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Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
Unit 8 chapter 44 diabetes mellitus
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Unit 8 chapter 44 diabetes mellitus

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  • 1. Unit 8: The Endocrine System Chapter 44: Drugs for Diabetes Mellitus
  • 2. Pancreas <ul><li>Describe the secretory function of the pancreas. </li></ul><ul><li>Which pancreatic cells are essential to the endocrine function? </li></ul><ul><li>Why is the endocrine function of the pancreas so important? </li></ul>
  • 3. Insulin <ul><li>Secretion regulated by chemical, hormonal, and neural factors </li></ul><ul><li>Key to metabolic process in most body cells </li></ul><ul><li>Transport vehicle for glucose (except brain) </li></ul><ul><li>Why does glucose not need a transport vehicle into brain cells? </li></ul><ul><li>What is the most important regulator of insulin secretion? (Think about the negative feedback loop) </li></ul>
  • 4. Contributors to Glucose Homeostasis <ul><li>Hyperglycemic effects </li></ul><ul><li>Hormones </li></ul><ul><ul><li>Epinephrine </li></ul></ul><ul><ul><li>Thyroid hormone </li></ul></ul><ul><ul><li>Growth hormone </li></ul></ul><ul><ul><li>conticosteroids </li></ul></ul><ul><li>Drugs </li></ul><ul><ul><li>Phenytoin </li></ul></ul><ul><ul><li>NSAIDs </li></ul></ul><ul><ul><li>Diuretics </li></ul></ul><ul><ul><li>Steroids </li></ul></ul><ul><li>Hypoglycemic effects </li></ul><ul><li>Drugs </li></ul><ul><ul><li>Alcohol </li></ul></ul><ul><ul><li>Lithium </li></ul></ul><ul><ul><li>ACE Inhibitors </li></ul></ul><ul><ul><li>Beta-adrenergic blockers </li></ul></ul>
  • 5. Diabetes Mellitus <ul><li>Chronic metabolic disorder characterized by hyperglycemia </li></ul><ul><li>Etiology: combination of genetic and environmental factors </li></ul><ul><li>Increasing incidence </li></ul><ul><li>Group of disorders caused by: </li></ul><ul><ul><li>Deficient to absent insulin secretion </li></ul></ul><ul><ul><li>Decreased insulin receptor sensitivity </li></ul></ul>
  • 6. Type I Diabetes Mellitus <ul><li>Usually presents during childhood </li></ul><ul><li>Aka: insulin dependent diabetes mellitus </li></ul><ul><li>Etiology: </li></ul><ul><ul><li>autoimmune destruction of pancreatic beta cells </li></ul></ul><ul><ul><li>Interaction of genetic, immunologic, and environmental factors </li></ul></ul><ul><li>Consistent presenting signs/symptoms </li></ul><ul><ul><li>Hyperglycemia, polyuria, polyphagia, polydipsia, glycosuria, weight loss, fatigue </li></ul></ul>
  • 7. Potential Complications <ul><li>Arterial damage </li></ul><ul><li>Altered peripheral circulation </li></ul><ul><li>Nerve degeneration </li></ul><ul><li>Impaired lipid metabolism </li></ul>
  • 8. Pharmacotherapy for Type I Diabetes Mellitus <ul><li>What are the current options for Insulin therapy? </li></ul><ul><li>What is the therapeutic goal and desired outcome of insulin therapy? </li></ul><ul><li>What additional measures are used with insulin pharmacotherapy to control Type 1 DM? </li></ul>
  • 9. Insulin Therapy <ul><li>Fundamental Principle: </li></ul><ul><li>“ the right amount of insulin must be available to cells when glucose is available in the blood.” </li></ul><ul><li>What is the consequence of administering insulin when glucose is not available? </li></ul><ul><li>What is the consequence of forgetting or skipping scheduled insulin dosage? </li></ul>
  • 10. Insulin Therapy <ul><li>What is the primary adverse effect of insulin therapy? </li></ul><ul><li>Other adverse effects include: </li></ul><ul><ul><li>Localized allergic reaction </li></ul></ul><ul><ul><li>Generalized urticaria </li></ul></ul><ul><ul><li>Swollen lymph glands </li></ul></ul>
