52/53 Female Reproduction (Henry) Flashcards
Review anatomy of the female reproductive system
Ovaries produce estrogen and progesterone. Uterus has 3 layers – serous, muscular and mucous. Mucous layer (endometrium) undergoes proliferation/differentiation/shedding every 28 days. Fallopian tubes are secretory and ciliated cells for sperm movement, fertilization, and zygote transport to uterus.
Differentiate between peptide and steroid hormones of the female reproductive system. Know the site of biosynthesis /secretion, cellular mechanism of action, mechanism of blood transport, mechanism of degradation, and target sites for each hormone (GnRH, LH, FSH, inhibin, estrogen, & progesterone).
Peptide Hormones: 3-200 AAs in size, synthed as pre-prohormone, post translational processing, vesicle storage, Ca dependent release, hydrophilic, bind cell surface receptors, circulate free.
• Hypothalamic: GnRH, OT
• Pituitary: FSH, LH, PRL
• Ovarian: Inhibin
Steroid Hormones: Derived from cholesterol, lipophilic, circulate bound, cross plasma memb. Are conjugated in the liver by glucuronidation and sulfation and then excreted in the urine or bile (about 1/5 in bile).
• Ovarian: estradiol, progesterone, androstenedione, testosterone
GnRH: Acts on ant. pit. to release gonadotropins.
LH: Act on ovary to increase estrogen/progesterone/inhibins.
FSH: Act on ovary to increase estrogen/progesterone/inhibins.
Inhibin:
Estrogen: Increases size of uterus, ovaries, vagina, breasts (does not convert them to milk producing organs). Proliferation of endometrial stroma lining. Inhibits osteoclast activity. Increases body protein and fat deposition. Sodium and water retention. Makes mucous thin and stringy which can help guide sperm.
Progesterone: Promotes secretory changes of uterus, prepares it for implantation. Decreases uterine contractions. Decreases prostaglandin production. Secretes fluid in fallopian tubes. Secretory development of breast tissue. Opposite effect on cervical mucous – increased viscosity.
Describe oogenesis and its relationship to changes in the ovarian follicle. Explain the roles of FSH, LH, estradiol, and inhibin in oogenesis and follicular maturation.
In development, oogonia undergo mitotic rounds of division, by birth around 2 mil oogonia. By puberty around 400k. Diploid oocyte is arrested until signaled to apoptose or develop to secondary oocyte. Meiotic division resumes at ovulation yielding haploid gamete.
Primary oocyte is surrounded by granulosa cells and is referred to as primordial follicle. Granulosa cells secrete oocyte-maturation inhibiting factor that halts further maturation. Hormone changes in repro years lead to proliferation of granulosa cells and it’s now referred to as a primary follicle.
Two phases of follicular development. Follicular phase – endometrial proliferation, follicle development. Luteal phase – occurs after ovulation. Corpeus luteum forms, endometrial differentiation, and then menses. Inhibin A low in follicular phase and high in luteal. Inhibin B moderate in follicular phase, spikes at beginning of luteal, then is low. Estradiol is low in follicular and luteal phase but spikes inbetween. LH and FSH low in follicular, spikes at beginning of luteal and then is low again.
In follicular phase LH causes theca cells to synth androstenedione, which is converted to estradiol in granulosa cells (controlled by FSH).
There is a slight spike in follicular phase of FSH and the secondary follicle is formed – granulosa and theca cells proliferate. Results in increased steroid (estradiol) production. Estradiol increases FSH receptors increasing granulosa cell sensitivity to FSH and increasing follicular secretions. FSH and estradiol increase LH receptors on theca cells also increasing follicular secretion. REALLY NEED TO KNOW THAT STEROIDOGENESIS INCREASES DESPITE NEG FEEDBACK.
One mature follicle is ready to ovulate, the other 5-11undergo atresia. Granulosa cells secrete inhibin B -> neg feedback on ant. pit. for FSH.
