Hormones

Home > Preview

The flashcards below were created by user kimiko on FreezingBlue Flashcards.


  1. What are the four hormone classes (classified by where they are secreted from)
    • 1. hypothalamic and pituitary hormones
    • 2. thyroid hormones
    • 3. corticosteroid hormones
    • 4. pancreatic hormones
  2. what are the 2 receptors that hormones use?
    • GCPR
    • TKR
    • intracellular
  3. can hormones bind to ion channel receptors?
    no because hormone responses are long maintenance and ion channels are for fast responses
  4. which hormones come from the anterior pituitary?
    • TSH
    • GH
    • ACTH
    • prolactin
    • LH/FSH
  5. Which hormones come from the posterior pituitary?
    • ADH
    • oxytocin
  6. where are the hormones (ADH and Oxytocin) that are stored in the posterior pituitary synthesized?
    hypothalamus
  7. what does ADH (antidiuretic hormone) do?
    promotes the retention of H2O by the kidneys
  8. what two things does oxytocin do?
    • 1.stimulates smooth muscle contraction of the uterus during parturition
    • 2. stimulates contractions of the mammary myoepithelial cells (milk ejection reflex)
  9. can ADH and oxytocin bind to each other receptors?
    yes, because they are similar in structure
  10. what is the mechanism of action of AVP (argentine vasopressin?
    • vasopression binds to v1 receptors--> phospholipase c--> ip3, Ca2+--> conraction of vascular and GI smooth muscle
    • Vasopressin binds to v2 --> adenylate cyclase --> increase in CAMP --> insertion of aquaporin into luminal membrane of renal medullary collecting ducts
  11. what is the Oxytocin mechanism of action?
    oxytocin binds to the OT receptor--> phospholipase C --> IP3, Ca2+ --> contraction of uterine smooth muscle and mammary myoepithelial cells
  12. what are the clinical uses of vasopressin?
    • 1. emergency treatment of bleeding esophageal varicose (varicose veins)
    • 2. acute hemorrhagic gastritis
    • 3. Diabetes insipidus
  13. what are the side effects of using vasopressin?
    headache, broncho-constriction, sweating, constriction of coronary arteries
  14. what are the clinical uses of oxytocin?
    • 1.induction of term labor
    • 2. control of postpartum bleeding
    • 3. maintain uterine tone
    • 4. increasing milk ejection
  15. how is oxytocin administered?
    nasal spray 2-3 min before breast feeding
  16. what are the sites of action of oxyctocin?
    uterus and mammary glands
  17. what are the side effects of oxytocin?
    • hypertension
    • water retention
    • fetal death
  18. what is GHRH do?
    growth hormone releasing hormone binds to the Gs -protein coupled receptors and stimulates the release of GH
  19. what does GHIH do?
    growth hormone inhibiting hormone inhibits the release of GH
  20. which type of receptor does GH bind to?
    tyrosine kinase receptors
  21. what does somatostatin do?
    factor that inhibits the release of insulin and glucagon
  22. what are the direct effects of GH?
    • 1. induce liver and other tissues of create IGFs
    • 2. anti-insulin actions--> increased lipolysis and increased blood sugar
  23. what are the effects of IGFs (aka indirect effects of GH)?
    • 1. increased cartilage formation and skeletal growth
    • 2. increased protein synthesis and cell growth and proliferation
  24. what happens when there is hyper secretion of GH in children?
    gigantism
  25. what happens when there is hyper secretion of GH in adults?
    acromegaly - progressive enlargement of head, face, hands, feet, thorax, heat intolerance, sweating, fatigue
  26. what causes hyper secretion of GH in adults?
    tumor in the brain or pituitary gland
  27. that happens when there is a deficiency of GH?
    postnatal growth retardation
  28. what are the 3 treatments of GH deficiency?
    • 1. somatropin (GH)
    • 2. IGF
    • 3. Sermorelin (GHRH receptor agonist)
  29. why would you give IGF-1 rather than GH?
