1. 1. Why DIABETES? One of the commonest health problem Affects almost all systems of the body 5% 10% of total health care expenditure is spent on DM
2. 2. Trend of The disease Each year 7 million people develop diabetes (each 10 seconds 2 people develop DM) 2.3.8 million people die out of DM each year (one person per each 10 seconds)
3. 3. Future By 2007,246 million people were affected worldwide By 2025 380 million people are expected to have the disease
4. 4. Content Introduction -Group 1& 2 Regulation of blood glucose-Group 3 & 4 Predisposing factors of DM -Group 5 & 6 Clinical presentation-Group 7 & 8 DM and pregnancy -Group 9 & 10 Diabetes ketoacidosis-Group 11 & 12 Complications of DM-Group 13 & 14 Diagnosis-Group 15 & 16 Dietary management of DM -Group 17 & 18 Prevention of DM -Group 19 & 20
5. 5. Groups 1 & 2
6. 6. What is Diabetes mellitus ? DM is the most common metabolic disorder encountered in clinical practice. Diabetes - Greek word means a passer through a siphon. Mellitus Greek word for sweet
7. 7. Classification of DM Type 1 - Insulin dependent DM Insulin deficiency due to autoimmune mediate pancreatic islet cell destruction. Type 2 - Non insulin dependent DM Due to tissue insulin resistance. Associated with ; - increasing age - obesity - ethnicity - family history.
8. 8. Clinical differences between Type 1 and Type 11 DiabetesType 1Type 11Ketosis proneYes UncommonInsulin requirementYes- absolute insulin Often later in disease-deficiencyinsulin deficiency+_deficiency Onset of symptomsAcute Often insidiousObeseUncommonCommonAge at onset - years Usually < 30>30Family history of10% 30% diabetes Concordance in 30- 50% 90-100% monozygotic twins
9. 9. Epidemiology More than 120 million people worldwide are suffering from DM. It is estimated that it will affect 220 million by year 2020.
10. 10. Prevalence of diabetes in Sri Lanka
11. 11. Symptoms Weightloss. Polyuria increased urine excretion. Polydipsia excessive thirst and water ingestion.
12. 12. Causes Increased prevalence of DM is related to; excessive caloric intake reduced physical activity.
13. 13. Nature of the Disease Usually irreversible. Strongly linked to obesity. Patients can have a reasonably normal life style.
14. 14. Insulin Coded by chromosome 11 and synthesized in the beta cells of the pancreatic islets. About 50% of secreted insulin is extracted and degraded in the liver and kidney
15. 15. Action of Insulin Prime target organ is the liver. Is the key hormone involved in the storage and controlled release of the chemical energy available from food within body.
16. 16. Metabolic Changes Abnormal carbohydrate metabolism.(Normal blood glucose level 3.6- 6.1 mmol /l) Abnormal lipid homoeostasis.Hyperglycemia
17. 17. Complications of Diabetes Macrovascular diseases Coronary heart disease Peripheral vascular disease Amputations Microvascular diseases Retinopathy Nephropathy Neuropathy
18. 18. Prevention & Treatment Combination approach. Increased exercise Decreases need for insulin Reduce calorie intake Improves insulin sensitivity Weight reduction Improves insulin action
19. 19. Group 3/4
20. 20. Normal plasma glucose: 3.9-8.3 mM Plasma glucose is tightly regulated by hormones: Insulin: Plasma glucoseGlucagon Epinephrine Cortisol Plasma glucose Growth hormone
21. 21. Correlation Between Plasma Glucose & Insulin Levels
22. 22. Metabolism of InsulinInsulin has no plasma carrier proteins Short plasma half-life (3-5 min) ~50% of insulin is removed during thefirst pass through the liver
23. 23. Biological Effects of Insulin Major target tissues for insulin: liver, skeletal muscle, & adipose tissue. Insulin glucose uptake in muscle and adipose tissue by regulating glucose transporter (GLUT4). Glucose transporter in the liver (GLUT 2) is not regulated by insulin.
24. 24. GLUCAGONThe most important hormone in increasing plasma glucose.Glucagon is a single chain polypeptide (29 amino acids).
