Pharm Chapter 32

  1. T/F: Pancreas functions as endocrine and exocrine gland.
    • TRUE!
    • Exocrine: excretes digestive enzymes into duodenum via pancreatic duct
    • Endocrine: Insulin and glucagon regulate blood glucose (Insulin also plays a role in protein and lipid metabolism and several aspects of growth and development)
  2. What synthesizes and secretes pancreatic hormones?
    • Islets of Landerhans
    • Four primary cell types
    • 1. Alpha (A) cells: produce glucagon
    • 2. Beta (B) cells: produce insulin
    • 3. Delta (D) cells: produce somatostatin (regulates GI absorption and motility)
    • 4. F cells: produce pancreatic polypeptide
  3. What is the primary effect of insulin?
    • Lower blood glucose by facilitating entry of glucose into peripheral tissues
    • Stored in liver: Hepatic cells permeable to glucose, even w/o insulin
    • Stored in other tissues: Most relatively impermeable to glucose and need facilitated diffusion
  4. How does insulin effect the glucokinase system?
    • Stimulates it!
    • Phosphorylates glucose and traps molecule in hepatic cell
    • ↑ activity of enzymes promoting glycogen synthesis, inhibits those promoting glycogen breakdown
  5. How does insulin promote storeage of protein and lipid in muscle and adipose tissue?
    • Protein: stimulates aa uptake, ↑ DNA/RNA activity, inhibits protein breakdown
    • Adipose: stimulates TG synthesis, inhibits hormone sensitive lipase (which breks down stored lipids)
  6. What is the hormonal antagonist of insulin, and what is its primary effect?
    • Glucagon
    • Increases blood glucose to maintain levels and prevent hypoglycemia
    • Produces ↑ in glycogen breakdown in liver (glycogenolysis)
    • Stimulates ↑ in hepatic glucose production (gluconeogenesis) to sustain blood glucose levels
  7. How does Glucagon affect the cAMP system in the liver cells?
    • Binds to hepatic cell membrane and stimulates activity of adenyl cyclase enzyme
    • Transforms ATP to cAMP (this stimulates enzymes to ↑ glycogen breakdown and stimulates gluconeogenesis)
  8. What is normal blood glucose levels? What maintains these levels? What happens if it gets too high/low?
    • 80-90mg/100mL of blood
    • Insulin and glucagon maintain blood glucose withing finite range
    • Hypoglycemia: can result in coma or death
    • Hyperglycemia: can result in neural and vascular changes
  9. What is the primary factor affecting pancreatic hormone release?
    • Level of glucose in the bloodstream
    • Blood glucose rises: insulin released from beta cells
    • Blood glucose falls: glucagon released from alpha cells
  10. What is type 1 diabetes?
    • Unable to synthesize enough insulin
    • Destruction of beta cells
    • Need exogenous insulin to survive
  11. What is diabetes mellitus and what are the types?
    • Insufficient insulin secretion or decrease in peripheral effects of insulin
    • Type I: Insulin-dependent diabetes mellitus (IDDM)/ Juvenile diabetes
    • Type II: Non-insulin dependent diabetes mellitus (NIDDM)
  12. What causes Type II diabetes?
    • Genetic predisposition
    • Poor diet, obesity, lack of exercise
    • Usually in older individuals
  13. What is the primary problem in type II diabetes?
    • Decreased sensitivity of peripheral tissues to circulating insulin (insulin resistance)
    • Target cell defect causes decreased resonse of cell to insulin
    • Cellular response is inadequate
  14. What is a secondary problem in type II diabetes aside from insulin resistance?
    • Pancreatic beta cells intact, can produce insulin
    • Insulin is release continuously, even when fasting
    • After meal, beta cells don't ↑ insulin release in proportion to ↑ glucose levels
  15. What are complications of DM?
    • Most common: hyperglycemia
    • Glycosuria: ↑ glucose excretion by kidneys (kidneys can't adequately resorb glucose)
    • Dehydration/electrolyte imbalance: osmotic force promotes fluid excretion
    • Ketoacidosis: Loss of glucose in urine causes shift towards fat and protein mobilization for energy
    • Microangiopathy: Abnormalities in small blood vessels leads to occlusion (can damage retina and kidneys)--->poor wound healing and ulcers!!
  16. T/F: Exogenous insulin is used for both type I and type II diabetes.
    TRUE: used in type 2 b/c other interventions may not be adequate to control disease
  17. What is a type of insulin preparation?
    • Lispro (Humalog)
    • Slower than endogenous insulin
    • Preparations can be fast or slow acting; slow acting allows more sustained levels
  18. What are ways of administering insulin?
    • Nasal spray (Exubera)
    • Subcutaneous
    • IV in emergency
  19. T/F: Insulin is often administered orally.
    FALSE: b/c of large polypeptide structure
  20. What is done in intensive insulin therapy?
    • Self-administering 3 or more dosages/day
    • Monitor blood glucose levels
    • Reduces long-term complications
  21. What are adverse effects of Insulin Therapy?
    • Primary problem: hypoglycemia
    • Strenuous activity can cause this by having insulin-like effect
    • Avoid by decreasing insulin by 30-35%
    • 10-15 g D-glucose restores blood glucose in early hypoglycemia
  22. T/F: Oral antidiabetic drugs are effective for type I and type II diabetes.
    FALSE: only type 2 (by mouth)
  23. What do Sulfonylureas do? Examples?
    • Act on beta cells to stimulate release of insulin
    • Released into hepatic portal vein to liver to inhibit glucose production
    • Early stages of type II
    • Glipizide (Glucotrol)
    • Glyburide (DiaBeta)
  24. Azathioprine
    • (Imuran)
    • Type of Immunosuppressant
    • Minimizes beta cell loss
  25. Exenatide
    • (Byetta)
    • Type of Glucagon-like Peptide 1
    • Released after meal
    • Increases after meal
    • ↑ ability of blood glucose to stimulate insulin release from beta cells
  26. What is sometimes used to Rx acute hypoglycemia?
  27. Nonpharmacologic Intervention in DM
    • Diet, weight loss
    • Exercise
    • Tissue transplants and gene therapy of pancreas
Card Set
Pharm Chapter 32