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26 Cards in this Set
- Front
- Back
endocrinology
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study of hormones, receptors, and the intracellular signaling pathways they stimulate
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hormone usually stimulates ___ cells
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target (specific); travel via blood
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types of hormonal communication
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endocrine (travel long distance thru blood --> traget); paracrine - local action, diffuse to neighboring target cells (ex testost from lytic cells --> affect sertoli cells or granulosa cells from estrogen); autocrine - acts on same cell (self, often case w/ reproductive cancer)
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hormone agonists
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(often natural), bind to receptor + stimulate post-receptor events that lead to bio effect - can have dif potencies
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hormone antagonist
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bind to receptor + repress activation by hormone or agonist + fail to trigger intracellular signaling events (used to halt cancers)
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# receptors per cell
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1,000- 10,000 recep molecs per cell but only 10^-9 M hormone concentration in blood
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dif b/w production of peptide and steroid hormones
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peptide hormones translated from RNA; steroid hormones = lipids made from cholesterol by series of enzymatic rxns
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conventional numbering and lettering of steroids goes:
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from bottom left to top right
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3 domains of nuclear receptors
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variable - "functional", changes in AA and composition based on the receptor, job is to bind to accessory proteins used in transcription (like RNA polym + coactivators/repressors); DNA-binding - highly conserved - binds to HRE (Hormone Response Elements) = specific regions on DNA (can be ARE = androgen response or ERE = estrogen response); Steroid-binding - steroid specific
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can steroid hormone receptors act w/o hormone?
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yes! some bind to HRE (hormone response elements - ex androgen or estrogen response elems) and repress transcrip in absence of hormone, others use chems (enviro,drugs,etc) to activate or repress activity of receptor and modify hormone-regulated gene trasncription
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what are natural bodily sources of estrogen?
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from uterus or from testosterone converted via adipose fat (esp in breast)
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discuss tamoxifen
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anti-estrogenic in breast but estrogenic in uterine walls (can cause uterine cancer)
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what does SERMS stand for?
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selective estrogen receptor modulators
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how do progestins and antiprogestins avoid pregnancy?
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progestins inhib LH surge + ovulation. antiprogestins can stim abortion by inhibiting activity of progesterone to maintain uterine lining
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what is androgen insensitivity syndrome?
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result of androgen receptor gene mutation - inability to respond to testosterone (androgen = male steroid hormone) that body produces - ex. even with Sry gene have testis (undescended) + breasts but no underarm hair, descended testes, scrotum b/c these happen in response to androgens
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domains of peptide hormone receptors
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extracellular (bind to peptide hormone); intracellular (bind to cytoplasmic proteins involved in signaling pathways); transmembrane (position receptor in lipid bilayer)
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G-proteins
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closely coupled to receptors (initiate signal transduction cascade)
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types of 2ndary messengers
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cAMP, IP3, DAG, Ca2+
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LH and FSH receptors localized to steroidogenic cells in gonads such as..
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Leydig cells in testis, granulosa in ovaries
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7-transmembrane receptor also known as
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G-protein coupled receptor
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True/False G-proteins always activate adenylate cyclase + therefore cAMP production
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false - depends on which G protein
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how is a G-protein's activity initiated?
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by turning GDP --> GTP and activating adenylate cyclase to make cAMP by cleaving ATP --> kinase's activity (GDP eventually regenerated)
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how does Viagra work?
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cGMP (like cAMP) increases blood flow to penis so viagra inhibs enzyme that degrades cGMP
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explain gonadatropin signal transduction cascade
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once LH and FSH are in blood, act on receptors --> stim adenylate cyclase --> make cAMP --> stim Protein Kinase A
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explain GnRH intracellular signal transduction cascade
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end goal: GnRH stims release of gonadatropins LH and FSH: GnRH attaches to receptor on gonadatrophs in ant pituitary --> activates phospholipase C --> produces secondary messengers IP3 and DAG --> DAG stimulates protein keinase C and IP3 stimulates release of Ca+ into cytoplasm which --> stims release of LH and FSH by exocytosis into blood
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clinical examples of peptide hormone-related pathology
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hypogonadotropic and/or hypogonadal = infertility; precocious puberty = too much steroid hormone (in males due to testototoxosis from too much cAMP --> too much Leydig activiation --> too much testost) hastens bone growth + aging so epiphyseal plate seals + adult height stunted
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