25. 25. REGULATION OF GLUCAGON SECRETION
26. 26. ROLE OF GLUCAGON IN GLUCOSE REGULATIONGlucagon opposes the metabolic actions of insulin.The major site of action: liver.The important metabolic effects of glucagon in the liver include:Carbohydrates: gluconeogenesis(glucose production) glycogenolysis(glycogen breakdown) glycogen synthesis
27. 27. Fat: Ketogenesis(ketoneproduction)Protein: Hepatic protein synthesis protein catabolism in the liver Glucagon DOES NOT affect muscle proteins.
28. 28. REGULATION OF BLOOD GLUCOSE BY INSULIN & GLUCAGON
29. 29. Overall:Insulin plasma glucose by promoting glucose uptake& its storage.Glucagon plasma glucose by increasingliver glucose output.
30. 30. GLUCOSE REGULATION DURING EXERCISE- ROLE OF EPINEPHRINE
31. 31. Group 5 & 6
32. 32. DietStarch White bread, sugared breakfast cereals & potatoes, which all have especially high glycemic index values & low fiber contents predispose diabetes. Potatoes ,in particular, can become dietery handgrenades for diabetics when served as French fries.
33. 33. Diet continue... Refined sugars Nothing increases blood sugar more readily than ingesting sugar. So high fructose corn syrup, candy & sweets suchas cakes are not good for diabetics at all . Saturated fats Fats do compound many risk factors for & complications from diabetes such as obesity, hardening of arteries & heart attack or stroke. Eg: butter, margarine, whole milk
34. 34. Emotional Stress Highly stressed life deeply influences the metabolism of the body. Even grief, anxiety, worry, death of any close person, etc. may alter the blood sugar level and lead to the disease. Energy mobilization is a primary result of the fight & flight response. So stress stimulates the release of various hormones like glucocorticoids which elevate blood glucose level.
35. 35. Obesity When a person is overweight, the cells in the body become less sensitive to the insulin due to the high circulating levels of leptin. There is some evidence that fat cells are more resistant to insulin than myocytes.If a person has more fat cells than muscle cells, then the insulin become less effective overall,& glucose remain circulating in the blood instead of being taken in to the cells to be used as energy.
36. 36. Sedentary Life A sedentary life style isdamaging to health & bearsresponsibility for the growingobesity problems. Inactivity & being overweightgo hand in hand towards adiagnosis of type 2 diabetes. Muscle cells have more insulinreceptors than fat cells, so aperson can decrease insulinresistance by exercising.
37. 37. Smoking smoking 16 to 25 cigarettes a day increases your risk for Type 2 diabetes to three times that of a non-smoker.. Increases complications esp. Retinopathy, Cardiovascular conditionsThere is also evidences thatlinks cigarette smoking withmicrovascular diseases indiabetes.Smoking can cause chronicpancreatitis which leads todiabetes.
38. 38. Ethnicity Incidence high in African, Americans, Asians, American Indians, Hispanic, Caucasians, Latinos, Mexican-American, EuropeansAge It has been observed that as one grows older, particularly above 45 years of age, in them the chances to develop diabetes are increased.It is chiefly because due to old age, the person becomes less active, tends to gain weight, leading to pancreatic dysfunction.
39. 39. Genetic Predisposition People who belong to family background having history of diabetes are 25% more prone to develop diabetes. The concordance of type 1 DM in identical twins ranges between 30% and 70%The major susceptibility gene for type 1DM is located in the HLA region onchromosome 6 The concordance of type 2 DM in identical twins is between 70% and 90% if both parents have type 2 DM, the risk approaches 40%
40. 40. Gestational DiabetesHuman placental Peripheral tissuesLactogenInsulin resistanceEstrogen PancreasProgesterone Increased Fat stores Prolactin Changes in insulin receptormost women revert to normal glucose tolerance post-partum, but have a substantial risk (30 60%) of developing diabetes mellitus later in life.
41. 41. Infections Mumps, Coxsackie B, Cytomegalovirus, Kilham rat virus and rubella infections can damage the pancreas. Coxsackie virus is the commonest viral cause Some viruses can trigger or maintain autoimmune beta cell damage.
42. 42. Barker and Hales hypothesis Evidence, mainly from animals, suggests that maternal and therefore fetal malnutrition during a critical early phase of fetal development can reduce Beta-cell mass and permanently impair insulin secretory reserve.
