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