Female Sexual Reproduction

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theca cells produce androgens

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and granulosa aromatize them.

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ova production

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as related to the follicle and the corpus luteum

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and the fetal maintenance

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as assocaited with the corpus luteum and progesterone production.

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these two systems operate sequentially

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28 day menstrual cycle.

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follicular phase

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ovum is readied for fertilization and is variable in lenght. first phase.

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luteal phase.

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second phase with a fixed lenght of 13 days because the lifespan of the corpus luteum is fixed; during this phase the tract is prepared for preganncy.

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thea interna cells

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are the target of LH and have LH receptors. LH is trophic to the theca cells and induced the synthesis of steroid. The prinicpal steroid product of theca cells is androgen.

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granulosa have

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fsh receptors, is trophic and enduces aromatase to convert the androgens of the theca cells.

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Oogonia

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proliferate in early gestation. 6-7 million formed. Mid gestation will enter the prophase of metaphase wih homologs forming chromosome tetrads. These oocytes become primordial follicles. They are surrouded by a single layer og spindle shaped pre-granulosa cells and enclosed by a basal lamina.

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Primordial follicle

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starts meiosis again just before ovulation. Follicles are arrested at this stage then for 12-50 years, probably by a maturation inhibiting factor.AT puberty only 500,000. BOth x chromosomes are required in the ovary for oocyte meiosis and survival!!!!!!

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Later in gestation

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some of the primordial follicles develop more. the spindle shaped cells change to cuboidal granulosa cells and a unilamiar primary follicle is formed. The granulosa cells become multilayered, form the zona pellucida, and the follicle increases in size.

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Precursor cells of the theca interna form outside the basal lamina and the granulosa cells extrude fluid forming a secondary or vesicular follicle.

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This is the maximal degree of development in the prepubertal ovary.

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Stage two of follicle development.

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Requires 70-85 days. Past the midpoint of each menstrual cycle, a ohort of secondary follicles is recruited to enter the next sequence which spans 2.5 cycles.

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Growth of the secondary follicles is quite rapid

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with their fsh receptorws. Only some of the follicles continue to grow under the direction of LH and FSH. the others undergo atresia.

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FLuid coalesces in the antrum, which is between the ovum and the granulosum

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and contains about everything you cn thing of like steroids, fsh, activin, inhibin, cytokines, etc.

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all the while of stage two Granulosa cells

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continue to proliferate, theca interna cells become secretory, theca externa grow togethor with blood vessels and the follicle is now a ANTRAL or GRAAFIAN FOLLICLE>

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STAGE 3

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most rapid. FIVE TO 7 days after the onset of menses. A single GRAAFIAN follicle is selected from its cohort and becomes the dominant follicle. This process occurs only in a single ovary each month. There is an increase in cellular growth and the production of antral fluid as the follicle progresses toward ovulation each month.

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Follicular ATRESIA.

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most follicles are destined to atresia.

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Ovulation and fertilization

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under the influence of LH just before ovulation. Granulosa cells of the follicle become able to make steroid; estrogen secretion is decreased and progesterone is production is initiated.

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AN increase in fluid movement as well as coolagenase activity causes the

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wall to rupture, meiosis resumes again before ovulation and the first polar body is expelled at the time of ovulation.

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Meiosis is not completed unless

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fertilization occurs which triggers the expulsion of the second polar body.

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when graafian follicle busts it releases the ovum into the oviduct---

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OVULATION

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Granulosa cells hypertrophy after ovulation and ---LUTEINIZATION

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form a corpus luteum four days after ovulation. These cells secrete progesterone and estrogen which prepare the endometrium for implanatation of the oocyte if it is fertilized by the sperm.

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If fertilization does not occure

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the corpus luteum is replaced by fribrous tissue 14 days after ovulation.
Corpus albicans

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oviduct development requires the

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absence of MIH

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The oviducts functionally form the

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connection with ovaries and the uterus.

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outer layer is smooth muscle and the

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inner mucosal lining has both ciliated and secretory epithelium that function in transport and nourishment.

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Uterus has a well developed

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mucosal wall and an inner mucosal endometrium.

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The neck of the uterus the cervix

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is lined with mucous secreting epithelium; the mucous forms a barrier that helps prevent bacterial infection from entering the uterus.

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The vagina is usually collapsed

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and is very elastic musculature. EPithelial cells lining the vagina release glycogen into the lumen where vaginal bacterial metabolize it.

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FSH

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is responsible for follicle development, conversion, including the preovulatory surge of estrogen!!!!!!!! graph

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LH is responsible for follicular development of androgens, the event preceeding ovulation, and the production of steroid hormones by the corpus luteum.

