Diabetes Diagnosis and Classification


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Diagnosis and classification of diabetes

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  • Glucose monitoring systems have come a long way. In the past, ants were utilized to detect diabetes. High concentration of sugar spilled into the urine would attract these insects. So, we can call it the ANTcient method. Currently, there are faster and more effective methods, which include continuous wireless transmission of the blood glucose readings from the sensor on the skin to the portable receiver. The quality of this modern technology has significantly improved diabetes management.
  • Implications for the menu of items offered…
  • 1 can of sugary pop per day in excess of what they need will put on 3 stone in weight over childhood
  • Type 2 diabetes is up to 6 times more common in people of South Asian descent and 3 times more common in those of African and African-Caribbean descent, compared with the white population More than one quarter of people of Asian origin aged over 40 years suffer from diabetes Diabetes National Service Framework: Standards – Department of Health 2001; Audit Commission – Testing Times (2000)
  • Diabetes Diagnosis and Classification

    1. 1. Dr. Vivek Arya MD, DM(Endo.), SGPGI, Lucknow Asst. Prof. Smt. NHL Medical College & VS Hosp. Formerly Asst. Prof. Nizam’s Institute, Hyderabad Formerly, Chief Consultant and Head, Belhoul Apollo Hospital, DUBAI Senior Consultant Endocrinologist & SAL/Sterling/Shalby/Apollo/Nidhi Hospital Investigating Type 2 Diabetes & ADA EASD recommendations enter for ndocrine Disease and Diabetes
    2. 2. (Answer: detect sugar) What do these pictures have in common?
    3. 3. The Size of the Problem <ul><li>80% of people with DM will die prematurely from long term complications </li></ul><ul><li>Patients with DM can expect to live 5-10 years less than someone without diabetes </li></ul><ul><li>70-75% of Type 2 DM will die of CVD </li></ul><ul><ul><ul><ul><ul><li>(BDA - Counting the Cost - 1996) </li></ul></ul></ul></ul></ul><ul><li>Cardiovascular mortality </li></ul><ul><ul><li>2-3 Xs higher in men with DM </li></ul></ul><ul><ul><li>3-5 Xs higher in women with DM </li></ul></ul><ul><ul><ul><li>(UKPDS, 1998) </li></ul></ul></ul>
    4. 4. Featuring……… <ul><li>Definition </li></ul><ul><li>Diagnosis </li></ul><ul><li>Classification </li></ul><ul><li>Evaluation </li></ul><ul><li>Case scenarios </li></ul>
    5. 5. Level of Evidence <ul><li>A </li></ul><ul><ul><li>Clear evidence from well-conducted, generalizable, randomized controlled trials that are adequately powered. </li></ul></ul><ul><ul><li>Compelling non-experimental evidence, i.e., the “all or none” rule developed by the Centre for Evidence-Based Medicine at Oxford. </li></ul></ul><ul><ul><li>Supportive evidence from well-conducted randomized controlled trials that are adequately powered. </li></ul></ul><ul><li>B </li></ul><ul><ul><li>Supportive evidence from well-conducted cohort studies. </li></ul></ul><ul><ul><li>Supportive evidence from a well-conducted case-control study. </li></ul></ul><ul><li>C </li></ul><ul><ul><li>Supportive evidence from poorly controlled or uncontrolled studies. </li></ul></ul><ul><ul><li>Conflicting evidence with the weight of evidence supporting the recommendation. </li></ul></ul><ul><li>E </li></ul><ul><ul><li>Expert consensus or clinical experience. </li></ul></ul>
    6. 6. Definition <ul><li>Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both. </li></ul>Diagnosis and Classification of Diabetes Mellitus American Diabetes Association Diabetes Care 33: 2010
    7. 7. Prevalence of retinopathy by deciles of the distribution of FPG, 2hrPPG and HbAlc National Health And Nutritional Epidemiologic Survey (NHANES III).
