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23 Cards in this Set
- Front
- Back
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where are the greatest # of GnRH producing neurons?
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arcuate nucleus of hypo
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release of GnRH
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GnRH releaseed in pulsatile fashion:
*follicular phase-1 pulse/hr *luteal phase- 1 pulse/3hr -increasing to 5 pulse/hr (as in GnRH analogs) suppresses gonadotropin (LH/FSH) secretion (Tx hormone-dep processes like prostate and breast cancer, precocious puberty, uterine fibroids, endometriosis) |
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-what do you use GnRH analogs to Tx?
-why? |
Tx hormone-dep processes like prostate and breast cancer, precocious puberty, uterine fibroids, endometriosis
-GnRH analogs increase GnRH to 5 pulse/hr, which suppresses gonadotropin (LH/FSH)secretion |
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gonadotropins
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LH, FSH
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what drugs can interfere with GnRH pulsatile secretion
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TCA's and neuroleptics (typical antipsychotics)
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how are LH and FSH released?
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GnRH binds to receptors on gonadotroph cells (ant pit)==>syntthesis AND release of LH, FSH
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how are LH and FSH synthesized?
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GnRH binds to receptors on gonadotroph cells (ant pit)==>syntthesis AND release of LH, FSH
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which has longer half-life: Lh or FSH?
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FSH (half-life is 4 hr, vs LH-30 min), thus GnRH pulsatility measured by peripheral measures of LH
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-what does LH act on
-where are LH receptors found |
LH acts on ovarian theca cells to induce steroidogenesis
-LH receptors found on theca cells throughout the menstrual cycle Under influence of FSH and estradiol, LH receptors also found on granulosa cells after the follicle matures. also found on corpus luteum. |
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fxn of FSH
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FSH promotes follicular growth
-FSH receptors found on granulosa cells |
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Two-cell theory
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(First Aid p. 412)
1. Theca cell: LH activates desmolase, which converts chol==>androstenedione/testosterone (androgen) 2. Granulosa cell: androstenedione/test(androgen) binds to FSH receptors on granulosa cells. Receptor binding induces production of aromatase and stim production of 3-beta-hydroxysteroid dehydrogenase delta-4,5-isomerase. Aromatase catalyses the conversion of 19C-androgen (androstenedione/test) ==>18C-estrogens |
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inhibin:
-fxn? -produced by? -structure? |
-mneum: "inhibits" FSH==>
decr FSH secretion from gonadotroph (ant pit); enhances LH-stimulated androgen synthesis -produced by granulosa cells, FSH stimulates its production -glycoprotein made of alpha and beta subunits -follicular phase: Inhibin B -luteral phase: Inhibin A |
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activin:
-fxn? -produced by? -structure? |
-mneum: "activates" FSH==> augments FSH activitym, incl: incr FSH receptor expression, aromatization, inhibin/activin production, LH expression
-produced by granulosa cells, FSH stimulates its production -composed of beta subunits of inhibin |
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development of dominant follicle (Obj 3)
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FSH causes:
-incr # granulosa cells -androgens from theca cells get aromatized to estrogens in granulosa cells. ==>Estradiol stimulates follicular growth and incr # FSH receptors ==>prevents follicular atresia (In contrast, test incr rate of follicular atresia) *the dominant follicle secretes estrogen and inhibin ==>decr FSH production ==>causes other follicles to atrophy, but dominant follicle still grows b/c can thrive even without much FSH b/c it has incr # granulosa cells w/incr density of FSH receptors -also, as dominaat follicle develops, its theca cells become more vascularized ==>follicle can produce more steroid hormones |
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what causes LH surge
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Dominant follicle controls timing of LH surge. This is shown b/c just before ovulation:
1. small incr progesterone 2. peak in estradiol levels. These cause LH surge==>then ovulation. |
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fxn of LH surge
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1. resume meiosis (final meiotic division occurs following fert)
2. ovulation 3. luteinazation of follicle==>shift in steroidogenesis in favor of progesterone production (LH causes corpus luteum to secrete progesterone) -high levels of progeest and estradiol==>neg feedback and decr prod of LH and FSH |
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Luteal Phase: levels of LH, FSH, estradiol, progest
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high levels of progest and estradiol==>neg feedback: decr LH and FSH
(Obj 2: negative feedback) |
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what causes follicular phase to begin
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at end of luteal phase, corpus luteum produces less progest, estradiol, and inhibin
==>loss of neg feedback on hypothalamic-pit axis |
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hCG
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identical to LH except for a minor difference
-if egg fertilized, hCH (producd by synctiotrophoblast) continues to stimulate corpus luteum |
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what is most variable portion of woman's cycle (follicular or luteal phase)?
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follicular phase
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layers of endometrium;
what happens after menstruation? after ovulation? |
2 layers:
1. Stratum basalis: not shed at menses 2. Stratum functionalis: grows and is shed at menses, consist of stratum spongiosum and strum compactum -Following menstration (thus 1st half of cycle: follicular/proliferative/estrogen phase): stratum basalis and fragments of stratum functionalis remain. Under influence of estrogen, stratum functionalist prolifeaates via mitosis of both glands and stroma. -Following ovulation (thus 2nd half of cycle=luteal/secretory/progesterone phase): *Under inf of progest, secretion of glycogen-rich material. *Decidualization: endometrial stromal cells become more polygonal and accumulate eoisinophilic substance rich in glycogen and lipid |
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decidualization?
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-after ovulation
-endometrial stromal cells become more polygonal and accumulate eoisinophilic substance rich in glycogen and lipid |
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what causes menstruation
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As est and progest levels fall in late luteal phase, waves of vasoconstriction of spiral arterioles
==>necrosis of superficial endometrium ==>shed stratum compctum & portions of stratum spongiosum |
