Talk on Diabetes and its Management

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A talk (in two parts) given to Diabetes Patients, Medical Representatives and Doctors

A talk (in two parts) given to Diabetes Patients, Medical Representatives and Doctors

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  • 1. Diabetes Mellitus and its Management Talk by Dr Anshu P Gokarn MBBS, MD(Pharmacology)
  • 2. How My Talk Is Structured PART - 1 1. Symptoms of Diabetes Mellitus 2. About our body & our pancreas 3. Glucose Metabolism : Role of Insulin 4. When Insulin Does Not Do Its Job - Diabetes Mellitus 5. Why is Diabetes Mellitus a Silent Killer Dr Anshu P Gokarn 2
  • 3. How My Talk Is Structured PART - 2 1. Diagonizing Diabetes Mellitus 2. Management of Diabetes Mellitus : 1. Diet & Excersise 2. Oral Medication 3. Insulin 3. Diabetes Management Algorithm 4. Hypo & Hyper Glycemia 5. Preventing & Controling Diabetes Mellitus - What you can do ? Dr Anshu P Gokarn 3
  • 4. Most of us have a close friend or relative who is suffering from “sugar” or “diabetes”. Let us understand a little more about the disease that suddenly seems to be all around us….Dr Anshu P Gokarn 4
  • 5. Diabetes Mellitus  Affects over 300 million people globally.  India leads the world – 50 million Indians suffer from it.  Incidence increasing rapidly … specially in the developing world : India & China – due to lifestyle changes.  Affects the middle class and the rich – is a lifestyle disease – high caloric diet and lack of physical excersise.Dr Anshu P Gokarn 5
  • 6. How My Talk Is Structured PART - 1 1. Symptoms of Diabetes Mellitus 2. About our body & our pancreas 3. Glucose Metabolism : Role of Insulin 4. When Insulin Does Not Do Its Job - Diabetes Mellitus 5. Why is Diabetes Mellitus a Silent Killer Dr Anshu P Gokarn 6
  • 7. PART 1 Symptoms of Diabetes MellitusDr Anshu P Gokarn 7
  • 8. Diabetes Mellitus  Person has high blood sugar, • either because the pancreas does not produce enough insulin, • or because cells do not respond to the insulin that is produced.  High blood sugar produces classical symptoms : • Frequent urination – polyuria • Increased thirst – polydipsia • Increased hunger – polyphagiaDr Anshu P Gokarn 8
  • 9. Symptoms of Diabetes MellitusDr Anshu P Gokarn 9
  • 10. Hyperglycemia Can Cause Serious Long-Term ProblemsDr Anshu P Gokarn 10
  • 11. About our body & our pancreasDr Anshu P Gokarn 11
  • 12. Pancreas  Is a solid organ lying in the abdomen.  The head of the pancreas fits in the C-shaped C- curve of the duodenum  Pancreas is a mixed gland with • Exocrine part • Endocrine part  The endocrine part consists of groups of cells called as Islets of LangerhansDr Anshu P Gokarn 12
  • 13. Islets of Langerhans  Consist of different types of cells which secrete different hormones  -cells : secrete glucagon  -cells : secrete insulin  -cells : secrete somatostatin  F-cells : secrete pancreatic polypeptideDr Anshu P Gokarn 13
  • 14. Secretions of Islets of Langerhans  Glucagon  Increases blood glucose levels  Insulin  Decreases blood glucose levels  Somatostatin  Inhibits secretion of glucagon and insulin  Pancreatic polypeptide  Released in response to high protein dietDr Anshu P Gokarn 14
  • 15. Glucose Metabolism : Role of InsulinDr Anshu P Gokarn 15
  • 16. Normal Body : Glucose/Insulin Self CorrectionDr Anshu P Gokarn 16
  • 17. Insulin Insulin is a hormone secreted by the -cells of the islets of Langerhans of the pancreas The -cells synthesize a prehormone called Preproinsulin Preproinsulin gets processed to form Proinsulin Proinsulin splits to form Insulin and C-peptideDr Anshu P Gokarn 17
  • 18. What is C-peptide ? C- C-peptide means Connecting peptide. It is the portion of proinsulin which gets split off during formation of insulin Levels of C-peptide are measured C- to assess -cell function C-peptide levels are measured instead of insulin levels because insulin gets metabolized in the liver but C-peptide stays in circulation C- for a long time Dr Anshu P Gokarn 18
  • 19. What Are The Actions Of Insulin? Insulin exerts it’s effects on carbohydrate, fat and protein metabolism Effect on Carbohydrate metabolism • Glucose transport : uptake / entry of glucose into cells • Glycogenesis : formation of glycogen from glucose • Glycolysis : breakdown of glucose to produce energy All these actions help in removing glucose from blood and hence reduce blood glucose levels. levels.Dr Anshu P Gokarn 19
  • 20. Actions of Insulin….  Effect on Fat / Lipid metabolism • Triglyceride synthesis in adipose tissue • Fatty acid synthesis in liver • Enhances lipoprotein lipase activity  Increases entry of fatty acids and triglycerides from lipoproteins into adipose cells AdipocytesDr Anshu P Gokarn 20
  • 21. Actions of Insulin… These actions help in removal of fats from blood and help them to get deposited in adipocytes. adipocytes. Effect on Protein metabolism • Increased transport of amino acids into cells • Enhances protein synthesisDr Anshu P Gokarn 21
