Pituitary Physiology Flashcards
anterior pituitary
glandular portion
contains epithelial cells
posterior pituitary
neural portion
contains neural axons
hypothalamus
located between optic chiasm and mammillary body
extends axons into the pituitary
magnocellular neurons
hypothalamic neurons that extend into the posterior pituitary
release hormones DIRECTLY into circulation via the inferior hypophyseal artery
parvocellular neurons
hypothalamic neurons that extend to the median eminence and release hormones into the hypothalamic-hypophyseal portal system to travel to the anterior pituitary to regulate hormone release
what hypothalamic nuclei contain magnocellular neurons
SON (supraoptic)
PVN (paraventricular)
what hypothalamic nuclei contain parvocellular neurons
PVN (paraventricular)
POA (pre optic)
ARC (arcuate)
what hormones does the SON release
vasopressin
oxytocin
what hormones does the PVN release
magnocellular: vasopressin, oxytocin
parvocellular: TRH, CRH, somatostatin
what hormones does the POA release
GnRH
what hormones does the ARC release
GHRH, dopamine
adrenocorticotropic hormone (ACTH)
stress response hormone
stimulates the adrenal cortex
ACTH stimuli
stress, hypoglycemia, hypotension, trauma, infection, inflammation
ACTH inhibitors
feedback loops
short: ACTH inhibits CRH
long: cortisol inhibits CRH + ACTH
HPA axis
- hypothalamus (PVN) –> CRH
- anterior pituitary –> ACTH
- adrenal cortex –> cortisol, aldosterone, androgens
growth hormone (GH)
regulates growth and body size
indirect/anabolic: stimulates liver to produce IGF-1
direct/catabolic: stimulates gluconeogenesis (liver), lipolysis (adipose), and inhibits glucose uptake (muscle)
GH stimuli
sleep, stress, starvation, exercise, hypoglycemia, high protein meal
GH inhibitors
feedback loops + somatostatin (PVN)
short: GH inhibits GHRH
long: IGF-1 inhibits GHRH + GH
pathway for GH
- hypothalamus (ARC) –> GHRH
- anterior pituitary –> GH
- GH –> liver, muscle, adipose
effect of IGF-1
anabolic
promotes protein synthesis, bone elongation, cell proliferation, organ growth
congenital pituitary dwarfism
congenital growth hormone deficiency
causes proportionate dwarfism
common in GSDs
cretinism
inadequate fetal thyroid hormone
causes disproportionate dwarfism
Laron dwarfism
failure of GH to stimulate IGF-1
gigantism
excess GH before growth plate closure
causes proportionate elongation
acromegaly
excess GH after growth plate closure
causes proliferation of bone, cartilage, and soft tissues in head/extremities
cats: prognathia (jutting out of lower jaw)
can lead to insulin resistance + glucose intolerance (diabetes)
GH responsive dermatosis
endocrine alopecia that develops with GH deficiency
- symmetric alopecia
- non-inflammatory
- truncal
- hyperpigmentation
prolactin
stimulates milk production in breast tissue
prolactin stimuli
suckling, changes in estrogen/progesterone at end pregnancy
prolactin inhibitors
dopamine
tonically inhibits prolactin secretion - release from hypothalamus (ARC) must be stopped during prolactin secretion
pathway for prolactin
- hypothalamus (PVN) –> TRH (& dec. dopamine)
- anterior pituitary –> prolactin
- breast tissue –> milk production
thyroid stimulating hormone (TSH)
stimulates thyroid hyperplasia/hypertrophy
promotes iodine uptake and hormone production/release
function of thyroid hormones
temperature regulation (increase metabolic rate), promote GH secretion
TSH stimuli
decreased temperature, increased nutritional status
TSH inhibitors
feedback loops + somatostatin
short: TSH inhibits TRH
long: T3/4 inhibits TSH + TRH
pathway for TSH
- hypothalamus (PVN) –> TRH
- anterior pituitary –> TSH
- thyroid –> T3 + T4
what are the posterior pituitary hormones
vasopressin + oxytocin
where are the posterior pituitary hormones produced
hypothalamus (SON + PVN) and released directly into posterior pituitary
vasopressin (AVP/ADH)
stimulates vasoconstriction and water retention
AVP stimuli
hypotension + hyperosmolarity (dehydration)
AVP inhibitors
ethanol, hypotonic water (over hydration)
pathway for AVP
- hypothalamus –> AVP production
- posterior pituitary –> AVP secretion
- vessels –> vasoconstriction
- kidneys –> water retention
V1 receptors
vasopressin receptors in vascular smooth muscle
causes vasoconstriction
V2 receptors
vasopressin receptors in kidneys
causes AQP-2 translocation to collecting duct membrane to promote water reabsorption
diabetes insipidus
deficiency in AVP action or production
clinical signs: PU/PD, hypotonic urine
neurogenic: inability to synthesize/secrete AVP
nephrogenic: inability to respond to AVP
oxytocin (OT)
stimulates milk let down and uterine contraction
oxytocin stimuli
suckling, vaginal/cervical distention, estrogen, neonate presence
oxytocin inhibitors
stress, epinephrine, ethanol
pathway for oxytocin
- hypothalamus –> OT production
- posterior pituitary –> OT secretion
- mammary gland + uterus