1.11.3 endocrine glands III

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efrain12
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295082
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1.11.3 endocrine glands III
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2015-02-06 15:32:42
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Endocrine glands III
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  1. What do f cells produce?
    Pancreatic polypeptide
  2. Glucagon is a
    Polypeptide made of 29 AA a
  3. Function of glucagon (4)
    -glycogenolysis

    -glucoeneogenesis

    -increase sblood glucose

    -lipolysis
  4. glycogenolysis
    Breakdown of glycogen
  5. gluconeogenesis
    Synthesis of glucose from AA or lipids
  6. lipolysis
    Breakdown of stored lipids in adipose cells
  7. Glucagon) PKA/camp system
    Main target organ is the liver
  8. Regulation of glucagon) 3
    1. Gland pancreas secretes glucagon ot target organ liver

    2. If blood lguose high then it will inhibit the pancreas

    3. If blood glucose low then it will stimulate pancreas
  9. Insulin) structure (3)
    Protein made up of 51 AA

    2 chains that are held together by disulfide bonds

    proinsulin that is later cleaved
  10. Insulin) functions (4)
    -lipogenic

    -glycogenic

    -blood glucose decreases

    -increase glucose trassnprot

    -increase protein synthesis
  11. Insulin) lipogenci
    Glucose converted to fat
  12. Insulin) glycogenic
    Storage of glucose as glycogen
  13. Insulin) blood glucose decr3eases
    Transfers glucose in blood to cells
  14. Regulation of insulin) 4
    1. Pancreas releases into blloood

    2. Glucose absorbed by muscle, liver etc

    3. If glucose, fatty acids, pro are high then it will stimulate pancreas

    4. If glusoe low, then it will inhb9it pancreas
  15. Insulin is secreted
    After meals
  16. Glucagon is secreted
    Between meals
  17. Regulation of blood glucose by insulin
    Glucose trasnproter
  18. Regulation of blood glucose by insulin) receptor
    Tyrosine Kinase which is embedded in cell membrane
  19. Regulation of blood glucose by insulin) insulin binds to
    Tyrosine kinase
  20. Insulin does not work though
    pka/cAMP nor steroid mechanism
  21. When insulin binds to tyrosine Kinase, glucose transporters are recruited to go into membrane to suck up the glucose
  22. DM) type 1
    Insulin dependent where very little insulin I sporduced
  23. DM) how is type 1 caused?
    Destruction of beta cells of islets
  24. DM) Type ii
    Non- insulin dependent

    *insulin resistant
  25. DM) type ii  
    causes of insulin resistant (3)
    • -ineffective insulin receptor
    • *not being able to bind to insulin

    -decrease production of glucose transporter

    • -some decrease in insulin productions
    • *not to the extent of type 1
  26. Onset of DM
    Even thugh there is a lot of glucose in the blood, the cells can't absocrb it so the body reacts as it is starving and looks for other sources of fuel
  27. 3 main pathways body resorts when onset of DM
    -lipolysis

    -glycogenolysis

    -gluconeogenesis


    ****all 3 are so body can fuel itself
  28. Onset of DM) lipolysis
    If glucose isn't used as fuel, then body will mobilize fats in this case. Fatty acids start to accumulate creating ketoacidosis
  29. ketones are
    STRONG ACIDS
  30. If there are excessive amounts of ketones then
    It will spill into urine
  31. The pathways body uses is to use glucose for fuel but with no insulin can't baostr it so it ssatrts to accumulate
  32. Why does kidneys allow glucose and ketones in urine?
    Too much to reabsorbed
  33. Wit excess ketones and glucose spilling into urine) polyuria
    • Excess urine production
    • *osmotic effect of glucose, ketones,
    •  bc water will be attracted to it
  34. Wit excess ketones and glucose spilling into urine) glucosuria
    Excess glucose in urine
  35. Wit excess ketones and glucose spilling into urine) polidypsia
    Excess drinking bc body gets dehydrated by peeing everyhting
  36. Wit excess ketones and glucose spilling into urine) polyphagia
    Excess eating but the person reamind weak, tired, loses weight bc body thinks its starving bc of lack of glucose uptake
  37. DM results in (4)
    -dehydration

    -acidosios leading to increase respiration rate

    -tissue breakdown

    -death if untreated
  38. hyperinsulinemia
    Opposite problem of DM
  39. hyperinsulinmia reuslts
    From too much insulting or being released to quickly leads to drop in blood glucose
  40. How do you treat hyperinsulimain?
    Giving CHO containing foodfs

    And frequent meals
  41. What population is hypoglycemia common in?
    ahtletes
  42. Gonads ) ovaries secrete
    -estrogen

    -progesterone
  43. Gonads ) what does estrogen and progesterone allow (3)
    -maturation of reproductive tract

    -breast developemtn

    -ovarian cycling
  44. Gonads ) testes secret
    test
  45. Functions of test (4)
    -maturation of male repro organs

    -secondary sex characteristics

    -sperm production

    -sex drive
  46. Regulation of gonadotpriic hormone ) 4
    1. Hypo release GnRH

    2. Pit release FSH, LH

    3 gonads release estro, pro, test

    4. If levels get oo high they inhibit fish/lh and gnRH
  47. Pineal gland
    Receives indirect stimulating from visual pathways
  48. Pineal gland: melatonin
    Regulation of sleep wake cycles
  49. Thymus glands) helps maturation of immune system (2)
    -thymosin= t-lymphocytes

    thymopoietin= t-lymphocytes

    **responsible for wbc
  50. Heart)
    Atria contain specials muscle cells
  51. eart) atrial natriautic factor (4)
    -reduces blood volume

    -blood pressure

    -blood sodium concentrations

    -inhibits aldosterone relaxes from adrenal ortex
  52. Placenta) secrets 3 hormones during pregnancy
    -HCG

    -estrogen

    -progesterone
  53. kidney) erythpotiein
    Signals bone marrow in increase production  of reed blood cells
  54. Skin) cholecalciferol
    Inactive form of vitamin D3 that heps in absorption of calcium and works in concert with parathyroid bromine to absorb calcium
  55. GI tact )
    potmote and coroditae digetion
  56. GI tarts secracrte (4)
    -gastrin

    -serotoning

    secretin

    Cholecystokinin




    These will promote and coordinate digestion

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