  • 22. How does glucose enters cells? Insulin acts on Insulin Receptors present on cell membrane Glucose Transporters [GLUTs] come to the [GLUTs] cell surface Glucose enters the cells through GLUTsDr Anshu P Gokarn 22
  • 23. INSULIN RECEPTOR GLUTDr Anshu P Gokarn 23
  • 24. What are Insulin Receptors These are the receptors present on cell membrane which bind the circulating insulin Actions of insulin are mediated by insulin receptors The number and sensitivity of insulin receptors varies with insulin levels, exercise, food and other factors If number and/or sensitivity of insulin receptors is reduced, the individual develops Insulin ResistanceDr Anshu P Gokarn 24
  • 25. When Insulin Does Not Do Its JobDr Anshu P Gokarn 25
  • 26. What is Insulin Resistance?  Insulin Resistance is the inability of insulin to act effectively on peripheral target tissues [especially muscles and liver]  Resistance to action of insulin impairs glucose utilization by peripheral cells and increases hepatic glucose output  This further signals the pancreas to release more insulin  Hence, excessive levels of insulin build up in the plasma [Hyperinsulinaemia] [Hyperinsulinaemia]Dr Anshu P Gokarn 26
  • 27. Insulin Resistance….. Insulin Resistance is a prominent feature of type 2 diabetes. Obesity contributes to insulin resistance. Insulin resistance is a part of Syndrome X. X.Dr Anshu P Gokarn 27
  • 28. Syndrome X ? Syndrome X is a condition which includes:  Insulin Resistance  Hypertension  Dyslipidaemia  Central Obesity  Endothelial dysfunction  Accelerated cardiovascular diseaseDr Anshu P Gokarn 28
  • 29. What happens due to lack of Insulin ? Lack of insulin affects:  Carbohydrate metabolism  Fat metabolism  Protein metabolism Leading to various biochemical abnormalities….Dr Anshu P Gokarn 29
  • 30. What happens due to lack of Insulin ? These biochemical abnormalities include…. Reduced entry of glucose into various peripheral tissues. tissues. Glycogenolysis [breakdown of glycogen to glucose] Increased liberation of glucose into circulation from liver Gluconeogenesis [synthesis of glucose from fatty acids and amino acids] Leading to Hyperglycaemia [excessive glucose in blood] Lipolysis. Lipolysis. Reduced entry of fatty acids and triglycerides into adipocytes Leading to Dyslipidaemia [disturbed lipid profile] Decreased in entry of amino acids into muscle. muscle. Leading to Muscle WastingDr Anshu P Gokarn 30
  • 31. More About Diabetes MellitusDr Anshu P Gokarn 31
  • 32. Diabetes Mellitus Is a clinical syndrome characterized by Hyperglycaemia due to Absolute or Relative lack of Insulin.Dr Anshu P Gokarn 32
  • 33. Recap : Signs & Symptoms of Diabetes Polyuria [increased urination] Polydipsia [increased thirst ] Polyphagia [increased hunger] Hyperglycaemia [increased blood glucose levels] Glycosuria [excretion of glucose in urine] and in uncontrolled cases - ketosis, acidosis and comaDr Anshu P Gokarn 33
  • 34. Types of Diabetes MellitusDr Anshu P Gokarn 34
  • 35. Types of Diabetes?According to the American Diabetes Association [2000]; diabetes is classified as follows:I. Type 1 diabetesII. Type 2 diabetesIII. Other specific types of diabetes a. Genetic defects of -cell function b. Genetic defects in insulin action c. Diseases of exocrine pancreas d. Endocrinopathies e. Drug- Drug- or chemical-induced chemical- f. Infections g. Uncommon forms of immune-mediated diabetes etc. immune-IV. Gestational diabetes [GDM]Dr Anshu P Gokarn 35
  • 36. What is Type 1 Diabetes? Type 1 DM is characterized by destruction of -cells, cells, usually leading to absolute insulin deficiency It is further classified as:  Type 1A : results from autoimmune -cell destruction  Type 1B : immunologic markers are not found, hence cause of - cell destruction is not known Type 1 was previously known as IDDM or Juvenile Onset of Diabetes. However, these terms are now considered obsolete because type 2 patients eventually require insulin and 5-10% of type 1 5- DM develops after 30yrs of age Dr Anshu P Gokarn 36
  • 37. What is Type 2 Diabetes?  Type 2 DM is characterized by  Variable degrees of insulin resistance  Impaired insulin secretion  Increased glucose production  Type 2 DM has a strong genetic component  Obesity, particularly central obesity, is very common in type 2 DM  Type 2 was previously called NIDDM or Maturity onset diabetes  Now obsolete as :  Type 2 patients eventually require insulin  Type 2 seen even at young age, particularly in obese adolescentsDr Anshu P Gokarn 37
  • 38. Gestational diabetes  A form of glucose intolerance that is diagnosed in some women during pregnancy.  Gestational diabetes occurs more frequently among African Americans, Hispanic/Latino Americans, and American Indians. It is also more common among obese women and women with a family history of diabetes.  During pregnancy, gestational diabetes requires treatment to normalize maternal blood glucose levels to avoid complications in the infant.  After pregnancy, 5% to 10% of women with gestational diabetes are found to have type 2 diabetes.  Women who have had gestational diabetes have a 20% to 50% chance of developing diabetes in the next 5-10 years.Dr Anshu P Gokarn 38