    8. 8. HbA1c : Glycosylated haemoglobin <ul><li>Average blood glucose over last 8-12 weeks </li></ul><ul><li>A1C >=6.5% is diagnostic </li></ul><ul><li>The test should be performed in a laboratory using a method that is National Glycohemoglobin Standardization Program (NGSP) certified </li></ul>
    9. 9. Criteria for diagnosis <ul><li>Fasting PG > 126mg% (8 hrs. non caloric intake) </li></ul><ul><li>Postprandial PG > 200mg% ( glucose load containing the equivalent of 75 g anhydrous glucose) </li></ul><ul><li>Symptoms of diabetes plus Random Blood Glucose > 200mg% </li></ul><ul><li>Check a second time </li></ul>
    10. 10. Categories of increased risk for Diabetes <ul><li>Impaired fasting Glycaemia (IFG) 100-125mg% </li></ul><ul><li>Impaired Glucose Tolerance (IGT) 140mg-199mg% </li></ul><ul><li>A1C 5.7–6.4% </li></ul>
    11. 11. What do the terms impaired fasting glycaemia AND impaired glucose tolerance imply ?
    12. 12. It means <ul><li>Increased risk for </li></ul><ul><li>cardiovascular /cerebrovascular disease </li></ul><ul><li>A predictor for subsequent diabetes mellitus </li></ul><ul><li>Diabetic range glucose values unmasked with stress </li></ul>
    13. 13. Testing in asymtomatic patients <ul><li>adults who are overweight (BMI 25 kg/m2*) and have additional risk factors: </li></ul><ul><ul><li>physical inactivity </li></ul></ul><ul><ul><li>first-degree relative with diabetes </li></ul></ul><ul><ul><li>members of a high-risk ethnic population (e.g., Asian American, Afro-american) </li></ul></ul><ul><ul><li>women who delivered a baby weighing 4 kg or were diagnosed with GDM </li></ul></ul><ul><ul><li>hypertension (140/90 mmHg or on therapy for hypertension) </li></ul></ul><ul><ul><li>HDL cholesterol level 35 mg/dl &/or a triglyceride level 250 mg/dl </li></ul></ul><ul><ul><li>women with polycystic ovary syndrome </li></ul></ul><ul><ul><li>A1C 5.7%, IGT, or IFG on previous testing </li></ul></ul><ul><ul><li>other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans) </li></ul></ul><ul><ul><li>history of CVD </li></ul></ul>
    14. 14. <ul><li>In those without these risk factors, testing should begin at age 45 years. (B). </li></ul><ul><li>If tests are normal, repeat testing should be carried out at least at 3-year intervals. (E). </li></ul><ul><li>In those identified with increased risk for future diabetes, identify and, if appropriate, treat other cardiovascular disease (CVD) risk factors. (B) </li></ul>Testing in asymtomatic patients
    15. 15. Testing for T2DM in asymptomatic Children <ul><li>Criteria : Overweight (BMI 85th percentile for age and sex, weight for height 85th percentile, or weight 120% of ideal for height) </li></ul><ul><li>Plus any two of the following risk factors: </li></ul><ul><ul><li>Family history of type 2 diabetes in first- or second-degree relative </li></ul></ul><ul><ul><li>Race/ethnicity (African American, Asian American) </li></ul></ul><ul><ul><li>Signs of insulin resistance or conditions associated with insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or small for gestational age birthweight) </li></ul></ul><ul><ul><li>Maternal history of diabetes or GDM during the child’s gestation </li></ul></ul><ul><li>Age of initiation : Age 10 years or at onset of puberty, if puberty occurs at a younger age </li></ul><ul><li>Frequency : Every 3 years </li></ul>