43. 43. Other factors Endocrine Acromegaly 25% Cushings Disease 30% Glucagonoma 90% Drugs that decrease insulin sensitivity Glucocorticoids Beta-2 receptor antagonists OCP
44. 44. Groups 7 & 8
45. 45. The history of diabetic symptomsis of the greatest importance and an accurateappreciation of their severity far exceeds anestimation of the blood sugar as a means ofassessing the need for treatment.(John Malins, Clinical Diabetes Mellitus, Eyre & Spottiswoode, 1968)
46. 46. Clinical presentationAcuteSub acuteSymptoms Symptoms Acute & Sub acute presentations often overlap.But, Asymptomatic diabetes can occur.
47. 47. Acute presentationYoung people often present with a 2-3 weeks history and report the classical triad of symptoms.ThirstPolyuria1.Thirst2.Polyuria3.Weight lossIf not Ketonuria treated Ketoacidosis
48. 48. Sub acute presentation Clinical onsetover several months, years In older patients Classical triad of symptoms are typically present.But complain of, visual blurring pruritus vulvae (female) balanitis (male) lack of energy dry mouth dysphagia
49. 49. balanitis Visual blurring Pruritus vulvae
50. 50. Other symptoms Somnolence (the tendency to fall asleep) Myopia Nausea, headache Tiredness, fatigue Malaise Hyperphagia - predilection for sweet foods
51. 51. Complications Macrovascular Microvasculardiseasesdiseases Cardiovascular diseases NehpropathyEg: Coronary arterydiseases NeuropathyStroke Retinopathy Foot infections Erectile dysfunctions gangrene
52. 52. Asymptomatic diabetes No symptoms or ill health. Accidently detected ;as glycosuria or hyperglycemia on routine investigations (for other purposes). Both are not diagnostic of diabetes but indicates a high risk of developing diabetes.
53. 53. Diabetes and pregnancy Group 9 and 10
54. 54. 1. Already diagnosed diabetes mellituswoman getting pregnant Preexistingdiabetes.2. A woman who hasnt been diagnoseddiabetes, exhibit high blood glucoselevels during pregnancy Gestationaldiabetes
55. 55. Gestational diabetes Gestational diabetes is defined as Any degree of glucose intolerance with onset or first recognition during pregnancy" Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy..
56. 56. Gestational diabetes DuringHuman placental lactogen pregnancy level & Cortisol level increase Both are insulin antagonists. Cortisol gluconeogenesisglucose utilizationBlood glucose HPLinsulin sensitivityglucose utilization
57. 57. Risk factors ObesityBMI > 30 Family history of diabetes Previous babies having high birth weight ( >4.5kg ) Previous still birth Previous babies with congenital abnormalities
58. 58. Maternal complications Pre-eclampsia (pregnancy induce hypertension ) Antepartum hemorrhage due to placental abbruption Microvascular Nephropathy Retinopathy Neuropathy Macrovascular Coronary artery disease Hyperglycaemia / hypoglycaemia / ketoacidosis Infection Thrombo embolic disease
59. 59. Fetal & neonatal complications Increase risk of miscarriage & congenital fetal abnormalities Neural tube defects, congenital heart diseases & spinal anomalies Sacral agenesis (caudal regression syndrome) Fetal macrosomia Late still birth Respiratory distress syndrome Hypoglycaemia Polycythaemia Hyperbilirubinaemia Hypomagnesemia Macrosomia
60. 60. Diagnosis of maternal diabetes Glucose challenge test (>140mg/dl) Oral glucose tolerance test. Random blood sugar. Normal fasting glucose -7mmol/l
61. 61. Management Diabetic women are advised to maintain the blood sugar level close to normal range for 2 to 3 months in advance, before planning for pregnancy. Antenatal care Frequent review Increase insulin dose Vigorous treatment for infection Regular urine analysis to detect nephropathyAt term, Should not be allowed to continue beyond 38 weeks. Caesarean section if needed. Delivery before 36 weeks Dexamethasone. Monitor the blood glucose & urine ketone body regularly
62. 62. Newborn, Anticipate & treat asphyxia Cross monitoring blood glucose level for the first 72h Early breast feeding Look for congenital malformation. Random blood sugar and give dextrose if necessary. On descharge Check the fasting blood sugar Complete family early & follow family planning method.
