenesis Oxidationin extra hepatic tissues 21
  • 22. Insulin ResistanceClinical features 22
  • 23. Insulin ResistancePhysical signs such as– Acanthosis Nigricans– Acrochordons : multiple skin tags– Hyperandrogenism– Acromegaloid features 23
  • 24. β cell dysfunction 24
  • 25. β cell dysfunction in Type 2 Diabetes 25
  • 26. 26
  • 27. 27
  • 28. Pathogenesis of Type 2 DM The progression to Type II DMEnvironment Genetic Insulin Resistance Hyperinsulinemia Compensated insulin resistance Normal glucose tolerance Beta cell exhaustion Impaired glucose tolerance Beta cell failure DIABETES MELLITUS 28
  • 29. Clinical presentation of T2DM• Estimated to occur at least 4-7 years before the clinical presentation• 3rd NHNES showed that 2.7% of the general adult population and 6 % of the population above 60 were undiagnosed diabetics• Previously undiagnosed hyperglycemia was discovered in 1/3rd of hospitalized patients – Levetan et all 29
  • 30. Clinical presentation of T2DM Nocturia PolyuriaDry mouth/thirst Mean age range Fatigue 52 (25 – 65) 66 (50 – 74) Blurred vision Pruritis Paraethesias 0 20 40 60 80 30 100 Adapted from Bulpitt et al; Ruige et al
  • 31. Clinical presentation of T2DM• In symptomatic patients , obese individuals are less likely to present with common symptoms than lean individuals• Also they are less likely to have weight loss than lean individuals Melton et al. Incidence of Diabetes Mellitus by clinical type. Diabetes Care 1983;6:75 - 86 31
  • 32. Type 1 or Type 2?A diagnostic dilemma… 32
  • 33. 33
  • 34. Criteria for Diagnosis 34
  • 35. 35
  • 36. Who should be screened for Diabetes? 36
  • 37. Screening• Asymptomatic individuals – Age > 30 years – Overweight BMI > 23 kg/m 2 – Central obesity i.e. waist hip ratio: men > 0.90 women > 0.85 – Family h/o Diabetes – Sedentary lifestyle – Previously identified IFG or IGT – h/o GDM, recurrent fetal loss or delivery of large baby – Hypertension – Dyslipidemia 37
  • 38. Screening• Individuals at high risk – Any patient with symptoms of hyperglycemia or complications of diabetes – Adults with tuberculosis – Patients on diabetogenic drugs – Women with PCOS – History of premature vascular disease 38
  • 39. Screening for Type 2 Diabetes in children and adolescents• Overweight (weight > 120% of ideal body weight) plus any one of the following risk factors :- – Family history of type 2 diabetes in first or second degree relative – Signs of insulin resistance or conditions associated with insulin resistance (viz. Acanthosis nigricans, hypertension, dyslipidemias or PCOS). 39
  • 40. Targets 40
  • 41. Targets for lipids 41
  • 42. Monitoring and follow up of patientswith diabetes 42
  • 43. • Urine sugar should not be used alone• Fasting and postprandial or casual plasma glucose• Individualized regimens of SMBG• Hb1Ac every 3- 6 months.• Clinical examination every visit at least 3 months• Optimizing weight, blood pressure and lipids• Screening for long term complications like retinopathy, nephropathy and neuropathy• Encourage foot care• Discourage tobacco 43
  • 44. About SMBG 44
  • 45. • Ideal for every diabetic for optimal long term control• All diabetics on insulin• Brittle diabetics• Ketosis and/or hypoglycemia prone diabetics• Hypoglycemic awareness• Whenever tight control is advocated e.g pregnancy, infections, advanced complications 45
  • 46. What to do annually?• Lipid profile• Opthalmology check up with dilated pupil• Blood urea/ creatinine• Urine for protein/albumin/microalbuminuria• ECG in patients above 40 years of age 46
  • 47. Thank You 47
  • 48. Metabolic Syndrome 48
  • 49. Metabolic Syndrome Metabolic syndrome is defined by the National Cholesterol Education Program - Adult Treatment Panel III as the presence of at least three out of five key risk factors. The greater the number of risk factors, the more at risk a patient is. The five risk factors are:1. Increased waist circumference (greater than 102 cm for men; greater than 88 cm for women)2. Elevated levels of triglycerides (blood fats)3. Low levels of HDL (good) cholesterol4. Blood pressure (greater than or equal to 130/85 mmHg)5. Impaired fasting glucose (insulin resistance) 49
  • 50. Metabolic Syndrome WHO Criteria Anyone who has diabetes or insulin resistance and two of the following:1. High waist-to-hip ratio;2. High triglycerides or low HDL cholesterol;3. High blood pressure;4. High urinary albumin excretion rate. 50
  • 51. Metabolic Syndrome• Candidate definitions of MS were proposed by modifying the NCEP ATPIII definition. These modifications included the following: waist circumference cutoffs as >90 cm in men and >80 cm in women, BMI cutoff as >23 kg/m2, and a measure of truncal subcutaneous fat (subscapular skinfold thickness [SST] >18 mm). Diabetes Care 28:398-403, 2005 51
  • 52. Metabolic SyndromeMetabolic Syndrome: a MisleadingDiagnosis Diabetes Care and Diabetologia, ADA and EASD 52
  • 53. Metabolic Syndrome"But there is no combination of risk factors that boosts apersons cardiovascular risk beyond the sum of the parts,or constitutes a separate disease,"Ele Ferrannini, MD, President of the European Association for the Study ofDiabetes. 53