Drugs affecting Blood Glucose Levels

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NurseNatalie
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Drugs affecting Blood Glucose Levels
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2011-02-03 15:06:44
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  1. When does type I diabetes usually develop and what is the speed of onset
    • childhood and adolescence
    • abrupt
  2. When does Type II diabetes usually develop and what is the speed of onset
    • usually after age 40
    • gradual
  3. What is the primary defect in Type I diabetes?
    Loss of pancreatic Beta Cells
  4. What is the primary defect in Type II diabetes?
    Insulin resistance and inappropriate insulin secretion
  5. Which type of Diabetes carries a greater risk of ketoacidosis?
    Type I
  6. What are the target tissues of insulin
    • liver
    • adipose tissue
    • muscle
  7. **In type II:
    Over time, hyperglycemia leads to destruction of pancreatic beta cells, and hence insulin production and secretion eventually decline.
  8. What are the acute problems seen with Type I diabetes?
    • Hyperglycemia results when insulin dosage is insufficient.
    • Conversely, hypoglycemia results when the insulin dosage is excessive.
    • Ketoacidosis develops when hyperglycemia is allowed to persist.
  9. What are the longterm problems seen with pts with diabetes
    • Macrovascular Damage: Cardiovascular disease mainly due to atherosclerosis, hyperglycemia, and altered lipid metabolism
    • Microvascular Damage: Destruction of small blood vessels contributes to kidney damage, blindness, and various neuropathies. Microvascular injury is directly
    • related to the degree and duration of hyperglycemia.
  10. ***Of note, ACE inhibitors and ARBs have an additional benefit: they can help control hypertension, a common complication of diabetes.
    • ***Treatment with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) can delay the onset of nephropathy, and can slow progression of nephropathy that is already present
    • *** ACE inhibitor (eg, captopril) or an ARB (eg, losartan) can help protect against diabetic nephropathy.
  11. What Three tests diagnose diabetes?
    • a fasting plasma glucose (FPG) test,
    • a casual plasma glucose test,
    • and an oral glucose tolerance test (OGTT).
  12. If diet and exercise fail for Type II diabetic pts, what are some other options?
    • Options include oral antidiabetic agents,
    • the new injectable hypoglycemic drugs—pramlintide and exenatide—
    • and, if needed, daily insulin
  13. What are the target values for glucose before meals?
    at bedtime?
    • 90 to 130 mg/dL before meals
    • 100 to 140 mg/dL at bedtime.
  14. What is the principle stimulus for a rise in glucose
    • The principal stimulus for insulin release is a rise in blood glucose.
    • ***however, Insulin release may also be triggered by amino acids, fatty acids, and ketone bodies.
  15. What receptor promotes secretion of insulin
    beta2-adrenergic receptors in the pancreas
  16. What receptor inhibits secretion of insulin
    alpha-adrenergic receptors in the pancreas
  17. Is insulin primarily anabolic or catabolic?
    The metabolic actions of insulin are primarily anabolic (ie, conservative or constructive). Insulin promotes conservation of energy and buildup of energy stores. The hormone also promotes cell growth and division.
  18. First, insulin stimulates cellular transport (uptake) of ______, ______, ______, and _____. Second, insulin promotes synthesis of complex organic molecules. What 3 complex molecules are created?
    • glucose, amino acids, nucleotides, potassium
    • glucose is converted into glycogen, amino acids are assembled into proteins, and fatty acids are incorporated into triglycerides.
  19. How is insulin deficiency catabolic
    • glycogen is broken down to glucose
    • protiens are broken down into amino acids
    • and tryglicerides are broken down into fatty acids
  20. How does insulin deficiency promote hyperglycemia?
    • (1) increased glycogenolysis,
    • (2) increased gluconeogenesis,
    • (3) reduced glucose utilization. Glycogenolysis, by definition, generates free glucose by breaking down glycogen
  21. What is the standard source of insulin in the U.S.?
    Recombinant DNA
  22. What three of the modified insulins act more rapidly than natural insulin but have a shorter duration of action.
    —insulin lispro, insulin aspart, and insulin glulisine—
  23. When the insulin molecule has been altered (to induce a longer effect), we refer to the product as ?
    human insulin analog
  24. Short duration insulins are divided into 2 groups
    • rapid acting (insulin lispro, insulin aspart, and insulin glulisine)
    • and slower acting (regular or “natural” insulin).
  25. What is the trade name of lispro?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Humalog
    • 15-30 min
    • .5-2.5 hr
    • 3-6.5 hr
    • SQ, IV
    • 15 minutes before food
  26. What is the trade name of aspart?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Novalog
    • 10-20 min
    • 1-3 hours
    • 3-5 hours
    • SQ, IV
    • 5-10 min before meals
  27. What is the trade name of glulisine?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Apidra
    • 10-15 min
    • 1-1.5 hr
    • 3-5 hr
    • SQ, IV
    • 15 min before meal, no later than 20 min after starting
  28. What is the trade name of Regular insulin?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Humulin R, Novolin R
    • 30-60 min
    • 1-5 hr
    • 6-10 hr
    • SQ, IV, IM
    • 30 min before meals
  29. What is the trade name of 70% Insulin aspart/30% Insulin aspart?
    What is the onset?
