Hypothalamic and Pituitary Relationships Pt. 1 (Creamer) Flashcards

1
Q

What are the sub-structures a/w the pituitary gland and how is it connected to the hypothalamus?

A
  • pituitary gland (hypophysis)
  • anterior pituitary (adenohypophysis): epithelial portion
  • posterior pituitary (neurohypophysis): neural portion
  • hypophysial stalk: physical connection between hypothalamus and post pit; hormonal connection between hypothalamus and ant pit (sends releasing hormones to ant pit)
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2
Q

What effects would be seen with damage to the hypophysial stalk, and with tumors in the pituitary?

A
  • hypophysial stalk damage: would inhibit releasing hormones to ant pit, leading to loss of function in this area; oxytocin and vasopressin would still go to post pit, thus function may be reduced but still retained
  • pituitary tumor: due to anatomical location in close a/w optic nerve, sx may include visual problems and dizziness
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3
Q

How are the hypothalamus and posterior pituitary connected?

A
  • post pit is neural tissue, w/ its cell bodies located in hypothalamus (supraoptic nucleus (SON) and paraventricular nucleus (PVN))
  • the hypothalamus produces neuropeptides in these nuclei and, via axons, sends the hormones (vasopressin and oxytocin) to the post pit
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4
Q

How is the hypothalamus connected to the anterior pituitary gland?

A
  • communications between the two are both neural and hormonal
  • hypothalamic neurons produce releasing/inhibiting hormones
  • the hormones are secreted via the hypothalamic-hypophysial portal blood vessels into the anterior pituitary where they either cause release/inhibition of downstream hormone production in ant pit
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5
Q

Compare and contrast the connections between the hypothalamus and posterior pituitary vs the anterior pituitary:

A
  • posterior pituitary: connections are neural only, hormones are produced in hypothalamus and projected via axons to the posterior pituitary (aka no hormones are actually prod in post pit)
  • anterior pituitary: connections are both neural and hormonal, releasing/inhibiting hormones are prod in hypothalamus that are secreted via hypothalamic-hypophysial portal to the anterior pituitary where hormone production is either stim/inhibited
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6
Q

How are the hormones of the anterior pituitary organized?

A

(via structure and function homology)

  • ACTH family:

hypothalamus releases CRF (+) > corticotrophs > ant pit secretes ACTH

  • TSH, FSH, LH family:

hypothalamus releases TRH (+) > thyrotrophs > ant pit secretes TSH

hypothalamus releases GnRH (+) > gonadotrophs > ant pit secretes LH and FSH

*hormones in this family all share same alpha subunit, the beta subunit is the part that differs*

  • GH and prolactin family:

hypothalamus releases GHRH (+) or somatostatin (GHIH) (-) > somatotrophs > ant pit secretes GH

hypothalamus releases PIF (dopamine) (-) or TRH (elevated) (+) > lactotrophs > ant pit secretes PRL

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7
Q

Define primary, secondary, and tertiary endocrine disorders:

A
  • primary: defect of hormone production/release within peripheral glands
  • secondary: defect of hormone production/release within pituitary gland
  • tertiary: defect of hormone production/release within hypothalamus
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8
Q

Describe the HPG hormonal axis in terms of the testes:

A
  • hypothalamus releases GnRH in pulsatory waves
  • GnRH stimulates anterior pituitary to produce/release LH and FSH
  • LH acts on Leydig cells of the testes, causing them to produce testosterone
  • testosterone along with FSH act on the Sertoli cells of the tests to produce androgen-binding proteins and activate spermatogenesis
  • this is a negative feed back system:

testosterone inhibits ant pit production of LH and hypothalamic production of GnRH

inhibin (prod by Sertoli cells) inhibits ant pit production of FSH

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9
Q

Describe the HPG hormonal axis in a female:

A

most phases of the menstrual cycle follow negative feedback system:

  • hypothalamus releases GnRH in pulsarory waves
  • GnRH stimulates anterior pituitary to produce/release LH and FSH
  • LH acts on Theca cells of the ovaries, causing them to produce androgens
  • androgens along with FSH act on the Granulosa cells of the ovaries to produce progestins and estrogens
  • feedback: progestins, estrogens, and inhibin produced by granulosa cells inhibit hypothalamic production of GnRH and ant pit production of LH and FSH

ovulation portion of the menstrual cycle follows a positive feedback system:

  • hypothalamus releases GnRH in pulsatory waves
  • GnRH stimulates anterior pituitary to produce/release LH and FSH
  • LH acts on Theca cells of the ovaries, causing them to produce androgens
  • androgens along with FSH act on the Granulosa cells of the ovaries to produce estrogens
  • feedback: estrogens produced by the granulosa cells increase production of GnRH in hypothalamus and LH and FSH in the ant pit
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10
Q
  • condition caused by excessive exposure to growth hormone by anterior pituitary causes liver to over-produce IGF-1 after closure of growth plates
  • can cause insulin-insensitivty in peripheral organs/cells which leads to TIIDM
  • sx: enlarged hands, feet, face along w/ a slew of other sx
A

acromegaly

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11
Q

Describe the growth hormonal axis:

A
  • hypothalamus releases GHRH (+) or somatostatin (GHIH, (-))
  • anterior pituitary is activated by GHRH and produces/releases GH (somatotropin)
  • GH activates JAK-STAT (tyrosine kinase associated PW) within liver and bones
  • direct effects on liver and bones causes cell growth/metabolism
  • liver and bones also produce IGF-1 (somatomedin C) which has growth stimulating and repair effects on bone, muscle, and adipose tissues
  • IGF-1 is inhibitory on ant pit prod of GH
  • IGF-1 is indirectly inhibitory by stimulating on hypothalamic prod of GHIH
  • GH is inhibitory on hypothalamic prod of GHRH
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12
Q

How is growth hormone (GH) from anterior pituitary secreted throughout the day?

