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An Emerging Disaster DIABETES MELLITUS. Session Objectives Identify the prevalence of diabetes mellitus (DM) in the Saudi community. Discuss the classification.

Mar 31, 2015

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Jazmin Darley
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An Emerging Disaster DIABETES MELLITUS Slide 2 Session Objectives Identify the prevalence of diabetes mellitus (DM) in the Saudi community. Discuss the classification of DM. Discuss the diagnostic criteria for DM. Identify the patho-physiological changes in a diabetic patient. Enumerate and discuss the importance presenting signs & symptoms of DM. Slide 3 Session Objectives (cont...) Investigate appropriately a patient with DM. Advice initial management plan for a patient diagnosed first with DM. Discuss different medication used in DM management. Identify importance of life style changes in diabetic patients. Discuss screening criteria for DM. Slide 4 Genetic predisposition IGT Insulin Resistance (Hyperinsulinemia) Cell Defect Usually 50% of cells are functioning at time of diagnosis Type 2 Diabetes Slide 5 Prevalence of DM in Saudi Arabia A community based study of 17232 subjects conducted between 1995 and 2000 in KSA. The examining age group, 30-70 years of selected households during 5-year period Mansour M. Al-Nozha et al,The prevalence of CAD among Saudis of both sexes, in rural as well as urban communities, as well as modifiable risk factors for CAD. Saudi Medical Journal 2004; Vol. 25 (9): 1165-1171 Slide 6 Prevalence of DM in Saudi Arabia The overall prevalence of DM obtained from this study is 23.7% in KSA. The prevalence in males and females were 26.2% and 21.5% respectively (p 7 % Acarbose PP Hyperg 50-100 mg TDS Acarbose PP Hyperg 50-100 mg TDS Flatulence Diarrhoea Acarbose NB : PP hyper post pyramidal hyperglycemia Slide 19 : 1- Metformin Effective & well validated therapy Choice as initial therapy Acts by reducing hepatic glucose production Other Reduces appetite & may delay absorption Improves peripheral insulin sensitivity No hypoglycemia and mild weight loss Start with 500 mg once or twice per day with meals and increase every few days till reach maximum dose of 2 gm per day. Slide 20 Oral Medication in Type 2 DM 4- Thiozolidinediones: PIOGLITAZONE (15mg) Reduce insulin resistance Promotes glucose uptake by skeletal muscles and adipose tissue Inhibits hepatic gluconeogenesis Used in combination with metformin and sulphonylurea Periodic monitoring of liver enzymes Not given in patients with heart failure Recently, Debate about increase incidence of Cancer bladder ?? Slide 21 INCRETINS - Slide 22 Glucose in Intestine DPP-4 Plasma Mixed Meal Active Incretins Stimulate B cells (Pancreas) to secrete Insulin Inactive Incretin Renal Clearance Slide 23 Physiological effects of GLP-1 Bunck MC, et al. Diabetologia. 2010;53 (Suppl 1):S338. Slide 24 Glucagon-like Peptide-1 (GLP-1) GLP-1 is secreted throughout the day by intestinal mucosa in response to oral glucose in the gut. GLP-1 causes anabolic actions on the synthesis of insulin in beta cells by stimulating all steps of insulin biosynthesis. GLP-1 provides continued and augmented release of insulin for secretion in response to glucose without overproduction that could lead to hypoglycemia. GLP-1 also acts on islet alpha cells, causing strong inhibition of postprandial glucagon secretion. GLP-1 slows gastric emptying and acts on brain to promote early satiety with reduced food intake Slide 25 Dipeptidyl Peptidase-4 (DPP-4) Within minutes of secretion or exogenous administration, GLP-1 is rapidly degraded by dipeptidyl peptidase-4 (DPP-4). DPP-4 is found in many body tissues, including liver, renal, and intestinal brush- border membranes; lymphocytes; and endothelial cells. Slide 26 INCRETINS The incretin system is impaired in patients with T2DM, which, as a consequence of its insulinotropic actions, contributes to fasting and postprandial hyperglycemia. The impairment of GLP-1 secretion varies directly with the degree of insulin resistance; those who are more insulin resistant