    16. 16. Screening for GDM <ul><li>Women at very high risk should be screened for diabetes as soon as possible after the confirmation of pregnancy. </li></ul><ul><li>Criteria for very high risk are: </li></ul><ul><ul><li>Severe obesity </li></ul></ul><ul><ul><li>Prior history of GDM or delivery of large-for-gestational-age infant </li></ul></ul><ul><ul><li>Presence of glycosuria </li></ul></ul><ul><ul><li>Diagnosis of PCOS </li></ul></ul><ul><ul><li>Strong family history of type 2 diabetes </li></ul></ul>
    17. 17. GDM Criteria *2 or more criteria met = positive diagnosis (cutoff points in mg/dl) † 1 or more criteria met = positive diagnosis 140 - 140 145 3 hours 155 ≥ 140 155 165 2 hours 180 - 180 190 1 hour 95 ≥ 126 95 105 Fasting Carpenter and Coustan* World health Organization † American Diabetes Association* National Diabetes Data Group*
    18. 18. Classification <ul><li>Type 1 Diabetes/LADA </li></ul><ul><li>Type 2 Diabetes </li></ul><ul><li>Other Specific Types </li></ul><ul><li>Gestational Diabetes </li></ul>
    19. 19. Type 1 Diabetes <ul><li>ß-cell destruction, leading to absolute insulin deficiency </li></ul><ul><li>Immune-mediated diabetes (common) </li></ul><ul><li>Idiopathic diabetes. </li></ul>
    20. 20. Type 1 Diabetes Insulitis
    21. 21. Pathogenesis of Type I DM Environment ? Viral infe..?? Genetic HLA-DR3/DR4 Severe Insulin deficiency ß cell Destruction Type I DM Autoimmune Insulitis (GAD,ICA IAA)
    22. 22. LADA(Latent Autoimmune Diabetes of the Adult)
    23. 23. Type 2 Diabetes <ul><li>May range from predominantly insulin resistance to predominantly an insulin secretory defect. </li></ul>
    24. 24. Type 2 Diabetes <ul><li>Loss of ß cells </li></ul><ul><li>Amyloid deposits </li></ul><ul><li>Hyalinization </li></ul>
    25. 25. Pathogenesis of Type 2 DM Environment Low Birth Weight Obesity Genetic ß cell defect Genetic ß cell exhaustion Type 2 DM Insulin resistance Relative Insulin Def. May require Insulin Secretory Defect
    26. 26. Physical Activity on the decline…………..
    27. 27. Physical Activity on the decline…………..
    28. 28. The economic driving factors…… Adam Drewnowski and SE Specter. Poverty, obesity, and diet costs. Am J Clin Nutr 2004;79:6 –16 40/- per kg 90/- per kg … Consumer Price Index shifts favour unhealthy products
    29. 29. Obesity and Type 2 Diabetes <ul><li>As a country becomes wealthier so does the incidence of obesity and diabetes </li></ul><ul><ul><li>‘ Coca Colonisation’ </li></ul></ul><ul><ul><li>‘ McDonaldisation’ </li></ul></ul><ul><li>Type 2 diabetes now seen in children due to obesity </li></ul>
    30. 30. Coca-colonisation
    31. 31. McDonaldisation
    32. 32. Other Specific Types <ul><li>A. Genetic defects in Beta Cell </li></ul><ul><li>Function/Insulin secretion </li></ul><ul><li>B. Genetic defects in Insulin Action </li></ul><ul><li>C. Diseases of the Exocrine Pancreas </li></ul><ul><li>D. Endocrinopathies </li></ul><ul><li>E. Drug or Chemical Induced </li></ul><ul><li>F. Infections </li></ul><ul><li>G. Uncommon Immune forms </li></ul><ul><li>H. Genetic Syndromes with Diabetes </li></ul>
    33. 34. Genetic defects of insulin secretion <ul><li>Maturity Onset Diabetes of the Young(MODY) </li></ul><ul><li>Six genetic loci on different chromosomes have been identified to date. </li></ul><ul><li>Glucokinase related MODY(MODY 2) is common….but in India….HNF-4 alfa. </li></ul><ul><li>Usually Nonketotic /Nonobese </li></ul><ul><li>Often in sucessive generations </li></ul>
