Pituitary & Growth Hormone Flashcards
what 3 glands are connected to the hypothalmus by the pituitary stalk
explain the connection between the anterior pituitary and how signals get to and move from here
- anterior pituitary: an endocrine gland
- intermediate pituitary: vestigial (not usedin humans)
- posterior: neuroendocrine (nerve to circulation)
Anteroir Pituitary
- NO DIRECT innervation: hypothalmic neuron terminal ends at the medial eminence connect to where the blood feeds into the anterior pituitary (a portal system)
- this connection allows for hormones to be synthesized from the hypothalmus and communicate directly with the pituitary through the median eminence, through a long portal vein and into the pituitary stalk
- then they are delivered through a capillary bed that perfused the anterior pituitary lobe
from the pituitary: it connects through another capillary bed to the general circulation
there is a short portal system that allows anterior and posterior pituitary to communiate
how does the hormone from the hypothalmus regulate the hormone release from th epituitary (concentrations)
- regulatory proteins (hormones) synthesized in the hypothalamic neurons: release to the median eminence , carried on long portal veins to the anterior pituitary
these proteins from the hypothalmus either stimulate or inhibit hormone secretion from the pituitary
the RATIO of stimulation:inhibition: is determined by the hypothalmic hormones: concentration of the hormone released from pituitary is determined by the release from hypothalmus
how does the posterior pituitary communicate with the hypothalmus
a neuroendocrine hormone release pathways (for oxytocin or ADH)
from hypothalmus
- supraoptic nucleus syntehsizes ADH
- paraventricaul nucleus syntehsizied oyxtonin
ADH and oxytocin then from the neuron travel down APs until they’re released at a positerior pititary capillary: enter the blood capillary at the post. pituitary & then enter venous circulation
what are the hormones secreted by the hypothalmus? what do they tirgger within the pituitary
Hypothalmus (to anterior pituitary releasing)
CRH: corticotropinin releasing hormone
TRH: thyroitropinin releasing hormone
somatostain
GnRH: Gonadotropin releasing hormone
GHRH: Growth hormone releasing hormone
PRF: prolactin-releasing factor
PIH: prolactin inhibitory factor
ADH –> to posterior pitutitary via neurons
oxytocin –> to posterior pituitary via neurons
Anterior Pituitary then..
- CRH = ACTH: adrenocorticotropin
- TRH = TSH: thyroid stimulation
- GnRH = LH Lutenizing hormone, FSH: follicle-stmualtion hormone
- GHRH = GH: growth hormone
- PRF = PRL: prolactin
50% is GH, 20% ACTH, 5% TSH
The role of ADH: Antidiuretic hormone
anti-diuretic: stop excretion: increased absorbtion of water
- whtn ADH is released: the cells fo teh collecting duct become permiable to water (by way of aquaporins)
- water is reabsorbed into medualary interstitum and then into blood
- urine becomes more concentrated when ADH is released
Specifically
- ADH binds to the V2 receptors on the collecting duct cells
- this inititaes the insertion of aquaporin 2 channels
- without ADH these are stored in endosomes
Growth Hormone
- what does it regulate
- how is it synthesized
- secretion pattern
- circulation
- feedback
- role of IGF-1 and GH on itse own
Synthesis
- anterior pituitary
- prehormone: then removed before its stroed: a single chain but peptide = therefore water soluable and receptors on the membrane
Regulates
- long bone growth
- glucose
- amino acids
- fatty acid metabolism
Secretion pattern
- pulsitile
- amount ranges from < 1 - 50!
- 70% during slow wave sleep = sleeping = big and strong!
- (needs to be pulsatile becuase absence of GH is necessary to insure insulin has its own time to work too)
Circualtion
- metabolize via liver
- lastts a SHORT amoutn: 6-20 minutes!
Feedback
- negative feedback loop
- GH secreted: goes to liver to promote secretion of IGF-1
- wheen excess GH –> goes back to turn off (via altering secondary messengers in hypothalmus) hyopthalmus and pituitary
- somatostain is also a NEGATIVE feedback mechanism (downregulates secondary messengers)
IGF-1 : promotes growth, resembles proinsulin and circualtes on carrier proteins
IGF-1 has effects on organs, muscle and bone
the GH ALSO has it sown affects: acts like glucagon (its a counterreg. hormone) = increase lipolysis, and carbhydrate metabolism (increase blood glucose)
Mediators of GH
Stimulators
estrogen increases womens response to GH
taller people more response thant average height
Stimulators of GH
- hypoglycemia
- slwo wave sleep
- amino acids
- exercise
- sleep
- pubery
inhibitors
- glucose
- REM
- somatostatin
- GH
- IGF-1
Describe the GH receptor
GH receptor: found in most tissues of the body
- a single chain protein receptor: binds to different domains of the GH: therefore too MUCH GH will actually have a decreased effectiveness (two receotrs will bind but less effective)
- syntehsis stimulated by low GH, insulin (?) , estrogen
- syntehsis inhibited by high GH (down regulation)
GH binding proteins: extracellulary domains
IGF-1 Hormone, binding protein and Receptors (action)
Hormone
- synthesized in the liver
- looks like proinsulin
- resonsible for most og the GH growth-promoting activity that occurs 12-18 hours after GH is released and triggers it
IGF-1 is bound to proteins: IGF Binding Protiens) = this helps so that the IGF-1 isnt degraded too quickly within the serum
- approx. 75% is bound and it helps increased the haf life
Receptors
- once bound: goes to bone and other organs/tissues
- in the bones: increase collagen, protine and cell proliferation
- increases linear growth = closed growth plate = outward growth (sideways)
- goes to other tissues to increased organ growth and size
Explain the difference between giantisism and acromegaly
Clinical Features
treatment
Giantism: excess GH secretion occuring during childhood to puberty
Acromegaly: onset of excess GH secertion after puberty
due to a pituitary tumor secreteing GH
Clinical
- accelerated growth, insulin resistance & mild carb intolerance
Features
- widened fingers, toes, hands and feet
- boney ridge above eyes
- prominent lower jaw
- coarse facial features
- thick skull
- enlarged tongue
- subcut. fat think
- enlarged organs (heart)
- atherosclerosis
Treatment
- tumor removal
- octreotide, lantreotide (somatostatin anologs)
radiation, DA agonists GHR antagonist
always with pituitary tumors risk of bitemporal hemianopsia
GH Tumor
Dwarfism
patho
clincal features
treatment
Impaired Function (could be ANY of these)
- hypothalmus = NO GHRH
- pituitray = no GH or non-functional GH
- liver: no IGF-1 or II
- target receptors: defect in number, binding or signalling
symptms
- short stature
- delyed bone maturation
- obesity (mild)
- delayed puberty
Treatment
- replacement thearpy
- helps lean body mass, decrease adipose & increased gorwth for kids, pubescence and fertibilit with these meds
seen in Laron’s syndrome: inbred parents
- have severe GH def.
- elvated cirucalting GH but low IGF-1
- means impaired GH rectors
see in pygimes african
- IGF-1 failed to increased in puberty
seen in kwashiokor
- GHR defects: no receptors for it to bind
