Hypothalamic-Pituitary Relationships Flashcards
What are the connections between the hypothalamus and posterior pituitary?
LO1
hypophysial stalk: physical connection between the hypothalamus and pituitary gland
communication: neural signal. collection of axons in posterior pituitary - cell bodies in hypothalamus
- Supraoptic nucleus (SON)
- Paraventricular nucleus (PVN)
What does the posterior pituitary secrete? (From which part of hypothalamus?)
ADH (SON)
oxytocin (PVN)
What are the connections between the hypothalamus and anterior pituitary?
LO2
neural and hormonal
-connected by hypophysial portal system
How are hormones delivered to the anterior pituitary?
LO2/LO3
-directly delivered to the anterior pituitary in high concentrations through the hypothalamic-hypophysial portal system
What is a primary endocrine disorder?
LO4
low or high levels of hormone due to defect in the peripheral endocrine gland
What is a secondary endocrine disorder?
LO4
low or high levels of hormone due to defect in the pituitary gland
What is a tertiary endocrine disorder?
LO4
low or high levels of hormone due to defect in the hypothalamus
What is in the ACTH family?
corticotrophs - secrete ACTH
What is in the TSH, FSH, LH family?
thyrotrophs - secrete TSH
gonadotrophs - secrete FSH and LH
What is in the prolactin family?
somatotrophs - secrete GH
lactotrophs - secrete Pro
Describe the HPA axis
LO5 overview
- corticotrophs in anterior pituitary produce ACTH
- ACTH is under the stimulatory control of hypothalamus - CRH
- ACTH targets adrenal gland
- stress is a regulator of the HPA axis: neurogenic (fear) or systemic (infection, surgery)
HPA axis
major hypothalamic and pituitary hormones
LO5a
hypothalamic: CRH
anterior pituitary: ACTH
HPA axis
peripheral target organ
LO5b
adrenal gland
HPA axis
peripheral hormone
LO5c
cortisol
HPA axis
regulation of the axis
LO5d
stress
- neurogenic (fear)
- systemic (infection, surgery)
HPT axis
overview
LO6
TSH is released by thyrotrophs in the anterior pituitary
-TSH is a glycoprotein hormone
TSH is under the stimulatory control of the hypothalamus: TRH
TSH stimulates thyroid gland
Stress inhibits TRH secretion
HPT axis
major hypothalamic and pituitary hormones
LO6a
hypothalamic: TRH
anterior pituitary: TSH
HPT axis
peripheral target organ
LO6b
thyroid gland
HPT axis
peripheral hormones
LO6c
T4, T3
HPT axis
regulation of the axis
LO6d
stress (physical stress, starvation, infection) inhibits TRH secretion
HPG axis
overview
LO7
- FSH and LH released by gonadotrophs in anterior pituitary
- secreted into different secretory granules allowing independent secretion by gonadotrophs
- FSH and LH are under the stimulatory control of the hypothalamus: GnRH
- FSH and LH regulate the function of the gonads
HPG axis
major hypothalamic and pituitary hormones
LO7a
hypothalamic: GnRH
anterior pituitary (gonadotrophs): FSH and LH
HPG axis
peripheral target organs
LO7b
gonads
HPG axis
peripheral hormones
LO7c
FSH
males: sperm maturation in Sertoli cells
females: follicular development and estrogen synthesis in ovaries
LH
males: testosterone
females: estradiol, progesterone
HPG axis
regulation of the axis
LO7d
negative feedback
Prolactin inhibits GnRH
Describe the relationship between growth hormone and insulin-like growth factor-1 in regulation of growth
LO8a
IGF-1 is a somatomedin that has a positive feedback loop to the hypothalamus to promote somatostatin and a negative feedback loop to the anterior pituitary to inhibit GH.
What is the role of GHRH on regulation of GH secretion?
LO8b
stimulates
What is the role of somatostatin (SRIF) on GH secretion?
LO8b
inhibits
What is the role of glucose on the regulation of GH secretion?
LO8b
inhibits
What is the role of insulin-like growth factor 1 (IGF-1) on the regulation of GH secretion?
LO8b
- stimulates somatostatin which inhibits growth hormone.
