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Diabetes Mellitus 101 for Medical Professionals

Diabetes Mellitus 101 for Medical Professionals. An Aggressive Pathophysiologic Approach to Cardiometabolic Therapy for Type 2 Diabetes :. Part 9. Stan Schwartz MD,FACP Clinical Associate Professor of Medicine, U of Pa. Cardiometabolic Institute Penn-Presbyterian Hospital, UPHS.

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Diabetes Mellitus 101 for Medical Professionals

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  1. Diabetes Mellitus 101 for Medical Professionals An Aggressive Pathophysiologic Approach to Cardiometabolic Therapy for Type 2 Diabetes: Part 9 Stan Schwartz MD,FACP Clinical Associate Professor of Medicine, U of Pa. Cardiometabolic Institute Penn-Presbyterian Hospital, UPHS

  2. Therapy for Type II Diabetes

  3. A1C (%) Normal: 4-6% Fasting/Preprandial (mg/dL)(plasma equivalent) Postprandial (mg/dL) (2-hour) ADA <7.0 90-130 <180* ACE <6.5 <110 <140 * Peak Targets for Glycemic Control Goals for individual patients may vary. Aim for the Lowest A1C Possible without Hypoglycemia. American Diabetes Association. Clinical Practice Recommendations. Diabetes Care. 2004,27:S15-S35 The American Association of Clinical Endocrinologists. Medical Guidelines for the Management of Diabetes Mellitus. Endocr Pract. 2002; 8(Suppl. 1): 40-82

  4. Relative Contribution of FBG and PPG Varies With A1C Range Inc PPG increases Micro- and macro- vascular disease Thus , to get to glycemic goals, one must control PPG as well as FBS. (incretins, alpha-glucosidase inhibitors, TZDs, glinides, fast-insulin analogues) Adapted from Monnier L, et al. Diabetes Care. 2003;26:881-885.

  5. Non-Insulin Therapy for Type II Diabetes

  6. Non-Insulin Therapy for Hyperglycemia in Type 2 Diabetes,Treating Defronzo’s Octet: Match Patient Characteristics to Drug Characteristics - - - Peripheral glucose uptake 1.Pancreatic insulin Secretion: Incretin, ranolazine 5.Gut CHO Absorption: Incretin, Pramlintide, Glucosidase inh. 7.Brain- TZD,INCRETIN, bromocryptine 2.Pancreatic glucagon Secretion- Incretin 8.Kidney- SGLT2 HYPERGLYCEMIA De 3.Muscle- TZD, Incretin Hepatic glucose production: Metformin, incretin 4.Liver 6.Fat- TZD, metformin

  7. Revised Treatment Algorithm At diagnosis: Lifestyle + metformin STEP 1 Tier 1* Tier 2† HbA1C >7.0% STEP 2 Add basal insulin Add sulfonylurea Add GLP-1 agonist Add pioglitazone ± SU Intensive insulin STEP 3 The New ADA Guidelines for Type 2 Diabetes:AKA- David Nathan’s Regimen- DNR NOT Glyburide, chlorpropamide NOT Rosiglitazone

  8. Simplified- AACE/ACE:Recommendations Based on A1C at Diagnosis Lifestyle Modifications Monotherapy Dual therapy Triple therapy A1C 6.5%-7.5% A1C 7.6%-9.0% A1C >9.0% If under treatment If drug naive Symptoms No symptoms Dual therapy Insulin plus other agent(s)* Insulin plus other agent(s)* Triple therapy Triple therapy *Pramlintide can be used with prandial insulin, but insulin secretagogues should be discontinued with multidose insulin Therapeutic Choice, based on Safety/ Efficacy, Should Match The Drug Characteristics With Patient Characteristics Rodbard HW, et al. Endocr Pract. 2009;15:540-559.

  9. Monotherapy Metformin Pioglitazone GLP-1 agonist Bromocriptine DPP-4 Inhibitor SGLT-2 Colsevelam AGI/Ranolazine Future AACE Guideline- Modest Proposal Asymptomatic 5.7 HbA1c Continuum 6.5%– if not at goal, advance Rx7.5% 9.0 12% Symptomatic Diet and Exercise • Insulin* • +/- Other agents • *Insulin analogs • Not NPH/regular •  If over 9.0% or above and symptomatic • If triple combo fails • Dual Combination • Metformin • Pioglitazone • GLP-1 agonist • Bromocriptine • DPP-4 Inhibitor • SGLT-2 • Colesevelam • AGI/Ranolazine • Triple Combination • Metformin • Pioglitazone • GLP-1 agonist • Bromocriptine • DPP-4 Inhibitor • SGLT-2 • Colesevelam • AGI/Ranolazine Prevention Pioglitazone [Incretin] [Bromocriptine] Metformin Colsevelam Therapeutic Choice Should Match The Drug Characteristics With Patient Characteristics

  10. Concurrent Therapy

  11. Aggressive medical therapy in diabetes ACE inhibitorsARBs β-blockersCCBsDiuretics Hypertension Atherosclerosis StatinsFibric acid derivatives Colsevalam Dyslipidemia MetforminTZDsSulfonylureas/GlinideRANOLAZINE colsevalam Incretins Insulin Hyperglycemia/ Insulin resistance ASAClopidogrelTiclopidine Platelet activationand aggregation Adapted from Beckman JA et al. JAMA. 2002;287:2570-81.

  12. Treating the ABCs Reduces Diabetic Complications 1 UKPDS Study Group (UKPDS 33). Lancet. 1998;352:837-853. 2 Hansson L, et al. Lancet. 1998;351:1755-1762. 3 UKPDS Study Group (UKPDS 38). BMJ. 1998;317:703-713. 4 Grover SA, et al. Circulation. 2000;102:722-727. 5 Pyŏrälä K, et al. Diabetes Care. 1997;20:614-620.

  13. Synergies In Therapy for the Cardiometabolic Syndrome ?√ ?√

  14. Summary Treat aggressively-benefit on cost and complications Treat elements of pathophysiology Resistance-glycemia,endothelial dysfunction,lipids,BP,coag. Secretion-first phase,incretin,importance of PPG Multi-hormonal issues Use SIDE-BENEFITS of the various agents Treat to new goals using combinations that make pathophysiologic sense Guidelines should help pick right drug(s) for right patients

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