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Early stages of preantal do not require FSH. development past requires FSH and estrogen. LH induces the theca interna cell to make androgens.

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the development of the capillary network in the latter part of the follicular phase allows systemic circulation

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of estrogen. Immediately prior to the LH surge, LH receptors are induced in G cells by continued FSH and estrogen stimulation. With the expression of LH receptors the G cells are capable of producing the massive LH surge.

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FSH and estrogen prime g cells for LH receptor induction for the LH surge. Response of the G cell to the the lh surge initiates

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ovulation

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the events that culminate in ovulation

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1. it terminates estrogen synthesis and stimulates progesterone synthesis
2. it reinitiates meiosis in the oocytes supressing oim release.
3. it triggers a large increase in prostaglandin release
4. and it causes differentiation of follicular cells into luteal phase.

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corpus luteum control

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only one horomen controls the develoment of the corpus luteum; LH.

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LH

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increases progesterone and estrogen production

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Low levels of LH

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are only required to keep the corpus luteum going. Steroid production goes up despite falling LH.

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midfollicular phase

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FSH controls more of the androgen to estrogen production

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in lutenizing granulosa cells

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LH drives progesterone secretion more than LH does estrogen production.

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WHen LH falls below a certain level

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luteolysis occurs.

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Estrogen is luteolytic.

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lifespan of luteum is determined by the ratio of LH to estrogen

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hcg

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plays a similar role to lh if cycle is fertile.

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estrogen vs. progesterone

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estrogen 18c one step away from androgens, progesterone is 21c is two steps away from cholesterol.

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3 physical important estrogens

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estradiol e2 is the most potent and is the primary estrogen in premenopause, estrone e1 is 1/10 as potent and is derived from adrenal androgens and is most important in postmenopause,
estriol is the least potent and is a metabolite important in pregnancy

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estradiol is the primary of the

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follicle. this rises dramatically as the dominant follicel matures and constitutes the preovulatory peak in estrogen. estradiol is also produced by corpus luteum, but progesterone is main product.

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estradiol

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varies from 6 early to 50 late. during mid luteal is about 20.

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progesterone

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progesterone rises beginning in ovulation, and peaks during luteal declining toward late luteal

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estradiol binds to ssbg tightly and albumin

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weakly

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progesterone binds primarily

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to albumin but also to cbg like cortisol. Its half life is short.

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estradiol

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is hydroxylated to estriol and O-methylated to 2-methoxyestrone. These compunds are then conjugated,

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pregnanediol

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is the major metab. of progesterone.

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estrogen

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induces progesterone receptors, but progesterone, but progesterone anatgonizes estrdiol .

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inhibin activates LH function, but

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activin potentiates the mitogenic action of FSH.

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estrodiol

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increases muscle contractions, the beating of cilia, and constricts the ishtmus. Contractions helps propel the sperm up the oviduct, and the cillia help transport the ovum from fimbria to the ampulla.

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Progesterone does the opposite by

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decreasing muscle contractions and relaxing constriction at the isthmus. Progestational. prepares the uterus.

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estrogen

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increases contractions of the myometrium and promotes growth during puberty and pregnancy.

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progest.

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decreases contractions of the myometrium.

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estrogen

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induces the proliferation of the endometrium, including blood vesels

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progesterone is responsible for the development of a secretory endometrium

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including blood vessels

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progesterone causes the spiral arteries

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to branch and become more tortuous.

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corpus luteum begins to regress

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and the decreased estrogen/progesterone secretion results in prostoglandin release. PGF2a causes vasosapasm---ischemia and necrosis.

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follicular phase

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endometrium thickens. uterine glands elongate and spiral arteries increase to supply the thickened endometrium.

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during the early luteal phase

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there is further thickening and the growth of coiled arteries and increased complexity of the uterine glands, remember ovulation between follicular and luteal phase.

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the corpus luteum wanes toward the end of the luteal phase

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the endometrium thickness is reduced and increases coiling of the spiral arteries causes sloughing of the endometrium .

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estrogen acts on cervical glands

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to increase their water content-a thin mucous that is stringy and can be drawn into strings on a slide. fern like pattern.

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progesterone causes the cervical glands to secrete

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a mucous like fluid that is antibacterial and anti sperm that does not give stringy apperance.

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estrogen in the absence of progesterone acts on vagina epithelial cells

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to flatten them making them pseudocornified. This protects the vagina during intercourse.

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preovulatory woman

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has stringly mucous because estrogen is high and progesterone low.

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estrogen

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causes proliferation of the duct system in mammary glands and causes fat deposition.