63. 63. References Obstetrics by Ten Teachers
64. 64. DIABETIC KETOACIDOSIS GROUP 11 & 12 07/08 BATCH
65. 65. Introduction Major medical emergency Principally with type 1 diabetes High blood sugar with ketones in urine and blood Body cant use glucose due to insulin shortage
66. 66. Main cause Type 1 diabetesUsually occurs in following circumstances Undiagnosed diabetes Interruption to insulin therapy Stress due to any illness (Also occurs in type 2 diabetes)
67. 67. Mechanism of Diabetes Ketoacidosis In adipose cells insulin inhibit the action of intracellular enzyme Hormone-sensitive lipase
68. 68. Development of Signs and Symptoms Diabetic ketoacidosis appears to require Insulin deficiency coupled with a relative or absolute increase in glucagon concentration Increased glucagon induces maximal gluconeogenesis and also impairs peripheral utilization of glucose resulting in severe hyperglycemia
69. 69. This induces osmotic diuresis that leads to volume depletion and dehydration that characterize the ketoacidotic state. Glucagon activates the ketogenic process and thus metabolic acidosis.
70. 70. Symptoms & signs Nausea Vomiting Excessive thirst Frequent urination Weakness Ketone / Fruity smelly breaths Hyperventilation Confusion Dry skin Abdominal pain
71. 71. Diagnosis Ketonuria or ketonemia is demonstrated Dipstick method for hyperglycemia Centrifugation blood for ketonemia ? Arterial blood gas analysis
72. 72. Investigations Urea & Electrolytes, Blood glucose, Plasma bicarbonate Arterial blood gases to assess the severity of acidosis Urinalysis for ketones ECG
73. 73. TreatmentReplace lost fluid & electrolytes suppressing high blood sugar & ketone production with insulin Fluid replacement Insulin therapy Potassium NaHCO3 .?
74. 74. Prevention Manage diabetes yourself Monitoring blood sugar levels Adjust insulin dose as needed Check urine for ketone levels Be prepared to act quickly
75. 75. References Kumar & Clark;Clinical Medicine Davidson;Clinical medicine Harpers illustrated biochemistry
76. 76. Groups 13-14
77. 77. Have a considerably reduced life expectancy 70%- due to cardio vascular diseases Followed by 10% -renal failure Pathophysiology Non enzymatic glycosylation of protains Polyoyl pathway Abnormal microvasculr pathway Other factors Haemodynamic changes
78. 78. Complications1.MacrovascularHypertensionSmoking Lipid abnormalities2.Microvascular Daibetic eye disese Diabetic kidney Diabetic neuropathyThe diabetic footInfectionsSkin & Joints
79. 79. Diabetic Retinopathy Impairment of loss of vision Due to damage to blood vessels of retina Cause of long standing diabetes Cataract Glucoma
80. 80. Diabetic nephropathy Important cause of morbidity mortality Among the most common causes of the end stage renal failure Management is frequently different & benefits of prevention are substantial
81. 81. Diabetic neuropathy Usually causing weakness & numbness Symptoms are depended on nerves which damage Most commonly affects legs
82. 82. Complications on foot Main cause of the AMPUTATION is diabetes mellitus Why it will end up with amputation ???? Diabetes. 1) Narrow & hardening the blood vesselsPoor circulationLess ability to fight with infections & healing also slow Foot ulcer Gangrene
83. 83. 2) Damage the nervesLoss of sensation (peripheral neuropathy)Injuries cannot be noticedSusceptible for infections 3) Damage to the nerves controlling oil & moistureSkin drynessEasy to getting cracksSusceptible for infections
84. 84. 4) Affects joints Making them stifferCharcots joints
85. 85. Effects of diabetes to blood vessels Diabetesmellitus Part of plaque GlucoseTravel through circulationCholesterol Breakage ofplaqueLodge in a vessel Deposit in damaged of brain (STROKE) vesselsLoss of blood supply to Atheroma ( in damaged inner layer)part of brain atherosclerosis Diameter of blood vessels Blood flow