    34. 35. Maturity Onset Diabetes in the Young (MODY) <ul><li>Uncommon – approx 2% of all diabetes </li></ul><ul><li>Relative insulinopenia </li></ul><ul><li>Before 25 years </li></ul><ul><li>Mutation in gene encoding for beta cell </li></ul><ul><li>Different types – 6 different genes identified </li></ul><ul><ul><ul><li>1- may not need any drug treatment </li></ul></ul></ul><ul><ul><ul><li>2 - may need insulin </li></ul></ul></ul><ul><ul><ul><li>3 - is often sulphonylurea sensitive </li></ul></ul></ul>
    35. 36. Type 2 or MODY Autosomal dominant Polygenic / Heterogen Inheritance rare frequent Obesity minimal considerable Role of environment beta cell dysfunction beta cell dysfunction + insulin resistance Patho-physiology child-young middle - old Age of onset MODY Type 2 DM
    36. 38. Genetic defects in insulin action     <ul><li>1. Type A insulin resistance        </li></ul><ul><li>2.Leprechaunism         </li></ul><ul><li>3. Rabson-Mendenhall syndrome         </li></ul><ul><li>4. Lipoatrophic diabetes         </li></ul><ul><li>5. Others     </li></ul>
    37. 39. Genetic defects in insulin action     <ul><li>1. Type A insulin resistance        </li></ul><ul><li>2.Leprechaunism         </li></ul><ul><li>3. Rabson-Mendenhall syndrome         </li></ul><ul><li>4. Lipoatrophic diabetes         </li></ul><ul><li>5. Others     </li></ul>
    38. 40. Adapted from F Karpe
    39. 41. Diseases of the pancreas <ul><li>Acquired causes include Pancreatitis, Trauma, infection, pancreatectomy, and pancreatic carcinoma. </li></ul><ul><li>Fibrocalculous pancreatopathy </li></ul><ul><li>Cystic fibrosis and Hemochromatosis </li></ul>
    40. 43. Fibrocalculous pancreatic diabetes <ul><ul><ul><li>The classical triad of clinical presentation in </li></ul></ul></ul><ul><ul><ul><li>tropical chronic pancreatitis: </li></ul></ul></ul><ul><li>Abdominal pain. </li></ul><ul><li>Maldigestion leading to steatorrhoea. </li></ul><ul><li>Diabetes (fibrocalculous pancreatic diabetes). </li></ul>
    41. 44. Drug induced diabetes. <ul><li>Drugs and hormones can impair insulin sensitivity and reduce insulin action. </li></ul><ul><li>glucocorticoids, phenytoin, thiazides & </li></ul><ul><li>interferons </li></ul><ul><li>Intravenous pentamidine can permanently destroy pancreatic ß-cells. </li></ul>
    42. 45. Component of Comprehensive diabetes evaluation <ul><li>Medical history </li></ul><ul><li>Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding) </li></ul><ul><li>Eating patterns, physical activity habits, nutritional status, and weight history; growth and development in children and adolescents </li></ul><ul><li>Diabetes education history </li></ul><ul><li>Review of previous treatment regimens and response to therapy (A1C records) </li></ul>
    43. 46. Component of Comprehensive diabetes evaluation <ul><li>Current treatment of diabetes, including medications, meal plan, physical activity patterns, and results of glucose monitoring and patient’s use of data </li></ul><ul><li>DKA frequency, severity, and cause </li></ul><ul><li>Hypoglycemic episodes </li></ul><ul><li>Hypoglycemia awareness </li></ul><ul><li>Any severe hypoglycemia: frequency and cause </li></ul>
    44. 47. Component of Comprehensive diabetes evaluation <ul><li>History of diabetes-related complications </li></ul><ul><li>Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of foot lesions; autonomic, including sexual dysfunction and gastroparesis) </li></ul><ul><li>Macrovascular: CHD, cerebrovascular disease, PAD </li></ul><ul><li>Other: psychosocial problems*, dental disease </li></ul>
