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2013-03-26 18:04:19

BC Boston College CRNA NU 672 Pathophysiology
Show Answers:

  1. How do hormones travel in the body?
    • Circulate as free, unbound molecules
    • Circulate as hormones attached to transport carriers
  2. What are the characteristics of the hormones that circulate unbound?
    • Water soluble.
    • Peptide hormones and protein hormones
    • Short half life (insulin 3-5 min)
  3. What are the characteristics of the hormones that circulate attached to transport carriers?
    • Liver synthesized proteins
    • most likely lipid soluble
    • half life is much longer (related to the degree of protein binding)
    • steroid and thyroid hormones are carried by specific carrier proteins from the liver
  4. How do unbound hormones affect change?
    • Because they are water soluble, they cannot enter the wells on their own.
    • They exert their effects via cell surface receptors and through second messengers (cAMP)

    • The hormone itself is the first messenger.
  5. How do bound hormone affect change?
    • Because they are lipid soluble, they can pass freely through the cell membrane. 
    • Nuclear or cytoplasm receptors receive it
  6. What are the three mechanisms of hormonal regulation?
    • Receptor modulation
    • Negative feedback
    • Neural regulation
  7. How does receptor modulation work?
    • The concentration of the hormone does NOT change, and it does not go inside.
    • It involves a change in target cell sensitivity
    • ---Up regulation: when low concentrations of a hormone increase the number of receptors per cell
    • ---Down regulation: when high concentrations of a hormones decrease the number of receptors per cell

  8. How does negative feedback work?
    • Think of the HPA axis!
    • The concentration of the hormone changes.
    • Basically a large concentration of a chemical eventually turns the whole cascade off.
  9. From where do "releasing" hormones come?
  10. From where do "tropic" hormones come?

    These hormones are typically the "mediating bridge."
  11. What is neural regulation?
    • Nervous system is involved in regulating the hormonal activity.
    • i.e. adrenal medulla releases epinephrine in response to SNS stimulation
  12. What hormones come from the anterior pituitary?
    • growth hormone
    • thyroid stimulating hormone
    • ACTH
    • FSH
    • prolactin
    • MSH
  13. What hormones come from the posterior pituitary?
    • ADH
    • oxytocin
  14. What is the function of oxytocin?
    Primary target organ is myoepithelial cells in mammary tissue, stimulates uterine contractions, may have a role in sperm motility
  15. What is the function of ADH?
    controls the serum osmolality by increasing water reabsorption in the distal tubules and collecting ducts of nephron
  16. SIADH has too much or too little ADH?
    too much!

    leads to water retention and specific gravity will be high
  17. What are the causes of SIADH?
    • ectopic secretion (paraneoplastic) in carcinomas
    • post-op crani/pituitary surgery
    • meds: antidepressants, anesthetics, barbiturates, morphine
  18. What is the treatment for SIADH?
    • Treat the underlying cause
    • Fluid restriction
    • Correct hyponatremia (water and Na go in the same direction)
  19. DI has too much or too little ADH?
    Too little!
  20. What are the two types of DI?
    • Nephrogenic: failure of the nephron to respond
    • Neurogenic: decreased synthesis
  21. Patient has urine specific gravity of 1.001-1.005. Do you expect DI or SIADH?
    DI! Patient is pouring out liters of urine, and so it will be very dilute.
  22. How do you treat DI?
    Vasopressin or DDAVP
  23. Endocrine hypofunction of posterior pituitary may mean what disorders?
    ADH and SIADH
  24. What problems might one expect to see with problems concerning anterior pituitary?
    Thyroid problems, prolactin problems (hyperprolactinemia), gigantism/acromegaly, etc.
  25. What does prolactin do?
    promotes breast development and lactation in women, helps with fertility and testosterone in men
  26. Growth hormone excess can affect kids and adults. How will they present?
    Kids will have proportional gigantism because it affects the whole body, not a specific organ.

    Adults will have large hands, nose, and coarse facial features. This is because hepatic secretion IGF-1.
  27. Does sleep affect growth hormone release?
    Yes you need at least two hours a day!
  28. What two pathways does growth hormone affect?
    Anti-insulin effects: decrease adiposity, increased blood glucose via CHO metabolism

    Growth-promoting actions via liver:IGF-1 > incr protein synthesis > increased linear growth of bone and cartilage, incr size and function of organs, incr lean muscle mass
  29. How does decreased growth hormone manifest?
  30. What does luteinizing hormone do?
    It promotes growth of testicular tissue and stimulates ovulation.
  31. What does follicle stimulating hormone do?
    stimulates spermatogenesis and testosterone production in men and ovarian follicles, estradiol and progesterone in women
  32. What does adrenocorticotropic hormone do?
    stimulates release of adrenal corticosteroids or androgens. It's secreted in response to low cortisol levels, diurnal rhythms, and stress
    • 1) cortex
    • 2) medulla
  33. What does the adrenal cortex secrete?
    • sex steroids
    • mineral corticosteroids
    • glucocorticoids
  34. What does the adrenal medulla secrete?
    Catecholamines (epinephrine, etc.)
  35. What are mineral corticosteroids responsible for?
    aldosterone secretion in response to angiotensin II >> increases the activity of the sodium pump (conserve Na, get rid of K)
  36. What are glucocorticoids responsible for?
    cortisol, numerous metabolic, anti-inflammatory effects, growth suppressing effects
  37. What are the immunologic and anti-inflammatory effects of glucocorticoids?
    • Decrease capillary permeability and stabilize lysosomal membranes to block inflammation
    • Suppress humoral and cell-mediated immune responses
    • Suppress fibroblast activity
    • Inhibit prostaglandin synthesis
  38. What might you see in adrenal cortex insufficiency?
    Primary insufficiency: Addison Dz (high ACTH)