have a lower rise in GLP-1 in response to a meal. Slide 27 Medication: Exenatide: GLP-1 receptor agonist, SC, twice-daily Liraglutide: GLP-1 analog, SC, once daily Sitagliptin (Januvia), (DPP-4) inhibitor, 100 mg OD Other DPP-4 inhibitors, Vildagliptin, Saxagliptin, Type 2 diabetes only Monotherapy or with Metformin or TZD Weight neutral Does not cause hypoglycemia Slide 28 Which antidiabetic Drugs are contraindicated or should be only very cautiously when the following Co-Morbidity is present? Chronic Kidney Failure: Metformin, Acarbose, Sitagliptin, Insulin & SUs (reduced dosage) Heart Failure: TZDs Osteoporosis: TZDs Myocardial Infarction: Hypoglycemias should be avoided when Insulin or SUs are taken. Elderly people (>70 years): Hypoglycemias should be avoided when Insulin or SUs are taken. Slide 29 Indication of Insulin in Type 2 DM If HbA1c is 9 % After maximum metformin and suphonylurea, you should consider adding Insulin and taper the Sulphonylurea. Slide 30 Strategies for Antidiabetic Treatment Oral Triple Combination Therapy plus Basal Insulin or plus GLP-1 Oral Monotherapy Oral Dual Combination Therapy Oral Triple Combination Therapy NPH, Glargine, Levemir Metformin + Sulfonylureas + TZDs Metformin + Sulfonylureas+DPP-4- Inhib. Metformin DPP-4 Inhibitors Glinides TZDs Sulfonylureas -Glucosidase-Inhibitors Metformin + DPP-4-Inhibitors Sulfonylureas + DPP-4-Inhibitors Metformin + Sulfonylureas Sulfonylureas + TZDs Metformin + TZDs Exenatide, Liraglutide Slide 31 Initiation of Insulin Therapy in DM2 Complete Replacement Keep Metformin + Basal + Bolus insulin Add on Basal insulin at bed time + oral medication Types of Insulin Basal insulin (NPH, Glargine ( Lantus ), Levimir) Premixed insulin (70/30, 75/25, 60/40, 50/50) Prandial insulin (bolus) Regular, Lispro, Aspart, NovoRapid SMBG Slide 32 Initiation and Adjustment of Insulin A1C 9% Long acting insulin (Basal) at bedtime 10 U or 0.2 U/Kg Check FG daily, increase by 2 4 U every 3 days until FG 70 130 mg/dl (3.9 7.2 mmol/L) if FBS > 250 mg/dl by 4-8 U. If hypoglycaemia occurs, or FG < 3.9 reduce bedtime by 4 units or 10 % which is greater If FG in range check before lunch, dinner and bedtime, add second injection. Begin with 4 -6 U of Bolus insulin before each. Adjust by 2-4 U every 3 days. Pre-bed is high add bolus insulin at dinner Pre-dinner is high add NPH at breakfast or bolus insulin at lunch Pre-lunch is high, add bolus insulin at breakfast Slide 33 Novorapid : do not cause hypoglycemia Slide 34 0600 0800 1800 12002400 0600 Time of day 20 4040 60 80 100 BLD Basal-Bolus Insulin Treatment With Insulin Analogues B=breakfast; L=lunch; D=dinner Glargine Lispro, or Aspart Normal pattern U/mL Slide 35 Glargine / Lispro Avoids fasting hyperinsulinaemia and hypoglycemia Can mimic pancreatic - cell insulin secretion 36% had hypoglycemia vs 50% on NPH. Glargine 50% and Lispro 50% Slide 36 Hypoglycemia Treatment Check BG if possible. IfSlide 37 Antiplatelet agents Consider Aspirin therapy (75162 mg/day) as a primary prevention strategy in those with type 1 or type 2 diabetes at increased cardiovascular risk (10-year risk 10%). This includes most men 50 years of age or women 60 years of age who have at least one additional major risk factor (family history of CVD, hypertension, smoking, dyslipidemia, or albuminuria). Slide 38 Statins and Diabetes Statin therapy should be added to lifestyle therapy, regardless of baseline lipid levels, for diabetic patients: with CVD. (A) without CVD who are over the age of 40 years and have one or more other CVD risk factors. (A) Slide 39 Statins and Diabetes Low risk patients (without CVD and age of < 40) Statin therapy should be considered in addition to lifestyle therapy: if LDL cholesterol remains above 100 mg/dl or with multiple CVD risk factors. Slide 40 Hypertension and Diabetes Goal: < 130 / 80 Choice of Medication: ACE inhibitors Angiotensin Receptor Blockers (ARP) Slide 41 Influenza vaccine (yearly) Pneumococcal vaccine (once in lifetime) Vaccination Slide 42 Targets in DM Bp < 130 / 80 (ACEi / ARB, if not achieved add Thiazide) HbA1C 7 % (European Diab. Soc. 6.5 %) LDL-C < 100 mg/dl (2.6 