  • 39. LADA - Latent Autoimmune Diabetes in Adults Latent Autoimmune Diabetes in Adults (LADA) is a form of autoimmune (type 1 diabetes) which is diagnosed in individuals who are older than the usual age of onset of type 1 diabetes. Alternate terms that have been used for "LADA" include Late-onset Autoimmune Diabetes of Adulthood, "Slow Onset Type 1" diabetes, and sometimes also "Type 1.5 Often, patients with LADA are mistakenly thought to have type 2 diabetes, based on their age at the time of diagnosis. Dr Anshu P Gokarn 39
  • 40. LADA - Latent Autoimmune Diabetes in Adults About 80% of adults apparently with recently diagnosed Type 2 diabetes but with GAD auto- antibodies (i.e. LADA) progress to insulin requirement within 6 years. The potential value of identifying this group at high risk of progression to insulin dependence includes:  the avoidance of using metformin treatment  the early introduction of insulin therapy Dr Anshu P Gokarn 40
  • 41. MODY - Maturity Onset Diabetes of the Young MODY – Maturity Onset Diabetes of the Young - is a monogenic form of diabetes with an autosomal dominant mode of inheritance: ◦ Mutations in any one of several transcription factors or in the enzyme glucokinase lead to insufficient insulin release from pancreatic ß-cells, causing MODY. ◦ Different subtypes of MODY are identified based on the mutated gene. Originally, diagnosis of MODY was based on presence of non- ketotic hyperglycemia in adolescents or young adults in conjunction with a family history of diabetes. However, genetic testing has shown that MODY can occur at any age and that a family history of diabetes is not always obvious. Dr Anshu P Gokarn 41
  • 42. MODY - Maturity Onset Diabetes of the YoungDr Anshu P Gokarn 42
  • 43. MODY - Maturity Onset Diabetes of the Young Within MODY, the different subtypes can essentially be divided into 2 distinct groups: glucokinase MODY and transcription factor MODY, distinguished by characteristic phenotypic features and pattern on oral glucose tolerance testing. Glucokinase MODY requires no treatment, while transcription factor MODY (i.e. Hepatocyte nuclear factor -1alpha) requires low-dose sulfonylurea therapy and PNDM (caused by Kir6.2 mutation) requires high-dose sulfonylurea therapy.Dr Anshu P Gokarn 43
  • 44. Diabetes Mellitus - Risk FactorsDr Anshu P Gokarn 44
  • 45. Risk Factors for Type 2 DM  Family history of diabetes  Obesity, esp. central  Age > 45 years  Race / ethnicity  Previously identified IFG [impaired fasting glucose] or IGT [impaired glucose tolerance]  History of GDM or delivery of baby over 9 lbs  Hypertension [BP > 140/90 mm Hg]  HDL- HDL-c < 35mg/dL and/or TG level > 250mg/dL 35mg/dL 250mg/dLDr Anshu P Gokarn 45
  • 46. Why is Diabetes Mellitus a Silent Killer Dr Anshu P Gokarn 46
  • 47. Complications due to Diabetes?Complications in diabetes occur due to • Excessive glucose in blood • Disturbed lipid profile • Insulin resistance • Increased rate of atherosclerosis, etc.Complications of diabetes can be :a. Acuteb. Long-term Long-Dr Anshu P Gokarn 47
  • 48. Acute Complications of Diabetes a. Acute Complications 1. Diabetic ketoacidosis : • Disturbed metabolism of glucose and fats leads to formation of excessive acetyl CoA • Excess acetyl CoA gets converted to ketone bodies • Ketone bodies reduce pH of body fluids • This leads to the condition called as diabetic ketoacidosis • Signs include: dehydration, hypertension, tachycardia, hypothermia. If untreated, it leads to ketoacidotic comaDr Anshu P Gokarn 48
  • 49. Acute Complications 2. Hyperglycaemic coma:  Excessive glucose in blood disturbs brain functions  Is accompanied by dehydration and uraemia  Management includes insulin and fluid & electrolyte replacement 3. Lacticacidosis: Lacticacidosis:  Excessive lactic acid production reduces pH of body fluids  Occurs due to anaerobic glycolysisDr Anshu P Gokarn 49
  • 50. Long- Long-standing Complications of Diabetes ?These develop over a period of months to years due to slowprogressive changes occurring in the blood vessels, nerves andvarious organs of the body. body.Long-Long-standing complications include: include: a) Microvascular Complications b) Macrovascular Complications c) Diabetic Neuropathies d) Diabetic foot e) Cataract f) Other complicationsDr Anshu P Gokarn 50
  • 51. Microvascular Complications of Diabetes  These are the complications involving the small blood vessels  Excessive glucose in blood gets converted to sorbitol, sorbitol, which is toxic and damages blood vessel walls  Excess glucose also binds to proteins in blood vessel walls by glycation reaction  These complications include • Diabetic Retinopathy • Diabetic NephropathyDr Anshu P Gokarn 51
  • 52. Microvascular Complications…. Diabetic Retinopathy Diabetic Nephropathy Damage to the retinal Damage to renal blood vessels due to blood vessels due to long- long-standing diabetes long- long-standing diabetes Later on, on, nephrons get damaged tooDr Anshu P Gokarn 52
