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UPDATE ON DIABETES AND INSULIN THERAPY BY Dr.M.SYED SULAIMAN.M.D; PHYSICIAN & DIABETOLOGIST.

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Presentation on theme: "UPDATE ON DIABETES AND INSULIN THERAPY BY Dr.M.SYED SULAIMAN.M.D; PHYSICIAN & DIABETOLOGIST."— Presentation transcript:

1 UPDATE ON DIABETES AND INSULIN THERAPY BY Dr.M.SYED SULAIMAN.M.D; PHYSICIAN & DIABETOLOGIST

2 DIABETES ENVIRONMENT IN INDIA Diabetes is no more an epidemic, it is a PANDEMIC. Diabetes related complications pose greatest risk of morbidity and mortality.

3 NoCOUNTRY2000COUNTRY2030 1INDIA31.7INDIA79.4 2CHINA20.8CHINA42.3 3U.S.A17.7U.S.A30.3 4INDONESIA8.4INDONESIA21.3 5JAPAN6.8PAKISTAN13.9 6PAKISTAN5.2BRAZIL11.3 7U.S.S.R4.6BANGLADESH11.1 8BRAZIL4.6JAPAN8.9 9ITALY4.3PHLIPPINES7.8 10BANGLADEH3.2EGYPT6.7

4 BURDEN OF DIABETES : MORBIDITY DIABETIC RETINOPATHY #1 Cause of blindness in working age adults DIABETIC NEPHROPATHY #1 Cause of ESRD DIABETIC NEUROPATHY AMPUTATIONS #1 Cause of non-traumatic amputations of lower Extremity. DIABETIC VASCULAR DISEASE 2 to 6 fold higher risk of CVD

5 DEFINITION Diabetes Mellitus is a group of metabolic diseases characterized by Hyperglycemia resulting from defects in Insulin secretion, Insulin action, or both.

6 ETIOLOGIC CLASSIFICATION OF DIABETES MELLITUS 1.Type 1 Diabetes A.Immune mediated B.Idiopathic 2.Type 2 Diabetes

7 3.Other specific types: a. Genetic defects of b-cell function b. Genetic defects in insulin action c. Disease of exocrine pancreas d. Endocrinopathies e. Drug/chemical induced f. Infection g. Uncommon immune mediated h. Other Genetic Syndromes 4.GESTATIONAL DIABETES MELLITUS(GDM)

8 IMPAIRED INSULIN SECRETION & INSULIN RESISTANCE GENES AND ENVIRONMENT IMPAIRED INSULIN SECRETION + INSULIN RESISTANCE IMPAIRED GLUCOSE TOLERANCE GENES & ENVIRONMENT IMPAIRED INSULIN SECRETION INSULIN RESISTANCE IMPAIRED GLUCOSE TOLERANCE TYPE 2 DM ETIOLOGY OF TYPE 2 DM

9 IFG -Impaired Fasting Glucose IFG -Impaired Fasting Glucose IGT -Impaired Glucose Tolerance IGT -Impaired Glucose Tolerance NORMALIFG/IGTDIABETES FPG<100100< hrPost Glucose Load <140140< DIAGNOSTIC CRITERIA OF DIABETES

10 What is pre diabetes? Abnormal blood glucose Values which is clearly Above the normal values but less than the Values diagnostic of Diabetes Abnormal blood glucose Values which is clearly Above the normal values but less than the Values diagnostic of Diabetes [IMPAIRED GLUCOSE METABOLISM] [IMPAIRED GLUCOSE METABOLISM]

11 MAJOR RISK FACTORS FOR TYPE 2 DM 1. Age>45 2. Race / Ethnicity (Asian / Asian American / Hispanics / etc) 3. Obesity (>30kg/m) 4. Family h/o Diabetes 5. Sedentary lifestyle 6. h/o GDM or delivered a baby weighing>4.5kg 7. PCOS

