NRSG351 Agents to treat Diabetes

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powerpoint presented to nursing students at Nell Hodgson Woodruff School of Nursing, Emory University, spring 2014

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  • The feedback loops of the insulin axis involve a number of different tissues. These tissues learn to communicate with each other during the late fetal and early postnatal stages of development. Signalling from the beta cells of the pancreas is via insulin (dotted lines). This acts on liver, muscle and adipose tissue to change levels of glucose in the circulation (solid lines). The development of liver, muscle and adipose tissue is regulated by gene nutrient interactions. If the nutritional balance is perturbed by changes in the maternal diet, the development of tissues is also changed altering the characteristics of this feedback loop. The communication between these organs is a complex web where subtle changes in just one component can influence the behaviour of the whole system. For example, decreased maternal nutrition may suppress beta cell development resulting in fewer fetal beta cells, resulting in reduced insulin release, requiring a corresponding increase in insulin sensitivity of fetal liver, muscle or adipose tissue to maintain glucose homeostasis.
  • NRSG351 Agents to treat Diabetes

    1. 1. Civility Clause…. Students are expected to behave toward lecturers and fellow students with courtesy and consideration. This means that talking and disruptive behavior will be kept to a minimum. Cell phones, pagers, and other electronic devices should be silenced in the classroom. I reserve the right to end a class at any time, for any reason, including the disruptive or rude behavior of anyone in the classroom.
    2. 2. Starting with insulin
    3. 3. Figure 3 The feedback loops of the insulin axis involve a number of different tissues. Maloney C A , and Rees W D Reproduction 2005;130:401- 410 © 2005 Society for Reproduction and Fertility
    4. 4. Goals of therapy in diabetes • To normalize blood sugar levels to minimize risk of long-term complications • To avoid instances of hypoglycemia • To promote normal carbohydrate, fat and protein metabolism
    5. 5. Non-insulin drugsInsulins Drugs for diabetes biguanides secretagogues sulfonylureas meglitinides α -glucosidase inhibitors TZDs amylin analogues incretin modulators GLP-1 analogues DPP-4 inhibitors Others
    6. 6. Therapy with insulin • Insulin is the PRIMARY treatment for Type 1 diabetes – insulin administration replaces insulin that is not produced by B cells • Also used in Type 2 as B cells fail and disease progresses
    7. 7. Therapy with insulin • USED TO TREAT – Type I or type 2 diabetes • CONTRAINDICATED IN – Allergy to a specific insulin product – hypoglycemia
    8. 8. Types of insulin • Ultra short acting or rapid acting – Rapid onset, short duration • Short-acting – Rapid onset • Intermediate-acting • Long-acting – Slow onset
    9. 9. Insulins Insulin aspart (Novolog®) - C Insulin lispro (Humalog®) - B Insulin glulisine (Apidra®) - C Pharmacology (Mechanism of action) Replaces insulin; Promotes cellular uptake of glucose, fatty acids and amino acids; Promotes storage of glycogen, triglycerides and proteins Adverse Effects Pharmacokinetics
    10. 10. Insulins Regular insulin (Humulin-R®, Novolin-R®) Pharmacology (Mechanism of action) Replaces insulin; Promotes cellular uptake of glucose, fatty acids and amino acids; Promotes storage of glycogen, triglycerides and proteins Adverse Effects Pharmacokinetics
    11. 11. Insulins Isophane insulin suspension (NPH®, Novolin-N®, Humulin-N) Insulin zinc suspension (Lente) (Humulin-L®; Novolin-L®) Pharmacology (Mechanism of action) Replaces insulin; Promotes cellular uptake of glucose, fatty acids and amino acids; Promotes storage of glycogen, triglycerides and proteins Adverse Effects Pharmacokinetics
    12. 12. Insulins Insulin glargine (Lantus®) Insulin detemir (Levemir®) Pharmacology (Mechanism of action) Replaces insulin; Promotes cellular uptake of glucose, fatty acids and amino acids; Promotes storage of glycogen, triglycerides and proteins Adverse Effects Pharmacokinetics
    13. 13. Insulins - Mixtures NPH70% + regular insulin 30% (Humulin 70/30 ®; Novolin 70/30®) NPH50% + regular insulin 50% (Humulin 50/50®) Insulin lispro protamine suspension 75% + insulin lispro 25% (Humalog Mix 75/25®) Pharmacology (Mechanism of action) Replaces insulin; Promotes cellular uptake of glucose, fatty acids and amino acids; Promotes storage of glycogen, triglycerides and proteins Adverse Effects Pharmacokinetics http://forecast.diabetes.org/files/images/InsulinChart_4.pdf