    sometimes when you give growth hormone it won’t work so you give IGF because growth is an indirect effect through IGF. some patients don’t have problems with having growth hormones but the receptors might be resistant to GH. growth is modulated by IGF not GH. IGF will bind to receptors in the bone.
  30. what is the treatment of hyper secretion of GH?
    octreotide--> act to increase secretion of GHIH
  31. where is the site of drug action for sermorelin?
    anterior pituitary
  32. where is the site of drug action for octreotride?
    anterior pitutiary
  33. where is the site of drug action for somatropin?
    liver and indirectly growth of peripheral tissue
  34. what is the secretion of prolactin inhibited by?
    dopamine
  35. what is a lactotroph?
    a structure that secretes prolactin from the anterior pituitary
  36. what is the primary target of prolactin?
    mammary gland
  37. what are the symptoms of hyperprolactinemia?
    • female: anovulation, oligomenorrhea, amenorrhea
    • male: decreased testosterone synthesis, decreased spermatogenesis
  38. what is the treatment for hyperprolactinemia?
    dopamine agonists (bromocriptine, pergolide) which bind to dopamine receptors and it will inhibit the anterior pituitary so prolactin is not secreted
  39. what are the gonadal steroid hormones?
    • estrogens
    • progestin
    • androgens
  40. what are the adrenocortical hormones?
    • glucocoritcoids
    • mineralcoritcoids
    • androgens
  41. what are steroid hormones synthesized from?
    cholesterol
  42. what does the hypothalamus secrete in response to stress?
    CRH (corticotropin releasing hormone) and ACTH releasing hormone
  43. What kind of cycle does the release of coritisol follow?
    circadian rhythym
  44. what is the mechanism of action of coritsol?
    cortisol binds to glucocoriticoid receptor in cytoplasm --> receptor is translocated into the nucleus --> binds to the DNA response element --> modulates the transcription of genes
  45. what are the physiological effects of glucocorticoids (9)?
    • 1. stimulation of gluconeogenesis from muscle protein
    • 2. peripheral muscle protein degradation is accelerated
    • 3. mobilization of amino acids from extra hepatic tissues
    • 4. inhibition of glucose uptake in muscles
    • 5. stimulation of fat breakdown in adipose tissue
    • 6. increase glycogen storage in liver
    • 7. breakdown of connective tissue and bone
    • 8. decreases immune response
    • 9. decreases antibody response
  46. what kind of drug is it if it ends in 'SONE'?
    glucocorticoid
  47. what are the 3 causes addison's disease?
    • 1.destruction of the adrenal glands by infection
    • 2. Destruction of the adrenal glands by and autoimmune attack
    • 3. An inherited mutation in the ACTH receptor on adrenal cells
  48. what are the symptoms of addison's disease?
    • hypoglycemia
    • Na/K imbalance
    • dehydration
    • hypotension
    • weight loss
    • weakness
    • loss of stress resistance
    • collagen diseases
    • dermatologic diseases
    • eye diseases
    • GI diseases
    • respiratory illness
    • allergic states
    • rheumatoid arthritis
    • organ transplant
    • autoimmune disorders
    • neoplastic diseases
  49. what are the side effects of glucocorticoids?
    • symptoms of cushiness
    • euphoria
    • increased weight
    • diabetes
    • hypertension
    • imbalanced na/k
    • hair growth
    • osteoporosis
    • gastric ulcers
    • thin skin
    • adrenal suppression
    • infections
  50. what causes cushing's syndrome?
    • hyper secretion of glucocorticoids
    • normally by a adrenal tumor or excess ACTH
  51. what are the symptoms of cushing's syndrome?
    • hyperglycemia
    • hypertension
    • muscle weakness
    • edema
    • loss of muscle and bone mass
    • abnormal fat disposition

Card Set Information

Author:
 kimiko
ID:
 276153
Filename:
 Hormones
Updated:
2014-06-09 05:57:38
Tags:
170b
Folders:

Description:
170b
Show Answers:

What would you like to do?

Home > Flashcards > Print Preview