12 ACUTE METABOLIC COMPLICATIONS OF DIABETES MELLITUS A.) DIABETIC KETOACIDOSIS B) HYPEROSMOLAR HYPERLYCEMIC STATE C) HYPOGLEMIA

13 Diabetes Mellitus and chronic complications Diabetes is a vascular disease Diabetes is a vascular disease Affects both small and medium sized arteries (micro vascular ¯o vascular) Affects both small and medium sized arteries (micro vascular ¯o vascular)

14 Chronic complications MICRO VASCULAR Retinopathy Retinopathy Nephropathy Nephropathy Neuropathy Neuropathy Macrovascular CVD CAD PVD

15 MANAGEMENT Diet Diet Exercise Exercise Insulin Insulin Oral Antidiabetic Drugs Oral Antidiabetic Drugs DPP 4 Inhibitors DPP 4 Inhibitors Amylin Analogues Amylin Analogues

16 ORAL ANTI DIABETIC DRUGS Secretogauges Secretogauges a) Sulphonylurias a) Sulphonylurias b) Non sulphonylurias b) Non sulphonylurias Biguanides Biguanides Alpha Glucosidase Inhibitors( A G I ) Alpha Glucosidase Inhibitors( A G I ) Thiozolidinediones Thiozolidinediones DPP 4 Inhibitors DPP 4 Inhibitors Amylin Analogues Amylin Analogues Exenatide Exenatide

17 SECRETOGOUGES Sulphonyluria Groups Sulphonyluria Groups First Generation SU First Generation SU 1.Tolbutamide 1.Tolbutamide 2.Chlorpropamide 2.Chlorpropamide Second Generation SU Second Generation SU 1.Glibenclamide(Daonil,Euglucon) 1.Glibenclamide(Daonil,Euglucon) 2.Glipizide(Glynase,Dibizide) 2.Glipizide(Glynase,Dibizide) 3.Gliclazide(Diamicron,Reclide) 3.Gliclazide(Diamicron,Reclide) 4.Glimipride(Amaryl,Glipride,Glimer) 4.Glimipride(Amaryl,Glipride,Glimer)

18 SECRETOGOGUES Currently available secretogogues stimulate Insulin secretion by causing closure of ATP dependent Potassium channel in Islet β cells.

19 Meglitinides Repaglinide(Novonorm) Repaglinide(Novonorm) NON SU SECRETOGOGUES

20 INSULIN SENSITIZERS Agents from this group enhances the effect of endogenous Insulin. Agents from this group enhances the effect of endogenous Insulin. A reduction in Insulin resistance at each and every stage of diabetes will improve Glucose metabolism. A reduction in Insulin resistance at each and every stage of diabetes will improve Glucose metabolism. Biguanide(Metformin),Thiozolidinedio nes(PIO,ROSI) Biguanide(Metformin),Thiozolidinedio nes(PIO,ROSI)

21 BIGUANIDES METFORMIN(Glyciphage,Glycomet). METFORMIN(Glyciphage,Glycomet). Primary site of action:Liver. Primary site of action:Liver. Reduces hepatic glucose output. Reduces hepatic glucose output. Reduce fasting hyperglycemia. Reduce fasting hyperglycemia.

22 THIOZOLIDINEDIONES Troglitazone Troglitazone Rosiglitazone(Rezult,Enselin) Rosiglitazone(Rezult,Enselin) Pioglitazone(Pioz,Pioglit) Pioglitazone(Pioz,Pioglit) Primary site of action : Adipose Primary site of action : Adipose Cells, Skeletal muscles. Cells, Skeletal muscles.

