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Type 2 Diabetes: A Fresh New Approach with Incretin AgentsAnswer online at www.CanadianHealthcareNetwork.ca April/May 2011ceContinuing EducationL e s s o n7com/dpp-iv_inhibitors.htm (accessed January 7, 2011).37. Noel RA, Braun DK, Patterson RE, et al. Increased risk of acute pancreatitisand biliary disease observed in patients with type 2 diabetes:a retrospective cohort study. Diabetes Care 2009;32:834-8.38. Parks M, Rosebraugh C, Weighing risks and benefits of liraglutide—the FDA’s review of a new antidiabetic therapy, NEJM. www.nejm.org/doi/full/10.1056/NEJMp1001578 (accessed January 7, 2011).39. McConnell EE, Solleveld HA, Swenberg JA, et al. Guidelines forcombining neoplasms for evaluation of rodent carcinogenesis studies.J Natl Cancer Inst 1986;76:283-9.40. Novo Nordisk Canada. Victoza (liraglutide) product monograph,May 21, 2010.41. Glucose tolerance and mortality: comparison of WHO and AmericanDiabetes Association diagnostic criteria. The DECODE studygroup. European Diabetes Epidemiology Group. Diabetes Epidemiology:Collaborative analysis of diagnostic criteria in Europe.Lancet 1999;354:617-21.42. Monnier L, Lapinski H, Colette C. Contributions of fasting andpostprandial plasma glucose increments to the overall diurnalhyperglycemia of type 2 diabetic patients: variations with increasinglevels of HbA(1c). Diabetes Care 2003;26:881-5.43. Evans J, Rushakoff R. Oral pharmacological agents for type 2diabetes: sulfonylureas, meglitinides, metformin, thiazolidinediones,α-glucosidase inhibitors, and emerging approaches. www.endotext.org/diabetes/diabetes16/diabetes14.html (accessedJanuary 7, 2011).44. Munro N. Modern management of hyperglycemia EPCCS 2009www.epccs.eu/default.aspx?id=23&subId=24&presentationId=9 (accessed January 7, 2011).45. Reid T. The importance and treatment of postprandial hyperglycemia.J Fam Pract 2010;59(5):S9-S14.46. Canadian Diabetes Association Clinical Practice Guidelines ExpertCommittee. Canadian Diabetes Association. 2008 clinical practiceguidelines for the prevention and management of diabetes inCanada. Can J Diabetes 2008;32(Suppl 1):S1-S201.47. Freeman J, Unger J. Why and when to implement incretin therapy.J Fam Pract 2008;57. www.jfponline.com/pages.asp?id=6688(accessed January 7, 2011).48. Nathan B, Buse J, Davidson M, et al. Medical management of hyperglycemiain type 2 diabetes: a consensus algorithm for the initiationand adjustment of therapy. Clin Diabetes 2009;27:14-5.49. Eli Lilly. Byetta (exenatide) prescribing information. http://pi.lilly.com/us/byetta-pi.pdf (accessed January 7, 2011).50. Buse JB, Drucker DJ, Taylor KL, et al. DURATION-1: exenatide onceweekly produces sustained glycemic control and weight loss over52 weeks. Diabetes Care June 2010;33(6):1255-61.51. LEAD-6: Liraglutide superior to exenatide in improving glycemiccontrol. www.endocrinetoday.com/view.aspx?rid=40742 (accessedJanuary 7, 2011).52. Hindsberger C, Jacobsen L, Robson R, et al. Effect of renal impairmenton the pharmacokinetics of the GLP-1 analogue liraglutide.Br J Clin Pharmacol 2009;68(6):898-905(8).53. Merck Frosst Canada. Januvia (sitagliptin) product monograph.Kirkland QC. 2009.54. Merck Frosst Canada. Janumet (sitagliptin phosphate monohydrateand metformin hydrochloride) product monograph. Kirkland QC.September 23, 2009.55. Onglyza Prescribing Information. www.onglyza.com/hcp/hcp.aspx(accessed January 7, 2011).Questions Answer online at www.CanadianHealthcareNetwork.ca, CE section, Quick Search CCCEP #1065-2010-050-I-P1. The natural progression ofT2DM can best be described aswhich of the following?a) An initial phase of insulinresistance that requires acompensatory increase ininsulin secretion to maintainnormal blood glucose levels.b) An initial phase of decreasedinsulin secretion which resultsin insulin resistance.c) An initial phase of increasedinsulin secretion which resultsin insulin resistance.d) An initial phase of decreasedglycogen production whichrequires increased insulinsecretion