Reproductive Physiology Flashcards
- The “Corpus Albicans” is the
(a) Degenerating corpus luteum
(b) Developing corpus luteum
(c) Implanted corpus luteum
(d) Secondary corpus luteum
(e) NOT the corpus luteum
(a) Degenerating corpus luteum
- What cells stimulate recruitment and development cells and where are they situated?
(A) thecal cells - inner layer of the corona radiata
(B) granulosa cells - peripheral layer of follicle post-primary stage
(C) thecal cells - on top of a basement membrane
(D) granulosa cells - on top of a basement membrane
(C) thecal cells - on top of a basement membrane
- Which of the following regarding the corpus luteum post-ovulation is INCORRECT?
a. the basement membrane breaks down
b. vasculature pervades through to provide a blood supply
c. becomes highly steroidogenic
d. layers become fused - thecal-luteal and granulosa-luteal cells
e. none of the above
e. none of the above
- In steroidogenesis, which is the MOST correct?
The enzyme 3-beta-HSD facilitates changes in…
a) progestagens to androgens
b) cholesterol to progestagens
c) progesterone to aldosterone
d) androgens to aldosterone
e) progestagens to progesterone
e) progestagens to progesterone
a) progestagens are converted to an intermediate (eg progesterone) by 3-beta-HSD, and then converted by other enzymes (eg 17-alpha-hydroxylase, 17,20 lyase) BEFORE conversion to androgens
b) cholesterol side-chain cleavage enzyme does this
c) in the adrenal cortex, 21-alpha-hydroxylase, 11-beta-hydroxylase and aldosterone synthase facilitates this transformation. 3B-HSD helps CREATE progesterone.
d) androgens cannot synthesise to aldosterone.
- Describe the functions of the Principal Ovarian Steroids.
Oestrogen (estradiol-17-beta): secondary sex characteristics, influences reproductive tract, development of breast ducts.
Progestagen (progesterone): activity of endometrium, implantation, maintain pregnancy - inhibits uterine contraction
Androgens (androstenedione): oestrogen synthesis
- Thecal cells produce ______ in response to _____.
_______ cells are stimulated by _____ to aromatise steroids to oestrogens.
This forms the two ____ - _ ________ hypothesis.
Rate of steroid production dependant on 4 key _____:
- CYP11A1 (aka ________ ___ ____-____ ____ enzyme)
- 3_______ (3 _____-________ _________
- CYP17 (steroid 17 alpha-hydroxylase)
- ar_______ (CYP19)
Thecal cells produce ANDROGENS (C19 steroids) in response to LH.
GRANULOSA cells are stimulated by FSH to aromatise steroids to oestrogens.
This forms the two CELL - 2 GONADOTROPHIN hypothesis.
Rate of steroid production dependant on 4 key ENZYMES:
- CYP11A1 (CYTOCHROME P450 SIDE-CHAIN CLEAVAGE enzyme)
- 3B-HSD (3 beta-hydroxysteroid dehydrogenase)
- CYP17 (steroid 17 alpha-hydroxylase)
- AROMATASE (CYP19)
- Prior to ovulation, Granulosa cells cannot synthesise progesterone. Explain.
Although Granulosa cells have side-chain cleavage enzyme to convert cholesterol to pregnenolone, and then 3BHSD to convert that into progesterone, they cannot get cholesterol to that region as the G cells are separated from a blood supply by the basement membrane of the follicle. Therefore:
- Cholesterol is minimum to those cells
Only post-ovulation when the structure changes in the CL (basement membrane degrades) and we become vascularised, that the granulosa-luteal cells left behind can obtain cholesterol and convert it to progesterone. This explains the progesterone-dominated response after ovulation, as opposed to estrogen pre-ovulation.
- Describe the phases of the OVARIAN cycle.
The menstrual cycle is defined as the time from commencement of one menstrual bleeding to onset of next, and is closely tied to the 2 phases of the OVARIAN cycle: the follicular phase and luteal phase, punctuated by ovulation.
Median length is 28 days, range 25-30 days (variable according to age). The follicular phase is also variable, but the luteal phase is a constant 14 days.
- What phases of the ovary and uterus correspond with each other?
FOLLICULAR phase (pre-ovulation) in ovary = MENSES and PROLIFERATIVE phase in uterus.
LUTEAL phase (post-ovulation) in ovary = SECRETORY phase in uterus (Establishment of an environment supportive of pregnancy).
- Explain the hypothesis on the physiological role of gonadotrophin surge-attenuating factor (GnSAF) during the normal menstrual cycle.
- GnSAF - in early follicular phase, cells of ovary secreting high amounts; working in concert with estradiol to provide nFB action on hypothalamus and pituitary.
- approaching the late follicular i.e. luteal phase (secretory), GnSAF levels drop off dramatically; lose the synergistic action with estradiol
Estrogen suddenly becomes POSITIVE in terms of the feedback of the system; promoting gonadotropin release and SURGE OF LH
- How does the combined pill work (estrogen + progesterone)?
- reduced FSH therefore follicles stopped from ripening and egg from maturing (++++)
- LH surge stopped so no egg release (++++)
- Cervical mucus thickens and forms a barrier to sperm (+++)
- Lining of uterus made less suitable for implantation of an embryo (+++)
- Uterine tubes perhaps affected so that they don’t transport egg so well (uncertain) (+)
Expected pregnancy rate per 100 women using the pill for one year (compared to no method of contraception = 80-90): 0.1-1
- Explain briefly hormonal control actions during puberty.
Driven by adrenarche and gonadarche: Maturation of reproductive tracts & gonads to facilitate the completion/production of gametes.
Prior to puberty - GABA suppresses GnRH, which then drops off due to a maturation in the brain - secretion of glutamate/neuropeptide Y.
Part thought to be established from maturation of Adrenal Gland - increase in activity gives rise to androgens, which stimulate secretion of kisspeptin/leptin, in turn stimulating GnRH, in turn LH and FSH, to drive GONADARCHE.
- Explain hormonal control actions during MENOPAUSE and HRT.
- Normal (/surgical) cessation of steroid production (steroidogenesis), resulting in no gamete production.
- HRT (hormone replacement therapy - combinations of estrogens and progestagens) works to combat the resulting physiological consequences of loss of sex steroids in women:
- Vaginal dryness
- Vaginal atrophy
- Breast atrophy
- Formication
- Skin thinning
Also - loss of nFB from steroid hormones on hypothalamus (GnRH) and pituitary, leads to increased gonadotrophins (LH in particular) = hot flushes.
- Explain the role of oxytocin during childbirth.
Oxytocin employs a positive feedback mechanism which stimulates the ejection of the baby from the uterus. In response to cervical receptors detecting stretch as a result of the foetus dropping lower in the uterus, oxytocin created in the nuclei of the hypothalamus is secreted by the posterior pituitary gland to further facilitate uterine contractions. Oxytocin further stimulates the release of prostaglandins from the uterine wall, which also stimulates uterine contractions. In an increasing positive feedback loop, the uterine contractions positively feedback on cervical stretch to further stimulate oxytocin release until full parturition is accomplished.
- Describe 4 features of the maternal brain.
- Hormonal changes responsible for extensive remodelling of the maternal brain during pregnancy.
- Oxytocin and prolactin stimulate maternal behaviour.
- Estrogen and progesterone of pregnancy prime the brain for these actions.
- Stress response is suppressed during parturition and during lactation.