23 AGI Acarbose(Glucobay,Acarb) Acarbose(Glucobay,Acarb) Miglitol(Misobit,Mignor) Miglitol(Misobit,Mignor) Voglibose(Volibo,Volix) Voglibose(Volibo,Volix) Blocks alpha glucosidase enzyme Blocks alpha glucosidase enzyme Targets postprandial hyperglycemia Targets postprandial hyperglycemia

24 DPP 4 Inhibitors (Dipeptidyl Pepsidase 4) Nateglinide Nateglinide Citagliptin Citagliptin Vidagliptin Vidagliptin DPP 4 Inhibits GLP 1.Thus extends Insulin action. DPP 4 Inhibits GLP 1.Thus extends Insulin action. Improves satiety,Increases β cell production,Inhibits β cell apoptosis delays gastric emptying,stimulate Insulin release Improves satiety,Increases β cell production,Inhibits β cell apoptosis delays gastric emptying,stimulate Insulin release

25 AMYLIN ANALOGUES Pramlintide Pramlintide

26 INSULIN First hormone to be First hormone to be Discovered Discovered Introduced in clinical practice Introduced in clinical practice Structurally characterized Structurally characterized Synthesized – chemically Synthesized – chemically Biosynthesized – by rDNA technology Biosynthesized – by rDNA technology

27 Insulin – Definitive Therapy for Diabetes In diabetes there is impaired insulin secretion and impaired insulin action In diabetes there is impaired insulin secretion and impaired insulin action Exogenously administered Insulin can overcome both defects Exogenously administered Insulin can overcome both defects Thus insulin is the definitive therapy for all types of diabetes Thus insulin is the definitive therapy for all types of diabetes

28 INSULIN ABSOLUTE INDICATIONS Regular Use Regular Use Type 1 Diabetes Patients Type 1 Diabetes Patients Type 2 Diabetes Patients with OHA failure Type 2 Diabetes Patients with OHA failure - Primary - Primary - Secondary - Secondary Intermittent Use Intermittent Use Type 2 diabetes patients during Type 2 diabetes patients during - major surgery - major surgery - pregnancy, labour and delivery - pregnancy, labour and delivery - myocardial infarction - myocardial infarction - acute infections - acute infections - acute metabolic crisis like hyperosmolar non - acute metabolic crisis like hyperosmolar non ketotic coma and lactic acidosis ketotic coma and lactic acidosis Gestational diabetesmellitus Gestational diabetesmellitus

29 Type 1 DM Insulin Therapy Initiating insulin therapy in uncomplicated ambulatory Type 1 patients Initiating insulin therapy in uncomplicated ambulatory Type 1 patients Initiating insulin therapy in ill patients with altered sensorium Initiating insulin therapy in ill patients with altered sensorium

30 Type 1 DM Insulin Therapy : Initiation In uncomplicated ambulatory Type 1 patients In uncomplicated ambulatory Type 1 patients Patients should preferably be admitted to hospital Patients should preferably be admitted to hospital Initiate with short-acting insulin [0.5 IU/Kg body weight per day] divided over 3 doses/day given pre-meal; subcutaneously Initiate with short-acting insulin [0.5 IU/Kg body weight per day] divided over 3 doses/day given pre-meal; subcutaneously

31 Type 1 DM Insulin Therapy : Initiation If hospital admission is not possible, close continuous monitoring of the patient is necessary If hospital admission is not possible, close continuous monitoring of the patient is necessary After adequate control is obtained with the above treatment a minimum of twice daily regimen with a short and intermediate-acting insulin may be given as per individual patient requirement After adequate control is obtained with the above treatment a minimum of twice daily regimen with a short and intermediate-acting insulin may be given as per individual patient requirement

32 ACTION PROFILE OF INSULIN TypeOnsetPeakDuration Rapid-Acting Analogues (Aspart, Lyspro) min h 4-5 h

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34 ACTION PROFILE OF INSULIN TypeOnsetPeakDuration Short-Acting (Regular) min 2-4 h 6-8 h

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36 ACTION PROFILE OF INSULIN TypeOnsetPeakDuration Intermediate- Acting(Basal) NPH 2-5 h 6-8 h h

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38 ACTION PROFILE OF INSULIN TypeOnsetPeakDuration Pre-Mixed (30/70,50/50 Regular/NPH) 30 min 2-8 h h

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40 ACTION PROFILE OF INSULIN TypeOnsetPeakDuration Long-Acting Analogue (Detemir,Glargine) 2-3 h No peak h