mmol/L) HDL-C > 40 mg/dl (males) > 50 mg/dl (females) Trig. < 150 mg/dl (1.7 mmol/L) Slide 43 Slide 44 Slide 45 UKPDS Aim: To determine whether intensified blood glucose control with either sulfonylurea or insulin reduces the risk of Macrovascular or Microvascular complications in type 2 diabet. Slide 46 UKPDS Results 1997 % decreaseP Conventiona l rate Intensive rateCause 120.0294640.9 Any Diabetes related 160.05217.414.7 MI -0.5255.6 Stroke -0.151.61.1 PVD 250.002911.48.6 Microvascular L ancet 1998;352:837-853 Slide 47 UKPDS Results 2007 Sulfonylurea / Insulin Intensive Bp lowering 2007 P 2007 RRR %1997 P 1997 RRR %End Point 0.001240.009925Microvascular Disease 0.014150.05216Myocardial infarction 0.007130.446All Cause Mortality 2007 P 2007 RRR %1997 P 1997 RRR %End point 0.20160.009237Microvascular Disease 0.18110.1321Myocardial infarction 0.18110.1718All Cause Mortality Slide 48 May 27, 2009 A new meta-analysis suggests that intensively controlling blood glucose levels (HbA 1c ) to < 7.0%, significantly reduces the risk of (MI) and (CHD) events and has no effect on all-cause mortality and Stroke. The findings include UKPDS, ADVANCE, VADT, ACCORD, and PROACTIVE studies. The concerns stemmed particularly from the (ACCORD) and (ADVANCE) and (VADT) which showed no significant response on Macrovascular outcomes. ACCORD, on the other hand, was stopped early because of an increased risk of death in patients who underwent intensive blood glucose lowering. Slide 49 PHYSICAL EXAMINATION Height and Weight (BMI) Blood Pressure (2 readings) Fundus Examination ( Hard and soft exudates, new vessel formation, macular oedema . ) Cardiac examination Lower Limbs: Skin Examination Evaluation of pulses Foot Examination Neurologic Examination Slide 50 LABORATORY EVALUATION FPG and 2 hr PP Midstream Urine (for Ketones, protein, pus cells,) Urea and Creatinine Lipid Profile (total cholesterol, LDLc, HDLc and triglycerides) HbA1C ( every 3 m for insulin / every 6 m for controlled ) Test for Microalbuminuria or Albumin to creatinine ratio / 24 hr urine collection for protein / Creatinine Clearance ECG Chest X-Ray Slide 51 Yearly Check Up: Investigations HbA1C Urea and Creatinine Lipid Profile ( Cholesterol, Triglyceride, LDL-C and HDL-C ) Albumin to creatinine ratio / 24 hour urine collection for protein Check : Eye: Fundus Examination / eye referral Feet : Visual inspection and Neurovascular status Slide 52 TREATMENT REGIMENS OF TYPE 1 DM Conventional Insulin Therapy Two injections of NPH and Regular Insulin Mixed Insulin Two injections of 70/30 or 60/40 or 50/50 Multiple Insulin Injections 1 or 2 injections of NPH plus 3 injections of Regular or Lispro Insulin. One injection of Glargine or Detemir plus 3 injections of Regular or Lispro Insulin. Slide 53 INSULIN GLARGINE (LANTUS) The first clear long-acting insulin Acidic (pH of 4) when injected it is neutralized by the body, causing Glargine crystals to be precipitated and slowly absorbed. It is taken once a day Being acidic, cannot be mixed with other insulin Slide 54 Initiation and adjustment of insulin regimens Long acting insulin at bedtime 10 U or 0.2 U/Kg Check FG daily, increase by 2 4 U every 3 days until FG 70 130 mg/dl (3.9 7.2 mmol/L) HbA1C 7% after 2-3 months If hypoglycaemia occurs, or FG < 3.9 reduce bedtime by 4 units or 10 % which is greater If FG in range check before lunch, dinner and bedtime, add second injection. Begin with 4 U before each. Adjust by 2 U every 3 days. Pre-bed is high add rapid acting insulin at dinner Pre-dinner is high add NPH at breakfast or rapid acting at lunch Pre-lunch is high, add rapid acting insulin at breakfast Slide 55 Insulin administration Do not mix Glargine with other insulin products. Insulin site should be clean, but wiping with alcohol is not needed. Syringe reuse acceptable but meticulous attention to cleanliness is needed. Insulin pens improve the dose accuracy. Injection site rotation reduces the lipoatrophy. Abdomen region has a faster absorption rate than the Arm, which is faster than the leg. Slide 56 American Diabetes Association Standards of Medical Care in Diabetes2012 Referrence Slide 57