CDE exam

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Author:
janeg70
ID:
285803
Filename:
CDE exam
Updated:
2014-10-14 16:56:51
Tags:
cde
Folders:
Diabetes basics
Description:
understanding diabetes
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  1. Amylin
    • a hormone formed by beta cells in the pancreas. hormone co-secreted with insulin (made in beta cells). This hormone helps in 3 ways:
    • 1. slows (normalizes) gastric emptying
    • 2. suppresses glycogen from the liver
    • 3. regulates food intake by centrally mediated

    first phase response
  2. Does the hormone amlyin help with pre or post prandial blood glucose?
    POST PRANDIAL GLUCOSE
  3. Incretin (gastrointestinal hormone)
    aka GLP-1 receptors that are secreted upon the ingestion of food from the GI tract. Increases insulin response from beta cells.

    first phase response
  4. what is the synthetic drug to mimic amylin?
    PRAMLINTIDE (SYMLIN)
  5. what meds try to mimic GLP-1 receptors?
    Exenatide (Byetta)

    liraglutide (victoza)

    bydureon
  6. what does GLP-1 stand for?
    Glucagon like peptide-1
  7. Functions of GLP-1?
    • -increase insulin secretion in pancreas
    • -decreases glucagon secretion
    • -
  8. Alpha cell
    Alpha cells make and release a hormone called glucagon. The body sends a signal to the alpha cells to make glucagon when blood glucose falls too low. Then glucagon reaches the liver where it tells it to release glucose into the blood for energy. (MAKES SUGAR!)
  9. beta cell
    a cell that makes insulin. Beta cells are located in the islets of the pancreas.-
  10. What hormones does beta cells release?
    insulin, C-peptide, and amylin
  11. What does C-peptide do?
    Helps to prevent neuropathy and other vascular deterioration
  12. DPP-4 Inhibitor (gut hormone)
    Blocks the action of DPP-4 enzyme which destroys incretin
  13. Basal rate
    a steady trickle of low levels of longer-acting insulin

    • (second phase insulin release)
    • Baseline insulin
  14. Bolus rate
    Insulin poured into bloodstream rapidly with a meal or snack to cover glucose entering blood (first phase insulin release)
  15. Pre-diabetes diagnosis
    • A1c= 5.7-6.4
    • FPG= 100-126
    • OGTT= 140-199
  16. Diabetes diagnosis
    • FPG= >126
    • A1c= >6.5%
    • OGTT= >200
  17. Signs/Symptoms of DKA?
    N/V/D,poluria,polydypsia,polyphagia,weight loss,high BS,lethargy,+ketones,fruit breath,dehydration,blurred vision
  18. Honeymoon phase
    When 10% of pancreas may produce insulin. Must be careful to avoid too much insulin dosing in beginning to prevent hypoglycemia. may last few weeks up to 1 year
  19. Target A1c?
    <7% ADA, <6.5% AACE
  20. Fasting pre-prandial glucose?
    70-130 ADA, <110 AACE
  21. Post prandial target?
    <180 ADA, <140 AACE
  22. HS glucose
    100-140 ADA, 100-140 AACE
  23. What is target BP for pt w/ dm?
    <130/<80

    • *start behavior therapy if 130-139 and 80-89
    • *start behavior + meds if >140/>90
  24. Target cholesterol?
    <200
  25. Target LDL?
    <100
  26. Target HDL
    • Men= >40
    • Women= >50
  27. target TG?
    <150
  28. What are microvascular side affects of diabetes complications?
    Nephropathy (kidneys), retinopathy (eyes), neuropathy (nerves)
  29. Macrovascular dm complications?
    CAD, STroke, PVD
  30. Gluconeogenesis
    Formation of new glucose from protein or fat
  31. Glycolysis
    breakdown of glucose for energy
  32. glycogen
    main form of carbohydrates storage in liver and muscle, readily converted to glucose to satisfy energy needs
  33. glycogenesis
    when glucose turns into glycogen for storage to use as energy later
  34. glycogenolysis
    the breakdown of glycogen to glucose in order to use the stored energy
  35. lipogenesis
    formation of lipids to store energy
  36. lipolysis
    breakdown of lipids to produce energy
  37. Why does insulin become ineffective in most type 2 diabetes patients?
    It starts with insulin resistance where body doesn't use insulin effectively which causes body to overcompensate and produce more than necessary which tires out the B cells and causes damage to proper function

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