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42 TYPES OF INSULINS TypeFormulationpreparation Onset (hr) Max. effect (hr) Duration (hr) ShortRegular H.Actrapid Actrapid Intermediate - NPH (Neutral protamine Hagedom)/ Isophane H.Insulatard Insulatard Intermediate - Insulin Zinc Suspension/ Lente H.Monotard Lentard Biphasic Regular (30%) + NPH (70%) H.Mixtard Mixtard

43 REGIMENS Should maintain normal blood glucose levels (Normoglycemia) Should maintain normal blood glucose levels (Normoglycemia) Mimic normal physiological profile Mimic normal physiological profile Regimens vary in Type 1 and type 2 diabetes because of different pathophysiology Regimens vary in Type 1 and type 2 diabetes because of different pathophysiology

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45 INSULIN REGIMENS – Type 1 Diabetes Insulin secretion totally absent Insulin secretion totally absent Insulin administration tailored to match demand Insulin administration tailored to match demand (food intake) (food intake) Need for multiple injections Need for multiple injections Popular Regimens Popular Regimens * Basal Bolus: Ideal but difficult to implement * Basal Bolus: Ideal but difficult to implement * Split mix therapy: Popular regimen; Patients find mixing insulins difficult * Split mix therapy: Popular regimen; Patients find mixing insulins difficult Premixed Insulins: Most popular regimen world- wide and in India Premixed Insulins: Most popular regimen world- wide and in India Right mix of compliance and control Right mix of compliance and control Insulin required Insulin required i.u/kg body weight/day i.u/kg body weight/day - Regimen depends on blood glucose profiles - Regimen depends on blood glucose profiles

46 BASAL BOLUS THERAPY At least four injections/day At least four injections/day Intermediate injection at bedtime Intermediate injection at bedtime soluble insulin before breakfast, lunch and dinner soluble insulin before breakfast, lunch and dinner Regular blood monitoring must Regular blood monitoring must Requires highly motivated patient Requires highly motivated patient

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48 SPLIT MIX REGIMENS Two injections (intermediate + soluble) per day Two injections (intermediate + soluble) per day before breakfast and before bedtime before breakfast and before bedtime Proportion/dosage of insulin titrated based on blood glucose profile Proportion/dosage of insulin titrated based on blood glucose profile Mixing insulin is tedious and problematic Mixing insulin is tedious and problematic

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51 A. COMPLIANCE Defective insulin regimen Defective insulin regimen Incorrect technique of mixing and measuring Incorrect technique of mixing and measuring Inconsistent eating and exercise habits Inconsistent eating and exercise habits Omission of insulin during inter current illness Omission of insulin during inter current illness Lack of awareness about diabetes at the beginning and during the course of illness Lack of awareness about diabetes at the beginning and during the course of illness Emotional and psychological disturbance Emotional and psychological disturbance

52 B. CHANGE IN INSULIN REQUIREMENTS Inactivity Inactivity Weight gain / Loss Weight gain / Loss Pregnancy and Post delivery phase Pregnancy and Post delivery phase Change in the exercise pattern Change in the exercise pattern Change in the food habits Change in the food habits Stress period Stress period

53 PREMIXED REGIMENS – Human Mixtard Very Popular regimen Very Popular regimen Most popular World-wide & in India Most popular World-wide & in India Right balance of convenience and control Right balance of convenience and control Improves compliance Improves compliance Popular schedule is Popular schedule is 2/3rd daily dose half an hour before breakfast 2/3rd daily dose half an hour before breakfast 1/3rd daily dose half an hour before dinner 1/3rd daily dose half an hour before dinner

54 Insulin Therapy for Type 2 DM Basal Insulin Supplementation: Bedtime NPH Basal Insulin Supplementation: Bedtime NPH Suppresses basal hepatic production Suppresses basal hepatic production Reduces fasting plasma glucose Reduces fasting plasma glucose Generally used in combination with OHA Generally used in combination with OHA Helps initiate the patient on insulin therapy with Insulatard NovoLet Helps initiate the patient on insulin therapy with Insulatard NovoLet

