16 | Pituitary, Growth Flashcards
lobes of the pituitary
- posterior lobe (neurohypophysis)
2. anterior lobe (adenohypophysis)
posterior pituitary - hormones (2) + travel
ADH + oxytocin
-signal impulse releases hormones into capillary plexus (inferior hypophyseal artery)
[one nerve cell for synthesis, storage and release. originates in hypothalamus]
anterior pituitary - hormones (6*2) + travel
[stim/releasing hormones] GnRH (gonadotropin RH), GHRH, SS, TRH (thyrotropin RH), DA, CRH (corticotropin RH)
-impulse release into primary capillary plexus (superior hypophyseal artery)
-hormones travel down portal vein
-enter pituitary at secondary capillary plexus and exit
-target specific endocrine cells (synthesize, store, secrete)
LH, FSH, GH, TSH, prolactin, ACTH [tropic hormones, w/out target glands atrophy]
-reenter secondary capillary plexus, travel in circulation to peripheral target cells
ADH (role)
conserve body water
regulate osmolarity
-lack of water stimulates ADH secretion, increased reuptake
-changes in osmolarity sensed by osmoreceptors which regulate ADH secretion
oxytocin (role, 2)
eject milk from lactating mammary gland
-suckling stimulates OCT release, which contraction myoepithelial cells of mammary gland, milk ejection
uterus contraction during birth
- cervix dilation stimulates OCT release, which enhances contraction, dilating cervix more
- positive feedback*
growth hormone (role, 4) [somatotrophs]
-muscle + skeleton: bone lengthening, protein synthesis (insulin like)
-stimulates gluconeogenesis, glycolysis, lipolysis, inhibits glucose storage (opp. of insulin/ diabetogenic)
-induces secretion if IGF-I (insulin growth facto)
(doesn’t regulate secondary endocrine organ)
-active somatotrophs inhibit thyrotrophs; inhibited by thyrotrophs
prolactin (role, 2 | excess, deficiency, inh/stim)
[mammotrophs]
increased levels associated with
- stress
- exercise
- estrogen
- suckling
- pregnancy
stimulates breast development
(no secondary endocrine gland)
excess: galactorrhea (milk discharge)
deficiency: failure to lactate
inhibited by DA, stimulated by TRH
ACTH (role, 4)
[adeno-corticotropic H]
[corticotrophs]
- circadian rhythm
- hypoglycemia, stress, fever, low glucocorticoid levels increase release
- stimulates cortisol release at adrenal glands
- inhibited by cortisol
FSH + LH (role, 4)
[follicular SH, luteinizing H)
[gonadotrophs]
-secreted by gonadotrophs
-stimulate germ cell development
-act on gonads to secrete sex hormones (E, P, T)
(glycoprotein)
-sex hormones provide stimulatory or inhibitory feedback (also on GnRH)
TSH (role, 1)
[thyroid SH]
[thyrotrophs]
travels to thyroid, stimulates release of TH’s
(glycoprotein)
-active thyrotrophs inhibit somatotrophs; inhibited by somatotrophs
GnRH (4)
[gonadotropin releasing hormone]
- stimulates pituitary synthesis and secretion of LH + FSH
- response to GnRH modulated by sex hormones (stimulate or inhibit)
- high, steady levels (vs. cyclic) block gonadal steroidogenesis
- inhibited by excess prolactin (also blocks ovulation)
GHRH (2)
- stimulates GH synthesis and release from pituitary
- negative feedback from GH and IGF-1
SS (3)
- inhibits release of GH from pituitary
- stimulated by GH and IGF-1
- stimulated by GHRH (brakes)
TRH (2.5)
- stimulates pituitary synthesis and secretion of TSH and prolactin
- negative feedback from T3, T4
PIF (prolactin inhibiting factor)/dopamine (2)
- tonically inhibits prolactin secretion
- stimulated by prolactin
CRH (3)
- stimulates pituitary ACTH synthesis and release
- short loop negative feedback from ACTH
- long loop negative feedback from cortisol
primary hyposecretion
endocrine gland secretes too little hormone, not functioning
-i.e. decrease TH secretion by thyroid gland due to lack of iodine
secondary hyposecretion
endocrine target gland okay, but tropic hormone from pituitary may be too low
- i.e. decreased cortisol b/c lack of ACTH
- i.e. decreased TH b/c lack of TSH
primary hypersecretion
dysfunctional endocrine gland, secretes too much hormone. usually due to tumor, independent of amount of tropic hormone
-i.e. thyroid tumor, hypersec of T3, T4
secondary hypersecretion
excessive stimulation by trophic hormone. independent of hypothalamus signaling/negative feedback
-i.e. Cushing’s disease, corticotroph tumor - hypersec of ACTH
hyporesponsiveness (receptors)
lack or deficiency or receptors for hormone
-i.e. T2D lack of insulin rec.
hyporesponsiveness (post-receptor)
post receptor defect in target cells
-normal receptor but activated receptor unable to cause formation of 2nd messenger, open channel, etc.
hyporesponsiveness (metabolic activation)
lack of metabolic activation of a hormone
-decreased conversion of T to DHT due to lack of 5a-reductase enzyme
hyporesponsiveness (general)
target cells don’t respond to third hormone
-hormone concentration is normal or elevated, but the response is low
