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autonomic final > lecture 16 > Flashcards

lecture 16 Flashcards

1
Q

list the function of prolactin

A
  • growth and lactogenesis in mammary glands during pregnancy
  • inhibits fertility
  • differentiation of hair cells (coat changes)
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2
Q

describe the hypothalamic releasing hormone for prolactin (name + function)

A
  • no specific stimulatory hypothalamic hormone: BUT secretion is increased by thyrotropin releasing hormone (TRH) and vasoactive intestinal peptide (VIP) (VIP increased during infant suckling)
  • dopamine inhibits secretion of prolactin (secreted by arcuate nucleus + binds inhibitory D2 receptors on lactotrophs)
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3
Q

describe the ant pit hormone (cells, hormone, target)

A
  • lactotrophs
  • prolactin
  • mammary glands, gonads, hair cells
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4
Q

describe the rate of secretion of prolactin

A

pulsatile
- increases w/ pregnancy, chest wall stim (suckling), trauma

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5
Q

describe prolactin during pregnancy

A
  • levels build up during pregnancy but milk secretion DOES NOT begin until after birth (why?)
  • lactation inhibited by high estrogen and progesterone during preg
  • prolactin is released into mother’s blood stream during infant suckling causing an increase in milk production
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6
Q

describe the mechanism of increased prolactin that leads to decrease fertility

A
  • increased prolactin during lactation and breastfeeding help suppress ovulation
  • high level prolactin inhibits GnRH > decreased fertility
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7
Q

what are the effects of pituitary tumors?

A

lead to elevated levels of prolactin
> hyperprolactinemia
= amenorrhea + male infertility (absence of menstruation + inhibition of testosterone and sperm production)

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8
Q

how is prolactinoma treated?

A
  • w/ dopamine agonist = bromocriptine
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9
Q

describe the hypothalamic output to posterior pituitary

A
  • comprised of axonal projections from magnocellular neurons with cell bodies located in hypothalamus (PVN and SON)
  • activation of hypoth neurons causes release of hormones directly into general circulation (axonally transported to posterior pit)
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10
Q

describe the effects of oxytocin (response to + effects)

A
  • released in response to:
  • birth of an offspring (stimulate uterine contractions during and after birth)
  • stim of mammary glands (causes milk let down)
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11
Q

describe the oxytocin receptor

A

GPCR > Gq > increase intra cal levels

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12
Q

describe oxytocin during birth

A
  • stim contractions of smooth muscles
  • SM cells of uterus increase expression of oxytocin R during gestation = increased estrogen (binds transcription factor R in target tissue) > increase OT R expr
  • oxy binds during labor > contractions of SM of uterus
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13
Q

describe oxytocin treatment during labor and birth + maternal

A
  • oxytocin analogs (pitocin) facilitates labor and delivery
  • facilitates the establishment of maternal behaviors ie increases nurturing behaviors in lactating females > attachment to offspring = important for survival
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14
Q

describe effects of oxytocin on mammary glands

A
  • stimulate milk ejection from alveoli (lined with SM cells called myoepithelial that expresses OT R)
  • binding > contraction > milk ejection
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15
Q

vasopressin effects + in response to

A
  • stimulate conservation of water primary effect = ADH increase plasma osmolarity (in response to increased plasma osmolarity increase BV > support blood pressure)
  • decrease in BP (causes vasoconstriction = secondary effect = very high levels of vasopressin release ie severe hemorrhage)
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16
Q

describe the AVP R (name, place of expression, mechanism)

A

V1A: expressed in blood vessels + couples via Gq to activation of phospholipase C

V 1B: expressed in the pituitary and CNS + couples via Gq to activation of phospholipase C

V2: Expressed in kidneys + Couples via Gs to activation of adenylyl cyclase

17
Q

describe vasopressin function in the kidney

A
  • increases reabsorption of water from distal tubule in kidney nephron
18
Q

how does the kidney work

A

blood enters kidney through renal arteries > through narrowing BV until reaches glomerulus (cap bed) > glom is surrounded by bowman capsule which filters excess water and sodium from blood stream > into tubules > the filtered fluid flows through tub > the collecting duct > into the bladder
- blood returns to circulation through renal veins (close proximity to tubules allow continuous reabsorption)

(structure of cap + tub = nephron)

19
Q

how does vasopressin regulate urine concentration

A
  • vasopressin promotes reuptake of water from distal tubule
  • by increasing expression of aquaporin on cells surface of distal tubule
  • water can pass through aquaporins out of tubules and back into interstitium
20
Q

detail the mechanism of vasopressin in regulation of aquaporins

A

VP binds V2 R on the renal interstitium side > V2 R couples to Gs > stim AC > increase cAMP > + PKA > insertion of aquaporins into membrane to transport water from the tubular side to the interstitial side.

21
Q

describe where on the tubules are VP R expressed and how this allows VP to exert control of water reabsorption

A

as filtered fluid passes down the descending loop of Henley water passively diffused out due to the concentration gradient
the ascending loop of Henley is impermeable to water so as the fluid enters the collecting duct it is here where VP Rs allow for further reabsorption of water

22
Q

how does VP cause vasoconstriction?

A

in response to BP decrease like (large volume loss): large amount of VP is released (baroreceptors of cartoid sinus stim SON and PVN) > VP release into BS in high enough quantity to activate V1A R expressed in SM surrounding the vasculature > Gq > PLC > contraction *note to elaborate on the mec later

23
Q

describe SNS innervation of J cells

A
  • JG cells receive input from SNS
    -Hypotension causes activation of SNS > Baroreceptors frequency of firing decreases at NTS > RVLM is activated > Descending sympathetics
  • JG cells express b adrenergic receptors = Binding of epinephrine results in release of renin
24
Q

what is SIADH and how is it treated?

A
  • syndrome of inappropriate ADH secretion; increased ADH release
    -Caused by patients with brain injury to hypothalamus
  • Causes hyponatremia (low Na+), nausea, vomiting, muscle cramps, etc.
  • Treated with ADH receptor antagonists
25
Q

what is diabetes insipidus and how is it treated

A

Nephrogenic: insensitivity of the kidneys to vasopressin cuz expression of defective ADH receptors = low water reabsorption = lar vol of dilute urine
Neurogenic: decrease in ADH expression (no effect on ADH receptors)
Can be treated with desmopressin (analog of ADH specific V2 receptor so less side effects)
Desmopressin can also treat bedwetting

26
Q

how is POTS treated

A

Desmopressin can be used to increase water retention → increase blood volume → increase blood pressure

autonomic final (8 decks)

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