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26 Cards in this Set
- Front
- Back
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What three transcription factors are necessary for normal gonadal development?
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SF-1 (steroidogenic factor 1): needed for normal adrenals and gonads
WT-1: Wilms Tumor Gene 1 required for urogenital dev't SRY: Testis determining factor on Y chromosome; regulates Anti-Mullerian Hormone--near centromere, common site of mutation (crossing-over)--bad (SOX9: Partner of SRY) |
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What role do Sertoli Cells play in the development of male genitalia? How does this differ in women?
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At 6 weeks of development, early testis (Sertoli Cells) release AMH which suppress Mullerian ducts in men. Testosterone synthesis determines male internal/external genitalia.
Women don't produce AMH, produce estrogen, women's genitalia develops. |
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By what week of gestation will the bipotential genital tubercle no longer be bipotential?
What would happen if a developing female were exposed to androgens prior to this period? |
By 12 weeks, raphe will be closed on boys, stay open on girls (fusion beigins at 9 weeks), and will be able to tell them apart.
If women exposed to androgens before this time, will virilize |
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What hormone changes allow for the onset of puberty?
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At puberty, pulsatile GnRH synthesized and secreted from hthal; stimulates pit:LH, FSH-->
Ovary; E, PG, ovulation Testis: Testosterone |
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Kisspeptin:
Role Regulated by? |
Increases at puberty, binds GPR54 on GnRH-secreting neurons, stimulates LH, FSH release
Regulated by leptin (made in fat)--if you have no body fat-->delayed puberty, delayed menses If lack GPR54-->no puberty |
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Describe the fluctuation of FSH, LH beginning with birth, peri-puberty and puberty.
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After birth, FSH>LH, declines by 2 years, inhibition of GnRH
Peri-puberty: GABA inhibition decreases as Kisspeptin increases Puberty: Peripheral signals leptin and IGF-1 promote GnRH-->FSH/LH |
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What effect do FSH and LH have on girls undergoing puberty?
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Increase ovarian E2, stimulate follicle development, ovulation, menses
Note: Ovarian E2 promotes breast and uterine growth, bone maturation, liver protein synthesis |
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What layers of the ovarian follicle produce E2?
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Granulosa and theca cells
(PUBIC HAIR HAS NOTHING TO DO WITH OVULATION) |
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Describe the follicular phase of menstruation.
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Follicular phase dominated by FSH
FSH: stimulate growth of 8-12 follicles, theca cells; stimulates granulosa cells to produce E2, Inhibin B (inhibits FSH to allow E2 to rise and for dom follicle to grow) LH: stimulates theca cells produce ANDROGENS; stimulates granulosa cells produce PG (late follic phase) Dominant follicle emerges, E2 production inhibits FSH E2 increases LH, small inc in FSH-->LH SURGE, PG Production Follicle swells, ruptures, discharges ovum post-LH surge |
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Describe the luteal phase of menstruation.
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Luteal phase dominated by LH
Collapsed follicle forms corpus luteum (follicle sans ovum) Corpus luteum makes Inhibin A, PG, E2 Without fertilization, corpus luteum involutes, E2, PG decline, WITHDRAWAL BLEEDING |
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Describe endometrial changes during menstruation.
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E2 promotes proliferation of cells, glands, vasculature
Post-ovulation, secretion of mucus, nutrients for fertilized egg Loss of PG, E2-->necrosis of cells, vessels, desquamation, menses |
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How does birth control prevent ovulation?
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Tonic level E, never stimulate LH--it's negative feedback
PG in pills allows for withdrawal bleed When hit placebo pills, mimics PG/E decline |
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Describe the effects of LH and FSH on the testes.
Describe regulatory points. What hormones are required for spermatogenesis? |
GnRH-->LH/FSH
LH/FSH-->Leydig Cells: Testosterone, E2 (negative regulators at pit (LH, FSH) and Hth (GnRH) FSH-->Sertoli Cells: Inhibin B (regulates pit LH/FSH), Activin stimulates FSH Spermatogenesis req FSH, Test |
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How do Leydig and Sertoli secretions differ as a fetus and in puberty? How do their effects differ?
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Sertoli cells (fetus): AMH to inhibit mullerian dev't
Sertoil cells (puberty): Androgen Binding Protein--get testosterone to developing sperm cell Leydig Cell (fetus): Testost to regulate (ALLOW WOLFFIAN!) wolffian duct dev't; DHT controls ext genitalia dev't Leydig Cell (puberty): Test increases, converted to DHT, controls virlization, spermatogenesis begins |
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Testosterone is converted in peripheral tissues to ______ which then ________.
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T-->DHT or E
DHT-->Virilization E-->Close epihphyses, promote breast dev't in 50% pubertal boys |
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Sex Hormone Binding Globulin has a large binding affinity for _____, allowing for its transport.
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T (less so for E)
If too much bound, not enough Free T. 60% T/DHT/E2 bind SHBG, rest binds albumin with low affinity |
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How does SHBG expression change in puberty in boys? in girls?
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Free T:SHBG decreases at puberty
Increase in testosterone in boys at puberty decreases SHBG (or won't have enough Free T!) Increase in estrogen in girls at puberty increases SHBG |
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Androgen receptors are encoded on the ___ chromosome and have a higher affinity for ___.
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X chrom, higher affin for DHT
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AR expression is highest in _______.
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Reproductive organs>skin>muscle
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AR is a steroid receptor and is UNBOUND in the ______.
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Nucleus
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How is spermatogenesis regulated?
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Hthal: GnRH-->Pit: LH/FSH
LH-->Leydig: T-->DHT FSH-->Sertoli: ABP ABP binds DHT, carries to spermatagonia |
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Girls have a growth spurt at the _____ of puberty, where as boys have it at the _____ of puberty.
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Girls: middle of puberty
Boys: end of puberty |
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Libido is the ________ and depends on ______.
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Desire/interest in sex
Testosterone |
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How do the roles of the parasympathetic and sympathetic nervous systems differ in sexual function?
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Psymp: Arousal: NO, ACh increases blood flow to erectile tissue (penis, clitoris)
Symp: Orgasm: emission and ejaculation in males, emission and contraction in females) via NE release in spinal cord reflex centers |
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Drugs affecting orgasm.
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Serotonin
Beta-blockers |
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Arrow relationships for:
Arousal Desire Orgasm |
Desire<-->Arousal-->Orgasm
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