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progesterone is responsible

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for the development of alveoli and lobules requiring very high levels of progesterone. so lobules not developed until pregnancy

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estrogen is responsible for

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the widening of the pelvic girdle, fat, especially on the buttocks. libido, axillary and pubic hair due to androgen

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estrogen is negative feedback on

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GnRH, LH, and FSH and POSITIVE feedback for the LH Surge.

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estrogen contibutes to the pubertal growth spurt

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and the closing of the epiphyseal plates

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e2

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promotes bone density

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estrogen decreases

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serum cholesterol and increases HDL levels.

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estrogen increases hepatic globulin (carrying protein production)

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and induces progest. receptros

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progesterone increases

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body temperature and antagonizes aldosterone

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Hormones in the early follicular phase.

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early----prog and estr are low, LH and FSH are elevated. INHIBIN is low so FSH>lh.
Mid----

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Mid follicular

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rising levels of estrogen induce proliferation of G cells and increase follicular estrogen production

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late follicular

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estrogen and inhibin rise causing FSH<lh. E2 causes increased FSH and LH storage and and hypothalamic GnRH availability.

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After the lH surge, just before mid cycle

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e2 levels start to fall since the granulosa cells in the follicle have acquired LH receptors and E2 is reduced.

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Midcycle events

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sustained levels of e2 triggeres the GnRH surge and subsequent LH surge. LH surge induces ovulation and the conversion of estrogen producing follicle to progesterone producing follicle----the corpus luteum.

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ovulation

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e2 up---gnrh up---lh up-----ovulation

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LH surge

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occurs about day 15 of 28 day cyle, folloed by ovulation and progesterone surge.

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Luteal phase to menses

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high estrogen and progesterone cause inhibtion of LH and FSH. Inhibin is high so FSH<lh. about 11 days after ovulation the low levels of LH and high estrogen cause luteolysis and as estrogen and progesteroen drop endometrial ischemia and necrosis begin, contractions of the myometrium and menses.

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early follicular phase LH and FSH begin to rise

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and stimulates the development of 6-12 primary follicles and the full maturation of a single graafian follicle

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growing follicles secrete large amounts of estrogen and lower amounts of progesterone and androstendione

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the rising blood estrogen stimultes growth of the endometrium of the uterus.

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rising blood estrogen stimulates growth

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of the endometrium of the uterus

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RISING estrogen ALSO stimulates GnRH

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which precipitates the luteal and FSH surge which precede ovulation

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JUST PRIOR to ovulation

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estrogen levels fall because follicle stops secreting

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The surge of LH

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induces ovulation

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following ovulation the

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remaining follicular cells become the corpus luteum and secrete large amounts of progesterone and lesser amounts of estrogen. Blood levels of THESE begin to rise.

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These horomones rising

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induce the secretory endometrium to grow more, this is around day 20. They also inhibit LH and FSH and these blood levels begin to fall.

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AS blood levels of FSH and LH begin to fall

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the signal for follicular growth diminishes and no new follicles develop

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ON DAY 8 following ovulation

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the corpus luteum begins to degenerate and secretes less estrogen and progesterone. These falling levels induce menses endometrium sloughing.

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AS the prog and estr

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fall, the inhibiton of GnRH, LH, FSH which was exerted is removed and these again begin to rise marking the start of the new cycle.

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low levels of E2 have negative feedback

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on GnRH during follicular and progesterone inhibits the high stimulatory effects of estrogen on GnRH during the luteal phase,

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exposure of the hypothalamus to high levels of estrogen above 150pg/ml for more than 36 hours

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will trigger an ovulatory surge of GnRH. If primed by estrogen then LH surge if GnRH high. MOre sensitive in late follicular (pit) to GnRH because of estrogen.

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estrogen

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increase spituitary reserve of LH in late follicular phase

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LH pulses increase in frequency during the late follicular phase

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reaching 1/hr before the surge.

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progesterone pills (minipil)

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blocks sperm transport by increasing cervical mucous viscosity and decreasing oviduct motility

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LOW DOSE oral contraceptives of estrogen and progesterone

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exert negative feedback on GnRH, follicular maturation and ovulatory surge.

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progesteone antagonsits

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block implantation

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Preven uses estradiol and progest

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at the same dose as birth control pills. first 2 taken within 72 hours and the second two 12 hours later.

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PLAN B

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uses high dose progesterone and is slightly more effective taken 120 hours after still good.

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pg. 149 is the

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best summary page.

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Adrenarche

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is the maturation of the adrenal cortex and precedes gonadal maturation and is independent of it.

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pg. 149

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is the best.