86. 86. Effect of diabetes to heartDiabetes mellitus AtherosclerosisBlood glucoseIn peripheralBlockage ofvesselscoronary vesselsblood flow blood supply Cardiac muscletopart of failure heartHeart has to pump (cardiomyopathy) more forcefully Ischemic heartdiseasehypertensionHeartattack
87. 87. GROUP 15-16 DIAGNOSIS of
88. 88. DIAGNOSIS OF DIABETES If patient complains of symptoms suggesting diabetes Test urine for GLUCOSE & KETONES Random Blood Glucose (normal 7.0mmol/l, 126mg/dL-DIABETES if (6.1 180mg/dL
89. 91. DIPSTICK METHOD A plastic strip coated with reagents Reagent strip measure glucose level using glucose oxidase method. GLUCOSE OXIDASE GLUCOSEH2O2 (Change the color of theindicator)
90. 92. BLOOD TESTS
91. 93. Random blood glucose level Measure the blood glucose level other than post prandial stage or fasting. If it is above 11.1mmol (200mg/dl) considered as diabetes. GLUCOMETER For rapid diagnosis of blood glucose levels (capillary blood )
92. 94. Fasting Plasma Glucose After 12hr fasting measure the blood glucose level in venous blood. 4 mmol/L 6.1 7.080 mg/dL mmol/Lmmol/L 110 126 mg/dL mg/dL Hypoglycemi Normal Impaired (Hyperglycemic)cFastingDiabetes Glucose
93. 95. OGTT (Oral Glucose Tolerance Test) Unrestricted carbohydrate diet for 3 days before test 8 Hour overnight fasting is required. 75g of glucose in 300ml of water is given orally within 5minutes. Measure plasma glucose BEFORE and 2 hours AFTERthe glucose load. Time Non Diabetic DiabeticImpaired Glucose _ Tolerance Fasting(07.0mmol/l 6.1-7.0mmol/l min) (110mg/dl)(126mg/dl) (110-126mg/dl) 120min 11.1mmol/l>7.8-11.1mmol/l(140mg/dl)(200mg/l)(140-200mg/dl)
94. 96. HbA1C Measure the glycated hemoglobin proportion which indicates the glycaemic condition Glycosylation of hemoglobin [glucose] This can reflect the glycaemic control of the patient over 2 to 3 months For every 1% increase of theHbA1c indicate 35mg/dl incease of blood glucose levels. 4.5% 6.5 % Reference range HbA1c > 8% Poor control
95. 97. HbA1 Mean plasma glucose c % mg/dl 6 135 7 170 8 205 9 240 10275 11310 12345
96. 98. Fructosamine Test Fructosamine = glycosylated plasma proteins,mainly albumin Indicate previous 2-3 week glyceamic control Impaired in patients with anemia , hemoglobinopathies & pregnancy.
97. 99. DIAGNOSIS OF COMPLICATIONS OF DIABETES Diagnosis of Diabetic Neuropathy Lower limbs Peripheral pulses Tendon reflexes Perception of vibration sensation, light touch and proprioceptionFeet Callus skin indicating pressure areas Nails Need for podiatry Ulceration DeformityDiabetic Nephropathy
98. 100. Diagnosis of Diabetic Nephropathy Microalbuminuria test In normal peopleAlbumin excretion =30mg/day In kidney damage > 300mg/day In diabetic nephropathy ;Albumin excretion =30-300mg/daymicroalbuminuria
99. 101. Diagnosis of Diabetic RetinopathyEye examination Visual acuities (near and distance) Ophthalmoscopy (with pupils dilated) Digital photography
100. 102. Group 17 & 18
101. 103. Diet is an essential part ofthe management of diabetes Diet is based on healthy eating principles
102. 104. Reasons for diet Weight controlBlood glucose controlPrevention and management of short-term and long-term complications of diabetes
103. 105. Basic Principles of Diabetic DietEnsure regular meals Base meals on starchy carbohydrates Aim for more fruit and vegetables Cut down on sugar and sugary foods If in doubt read food label Encourage relatives to bring low sugar foodsReduce salt
104. 106. Eat starchy foods regularly Bread Potatoes Rice Cereals Plantain CHO to form 45-60% of total energy [cereals,vegetables,legumes]better use foods which has low glycaemic index
105. 107. Eat fruit and vegetables Fresh Frozen Tinned Dried Juice Encourage food rich in antioxidants - vitamins