    45. 48. Component of Comprehensive diabetes evaluation <ul><li>Physical examination </li></ul><ul><li>Height, weight, BMI </li></ul><ul><li>Blood pressure determination, including orthostatic measurements when indicated </li></ul><ul><li>Fundoscopic examination* </li></ul><ul><li>Thyroid palpation </li></ul><ul><li>Skin examination (for acanthosis nigricans and insulin injection sites) </li></ul><ul><li>Comprehensive foot examination: </li></ul><ul><ul><li>Inspection </li></ul></ul><ul><ul><li>Palpation of dorsalis pedis and posterior tibial pulses </li></ul></ul><ul><ul><li>Presence/absence of patellar and Achilles reflexes </li></ul></ul><ul><ul><li>Determination of proprioception, vibration, and monofilament sensation </li></ul></ul>
    46. 49. Component of Comprehensive diabetes evaluation <ul><li>Laboratory evaluation </li></ul><ul><li>A1C, if results not available within past 2–3 months </li></ul><ul><li>If not performed/available within past year: </li></ul><ul><ul><li>Fasting lipid profile, including total, LDL- and HDL cholesterol and triglycerides </li></ul></ul><ul><ul><li>Liver function tests </li></ul></ul><ul><ul><li>Test for urine albumin excretion with spot urine albumin/creatinine ratio </li></ul></ul><ul><ul><li>Serum creatinine and calculated GFR </li></ul></ul><ul><ul><li>TSH in type 1 diabetes, dyslipidemia, or women over age 50 years </li></ul></ul>
    47. 50. Clinical Scenarios
    48. 51. CASE 1 <ul><li>36 year old Mr.R who had his blood glucose levels checked since he had a family history of diabetes </li></ul><ul><li>BMI : 31 kg/m 2 </li></ul><ul><li>His fasting plasma glucose(FPG) was 118 mg%, 2hr PPBG was 155 mg%. </li></ul><ul><li>DIAGNOSIS- </li></ul>
    49. 52. Case 2 <ul><li>20 year old gentleman was diagnosed to have diabetes on a </li></ul><ul><li>pre-employment check up. </li></ul><ul><li>He was born of non consanguineous marriage and his mother and his maternal grand father were having diabetes </li></ul><ul><li>His BMI was 21 kg/m 2 . BP =120/80mm Hg. </li></ul><ul><li>Probable Type - </li></ul>
    50. 53. Case 3 <ul><li>39 yr old Mr. Al was diagnosed to have diabetes.. </li></ul><ul><li>Polyuria and weight loss in previous 4 months. No recurrent abdominal pain/steatorrhea </li></ul><ul><li>BMI: 20 kg/m 2 . Urine ketones:negative. </li></ul><ul><li>Glycemic control for first one year achieved with OHAs. Required insulin thereafter. </li></ul><ul><li>GAD antibodies were positive </li></ul><ul><li>Type of diabetes- </li></ul>
    51. 54. Case 4 <ul><li>20 year old lady was diagnosed to have diabetes mellitus. </li></ul><ul><li>Menstrual irregularity+ </li></ul><ul><li>BMI =31 kg/m 2 </li></ul><ul><li>Proximal muscle weakness+, Purplish abdominal striae+ </li></ul><ul><li>Further work up- </li></ul>
    52. 55. Summarizing………. <ul><li>Diabetes Mellitus should be looked at as a whole with the metabolic syndrome. </li></ul><ul><li>Impaired fasting glycaemia and glucose tolerance should be given due importance </li></ul><ul><li>In the young the clinical features should be taken into account to determine the cause of diabetes. </li></ul>
    53. 56. Thank you Dr. Vivek Arya MD, DM(Endo.), SGPGI , Lucknow Asst. Prof. Smt. NHL Medical College & VS Hosp. Formerly Asst. Prof. Nizam’s Institute, Hyderabad Formerly, Chief Consultant and Head, Belhoul Apollo Hospital, DUBAI Senior Consultant Endocrinologist & SAL/Sterling/Apollo/Shalby/Nidhi Hospitals, Ahmedabad Mobile : 98795 37973 Phone : 2929 8877 enter for ndocrine disease and Diabetes