    14. 14. http://www.ourdiabetes.com/insulin-therapy.htm
    15. 15. Adverse Effects of Insulin • Hypoglycemia – Sympathatic activation produces palpitations, sweating, nervousness, weakness – Serious hypoglycemia produces CNS effects, including mental confusion, incoherent speech, blurred vision, coma • Weight gain
    16. 16. Role of the nurse (Abrams, pp. 726-730) • Teach the patient how to administer insulin correctly – Choice of administration techniques – Using a syringe – Choice of injection sites – When and how often to inject – How to store
    17. 17. Non-insulin drugsInsulins Drugs for diabetes biguanides secretagogues sulfonylureas meglitinides α -glucosidase inhibitors TZDs amylin analogues incretin modulators GLP-1 analogues DPP-4 inhibitors Others
    18. 18. Sulfonylureas Glyburide (Diabeta®, Micronase®) Glipizide (Glucotrol®) Glimepiride (Amaryl®) Pharmacology (Mechanism of action) Stimulate insulin release from the pancreas; Increases the number and sensitivity of insulin receptors; Decreases glycogenolysis and gluconeogenesis Adverse Effects Pharmacokinetics
    19. 19. K+ B cell basal state insulin glucose K+
    20. 20. Sulfonylureas • Inhibits (closes) a K+-ATP channel, leading to • Decreased K+ efflux from B-cells which • Depolarizes the B-cell membrane, leading to • Increased Ca++ influx and • Increased exocytosis of insulin from B-cells
    21. 21. glipizide sulfamethoxazole
    22. 22. Sulfonylureas • Serious adverse effects – Hypoglycemia – Hematological effects (thrombocytopenia, aplastic anemia, others) • Common adverse effects – Weight gain – Rash – Hypoglycemia
    23. 23. Biguanides metformin (Glucophage®) metformin / glipizide (Metaglip®) rosiglitazone / metformin (Avandamet®) Others…. Pharmacology (Mechanism of action) Decrease hepatic glucose production; Decrease glucose absorption from GI tract; Increases insulin receptor sensitivity Adverse Effects Pharmacokinetics
    24. 24. Biguanides • USED TO TREAT – Type 2 diabetes • CONTRAINDICATED IN – Hypersensitivity to biguanides – Hepatic or renal disease – Alcoholism – Cardiopulmonary disease
    25. 25. Biguanides • Serious adverse effects – Lactic acidosis (due to the inhibition of gluconeogenesis and the buildup of fatty acids) - rare • Common adverse effects – Nausea, vomiting – Flatulence
    26. 26. Thiazolidinediones (Insulin Sensitizers; glitazones; TZDs) Rosiglitazone (Avandia®) - C Pioglitazone (Actos®) - C Pharmacology (Mechanism of action) Enhances the effects of circulating insulin; Stimulates peripheral glucose uptake and storage Inhibits hepatic glucose production NO increase in insulin levels Adverse Effects Pharmacokinetics http://www.fda.gov/Drugs/DrugSafety/ucm255005.htm
    27. 27. Thiazolidinediones (TZDs) • Serious adverse effects – Congestive heart failure (new or exacerbated) due to increasing blood volume – BLACK BOX WARNING – Hepatic dysfunction or failure • Common adverse effects – Mild anemia – Moderate weight gain – Upper respiratory infection – Headache and myalgia
    28. 28. Secretagogues (meglitinides) Repaglinide (Prandia®) Nateglinide (Starlix®) Pharmacology (Mechanism of action) Stimulates insulin release from B-cell through inhibition of ATP-sensitive K+ channels; Adverse Effects Pharmacokinetics
    29. 29. Alpha-glucosidase inhibitors Acarbose (Precose®) Pharmacology (Mechanism of action) Reversibly inhibit alpha glucosidase Delays absorption of glucose in the intestine; Blunts postprandial elevations in glucose Adverse Effects Pharmacokinetics
    30. 30. Glucagon-like peptide 1 (GLP-1) Exenatide (Byetta®; Bydureon®) – C Liraglutide (Victoza®) Pharmacology (Mechanism of action) Incretin mimetic that binds to GLP receptors; Increases glucose- dependent secretion of insulin from pancreatic B cells Adverse Effects Pharmacokinetics Injected sc
    31. 31. Synthetic amylin analog pramlintide (Symlin®) Pharmacology (Mechanism of action) Amylin slows gastric emptying; suppresses glucagon; Modulates appetite in the CNS Adverse Effects Pharmacokinetics Injected sc
    32. 32. DPP-4 inhibitor Sitagliptin (Januvia®) Saxagliptin (Onglyza®) Pharmacology (Mechanism of action) Inhibits DPP-4, which slows inactivation of incretin hormones GLP- 1 and GIP Adverse Effects Pharmacokinetics Oral
    33. 33. Figure 1. Key sites of action of diabetes medications. Martin C L The Diabetes Educator 2007;33:6S-13S Copyright © by American Association of Diabetes Educators; Published by SAGE Publications

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