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58 Cards in this Set

  • Front
  • Back
(Hypothalamus & Pituitary)
L = Liver (endocrine gland)
HPL Axis
= growth hormone, is a tropic hormone
GH
testosterone, estrogen,
steroid hormones
-a group of protein hormones
growth factors
-will then enter portal system and seek out their target (somatotropes)
Axis GHRH
-AKA somatropin (RH) -> Liver is going to produce ->IGF (insulin-like growth factor)
GH
– promotes most of the growth, indirect actions of GH promotion by this hormone in Bones, cartilage, soft tissue (skin, internal organs)
IGF
If excess GH is present this occurs as a negative feedback mechanism
GH
If IGF is present it feeds back to the hypothalamus and this happens- - - -
feeds back to the hypothalamus, produces GH-anterior pituitary
These factors affect the secretion of growth hormone.
Exercise, sleep, nutrients (amino acids)
Argenine! Fatty acids –no-effect on ____ secretion.
GH
- is a protein anabolic hormone that increases cellular amino acid uptake, and incorporation of protein and represses proteolysis.
GH
High levels of growth hormone cause:
anti-insulin-effect can induce insulin resistance –diabetogenic
-GH develop of bone and cartilage initiated by IGF (once called somatomedin)
somatotropin
(genetic mutation) DWARFISM
GH- deficiency
(problem at target) Loran dwarfs -> IGF Resistant DWARFISM
GH-resistance
-is also a problem during growth phase (somatotrope tumor) adenoma –gigantism (can be over 8 ft. tall)
GH-excess
-GH excess more common- acomegaly- get bone thickening, thickening of cartilage in joints, (prominent in face), Hands/Feet (similar to arthritis) organs enlarged, anti-insulin, any insulin resistance -> type II diabetes mellitus.
Adulthood GHI defiency
-thyrotropin releasing hormone-> TSH= thyrotropin (thyroid stimulating hormone)-> thyroid-> thyroid hormones
TRH
prohormone for T3 (inactive)
T4
-are processings of T4 (active)
T3
- is reverse T3 (inactive)
rT3
-like all other anterior pituitary tropic hormones glycoprotein hormones- one member of a small group of 4 glycoproteins
TSH
- contains alpha and beta subunits
TSH
-common shared w/ all glycoprotein hormones
alpha subunit
-hormone specific
beta subunit
=thyroglobulin (Tg or Tgd)-creates gel-like material inside the follicle- highly concentrated thyroglobulin inside follicle.
Colloid
is made from tyrosine
thyroglobulin
=basolateral membrane- Na+/I- cotransporter “iodide trap”
I-transporters
-(aka pendrin) uniporter- only transports iodide
Apical
IPO- converts I to active iodide- > active iodide is converted into tyrosine residues in thyroglobulin –> incorporates iodide into tyr & tg -> MITs and DITs
Making of steroid hormones
constitutively secreted
thyroid hormones
TBG- tyrosine binding globulin. (T4)
carrier proteins
-bound hormone (99.96 %) binding is reversible which sets up eq’m
T4-TBG
T4-TBG<->
T4 free (enters targets) .04%
T4-TBG half-life
seven days
Permissive with growth hormones and catecholamines.
T3
responsible for development/growth –esp. in utero, also after birth particularly the brain
T3
-low thyroid hormone during pregnancy
cretinism
responsible for growth following birth- permissive = GH cardiovascular system- increases heart rate and blood pressure
Metabolism- setting BMR= basal metabolic rate
T3
- is a thermongenic hormone absence causes cold stress
T3
-enlargement of the thyroid- lump in the throat, most frequency cause – lack of iodine, I- defiency
Goiter
-normal function
Euthyroid
– lower than normal (low t4)
hypothyroid
- higher than normal (high t4)
hyperthyroidism
- hyperthyroid- auto-immune- mechanism, antibodies attack TSH receptor on the follicle cells of the thyroid. Abs. bind to receptor and activate it, and like TSH itself and stimulates T4.
Grave's Disease
- hypothyroid, autoimmune disease antibodies attack TPO- and inhibit it’s activity
Hashimoto's disease
– make catecholamines {Epi/Norepi} and secrete them – regulated and determined by autonomic nervous system (ANS)
chromatin cells
AKA- thoracolumbar division of ANS- spinal regions from which sympathetic nerves originate (spinal nerves from earlier)
Sympathetic division
- is and exception- innervated by pre-ganglionic neurons use acetyl choline (ACA) as neurotransmitter -> cholinergic responses.
Adrenal Medulla
- of ANS is activated by mass activation by stress – acute (sudden unexpected) “Fight or Flight responses”
sympathetic division
AKA craniosacral division- participates in what is called dual innervations of targets- both sympathetic and parasympathetic innervations of a target.
parasympathetic division
is an exception- -uses sympathetic neurons only no parasympathetic input both pre- and post- ganglionic neurons both use ACH as neurotransmitter
adrenal medulla
- gradual or grated response reset system after sympathetic system. Parasympathetic = “rest and digest” conditions!
no mass activation
“fight or flight” response->hypothalamus->sympathetic mass activation ( through neural network)
acute stress
- Ach. as neurotransmitter->Adrenal medulla->epi/norepi (hormone response)
Preganglionic
-norepi->(neurotransmitter)-> targets (mass activation- all at once)-> responses-> metabolism& genitor-urinary& cardiovascular& gastrointestinal& respiratory
Postganglionic
Ach-released from axon terminals (neuron –like cells) and go to chromatin cells w/ in adrenal medulla -> nictoni ach receptor-> ligand-gated ion channels (ACH)-> channels opens -> Na+ influx ->depolarization-> (inside becomes more positive) -> voltage dependent calcium 2+ channels-> ca 2+ influx-> tyrosine hydroxylase (increases it’s activity and release or secretion of epi/norepi)
MEMORIZE THIS