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Treatment of diabetes mellitus

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Treatment of diabetes mellitus

  1. 1. Treatment of Diabetes Mellitus Dr. Salman Iftikhar Department of Pharmacology UHS
  2. 2. Diabetes Mellitus <ul><li>Type 1 (IDDM): </li></ul><ul><ul><li>Early onset </li></ul></ul><ul><ul><li>Loss of pancreatic B cells  absolute dependence on insulin </li></ul></ul><ul><ul><li>Ketoacidosis – prone </li></ul></ul><ul><li>Type 2 (NIDDM) </li></ul><ul><ul><li>Usually adult onset </li></ul></ul><ul><ul><li> response to insulin </li></ul></ul><ul><ul><li>Not Ketoacidosis – prone </li></ul></ul>
  3. 3. Insulin
  4. 6. Oral Hypoglycemic Agents
  5. 7. Sulfonylureas
  6. 9. Sulfonylureas <ul><li>Mechanism </li></ul><ul><ul><li>The acute action of sulfonylureas is to block K + channels  depolarization  insulin release </li></ul></ul><ul><li>Effects of increased insulin </li></ul><ul><ul><li> glucagon release from pancreatic  cells </li></ul></ul>
  7. 10. Sulfonylureas <ul><li>Acetohexamide (active metabolite,  dose in renal dysfunction) </li></ul><ul><li>Tolbutamide (appropriate in renal dysfunction) </li></ul><ul><li>Chlorpropamide (long acting, SIADH/disulfiram reaction) </li></ul><ul><li>Glipizide (  dose in hepatic dysfunction) </li></ul><ul><li>Glyburide (active metabolite,  dose in renal dysfunction) </li></ul>
  8. 11. Sulfonylureas <ul><li>Adverse effects: </li></ul><ul><ul><li>Hypoglycemia </li></ul></ul><ul><ul><li>Weight gain </li></ul></ul><ul><ul><li>Hypersensitivity (possible cross allergy with sulfonamides) </li></ul></ul><ul><ul><li>Drug interactions mainly with first-generation drugs  hypoglycemia with cemetidine, insulin, sulfonamides, salicylates </li></ul></ul>
  9. 12. Metformin <ul><li>“ Euglycemic”,  postprandial glucose levels but does not cause hypoglycemia or weight gain </li></ul><ul><li>May involve  tissue sensitivity to insulin and/or  hepatic gluconeogenesis </li></ul><ul><li>Adverse effects: possible lactic acidosis; gastrointestinal distress is common </li></ul>
  10. 13. Acarbose <ul><li>No hypoglycemia </li></ul><ul><li>Mechanisms: inhibits  glucosidase in brush borders of small intestine   formation of absorbable carbohydrate   postprandial glucose   demand for insulin </li></ul><ul><li>Adverse effects: GI discomforts, flatulence and diarrhea; recent concerns over potential hepatotoxicity </li></ul>
  11. 14. Thiazolidinediones Pioglitazone & Rosiglitazone
  12. 15. <ul><li>Mechanism: </li></ul><ul><ul><li>Bind to nuclear peroxisome proliferator-activating receptors (PPARs) involved in transcription of insulin responsive genes  sensitization of tissues to insulin, plus  in hepatic gluconeogenesis and triglycerides and  insulin receptor numbers </li></ul></ul><ul><ul><li>Adverse effects: less hypoglycemia than sulfonylureas, but weight gain and edema reported </li></ul></ul>
  13. 16. BLOOD
  14. 17. New Drugs
  15. 18. PRAMLINTIDE <ul><li>Synthetic analog of amylin </li></ul><ul><li>Injectable: modulates postprandial glucose levels </li></ul><ul><li>Suppresses glucagon release via undetermined mechanisms, delays gastric emptying, and has central nervous system-mediated anorectic effects </li></ul><ul><li>Administered in addition to insulin in those who are unable to achieve their target postprandial blood sugars </li></ul>
  16. 19. <ul><li>Renal metabolism and excretion </li></ul><ul><li>Always be injected by itself with a separate syringe; it cannot be mixed with insulin </li></ul><ul><li>Adverse effects: hypoglycemia and gastrointestinal symptoms including nausea, vomiting, and anorexia. </li></ul>PRAMLINTIDE
  17. 20. EXENATIDE <ul><li>A synthetic analog of glucagon-like-polypeptide 1 (GLP-1), exenatide is the first incretin therapy to become available for the treatment of diabetes </li></ul><ul><li>Approved as an injectable, adjunctive therapy in persons with type 2 diabetes treated with metformin or metformin plus sulfonylureas who still have suboptimal glycemic control </li></ul><ul><li>Multiple actions </li></ul><ul><ul><li>potentiation of glucose-mediated insulin secretion </li></ul></ul><ul><ul><li>Suppression of postprandial glucagon release through as-yet unknown mechanisms </li></ul></ul><ul><ul><li>slowed gastric emptying, and a central loss of appetite </li></ul></ul><ul><ul><li>The increased insulin secretion is speculated to be due in part to an increase in beta-cell mass </li></ul></ul>
  18. 21. <ul><li>Adverse effects are nausea (about 44% of users) and vomiting and diarrhea. The nausea decreases with ongoing exenatide usage </li></ul><ul><li>Weight loss is reported in some users, presumably because of the nausea and anorectic effects. A serious and, in some cases, fatal adverse effect of exenatide is necrotizing and hemorrhagic pancreatitis. </li></ul><ul><li>Safety issues, however, may deter future use. </li></ul>EXENATIDE
  19. 22. SITAGLIPTIN <ul><li>Inhibitor of dipeptidyl peptidase-4 (DPP-4), the enzyme that degrades incretin and other GLP-1-like molecules </li></ul><ul><li>Its major action is to increase circulating levels of GLP-1 and GIP. </li></ul>
  20. 23. <ul><li>Decreases postprandial glucose excursions by increasing glucose-mediated insulin secretion and decreasing glucagon levels </li></ul><ul><li>Adverse effects include </li></ul><ul><ul><li>nasopharyngitis, upper respiratory infections, and headaches. Rarely, severe allergic reactions </li></ul></ul><ul><li>Dosage should be reduced in patients with renal impairment. Sitagliptin can be given as monotherapy or combined with metformin or Tzds. </li></ul>