  • 53. Macrovascular Complications…. These are the complications involving larger blood vessels due to long-standing diabetes long- Occur due to • accelerated atherosclerosis • Dyslipidaemia These include increased incidence of stroke, CHD [coronary heart disease, peripheral arterial diseases etc. disease, Dr Anshu P Gokarn 53
  • 54. Macrovascular Complications…. CHD [Coronary Heart Disease] Also called as IHD [ischaemic heart disease] [ischaemic Ischaemia = lack of blood supply to a tissue damage to coronary blood vessels increases risk of heart attacks CHD includes:  Angina – pain in chest due to lack of blood supply to heart muscles  MI [myocardial infarction] – death of cardiac tissue due to lack of blood supply Dr Anshu P Gokarn 54
  • 55. Macrovascular Complications…. Stroke Peripheral Arterial Damage to cerebral Disease arteries leads to lack of  Damage to arteries of legs blood supply to brain leads to pain while walking tissue  Increasing damage can lead Resulting neurological to ischaemic necrosis of dysfunction [paralysis tissues and may even etc.] is called stroke require amputation of leg Dr Anshu P Gokarn 55
  • 56. Long standing complications…. Diabetic Neuropathy Damage to nerves occurs due to excessive glucose and other factorsIncludes:  Peripheral neuropathy – damage occurs to nerves of arms and legs leading to loss of ability to sense touch, pain, temperature etc.  Autonomic neuropathy – damage to nerves of autonomic nervous system leading to GI disturbances, urinary incontinence, impotence etc. Dr Anshu P Gokarn 56
  • 57. Long standing complications…. Hypertension Sustained elevation of blood pressure above normal limits is called as hypertension. hypertension. Hypertension may develop in diabetics due to : • Increased rate of atherosclerosis • Insulin resistance • Endothelial dysfunction • Diabetic nephropathy, etc. etc.Dr Anshu P Gokarn 57
  • 58. Long standing complications…. Diabetic Foot Cataract Ulcers develop in feet  Lens of the eye becomes These are foul smelling and opaque become infected with  Due to glycation of lens bacteria proteinsDr Anshu P Gokarn 58
  • 59. Other Complications …..  Increased incidence of infections like • UTI • Skin infections • Fungal infections  Bone metabolism disorders  Fetal abnormalities in diabetic mothers, etc.Dr Anshu P Gokarn 59
  • 60. How My Talk Is Structured PART - 2 1. Diagonizing Diabetes Mellitus 2. Management of Diabetes Mellitus : 1. Diet & Excersise 2. Oral Medication 3. Insulin 3. Diabetes Management Algorithm 4. Hypo & Hyper Glycemia 5. Preventing & Controling Diabetes Mellitus - What you can do ? Dr Anshu P Gokarn 60
  • 61. PART 2 Diagonizing Diabetes MellitusDr Anshu P Gokarn 61
  • 62. Tests For Diagnosing Diabetes Tests involving measurement of glucose levels include:  Fasting blood glucose [ FBG ]  Post Prandial Blood Glucose [ PPBG ]  Glycosylated Haemoglobin { Hb A1C } levels  Glucose Tolerance Test { in selected cases } Other tests include:  Urine analysis – for glucose, proteins, ketone bodies  Other tests for screening of complications Dr Anshu P Gokarn 62
  • 63. Fasting & Post-Prandial Blood Glucose Post- FBG [fasting blood glucose] : level of glucose in blood glucose] on empty stomach (for at least 8 hours) hours) PPBG [post-prandial blood glucose] : blood glucose post- glucose] levels at 2 hours after mealsDr Anshu P Gokarn 63
  • 64. Glycosylated Haemoglobin HbA1C Glycosylation = enzymatic reaction in which glucose binds with a protein Haemoglobin present in the RBCs consists of a pigment ‘haem’ ‘haem’ and a protein ‘globin’ ‘globin’ Glucose normally binds with the globin of the Hb leading to formation of a complex called glycosylated Hb HbAic is the specific portion [1c] of adult haemoglobin [HbA] HbA] bound with glucose Normal levels of HbA1c are <6% In diabetes, due to high levels of glucose in blood, the levels of HbA1c are raised HbA1c is a more sensitive test than plasma glucose measurement Dr Anshu P Gokarn 64
  • 65. HbA1c formation  HbA1c is the complex formed when glucose combines with [the globin of] haemoglobin GLUCOSE RBC GLYCOSYLATED HbDr Anshu P Gokarn 65
  • 66. Diabetes Diagnostic Criteria Diabetes Diagnostic Criteria 2 Hour Glucose Fasting Glucose Hba1c Condition mg/dl mg/dl % Normal <140 <110 <6.0 Pre-Diabetes Impaired Fasting <140 ≥110 And <126 6.0–6.4 Glycaemia Impaired Glucose ≥140 < 126 6.0–6.4 Tolerance Diabetes ≥200 ≥126 ≥6.5 MellitusDr Anshu P Gokarn 66
  • 67. Hba1c and Blood GlucoseDr Anshu P Gokarn 67
  • 68. Pre-diabetes: Impaired glucose tolerance and impaired fasting glucose Pre-diabetes : people at increased risk of developing diabetes. People with : • Impaired fasting glucose (IFG) - fasting blood sugar level is elevated (100 to 125 milligrams per decilitre or mg/dL) • Impaired glucose tolerance (IGT) - blood sugar level is elevated (140 to 199 mg/dL after a 2-hour oral glucose tolerance test)Dr Anshu P Gokarn 68
