VI- ANT/POST PITUITARY Flashcards
magnocellular neurons
@ supraoptic and paraventricular nucleus of hypothalamus for ADH and OT
-large
> hypothalamic hypophysial tract to post pit
parvocellular neurons
@numerous nuclei in hypothalamus
-small bodied
-release hypophysiotropic hormones into hypophyseal portal system thru median eminence to ant pit
metabolism hormones
TRH (+) somatostatin (-)
on TSH
stress hormones
CRH and VP (+)
on ACTH
reproduction hormones
GnRH (+)
on LH and FSH
growth hormones
GHRH (+) and somatostatin (-)
on GH
lactation hormones
TRH (+) and dopamine (-)
on prolactin
oxytocin release
stretch receptors in cervix stim production for labor
-receptors are inc as approach full term
-exhibit pos feedback during labor
ADH release
- osmorecptors in resp to osmolality changes
- baroreceptors in resp to drops in blood vol
-usually more sensitive to osmolality than blood vol except if significant depletion
inc by ang II, pain, stress, nausea, hypoglycemia
dec by alcohol
oxytocin effect
contract uterine muscle
myoepithelial cells in mammary tissue
stim formation of prostaglandins
ADH effects
reg body fluid osmolality and ECF vol by inc water reabsorption
potent vasoconstrictor
stim release of ATCH
ADH mechanism
- bind V2 receptors
- induce AQP2 luminal insertion
- water moves into cell
- water moves into interstitial space thru AQP3-4
- vasculature
nephrogenic diabetes
renal resistance/insensitive to ADH from mutation of V2R or AQP2
-can also get from drugs (lithium) or hypercalcemia
dilute urine and dec renal water reabsorption
central/neurogenic diabetes
from ADH deficiency thru trauma, neoplasms, infections, inflamm, vascular
dilute urine and dec renal water reabsorption
response to desmopressin
nephrogenic will NOT resp bc resistant
-neurogenic WILL
SIADH etiology
from brain tumors that inc ADH, CNS injuries, lung tumors (ectopic)
lead to xs ADH without stimuli so xs water reabsorption and inc total body water vol, ECF expands and triggers pressure naturesis
SIADH clinical presentation
lethargy, nausea, vomiting, muscle cramps, coma, convulsion, death
SIADH values
dec plasma osmolality
inc urine osmolality
hyponatremia (from dilution and pressure natiuresis)
diabetes insipidius values
low urine osmolality
plasma hyperosmolality
hypernatremia (if water limited)
corticotropes release
ACTH from CRH stim
to adrenal cortex (MC2R) for glucocorticoids aka cortisol
thyrotropes release
TSH from TRH stim
to thyroid for T3 and T4
gonadotropes releas
LH and FSH from GnRH stim
to gonads
lactotropes release
prolactin PRL from TRH stim
to mammary tissue
inhibited by dopamine, pos feedback from suckling
somatotropes release
GH from GHRH stim
to liver for protein synthesis with IGF-1 and insulin too if fed state
or inc lipolysis and dec glucose uptake if fasting
stimulants of IGF
GHRH
stress
exercise
catecholamines (epine, norep)
TSH
hypoglycemia
amino acids (arg)
inhibitors of IGF
somatostatin
IGF-1
hyperglycemia
FFAs
osmolality points
set point is 280 , when release ADH
-human blood osmolality 285
what happens when osmolality falls under 280
need to concentrate plasma bc too dilute
-shut off ADH
-excrete water so urine maximally dilute (50-100)
-high urine production
what happens in osmolality above 295
need to dilute bc too concentrated
-ADH production inc
-less water excreted so urine max concentrated (1200) but production minimal
hyperprolactinemia
in women: prolactin neg feedbacks GnRH so hypogonadism, amenorrhea, galactorrhea, infertility
in men: diminished libido, infertility, osteopenia red muscle mass, dec beard grow
acromegaly features
somatotrope adenoma so inc growth hormone
-goiter, facies, barrel chest, abnormal glucose tolderance secondary to insulin resist
-inc size of hands, feet
-thickened skin