    54. 57. <ul><li>Parameters New Delhi </li></ul><ul><li>Region </li></ul><ul><li>Incidence of diabetes 33% </li></ul><ul><li>Incidence of hypertensives 48% </li></ul><ul><li>Incidence of both diabetes and hypertension 21% </li></ul><ul><li>Unaware they had diabetes 3% </li></ul><ul><li>Diabetics with no family history 31% </li></ul><ul><li>Patients with uncontrolled diabetes 62% </li></ul><ul><li>Diabetics with kidney complications 27% </li></ul><ul><li>Unaware they had hypertension 24% </li></ul><ul><li>Hypertensives with no family history 42% </li></ul><ul><li>Patients with uncontrolled hypertension 77% </li></ul><ul><li>Hypertensives with kidney complications 23% </li></ul>
    55. 58. Who Gets Diabetes? <ul><li>Diabetes is becoming more common </li></ul><ul><ul><li>Type 1 diabetes is increasing in children, particularly in under 5s </li></ul></ul><ul><ul><li>Type 2 diabetes is increasing across all groups, including young people, and particularly among black and minority groups </li></ul></ul><ul><li>Elderly </li></ul><ul><ul><li>1 in 20 over 65s </li></ul></ul><ul><ul><li>1 in 5 over 85s </li></ul></ul><ul><ul><li>7 – 25% of people in care homes </li></ul></ul><ul><ul><li>¼ of Asians over the age of 60 </li></ul></ul><ul><li>Diabetes National Service Framework: Standards – Department of Health 2001; Audit Commission – Testing Times (2000) </li></ul>
    56. 59. The Size of the Problem <ul><li>Microvascular complications - affecting the smaller blood vessels </li></ul><ul><ul><li>Eye (diabetic retinopathy), kidneys, (nephropathy) and nerves (neuropathy) </li></ul></ul><ul><li>Macrovascular complications – affecting the larger arteries </li></ul><ul><ul><li>Resulting in coronary heart disease (CHD), stroke, and peripheral vascular disease </li></ul></ul><ul><li>50% of patients already have one or more vascular complication at diagnosis to Type 2 diabetes (UKPDS, 1990) </li></ul>
    57. 60. The Concept of the Metabolic Syndrome
    58. 61. What is the metabolic syndrome ? <ul><li>&quot;Metabolic Syndrome&quot; </li></ul><ul><li>(also referred to as Syndrome X or Insulin Resistance Syndrome) </li></ul><ul><li>describes a cluster of CVD risk factors and metabolic alterations associated with excess body fat. </li></ul>
    59. 62. ATP III Operational Definition <ul><li>Occurrence of any 3 of the following abnormalities: </li></ul><ul><ul><li>Elevated fasting serum triglycerides (>150 mg/dL) </li></ul></ul><ul><ul><li>High blood pressure (>130/85) </li></ul></ul><ul><ul><li>Serum HDL Cholesterol <40 mg/dL (male) or 50 mg/dL (female) </li></ul></ul><ul><ul><li>Increased waist circumference >102 cm (male) or >88 cm (female) </li></ul></ul><ul><ul><li>Impaired fasting glucose ( > 100 mg/dL) </li></ul></ul>
    60. 63. WHO Definition <ul><li>IGT / IFG/T2DM + any of the two below </li></ul><ul><li>Increased Waist-Hip Ratio (M:>0.9, F: >0.85) </li></ul><ul><li>Elevated Blood Pressure>140/90 mm Hg </li></ul><ul><li>Elevated Triglycerides>150mg/dl </li></ul><ul><li>Low HDL cholesterol </li></ul><ul><li>Microalbuminuria </li></ul>
    61. 64. Prevalence of the Metabolic Syndrome Men 19 18 13 Men (n=279) 8 7 6 Women (n=289) IDF % ATPIII % EGIR % IDF EGIR ATPIII 14.7 2.7 22.1 11 11.9 20.2 17.4 IDF EGIR ATPIII 20.9 0 41.8 16.3 14 0 7 Women
    62. 65. BMI vs WHR in relation to CHD risk Yusuf S et al. Lancet 2005;366:1640-9
    63. 66. Klein S et al. NEJM 2004;350:2549-2557