106. 108. Reduce protein intake Restriction of protein intake to 0.6 -0.8 g/ kg/ day Replace red meat with chicken ,fish or vegetable protein To contribute 10-20% of total energy
107. 109. Aim for low sugar diet Not a sugar free diet Instead of sweet cakes/ biscuits offerfruit loaf, plain biscuits, teacakesCut down on sugar andsugary foods: Use low sugar foods Use drinks labeled diet, low calorie orsugar- free Choose diet or light yoghurts instead oflow-fat or whole yoghurts Use sugar free/ low sugar - jelly, custard, rice pudding as dessert ideas
108. 110. Nutrition Claims Sugar No added Sugar No sugar from any source added Low Sugar No more than 5gssugar/100gs Reduced Sugar 25% less sugar than regular productFREE SUGER do not exceed 50g per day
109. 111. Choose more high fibre foods To help maintain blood glucose levels and cholesterol levelsHelps to maintain a Fruit healthy gut Vegetables Pulses Wholegrain cereals Oats Wholemeal bread Brown rice FIBERS 40g per day or morehalf of fiber should be soluble
110. 112. Reduce animal or saturated fat intake Use low fat milk Use low fat spread instead of butter Use oil high in unsaturated fat, eg olive oil, rapeseed oil
111. 113. Use less fat in cooking Dry-roast Microwave Steam FAT - should not exceed 30 % of total energy restrict cholesterol to 300mg or less per day
112. 114. Choose the right sort of fatSATURATEDMONO- POLY-UNSATURATED UNSATURATED Full fat dairyproduce (eg Olive oil Sunflower oilcheese, butter,(products) Rapeseed oilfull cream milk) Oily fish Groundnut oil Biscuits Savoury snacks Lard Hard vegetablefat
113. 115. Nutrition Claims Fat Low Fat - . 3g Fat/ 100g or 100mls Less than 5% Fat - . 5g fat/ 100g Reduced Fat 25% less fat than similar products
114. 116. Reduce salt intake Cut down on added salt Use alternatives Look out for reduced/low sodium foods, eg bread Avoid salt substitutes SODIUM restrict to 6g per day
115. 117. Alcohol Alcohol in moderation can be included, no more than: 1-2 units/ day for women 2-3 units/ day for men Never give alcohol on an empty stomach Remember to use diet mixersCaution with sweet liqueurs
116. 118. Special diabetic foods Not recommended May contain more fat or energy than other foods May be low in fibers Has sorbitol may cause diarrhoea Excessive fructose may be used - Fruit sugar (fructose) when used excessively as asweetener will still affect blood sugarsin the same way as normal sugar!!
117. 119. If Residents Overweight Weight loss is desirable via exercising Encourage to cut down on fatty foodse.g. chips, pastry, crisps, biscuits, cheese and fried foods Encourage low-fat food options e.g. semi-skimmed milk, low-fat spread Offer fruit/ low fat yoghurt as a dessert Snacks not essential
118. 120. If residents malnourished Encourage small frequent meals and low sugar puddings and snacks: Glass of milk/ milky drinks Crackers and cheese Toast, butter and reduced sugar jam Breakfast cereals, nuts low fat yoghurt or low sugar milk pudding Plain biscuits, fruit cake, kurakkan bread,
119. 121. Recommended food meals for a diabetic patient Breakfast chickpea 1 cup or green gram 1 cup orbread two slices with polsambol 1 tsp.Lunch Rice two cups , Vegetables 6 tablespoons , green leaves cup, fish or chicken 1 piece, fruit 1 servingDinner Rice 1 cup, vegetable 3 tablespoons, Dhal3 tablespoons, Fruit 1 serving
120. 122. Key Points Ensure regular meals Base meals on starchy carbohydrates Aim for more fruit and vegetables Cut down on sugar and sugary foods If in doubt read food label Encourage relatives to bring low sugar foods
121. 123. Group 19-20
122. 124. CANNOT CURE. But can prevent. Kathmandu declaration- life cycle approach for prevention & care of DM. o Primary prevention o Secondary prevention
123. 125. THANK YOU!