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56 Guidelines for Initiating Insulin Alone or in combination with an OHA Alone or in combination with an OHA 0.2 units/kg body wt./day of intermediate acting insulin e.g. Insulatard NovoLet 0.2 units/kg body wt./day of intermediate acting insulin e.g. Insulatard NovoLet Increase dose by 2-4 u every 3-4 days if necessary. If requirement exceeds u, split the dose into two daily : 2/3 before breakfast, 1/3 before dinner Increase dose by 2-4 u every 3-4 days if necessary. If requirement exceeds u, split the dose into two daily : 2/3 before breakfast, 1/3 before dinner If postprandial glucose levels are high introduce short acting insulin in 30:70 or 50:50 ratio If postprandial glucose levels are high introduce short acting insulin in 30:70 or 50:50 ratio

57 Early Insulin Initiation Is therefore beneficial in: Is therefore beneficial in: Providing better control of hyperglycemia Providing better control of hyperglycemia Reversing other metabolic defects Reversing other metabolic defects Controlling inflammation which may initiate and aggravate development and progression of diabetes and diabetes-induced tissue damage Controlling inflammation which may initiate and aggravate development and progression of diabetes and diabetes-induced tissue damage Preserving beta cell function and thus helping maintain better glycemic control in the long-term Preserving beta cell function and thus helping maintain better glycemic control in the long-term Should be done when it can be useful to the patient Should be done when it can be useful to the patient

58 FACTORS AFFECTING INSULIN PHARMAKOKINETICS Injection site Injection site Exercise Exercise Depth of injection Depth of injection Insulin source Insulin source Potency Potency Insulin antibodies Insulin antibodies

59 Injection Site The absorption varies with change of area The absorption varies with change of area Rotation of site within the same area Rotation of site within the same area Short Acting - ABDOMEN - If rapid action desired Short Acting - ABDOMEN - If rapid action desired Suspensions - THIGH - for longer action Suspensions - THIGH - for longer action Random rotation of the site should be avoided Random rotation of the site should be avoided

60 Rotation of Site in a given area Blood flow Blood flow Temperature Temperature Heavy massage in the injected area Heavy massage in the injected area

61 Exercise Exercise following insulin injection increases the amount of insulin absorbed as well as the rate at which it is absorbed Exercise following insulin injection increases the amount of insulin absorbed as well as the rate at which it is absorbed Exercise increases the peripheral glucose utilisation by increasing the insulin sensitivity Exercise increases the peripheral glucose utilisation by increasing the insulin sensitivity

62 Depth of injection IM Vs SC inj Absorbed faster with IM injections Absorbed faster with IM injections IM injections are not recommended for routine use IM injections are not recommended for routine use Useful only in patients with subcutaneous insulin degradation or resistance Useful only in patients with subcutaneous insulin degradation or resistance IM injections are more painful IM injections are more painful SC is therefore ideal SC is therefore ideal Soluble [ Human Actrapid ] can be given IV during surgery and diabetic emergencies Soluble [ Human Actrapid ] can be given IV during surgery and diabetic emergencies

63 Source of insulin Human Insulin is absorbed quicker Human Insulin is absorbed quicker Bovine Insulin is the slowest Bovine Insulin is the slowest Porcine is absorbed little slower than Human Porcine is absorbed little slower than Human Auxiliary Substances Auxiliary Substances Preservative - phenol, metacresol Preservative - phenol, metacresol Retarding Agent – protamine, zinc Retarding Agent – protamine, zinc Water as solvent Water as solvent

64 Insulin Antibodies Circulating antibodies and exogenous insulin bind to form insulin antibody complex Circulating antibodies and exogenous insulin bind to form insulin antibody complex The antibody bound insulin may produce a delayed effect at an unexpected time The antibody bound insulin may produce a delayed effect at an unexpected time Resulting from Reduced absorption, Delayed clearance Resulting from Reduced absorption, Delayed clearance

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