- therefore, IGF-1 (somatomedin) inhibits the secretion of GH
What are the changes of IGF-1 and GH in the fasting state?
LO8c
GH is stimulated in the fasting state
-produces an increase in blood glucose = diabetogenic
-more GH = more IGF-1 –> mediates effects of GH
What are the metabolic and growth promoting actions of GH?
LO8d
- diabetogenic or anti-insulin effect (insulin resistance and decreased glucose uptake and utilization by target tissues; increases lipolysis in adipose tissue) –> increases blood insulin level
- increased protein synthesis and organ growth (increases amino acid uptake and stimulates DNA, RNA, and protein synthesis)–> increased lean body mass and increased organ size
- increased linear growth (mediated by somatomedins, GH stimulates DNA, RNA, and protein syntheis, promotes epiphyseal plate widening, chondrocyte proliferation, and bone formation)
Explain how the regulation of prolactin secretion differs from the secretion of most anterior pituitary hormones
LO9
hypothalamus secretes dopamine, a catecholamine, (the main regulator of prolactin) which INHIBITS prolactin secretion from the anterior pituitary.
-prolactin stimulates dopamine secretion so that prolactin is inhibited (feedback loop)
-TRH is a minor regulator that stimulates prolactin secretion
Describe the production and release of oxytocin from the posterior pituitary
LO10
Hypothalamus is made in the paraventricular nucleus of the hypothalamus (cell body of neurons) as prepro-oxyphysin –> cleavage of signal peptide and packaging in vesicles –> pro-oxyphysin –> cleavage of neurophysins and axoplasmic flow in hypothalamic hypophyseal tract (axons) –> posterior lobe of pituitary where stored as oxytocin with NP1 in granules –> oxytocin released into systemic circulation for breast and uterus
Describe the synthesis and release of ADH
LO11
supraoptic nuclei of hypothalamus (cell body of neurons) prepropressophysin – cleavage of signal peptide and packaging in vesicles –> propressophysin – hypothalamic hypophyseal tract (axon of neurons) cleavage of neurophysins and axoplasmic flow –> posterior lobe of pituitary ADH and NPII in granules –> ADH to systemic circulation for kidney and arterioles
What triggers ADH release?
LO12
- low blood pressure sensed by cardiac and aortic baroreceptors (sensory neuron to hypothalamus)
- low arterial stretch due to low blood volume sensed by atrial stretch receptors (sensory neuron to hypothalamus)
- increased osmolarity > 280 mOsm sensed by hypothalamic osmoreceptors (interneuron to hypothalamus)
Mechanisms of action of ADH on kidney and vasculature
LO13
vasculature: V1 receptors –> vasoconstriction
kidney: V2 receptors –> increased reabsorption of water
net result: increased BP and blood volume
Pathological changes in ADH secretion in diabetes insipidus
-overview
LO14
- lack of an effect of ADH on the renal collecting duct
- causes frequent urination
- large volume of urine is diluted
Central DI vs Nephrogenic DI
LO14a
central
- lack of ADH resulting from damage to pituitary or destruction of hypothalamus
- treatment: desmopressin (drug that prevents water excretion)
nephrogenic
- kidneys unable to respond to ADH (increased plasma ADH)
- caused by drugs like lithium or chronic disorders (polycystic kidney disease or sickle cell anemia)
- desmopressin treatment does not work
Impact of water restriction on urine osmolality in central and nephrogenic DI
LO14b
- allow fluids overnight before test and give breakfast w/out fluids
- weigh pt
- allow no fluid for 8 hrs. weigh pt every 1-2 hrs. pt empties bladder: measure urine volume and osmolarity. measure plasma osmolarity.
- If results suggest DI, allow pt to drink (no more than twice urine volume of perior of fluid deprivation) and administer desmopresin
- measure plasma urine osmolarity and urine volume
urine osmolarity will be much closer to normal for central DI with desmopressin
Pathophysiological changes in ADH secretion associated wtih SIADH
LO15
- excessive secretion of ADH
- excessive water retention
- hypoosmolarity fails to inhibit ADH release
- low plasma osmolality
- increase urinary osmolality
SIADH treatment
- fluid restriction
- IV hypertonic saline
- V2 receptor antagonist
- demeclocycline