During follicular phase estrogen regulates uterine endometrium. Proliferation of epithelial cells controlled by estrogen
. Describe the hormonal regulation of estrogen and progesterone biosynthesis by the ovary as well as identify the cell types and regulatory signals involved during steroidogenesis.
GnRH released in pulsatile fashion 5-25 mins every 1-2 hrs. Results in LH release around every 90 mins. Estrogen rises during follicular phase and peaks before dropping off at luteal phase. Progesterone rises during luteal phase and drops off at end.
Diagram the fluctuations in hormones (LH, FSH, Estrogen, Progesterone, Inhibin) during the female sexual cycle and how these changes correlate with endometrial changes. Describe the impact ovarian steroids have on the proliferative and secretory changes of the uterine endometrium.
Inhibin B is secreted from granuloma cells and exerts neg feedback on ant. pit. FSH secretion. Just after ovulation, inhibin B spikes to decrease FSH secretion. Inhibin A is high in the luteal phase and acts on the ant. pit. to inhibit gonadotropin secretion.
Describe the regulatory signals that control ovulation. Describe the formation and decline of the corpus luteum. Diagram the changes in basal body temperature during the sexual cycle and know the hormone responsible for this change. List the principle physiological actions of estrogen and progesterone.
At mid cycle, just before ovulation, estrogen spikes for 24-36 hrs and causes pos feedback on gonadotropins = surge. LH absolutely required for ovulation – stims rupture of follicle by changes in gene expression of cyclo-oxygenase II, etc.
Progesterone synth rises if ovulation occurs – is thermogenic and increases basal body temp slightly, can monitor this.
Thecal, granulosa, endothelial, lipids (cholesterol) and immune cells create the corpeus luteum which acts as a temp. endocrine gland secreting estradiol and progesterone. Theca cells convert cholesterol into androstenedione in response to LH. Androstenedione is converted to estradiol in luteinized granulosa cells which are controlled by LH. Additionally, granulosa cells create progesterone from LDL/cholesterol.
Progesterone is responsible for differentiation/secretory development of endometrial lining in luteal phase. Increased complexity of vascular/glandular structures, accumulation of substances, lipids, glycogens, etc.
Progesterone and inhibin A exert neg feedback on gonadotropins from ant. pit. Results in less steroid synth from corpus luteum -> leads to regression of corpeus luteum. Decline in estrogen and progesterone results in release of proteolytic enzymes which lyse tissue. Also increases prostaglandin production and thus myometrial contractions. Decline in steroid production leads to less neg feedback on HPG axis and gonadotropin production rises again and cycle starts over.
Describe the process of fertilization, including capacitation and the acrosome reaction, and the movement of the blastocyst to the uterus. Describe the key hormone changes that occur during the transition to pregnancy.
Sperm deposited. Capacitation (increased motility) and acrosome rxn (penetration of egg) occur. Blastocyst (fertilized egg) expresses enzymes that allow invasion into endometrium. Placenta releases hCG which stims ovarian steroidogenesis by binding to same LH receptor (remember because LH is decreasing). Corpus luteum also secretes relaxin which inhibits myometrial contractions. After week 8 the placenta can synth steroids and corpus luteum no longer needed. Progesterone suppresses uterine contractions, inhibits prostaglandin production, and impacts immune response. Estrogen stims uterine growth, thickens vag epithelium and growth/development of mammary epithelium.
Describe key age related hormone changes observed during puberty and menopause.
Puberty: Pulsatile release of GnRH at night between 8-13 yrs. Changes estrogen synth (increases), and female developments begin to take place. Menses begins around 13 yrs which indicates estrogen levels are high enough for endometrial growth.
Menopause: Begins around age 36 and sx of follicle loss begin around 51. Decrease in follicles results in decline in estradiol and inhibin -> loss of neg feedback and elevated LH/FSH. Extragonadal estrogen exists, however huge decline in estrogen production = hot flushes, night sweats, loss of libido, loss of bone mass, increased risk of heart disease.