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UNidentified factor

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increases DHEA synthesis from the z. reticularis and is responsible for the androgen surge and secondary sex characterisitics is female with some help from theca

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females begin puberty

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1-2 years earlier. Adrenal androgens cause growth spurt before breast development

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Rise in gonadotropins (FSH>lh)

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precedes rise in estradiol

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nocturnal bursts of fsh and lh

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begin at puberty

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average age of menarche is 12.5

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but first cycles are infertile.

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ration of fat to lean mass

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is required for puberty. tina no

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FSH and LH start rising around 9, peak at 15. estradiol rises at 10 and peaks at 15. breast develop from 11-15. peak growth is 12.

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menstural cycle 10-16.

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during neonatal and prepubertal

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fsh are greater than lh, and pulsatile lh is minimal

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as puberty approaches lh secretion

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increases during sleep. When puberty is completed LH secretion is greater than FSH secretion and cycles comense.

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at menopause

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cyclic GnRH release ceases and FSH and LH increase DRAMATICALLY with FSH again higher.

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at menopause

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progressively decreasing estrogen production by each successive developing follicle ultimaltey leads to the dominant follicle to fail to ovulate.

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estrogen however

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does not drop in years leading up. The decreasing number of follicles and build up of androgen producing cells make ovarian failure. androgens promote atresia.

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atresia----more androgen---atresia

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estrogen becomes low enough for endometrium to stop sloughing, 51 is the average onset of menopause.

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no negative feedback from estrogen cause FSH and LH to rise.

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FSH greater because inhibin removed. weak androgens from adrenal converted to estrone by fat cells. ovarian androgens contribute but eventually close down and cannot maintain reproductive tissue.

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highest needs for estrogen

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ovulation, menstruatio, cervical mucous, vaginal cornification, and vulvar tissue strnght.

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atrophy of female sexual tissue

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occurs as estrogen decreases.

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low estrogen can cause

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bad GH, atrophic conditions give rise to pain on intercourse. and increased cholesterol and decreased HDL.

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dymenorreah

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is painful menstruaitonischemia from uterine contractions.

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review tanner satge

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great test material

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you have to open the cervix and contract the myometrium

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to expel the fetus.

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oxytocin does this

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and its effects are enhanced by estrogen and relaxin increasing the number of receptors on the myometrium.

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relaxin from the CL

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causes the cervix to ripen by breaking down fibers and also loosesns the ligaments of the pelvic girdle.,

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estrogen to progesterone ratio

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also increases at end of preg to mke uterine contractions more likely. But no dramamtic change.

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progesterone being decreased by a number of mechanisms and placental CRH secretion initiaiting prostaglandin synthesis and estrogen synthesis in the fetal adrenal. ALSO RISE IN CORTISOL

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can increase uterine contraction that may initiate labor. After labor progesterone obviously falls,

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cortisol actually increases prostoglandin synthesis

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by upregulating COX2 and promotes uterine contractions and cervical ripening. IT IS IMPORTANT To know that PROGESTERONE HAS OPPOSITE EFFECT.

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cortisol may inhibit

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the inhibitory actino of progesterone on PLACENTAL CRH production.

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cortisol fetoplacental environment

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may overcome the inhibitory effects of progesterone to inhibt uterine contract.

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Parturition

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increased prostoglandin concentrations is the main stimulus for uterine contractions. estrogen and oxytocin both contribute.

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uterine dicidual cells r stimulated by oxytocin

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to increase prostoglandin synthesis.

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prostoglandins

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stimulate uterine smooth muscle contraction, potentiate oxytocin induced contractions by promoting the formation of gap junctions in SM. and soften and dilate the cervix.

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oxytocin binds to Gq receptors

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and stimulates calcium influx to contract uterine muscle and stimultate prostoglandin production.

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estrogen increases

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ocytocin receptors.

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uterus insensitive to oxytocin

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in beginning but increases as labor goes on.

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oxytocin bursts increases as labor progresses.

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and acts through a neuroendocrone reflex. The PRIMARY STIMULUS IS THE FERGUSON EFFECT WHICH IS PRESSURE AND DISTENTION ON THE CERVIX

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each uterine contraction

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begins in the fundus and extends to the cervix. relaxin helos dilate the cervix. SO positive feedback loop of oxytocin

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Uterus continues to contract after delivery and the

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placenta seperates from the myometrium and passes through the vagina. Bleeding is limited becasue continuing contractions restricts the maternal vessels. oxytocin is thus often injected.

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High doses of gonadotropin

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triggeres the development of many follicles that the physician needs to successfully perform in vitro fertilization. Must use anologs to prevent real ovulation exert neg. feedbck on pituitary.

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when estradiol levels and follicular growth indicate

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correct folliculageneissi then physician injects hCG to stimulate a LH surge, which completes the maturation. Physician harvests oocyte just prior to ovulation.