Endo - Hypothalamus-Pituitary Flashcards
things ant pituitary regulates
thyroid adrenals repro glands somatic growth lactation
things post pituitary regulates
water metabolism
ant pit aka
adenohypophysis
post pit aka
neurohypophysis
hypothalamus fxn
collect and integrate signals from diverse sources
relay to pituitary
pituitary tumor –> blindness how
optic chiasm right above pit
swelling/tumor in pit compress optic nerve –> loss of visual fields/acuity
pit embryology
floor of diencephalon grows downward (infundibulum)
secretes factors to induce upgrowth of oral ectoderm (–> Rathke’s pouch)
rathke’s pouch –> adenohypophysis and detaches from oral ectoderm
infandibulum –> neurohypophysis - stays connected by median eminence?
neurons of PP
cell bodies in hypothalamus:
suproptic nucleu (ADH)
paraventricular nuclei (oxytocin)
all are magnocellular
ADH fxns
maintain ECF osmolarity
maintain blood volume
ADH mech
open aquoporin channels in CD of kidneys –> reabsorb water
ADH stimulation mech
- up ECF osmolarity: sensed by osmoreceptors in hypo –> target V2 receptor in renal cells
- down blood vol or BP: sensed by baroreceptors in atria –> target V1 recepors in vascular SM
oxytocin fxns
uterine motility
milk release
oxytocin stim + action steps
- stretch vagina and cervix –> target uterine myometrium
2. suckling –> target myoepithelial cells aroound mammary glands
PP hormones
oxytocin
ADH
AP hormones
prolactin (PRL) growth hormone (GH) thyroid stimulating hormone (TSH) adenocorticotropic hormone (ACTH) follicle stimulating hormone (FSH) lutenizing hormone (LH)
AP cell types (+hormones)
corticotroph (ACTH) thyrotroph (TSH) gonadotroph (LH, FSH) somatotroph (GH) lactotroph (PRL)
hypo hormones to AP path
parvocellular neurons stim
secreted from terminals in median eminence
hormones into hypophyseal-portal system to AP
PRL inhibition
tonically inhibited
dopamine binds to D2 receptors on lactotrophs
things that cause hyperprolactinemia
drugs that block dopamine lesions that interfere w/ portal blood flow primary hyperthyroidism (high TRH) lactotroph adenomas (prolactinomas)
PRL actions
enhance breast development in pregnancy
induce milk production
PRL during preg
estrogen stim proliferation of pit lactotroph cells
but lactation is inhibited by high est and progest
PRL post partum
rapid decline of est and progest allows lactation to start
ovulation may be suppressed due to PRL suppressing gonadotropins
GH direct effects
action on tissues
lipolysis in adipocytes
GH indirect effects
anything done by IGF-1
liver/tissue release IGF-1 in response to GH
GH feedback loop
GHRH –> GH (AP) –> IGF
GHRH inhibit GHRH release, IGF inhibit GH release
IGF and GH –> SS
GH receptor
cytokine receptor
intracellular domain or receptor has protein tyrosine kinase (JAK)
Jak cascade protein phosphorylation –>
STAT proteins go into nucleus and alter DNA transcription
GH effects
postnatal growth of bones* (proliferate cart @ epi plates) up lean body mass down fat cell size (lipolysis) up blood gluc up organ size/fxn
GH stimulating factors
down glucose down FAs fasting puberty hormones (est, test) exercise stress alpha-adrenergic agonists
GH inhibitory factors
up glucose up FAs obesity SS beta adrenergic agonists pregnancy
GH pulses
10 pulses daily
peak 1 hr after stage 3 or 4 sleep
most in puberty
low in elderly/obese
GH deficiency (children)
dwarfism
retarded skeletal growth
poorly developed muscles
excessive subcutaneous fat
GH deficiency (adults)
reduced well-being increased fat mass (central obesity) dyslipidemia up CV disease down bone density
GH excess (before puberty)
gigantism glucose intolerance and hyperinsulinism CV problems (hypertrophy) up infections usually from pit tumors
GH excess (adults)
acromegaly
insidious onset
overgrowth of bone/CT –> course features
decreased subcutanous fat
metabolic derangements (glucose intolerance/diabetes)