    What is the Peak?
    Duration?Route?
    Administration in relation to meals?
    • NovoLog Mix 70/30
    • Rapid
    • 1-4 hours
    • Up to 24 hours
    • SQ
    • 15 min before or immediately after
  30. What kind of insulin is suitible to be mixed with short-acting insulins?
    Of the longer acting insulins in current use, NPH insulin is the only one suitable for mixing with short-acting insulins.
  31. What is the trade name of NPH insulin?
    What is the onset?
    What is the Peak?
    Duration?Route?
    Administration in relation to meals?
    • Humulin N, Novolin N
    • 60-90 min
    • 6-14 hours
    • 16-24 hours
    • SQ
    • used to provide glycemic control between meals
  32. What is the trade name of 70% Insulin NPH/30% Insulin regular?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Humulin 70/30, Novolin 70/30
    • 30-60 min
    • 1.5-16 hr
    • up to 24 hr
    • SQ
    • Not included.
  33. What is the trade name of Insulin detemir?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Levemir
    • Slower than NPH
    • 6-8 hrs
    • 12-24 hrs
    • SQ
    • for basal control
    • *Do not mix with other insulins. NO IV
  34. What is the trade name of Insulin glargine?
    What is the onset?
    What is the Peak?
    Duration?
    Route?
    Administration in relation to meals?
    • Lantus
    • 70 min
    • No Peak
    • 24 hours
    • SQ
    • For Basal Control
  35. Why is ultralente insulin rarely used?
    due to risk of hypoglycemia
  36. When mixing insulins, the short acting insulin should be drawn into the syringe first. Why?
    To avoid contaminating the stock vial of the short-acting insulin with NPH insulin.
  37. Which 4 insulins can be administered IV?
    insulin aspart [Novolog], insulin lispro [Humalog], and insulin glulisine [Apidra]
  38. IV insulin is used to treat what?
    diabetic ketoacidosis
  39. Tight Glucose Control
    The process of maintaining glucose levels within a normal range, around the clock
  40. What are the benefits of tight glucose control?
    • decrease in clinically significant kidney disease
    • decrease in neuropathy
    • decrease in serious ophthalmic complications.
  41. What are the drawbacks of tight glucose control?
    hypoglycemia
  42. What increases the need for insulin and possible dosage adjustment?
    infection, stress, obesity, the adolescent growth spurt, and pregnancy after the first trimester.
  43. What decreases the need for insulin and possible dosage adjustment?
    exercise and during the first trimester of pregnancy.
  44. What are the 6 main families of Oral Hypoglycemics?
    • biguanides,
    • sulfonylureas,
    • glinides (meglitinides),
    • thiazolidinediones (glitazones),
    • alpha-glucosidase inhibitors,
    • gliptins.
  45. In what 2 ways do the oral agents work?
    • Some of them—notably the sulfonylureas, glitazones, and glinides—actively drive blood glucose down.
    • Others—notably metformin (a biguanide) and the alpha-glucosidase inhibitors—don't drive blood glucose down; rather, they simply modulate the rise in glucose that happens after a meal.
  46. What is an example of a Biguanide?
    How does it work?
    • Metformin;
    • lowers blood glucose and improves glucose tolerance in three ways. First, it inhibits glucose production in the liver. Second, it reduces (slightly) glucose absorption in the gut. And third, it sensitizes insulin receptors in target tissues
  47. Metformin (Glucophage) is likely to....
    a rare effect is
    • cause weight loss
    • lactic acidosis
  48. What is an example of a Sulfonylurea?
    How does it work?
    • Glyburide (DiaBeta)
    • Stimulates insulin release and reduces glucagon levels
    • **avoid during pregnancy
  49. If you mix a Sulfonylurea and alcohol, what happens?
    If you mix a Sulfonylurea and an NSAID, what happens?
    If you mix a Sulfonylurea and a Beta Blocker, what happens?
    • nausea, vomiting, facial flushing, palpations
    • low blood sugar
    • diminishes effect of sulfonylurea
  50. What is an example of a Meglinatide?
    How does it work?
    • repliginide (prandin)
    • Stimulates insulin release
  51. What are some adverse effects of Meglinatides?
    • Hypoglycemia
    • *patients eat no later than 30 minutes after taking the drug.
  52. What is an example of a Thiazolidinedione?
    How does it work?
    • rosiglitazone (Avandia)
    • turns on insulin-responsive genes that help regulate carbohydrate and lipid metabolism. As a result, cellular responses to insulin are increased
  53. What are some adverse effects of a Thiazolidinedione?
    • fluid retention= edema
    • monitor liver function
    • Increase in LDL and TG
  54. What is an example of a Alpha glucosidase Inhibitor?
    How does it work?
    Adverse effects?
    • acarbose (Precose).
    • Delays the digestion of carbohydrates, resulting in a smaller postprandial rise of blood glucose.
    • GI: flatulence, cramps, diarrhea, etc
  55. What is an example of a Gliptin?
    sitagliptin (januvia)
  56. What is an example of Incretin Mimetic?
    How does it work?
    • exenatide (Byetta)
    • Slows gastric emptying
    • Stimulates glucose dependent release of insulin
    • Inhibits post prandial release of glucagon
    • Supresses appetite

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