  • 11. Hypoglycemia (Insulin Reaction) <ul><li>Symptoms occur when there is more insulin in the blood than needed. </li></ul><ul><li>Causes: </li></ul><ul><ul><li>Insulin levels peak during exercise </li></ul></ul><ul><ul><li>Received too much insulin </li></ul></ul><ul><ul><li>Skipped meal after taking dose of insulin </li></ul></ul><ul><li>May be treated with glucagon </li></ul><ul><ul><li>Can cause response in ≤ 20 min </li></ul></ul>
  • 12. Somogyi Phenomenon <ul><li>Rapid decrease in blood glucose (typically at night) </li></ul><ul><li>Stimulates release of hormones that increase blood glucose </li></ul><ul><li>Morning blood glucose is elevated </li></ul>
  • 13. Types of Insulin <ul><li>Most insulin given today is human insulin </li></ul><ul><li>Human insulin has been modified to produce a more rapid onset or longer duration. (Insulin Analogs) </li></ul><ul><li>Classified as rapid, short, intermediate, or long acting </li></ul>
  • 14. Nursing Considerations <ul><li>What are nursing considerations for insulin therapy? </li></ul><ul><li>What must the nurse be familiar with? </li></ul><ul><li>What teaching must be included? </li></ul>
  • 15. Type 2 Diabetes Mellitus <ul><li>Major type of diabetes mellitus </li></ul><ul><li>Endogenous insulin present in deficient amounts </li></ul><ul><li>Fundamental problem </li></ul><ul><ul><li>Insulin resistance </li></ul></ul><ul><li>Poor management results in same complications as Type 1 diabetes mellitus </li></ul><ul><li>Recommendation: preprandial glucose < 110 mg/dl </li></ul>
  • 16. Oral Hypoglycemics <ul><li>Lower blood sugar </li></ul><ul><li>Some may cause hypoglycemia </li></ul><ul><li>Classified based on structure and mechanism of action </li></ul><ul><li>Initially monotherapy </li></ul><ul><li>Insulin may need to be added to regimin </li></ul><ul><li>Some combination drugs are available. Why? </li></ul>
  • 17. Classes of Hypoglycemic Agents <ul><li>Sulfonylureas </li></ul><ul><li>Biguanides </li></ul><ul><li>Alpha-glucosidase Inhibitors </li></ul><ul><li>Thiazolidinediones </li></ul><ul><li>Meglitinides </li></ul><ul><li>New drugs </li></ul><ul><li>Develop a table to compare and contrast </li></ul>
  • 18. Incretin-Glucose Control Mechanism <ul><li>Incretin is a hormone secreted by the intestines in response to a meal when blood glucose is elevated. </li></ul><ul><li>Increased incretin levels signals the pancreas to increase insulin secretion and the liver to stop producing glucagon. </li></ul><ul><li>Why is this important? </li></ul>
  • 19. exenatide (Byetta) <ul><li>Mimics the action of incretin </li></ul><ul><li>Causes increased secretion of insulin, slows absorption of glucose, and reduces action of glucagon </li></ul><ul><li>Subcutaneously 1-2 times per day </li></ul><ul><li>Adverse effects: </li></ul><ul><ul><li>Significant nausea, vomiting, diarrhea </li></ul></ul>
  • 20. Additional New Drugs <ul><li>Dipeptidyl peptidase – 4 (DPP4) Inhibitors </li></ul><ul><ul><li>Sitagliptin phosphate (Januvia) </li></ul></ul><ul><ul><li>Inhibits destruction of incretin </li></ul></ul><ul><li>pramlinitide (Symlin) </li></ul><ul><ul><li>Resembles pancreatic hormone amylin </li></ul></ul><ul><ul><li>Assists with glucose regulation </li></ul></ul><ul><ul><ul><li>Slows absorption of glucose </li></ul></ul></ul><ul><ul><ul><li>Inhibits action of glucagon </li></ul></ul></ul>
  • 21. Nursing Considerations <ul><li>What are the nursing considerations for hypoglycemic agents? </li></ul><ul><li>What needs to be included in teaching? </li></ul>

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