  • 69. Pre-diabetes People with pre-diabetes are already at increased risk for other adverse health outcomes such as heart disease and stroke. Progression to diabetes among those with pre-diabetes is not inevitable. Studies suggest that weight loss and increased physical activity among people with prediabetes prevent or delay diabetes and may return blood glucose levels to normal.Dr Anshu P Gokarn 69
  • 70. Management of Diabetes MellitusDr Anshu P Gokarn 70
  • 71. Management of DM The major components of the treatment of diabetes are: A • Diet and Exercise • Oral hypoglycaemic B therapy C • Insulin TherapyDr Anshu P Gokarn 71
  • 72. Management of Diabetes The specific aims of treatment for type 2 diabetes are:  Glycaemic control • Diet/lifestyle changes • Exercise • Medication  Treatment of associated conditions • Hyperlipidaemia • Hypertension • Obesity • CHD  Screening and management of complications • Cardiovascular disease • Nephropathy • Retinopathy • NeuropathyDr Anshu P Gokarn 72
  • 73. Management of Diabetes A • Diet and ExerciseDr Anshu P Gokarn 73
  • 74. Dietary Guidelines The following principles are recommended as dietary guidelines for people with diabetes:  Dietary fat should provide 25-35% of total intake of calories but saturated fat intake should not exceed 10% of total energy. Cholesterol consumption should be restricted and limited to 300 mg or less daily.  Protein intake can range between 10-15% total energy (0.8-1 g/kg of desirable body weight). Requirements increase for children and during pregnancy. Protein should be derived from both animal and vegetable sources.  Carbohydrates provide 50-60% of total caloric content of the diet. Carbohydrates should be complex and high in fibre.  Excessive salt intake is to be avoided. It should be particularly restricted in people with hypertension and those with nephropathy.Dr Anshu P Gokarn 74
  • 75. A. Diet & Lifestyle Management • Regulating intake of carbohydrates and fat • Reducing weight if obese • Exercise • Dietary adjuncts to reduce absorption of carbohydrates e.g. guar gum etc.Dr Anshu P Gokarn 75
  • 76. Goals of eating right : Weight control & reducing body fat Blood glucose control Prevent and manage short-term & long- term complications of diabetes Providing nutritional requirementsDr Anshu P Gokarn 76
  • 77. Slimming tips  Be realistic about your target weight  Aim to lose weight gradually  Eat regular meals  Make small changes you can stick toDr Anshu P Gokarn 77
  • 78. Exercise  Physical activity promotes weight reduction and improves insulin sensitivity, thus lowering blood glucose levels.  Together with dietary treatment, a programme of regular physical activity and exercise should be considered for each person. Such a programme must be tailored to the individual’s health status and fitness.  People should, however, be educated about the potential risk of hypoglycaemia and how to avoid it.Dr Anshu P Gokarn 78
  • 79. Foods to Avoid/Reduce intake of :1. SALT: You get enough salt from vegetables in inorganic form, so reduce the intake of extra salt.2. SUGAR: Sucrose, a table sugar, provides nothing but calories and carbohydrates. Substitute sucrose with natural sugar, like honey, jaggery (gur), etc.3. FAT: Excessive fat intake is definitely not a good habit. Try and exclude fried items from the diet But, remember, a small quantity of oil is needed to absorb fat-soluble vitamins, especially vitamin E.4. WHOLE MILK AND PRODUCTS: Try to switch to low fat milk and its products like yogurt (curd).5. WHITE FLOUR (MAIDA) AND ITS PRODUCTS: Replace these with whole grains, whole wheat (ATTA) or soya breads and unpolished rice.6. FOODS WITH A HIGH CARBOHYDRATE (SUGAR) CONTENT: Avoid white rice, potatoes, carrots, breads and banana – they increase the blood-sugar levels. Dr Anshu P Gokarn 79
  • 80. Recommended food for diabetics  Bitter gourd (karela)  This vegetable contains a high dosage of plant insulin.  It lowers the blood sugar levels effectively.  Have the juice of three to four karelas early morning on an empty stomach.  As a vegetable, too, it can be taken on a regular basis.  Powder the seeds of karela (measuring 1 teaspoon), mix with water and drink it.  Fenugreek (methi)  It is the most common food used to control diabetes.  Gulp a teaspoonful of these seeds with a glass of water daily.  Soak the seeds overnight. Have the water in which the seeds were soaked.  You can make a chutney with methi seeds. You can also eat them sprouted, dried and powdered, or mix them in wheat flour to make chapattis.Dr Anshu P Gokarn 80
  • 81. Recommended foods for diabetics  Indian blackberry (jamun)  This fruit is very effective in preventing and controlling diabetes.  Powder the stone of the fruit and eat it -- it contains glucoside, which prevents the conversion of starch into sugars.  Garlic  This is used to lower blood-sugar levels. Garlic is rich in potassium and replaces the potassium which gets lost in urine. It also contains zinc and sulphur, which are components of insulin. Take about three to four flakes of freshly crushed garlic daily.  Onion  Because of its diuretic and digestive properties, onion works against diabetes. Raw onion is more useful.Dr Anshu P Gokarn 81