    Secondary insufficiency: HPA axis is not enough so there isn't enough ACTH; hypopituitarism, rapid withdrawal of glucocorticoids (lazy organ)

    Weakness, GI disturbances, hyperpigmentation (if ACTH is increased like in Addison), hypoglycemia, hypotension (lacking aldosterone)
  39. What will you see in Addison's Disease?
    nausea, weight loss, weakness, hyperpigmentation, hypotension, hyperkalemia, hypoglycemia
  40. Is Cushing Syndrome a result of hypo or hyper function?
    Hyperfunction of adrenal cortex, so you get hypercortisolism
  41. What is the difference between Cushing Syndrome and Disease?
    Syndrome: chronic hyperfunction of adrenal cortex

    • Disease: too much ACTH from pituitary
    • --Primary: problem with adrenal gland
    • --Secondary: pituitary adenoma
  42. How will a patient with Cushing Syndrome present?
    • Weight gain with abnormal distribution, abdominal striae, glucose intolerance (>>DM), protein wasting, osteoporosis, hypercalciuria, loss of collagen, HTN, mood disturbances, impaired inflammation and immune responses, poor wound healing, gastric bleeding
  43. How does adrenal medulla hyperfunction manifest?
    • Because the medulla secretes catecholamines, you may see very high BP
    • Pheochromocytoma
  44. How does adrenal medulla hypofunction manifest?
    It doesn't really. Other organs will take over to secrete catecholamines.
  45. What is the role of calcitonin?
    Decreases serum calcium by inhibiting osteoclastic activity and increase osteoblastic activity
  46. What do thyroid hormones do?
    Regulate metabolism
  47. Thyroid hyperfunction will look like:
    hypermetabolism with multisystem involvement: anxious, incr HR, weight loss, heat intolerance, dyspnea, sweating, goiter, exophthalmos, diarrhea...

    "Thyroid storm" or thyrotoxicosis or Grave's
  48. How does the autoimmune process of Grave's Disease work?
    Antibody binds to TSH receptors on thyroid. TSH cannot take control.
  49. How does one get hypothyroidism?
    Autoimmune destruction, Hashimoto thyroiditis, iodine deficiency, iatrogenic, congenital defects
  50. How does hypothyroidism present?
    Newborn screening: must be caught within 6 weeks or else they will have mental retardation and cretinism

    constipation, cold intolerance, depression, weight gain, dry/cold skin, slow reflexes
  51. What happens if you don't treat hypothyroidism?
    Myxedema: dry, pale ski, thinning of lateral eyebrows, puffy face...

    Myxedema coma: hypothermia, respiratory depression, cardiovascular collapse
  52. How do you diagnose diabetes?
    • Random glucose > 200
    • Fasting glucose > 126
    • GTT > 200
  53. What causes type 1 diabetes?
    • Autoimmune disease that likely is related to genetics. 
    • Presence of Islect Cell Antibodies
  54. How do people get DM2?
    Strong genetic link, strong obesity link
  55. How do people with DM2 react to insulin? Do they still make it?
    • Yes ppl can have high, normal, or low insulin levels.
    • People may develop insulin resistance accompanied by a relative insulin deficiency or impaired release of insulin in relation to glucose levels
  56. Metabolic syndrome is characterized by:
    • central obesity (apple, not a pear)
    • high BP
    • high triglycerides
    • low HDL
    • insulin resistance
  57. How do people typically present before they are diagnosed with DM?
    • polydipsia
    • polyuria
    • polyphagia
  58. What is a complication of type 1 diabetes?
  59. How does one get DKA?
    infection, stressors (trauma, surgery, MI), inadequate insulin dose
  60. What are the clinical manifestations of DKA?
    • Ketosis: Kussmauls respirations, fruity breath (ketones from liver), nausea, abdominal pain
    • Dehydration or electrolyte loss, polyuria, polydipsia, weight loss
    • Dry skin, sunken soft eyeballs
    • Lethargy, coma
    • Serum glucose > 250
    • serum and urine ketones: positive
    • serum pH < 7.3 (acidotic)
    • serum HCO3 < 15 (metabolic acidosis)
  61. How does DM2 patients tend not to have DKA?
    • Just a little bit of insulin will prevent ketone formation
  62. What is a complication of elderly people with DM2?
  63. How does a person with DM2 get HHNK?
    infection, stressors, poor PO intake

    Often occurs in profoundly dehydrated people with insufficient insulin
  64. What are the clinical manifestations of HHNK?
    • neurologic: confusion, seizures, hemiparesis
    • marked dehydration and fluid/electrolyte imbalances
    • serum glucose > 600
    • serum & urine ketones: negative
    • serum pH > 7.4
    • serum HCO3 > 20
    • hyperosmolar state
  65. What are chronic complications of DM?
    • Macrovascular: CAD, cerebrovascular, PVD, foot ulcers
    • Microvascular: nephropathy, retinopathy, neuropathy (caused by chronic hyperglycemia)