A
  • GH secretion varies throughout the day: primarily during sleep (sleep disturbances perturb secretion), peaks w/ exercise, also varies with meals
  • GH secretion varies throughout lifetime: avg secretion is high during early childhood, peaks at puberty, remains relatively stable throughout adulthood, then starts declining later in life
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13
Q

What lifestyle/physiological factors affect GH secretion?

A
  • fasting/hunger/starvation
  • hypoglycemia
  • hormones of puberty
  • exercise
  • sleep
  • stress
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14
Q

What are the direct and indirect effects of GH?

A
  • direct: stimulates response in bone/muscle, growth of cells in these tissues due to hypertrophy, increase in cell numbers/hyperplasia, increase in metabolism (glycogen/fat breakdown for increase in energy/protein syn)
  • indirect: acts upon liver to produce IGF-1 which causes proliferation/growth of many cells through hypertrophy/hyperplasia and increases metabolic effects in these cells
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15
Q
  • excessive production of growth hormone (GH) in anterior pituitary before growth plates close
  • sx: excess height and girth of body
A

gigantism

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16
Q

How would the following growth hormone (GH) deficiencies present:

  • GH insensitivity (primary deficiency):
  • secondary deficiency:
  • tertiary deficiency:
A
  • GH insensitivity (primary deficiency): problem w/ liver insensitivity to GH; increased systemic levels of GH (insensitivity of GH in liver reduces prod of IGF-1 limiting negative feedback on GH in ant pit) and low levels of IGF-1
  • secondary deficiency: GH not produced/released from ant pit; causes low IGF-1 levels due to low levels of GH
  • tertiary deficiency: GHRH not produced/released from hypothalamus; low levels of GHRH from hypothalamus causes low levels of GH
17
Q

How does growth promoting factors respond in a fed state w/ adequate protein intake?

A
  • increased carb intake = increased blood sugar = adequate insulin availability
  • increased protein intake = adequate amino acid availability

>

liver produces IGF-1

>

IGF-1 stimulates mitogenesis, lipolysis, cell differentation

18
Q

How do growth factors respond in a fed that w/ low protein intake?

A
  • increased carb intake = increased blood sugar = adequate insulin availability
  • decreased protein intake = inadequate AA availability

>

GH is inhibited, liver will not produce IGF-1

>

lack of IGF-1 leads to lipogenesis and carb storage

>

weight gain

19
Q

How do growth factors respond in a fasted state?

A
  • decreased carb intake = hypoglycemia = inadequate insulin availability
  • increased protein intake = adequate AA availability

>

peripheral metabolism shifts to lipids are energy source

>

GH levels increase

liver will produce IGF-1

>

lipolysis, ketogenic metabolism, diabetogenic (insulin insensitivity)

(GH raises blood glucose by decreasing peripheral glucose uptake and stim hepatic gluconeogenesis)

20
Q

What are the metabolic functions of growth hormone (GH)?

A
  • diabetogenic effect: increase in blood glucose (insulin resistance), decrease glucose uptake/utilization by target tissues, increase lipolysis in adipose tissue, decrease in blood insulin levels
  • protein synthesis and organ growth: increase uptake of AA’s, DNA/RNA/protein syn stimulated (mediated by somatomedins (IGF-1))
  • increased linear growth: stim syn of DNA/RNA/proteins, increased metabolism in cartilage-forming cells and chondrocyte proliferation
21
Q

Describe the general prolactin axis:

A
  • hypothalamus secretes dopamine which inhibits prolactin production (tonic inhibition)
  • during pregnancy (5th week), body starts secreting prolactin from ant pit lactotrophs in pulsatile form
  • prolactin stimulates mammilary gland growth and milk production
  • prolactin negatively inhibits GnRH apart of the HPG axis, and can cause lactating amenorrhea
22
Q

Describe the oxytocin axis of the posterior pituitary:

A
  • begins as production of prepro-oxyphysin in the cell body of hypothalamic neurons
  • prepro-oxyphysin is cleaved and packaged into vesicles as pro-oxyphysin
  • vesicles travel via the hypothalamic-hypophyseal tract (axons of neurons) where additonal cleavage of neurophysins occur
  • reaches posterior pituitary where it has been modified into final form, oxytocin
  • oxytocin is stored in vesicles until it is released into circulation w/ main effects being in breast and uterine tissues
23
Q

What are the 2 main functions of oxytocin?

A
  • milk ejection: milk letdown (stimulates contraction of myoepithelial cells lining milk ducts), major stimulus (suckling, but also sight/sound/smell of infant)
  • uterine contraction: stim by dilation of cervix/orgasm, stim uterine contractions, creates positive feedback loop