  • 82. Recommended foods for diabetics  Flaxseed  This is the richest source of Omega 3 fatty acids. It helps control diabetes because it maintains the sensitivity of the cell membrane, facilitates insulin, and thereby the uptake of glucose by the cells.  Fibre  Soluble fibre, found in apples, kidney beans (rajma), oatmeal, soyabean, etc, help control diabetes.  These aid slow digestion and absorption of nutrients, resulting in a slow and steady release of glucose.  They soak up excess bile acids found in the intestinal tract, the same acids that are converted to blood cholesterol.  They also help empty the stomach and bring about a feeling of satisfaction that can help Type 2 diabetics to achieve weight loss goals.Dr Anshu P Gokarn 82
  • 83. Recommended foods for diabetics  Cinnamon solution  Water extracts of cinnamon have been found to promote glucose metabolism and reduce cholesterol. You can boil cinnamon sticks in water and drink this water.  Antioxidants  Diabetes is often associated with conditions like heart disease, diabetic retinopathy, immune deficiency and  kidney disease. Many are caused by free radical damage. Therefore, make sure you include foods containing antioxidants, like amla, fresh seasonal fruits, pomegranates and green/black tea in your diet.Dr Anshu P Gokarn 83
  • 84. Management of Diabetes • Oral hypoglycaemic B therapyDr Anshu P Gokarn 84
  • 85. B. Oral Anti-Diabetic Agents Anti- These drugs depend on endogenous supply of insulin Include various classes like: • Sulphonylureas (Insulin Secretagogues) Secretagogues) • Biguanides • -glucosidase inhibitors • Meglitinides • Thiazolidinediones Used as adjunct to dietary and lifestyle modifications Used as monotherapy or in combinationDr Anshu P Gokarn 85
  • 86. B. Oral Anti-Diabetic Monotherapy Anti-  If glycaemic control is not achieved (HbA1c > 6.5% and/or; FPG > 7.0 mmol/L or; RPG >11.0mmol/L) with lifestyle modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should be initiated.  In the presence of marked hyperglycaemia in newly diagnosed symptomatic type 2 diabetes (HbA1c > 8%, FPG > 11.1 mmol/L, or RPG > 14 mmol/L), oral anti-diabetic agents can be considered at the outset together with lifestyle modification.Dr Anshu P Gokarn 86
  • 87. B. Oral Anti-Diabetic Monotherapy Anti- First line therapy:  Obese type 2 patients, consider use of metformin, acarbose or TZD.  Non-obese type 2 patients, consider the use of metformin or insulin secretagogues  Metformin is the drug of choice in overweight/obese patients. TZDs and acarbose are acceptable alternatives in those who are intolerant to metformin.  If monotherapy fails, a combination of TZDs, acarbose and metformin is recommended. If targets are still not achieved, insulin secretagogues may be added.Dr Anshu P Gokarn 87
  • 88. B.2 Combination Oral Agents Combination oral agents is indicated in:  Newly diagnosed symptomatic patients with HbA1c >10  Patients who are not reaching targets after 3 months on monotherapyDr Anshu P Gokarn 88
  • 89. B.3 Combination Oral & Insulin  If targets have not been reached after optimal dose of combination therapy for 3 months, consider adding intermediate-acting/long- acting insulin (BIDS).  Combination of insulin+ oral anti-diabetic agents (BIDS) has been shown to improve glycaemic control in those not achieving target despite maximal combination oral anti-diabetic agents.  Combining insulin and the following oral anti-diabetic agents has been shown to be effective in people with type 2 diabetes: ◦ Biguanide (metformin) ◦ Insulin secretagogues (sulphonylureas) ◦ Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is not an approved indication) ◦ α-glucosidase inhibitor (acarbose)  Insulin dose can be increased until target FPG is achieved.Dr Anshu P Gokarn 89
  • 90. How do Sulphonyl Ureas act? SUs stimulate the -cells of the pancreas and increase the secretion of insulin In long-term, they also improve insulin-sensitivity long- insulin- Useful for management of type 2 DM especially in non- non-obese patients Main adverse effects include: risk of hypoglycaemia, weight gainDr Anshu P Gokarn 90
  • 91. Examples of Sulphonyl Ureas FIRST GENERATION SECOND GENERATION Chlorpropamide  Glibenclamide  Gliclazide Tolbutamide  Glipizide Tolazamide, Tolazamide, etc.  Glipizide extended release  Glimepiride, Glimepiride, etc.  Second generation sulphonylureas are more potent than first generation  Glibenclamide should be avoided in elderly and renally impaired  Gliclazide has beneficial antiplatelet effects Dr Anshu P Gokarn 91
  • 92. How do Biguanides act ? Biguanides have peripheral actions only. i.e.,  Reduce hepatic glucose output  Enhance action of insulin on peripheral cells  Increases glucose utilization by peripheral cells No effect on pancreas or insulin secretion e.g. Metformin .g. Main adverse effects: GI disturbances, lactoacidosisDr Anshu P Gokarn 92
