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Diabetes Management Strategies: Practical Implementation with Patients

This discussion covers the practical use of SGLT-2 inhibitors in type 2 diabetes, including general principles, care processes, natural history, complications, and clinical trial summaries. It emphasizes delaying insulin therapy, avoiding hypoglycemia, and personalizing treatment approaches based on individual etiology. The focus on SGLT-2 inhibitors and core defects in diabetes management is highlighted.

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Diabetes Management Strategies: Practical Implementation with Patients

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  1. Practical Implementation as a Discussion with the Patient Practical Use of SGLT-2 Inhibitors in T2DM: Clinical Pearls- Perlas de Sabiduria Stan Schwartz MD, FACP Affiliate, Main Line Health System Emeritus, Clinical Associate Professor of Medicine, U of Pa. stschwar@gmail.com

  2. Structure of Our Discussion: • Following Flow of Discussion with Patient • General principles • SGLT-2 Principles • First Visit Process of Care • Follow-up Visit Process of Care

  3. Updated Natural History of Type 2 Diabetes EPIGENITICS EPIGENITICS Age 0-15 15-40+ 15-50+ 25-70+ Environmental Inflam. Triggers eg: viral,endocrine disruptors, food AGE’s, biome Macrovascular Complications IR Phenotype Disability Resistance inflammatory, adipokines MICVAAmp β-Cell secretion/mass Polygenic- other Monogenic (HLA) pp>7.8 IGT Type II DM Gene DEATH Polygenic Monogenic – MODY BlindnessAmputationCRF Resistance-FFA Poor diet, inactivity EyeNerveKidney ETOHBPSmoking Disability Microvascular Complications endocrine disruptors, food AGE’s ,biome Environmental Triggers Risk of Dev. Complications

  4. Treat Aggressivelyto Delay or Prevent Complications Pearl

  5. Impact of Intensive Therapy in Type 2 Diabetes Summary of Major Clinical Trials: BUT Subset Evaluations Show Reduced CV Outcomes if shorter duration of DM, without significant pre-existing complications Initial Trial Long Term Follow-up ↑- likely due to hypoglycemia and weight gain

  6. Early Treatment Decreases Micro and Macro Vascular RISK/ OUTCOMESAs long as do without Undue Hypoglycemia or Weight Gain Pearl

  7. Consequences of Hypoglycemia • Prolonged QT- intervals- Diabetologia 52:42,2009 • Can be of pronged duration IJCP Sup 129, 7/02 • Greater with higher catecholamine levels Europace 10,860 • Associated with Angina Diabetes Care 26, 1485, 2003 / Ischemic EKG changesPorcellati, ADA2010 • Associated with Arrhythmias • Associated with Sudden Death Endocrine Practice 16,¾ 2010 • Increased Variabilty- explains highest mortality in intensive group had highest HgA1c in ACCORD ( increases inflammation, ICU mortality Hirsch ADA2010) • Sulfonylureas block Ischemic Preconditioning

  8. There is No perfect Exogenous Insulin:All result in HyperInsulinemia and Potential Hypoglycemia Hypoglycemia/ Wt. Gain CONCLUSION: DELAY INSULIN THERAPY; AVOID BOLUS RX if possible NORMAL: Insulin into portal system and B-cell= Perfect glucose sensor- Insulin secretion modulator Exogenous Insulin

  9. Pearl No more Sulfonylureas or Glinides Delay Insulin Most will not need Bolus Insulin

  10. Beta Cell-Centric View of Diabetes: Matching Rx with Etiology use least number agents treating maximal # of modes of hyperglycemia FOCUS on SGLT-2 Inhibition- addresses 5/11 MOH Egregious Eleven 2. Unsuppressed glucagon secretion Incretins Pramlintide 1. Decreased insulin secretion Incretins Ranolazine 3. Decreased incretin effect Incretins 11. Immune System / Inflammation 4. Increased hepatic glucose production Anti-Inflam-matories, Immune modulators CORE DEFECT Metformin, TZDs 5. Decreased peripheral muscle uptake 10. Kidney SGLT2 Inhibitors Hyperglycemia Metformin, TZDs 9. Brain Incretin Dopa agonist 7. Stomach/Small intestine 6. Adipose 8. Colon / Biome GLP-1 RAs AGI Pramlintide Metformin, TZDs Incretins/Probiotics Resistance Issues New Construct Older Construct Islet Cell Issues

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