to maintain normalblood glucose levels.2. Nutrition therapy can reduceA1C by:a) 0.1–0.5% c) 1.0–2.0%b) 0.5–1.0% d) 2.0–3.0%3. Which of the following statementsis true?a) Insulin resistance will alwayslead to T2DM.b) At diagnosis of T2DM, mostpatients have already lost 50%of their beta-cell function.c) Intense research is underwayto develop new agentsto mimic the actions of GIP(glucose-dependent insulinotropicpolypeptide).d) According to the CDA 2008CPGs, if glycemic targets arenot achieved within six to 12months of lifestyle management(nutrition therapy andexercise recommendations),antihyperglycemic pharmacotherapyshould be initiated.4. Which of the followingstatements is true?a) A1C reduction is durable withsulfonylurea therapy.b) Metformin is an insulin sensitizerthat is capable of inhibitinghepatic gluconeogenesis.c) Weight loss is a side effect ofDPP-4 inhibitors.d) Insulin is a desired add-ontherapy to TZDs.5. Which of the followingstatements is true?a) Insulin therapy can reduceA1C by 0.5–1.5%.b) Sulfonylurea therapy canreduce A1C by 0.5–0.8%.c) Alpha-glucosidase therapy canreduce A1C by 0.5–0.8%.d) TZD therapy can reduce A1Cby 1–2%.6. As A1C levels decreasetowards the target, the importanceof postprandial glucosefor A1C reduction:a) increasesb) decreasesc) stays the samed) increases first then decreasesas the A1C is closer to target7. Which of the followingstatements about incretinhormones is true?a) “GLP-1” is an acronym for“glycogen-like peptide-1.”b) “GIP” is an acronym for“glucagon-dependentinsulinotropic polypeptide.”c) “GLP-1” is an acronym for“glucose-like peptide-1.”d) “GIP” is an acronym for“glucose-dependent insulinotropicpolypeptide.”8. Which of the following statementsabout incretin hormonesis true?a) GIP level and insulinotropiceffects are significantlyreduced in T2DM.b) GLP-1 level is normal but itloses its insulinotropic effectsin T2DM.c) GLP-1 level is reduced butinsulinotropic effects areretained in T2DM.d) GIP level is reduced butinsulinotropic effects areretained in T2DM.9. Native GLP-1 has anapproximate half-life of:a) 10–15 minutesb) four to six hoursc) two to three minutesd) two to three seconds10. Which of the followingstatements is true?a) GLP-1 receptor agonist therapywill result in physiologicconcentrations of GLP-1.b) DPP-4 therapy will resultin supraphysiologicconcentrations of GLP-1.c) GLP-1 receptor agonisttherapy will result in supraphysiologicconcentrationsof GLP-1.d) DPP-4 therapy will resultin supraphysiologicconcentrations of GIP.11. Treatment with exenatide, aGLP-1 agonist, is associated withall but which of the following?a) diminished appetiteb) improved beta-cell functionin rat modelc) decreased postprandialblood glucosed) weight gain12. Which of the followingmechanisms contributes tothe glucose-lowering propertiesof GLP-1 receptor agonists?a) continuous pancreaticbeta-cell stimulationb) enhanced postprandialinsulin secretionc) increased gastric emptyingd) increased glucagon secretion13. Which of the following statementsis true?a) Sulfonylureas stimulate insulinsecretion in a glucose-dependentmanner.b) Meglitinides stimulates insulinsecretion in a glucose-dependentmanner.c) DPP-4 inhibitors stimulateinsulin secretion in a glucosedependentmanner.d) DPP-4 inhibitors stimulateinsulin secretion in a glucoseindependentmanner.14. Which of the following agentshas the potential to reduce A1Cby the greatest amount?a) sitagliptin c) metforminb) exenatide d) pioglitazoneQuestions 15-18 pertain to thefollowing case:Roger, a 45-year-old male witha BMI of 35 kg/m2 presentsto your pharmacy and asks youto review his logbook. He wasdiagnosed with T2DM three yearsago (with an A1C of 8.5%) andhas been taking metformin eversince. He tells you that his A1Cis 10.1% and his logbook revealsthat his fasting sugars have beenquite high recently. Exercise isdifficult due to chronic backpain. He denies any othermedical conditions.15. According to the CDA 2008Clinical Practice Guidelines, whatis an appropriate A1C goal forthis patient?a)