  • 93. What are -Glucosidase Inhibitors? Agents which inhibit enzyme -glucosidase in the intestines and prevent absorption of carbohydrates Help in reducing the post prandial rise in glucose e.g. Acarbose, Voglibose .g. Acarbose, Used as adjunct to diet controlDr Anshu P Gokarn 93
  • 94. How do Meglitinides act? Meglitinides stimulate insulin secretion from pancreas by causing closure of ATP-sensitive K+ ATP- channels in -cells Effectiveness depends on number of -cells present e.g. Repaglinide, Nateginide .g. Repaglinide, Have a fast onset of action Should be used with caution in patients with liver dysfunctionDr Anshu P Gokarn 94
  • 95. How Do Thiazolidinediones Act? TZDs stimulate PPARs and improve insulin sensitivity Improve glycaemic control and also have beneficial effect on lipid profile They depend on presence of endogenous insulin for their action e.g. Rosiglitazone, Pioglitazone .g. Rosiglitazone, Troglitazone was withdrawn because of hepatotoxicityDr Anshu P Gokarn 95
  • 96. What Are PPARs ? PPARs = Peroxisome Proliferator Activated Receptors PPARs are a sub-family of nuclear receptors sub- Activation of PPARs stimulates the transcription of genes which are responsible for regulating glucose and fat metabolism Rosiglitazone activates PPAR- PPAR- Pioglitazone activates PPAR-  and PPAR- PPAR- PPAR-Dr Anshu P Gokarn 96
  • 97. Oral Hypoglycaemic MedicationsDr Anshu P Gokarn 97
  • 98. General Guidelines for Use of Oral Anti- Anti-Diabetic Agent in Diabetes In elderly non-obese patients, short acting insulin secretagogues can be started but long acting Sulphonylureas are to be avoided. Renal function should be monitored. Oral anti-diabetic agents are not recommended for diabetes in pregnancy Oral anti-diabetic agents are usually not the first line therapy in diabetes diagnosed during stress, such as infections. Insulin therapy is recommended for both the above Targets for control are applicable for all age groups. However, in patients with co-morbidities, targets are individualized When indicated, start with a minimal dose of oral anti-diabetic agent, while reemphasizing diet and physical activity. An appropriate duration of time (2-16 weeks depending on agents used) between increments should be given to allow achievement of steady state blood glucose control Dr Anshu P Gokarn 98
  • 99. Management of Diabetes C • Insulin therapyDr Anshu P Gokarn 99
  • 100. When is Insulin used? Exogenous Insulin is  Essential for treatment of type 1 DM  May eventually be required in type 2 DM where oral antidiabetic agents are not enough to control glucose levels  Is used during surgery in diabetics when oral drugs are withheld for sometime Dr Anshu P Gokarn 100
  • 101. Insulin Sources Sources  Bovine & Porcine – not used today  Human  Recombinant/synthetic Depending on duration of action :  Short acting  Intermediate acting  Long acting  Combination Dr Anshu P Gokarn 101
  • 102. Recombinant InsulinDr Anshu P Gokarn 102
  • 103. Where is insulin injected?Dr Anshu P Gokarn 103
  • 104. Insulin TherapyShort-term use: Acute illness, surgery, stress and emergencies Pregnancy Breast-feeding Insulin may be used as initial therapy in type 2 diabetes in marked hyperglycaemia Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma, lactic acidosis, severe hypertriglyceridaemia)Long-term use: If targets have not been reached after optimal dose of combination therapy or BIDS, consider change to multi-dose insulin therapy. When initiating this,insulin secretagogues should be stopped and insulin sensitisers e.g. Metformin or TZDs, can be continued. Dr Anshu P Gokarn 104
  • 105. Insulin regimens The majority of patients will require more than one daily injection if good glycaemic control is to be achieved. However, a once-daily injection of an intermediate acting preparation may be effectively used in some patients. Twice-daily mixtures of short- and intermediate-acting insulin is a commonly used regimen. In some cases, a mixture of short- and intermediate-acting insulin may be given in the morning. Further doses of short-acting insulin are given before lunch and the evening meal and an evening dose of intermediate-acting insulin is given at bedtime. Other regimens based on the same principles may be used. A regimen of multiple injections of short-acting insulin before the main meals, with an appropriate dose of an intermediate-acting insulin given at bedtime, may be used, particularly when strict glycaemic control is mandatory.Dr Anshu P Gokarn 105
  • 106. Overview of Insulin and ActionDr Anshu P Gokarn 106
  • 107. Dr Anshu P Gokarn 107
  • 108. Diabetes Management AlgorithmDr Anshu P Gokarn 108
  • 109. Diabetes Management AlgorithmDr Anshu P Gokarn 109
  • 110. Combination Therapy in Diabetes  Diabetes is a progressive disorder  Type 2 diabetics eventually require combinations of antidiabetic drugs for effective glycaemic control  The additional agents are added in a stepwise manner depending upon the quality of control of diabetic condition  The drugs used in Combinations have additive action and offer a better glycaemic controlDr Anshu P Gokarn 110
  • 111. Commonly Used Regimens in Diabetes  Sulphonylurea or Meglitinide + Metformin or Thiazolidinedione  Sulphonylurea + -glucosidase inhibitor  Insulin + Metformin or Thiazolidinedione  Metformin + ThiazolidinedioneDr Anshu P Gokarn 111
  • 112. Hypo & Hyper GlycemiaDr Anshu P Gokarn 112
  • 113. Hyperglycemia Hypoglycemia• When controlling diabetes, blood sugar can become too high or too low. These conditions should be taken seriously. Fortunately, one can easily re-establish control of blood sugar.• When there is too much sugar in the blood, this condition is called hyperglycemia. Hyper is Latin and means "more." Glycemia is also Latin and means "sugar in the blood."• Hyperglycemia is caused by eating too much food, eating sugary foods, or by not taking one’s medication. It can also occur when one is sick. If not treated, hyperglycemia can lead to a coma.Dr Anshu P Gokarn 113
  • 114. Hyperglycemia Hypoglycemia• Hypoglycemia occurs when too little sugar is present in the blood. Hypo is Latin and means "less."• Hypoglycemia usually occurs with patients who take insulin or other medications.• Taking too much insulin can cause it. That is why it is also known as insulin shock.• Hypoglycemia can also be caused when the food intake is reduced or a meal is skipped. . Signs of low blood sugar, or hypoglycemia .Dr Anshu P Gokarn 114
  • 115. Hyperglycemia Hypoglycemia• If not treated, low blood sugar can lead to fainting or seizures. Diabetics experience different signs when their blood sugar is low and they learn to recognize these signs.• Some patients do not experience any signs when their blood sugar is low. These patients must depend on blood sugar testing to find out if they have hypoglycemia..Dr Anshu P Gokarn 115
  • 116. Symptoms of HypoglycemiaDr Anshu P Gokarn 116
  • 117. Treatment of low blood sugar  If you sugar is 70 or lower you should treat it with….  ½ a glass of juice  ¼ glass of soft drink  2 or more glucose tablets if necessaryDr Anshu P Gokarn 117
  • 118. Symptoms of HyperglycemiaDr Anshu P Gokarn 118
  • 119. Treatment of high blood sugar If your sugar is above 240 you should do the followings: Drink lots of sugar-free fluids like water or diet drinks Eat the right food and the right amounts Check your blood sugars more often Check keytones if over 240 Call doctor or nurse if you have a positive keytones Dr Anshu P Gokarn 119
  • 120. Summing Up Preventing & Controling Diabetes Mellitus What you can do ?Dr Anshu P Gokarn 120
  • 121. B.E.A.T. DIABETES Be physical active…. Eat a healthy diet Abcs(know and control) Hb1ac, blood pressure, cholesterol, and smoking Take your medicationDr Anshu P Gokarn 121
  • 122. Getting regular medical care Schedule for routine medical care HbA1c 2-4 times/year Blood pressure At least 2 times/year Cholesterol At least every other year Dilated eye exam 1 time/year Foot exam At least 1 time/year Dental exam 2 times/year Urine microalbumin/ 1 time/year creatinine ratio Flu shot 1 time/year Pneumococcal vaccine Once (repeat at age 65)Dr Anshu P Gokarn 122
  • 123. ABC of Diabetes Care  A – A1c, or hemoglobin A1c test.  ADA goal is 7% or less.  AACE goal is 6.5% or less.  B – Blood pressure  < 130/80 mmHg for non-pregnant adults.  C – Cholesterol  HDL (good) cholesterol – >40 mg/dl (men); >50 mg/dl (women)  LDL (bad) cholesterol – <100 mg/dl  Triglycerides – <150 mg/dlDr Anshu P Gokarn 123
  • 124. Recap - Diabetes can be controlled by Healthy diet may include changing what one eats, quantities, and how often. Exercise helps diabetic patients in many ways - lowers glucose levels, helps weight loss, maintains a healthy heart and healthy circulation. In addition, exercising helps relieve stress and strengthens muscles. Blood/urine sugar testing is important in order to find out if the sugar level is where it should be. If the blood/urine sugar is too low or too high, a change in diabetes medication, diet, or exercise may be needed. Blood sugar should be checked often. In cases of very high blood sugar levels that do not respond to diet and exercise plans, medications may be needed. If insulin is needed, it can only be injected. Insulin is needed for all patients with Type 1 diabetes and for some patients with Type 2 diabetes.Dr Anshu P Gokarn 124
  • 125. Self- Self-Care Patients should be educated to practice self-care. This allows the patient to assume responsibility and control of his / her own diabetes management. Self-care should include: • Blood glucose monitoring • Body weight monitoring • Foot-care • Personal hygiene • Healthy lifestyle/diet or physical activity • Identify targets for control • Stopping smokingDr Anshu P Gokarn 125
  • 126. Avoid diabetic products  Cost  Laxative effects  Focus on ‘sugar free’  Still raise blood glucose levels  Still contain same caloriesDr Anshu P Gokarn 126
  • 127. Good News for Type 1Diabetes
  • 128. Thank You Queries ? anshu.gokarn@gmail.comDr Anshu P Gokarn 128