Control of Ovarian Function and the Menstrual Cycle

Question 1

Where are LH and FSH released from, and why?

Answer 1

From the Anterior Pituitary in response to GnRH.

Question 2

What does LH do?

Answer 2

Controls reproductive cycle and ovulation - stimulates oestrogens.

Question 3

What does FSH do?

Answer 3

Stimulates the growth and maturation of ovarian follicles.

Question 4

s of primary oocytes before birth, at birth, at puberty and at menopause?

Answer 4

Before birth - 7 million
At birth - 2 million
Puberty - 0.4 million
Menopause <1000

Question 5

Migratory Germ cells?

Answer 5

Divide by mitosis to form oogonia.

Starting from weeks 4-8 of foetal development.

Question 6

Oogonia?

Answer 6

Diploid cells, 46 chromosomes, divide by asymmetric division to form one oogonia and one primary oocyte.
Starts 10-20 weeks of foetal development till birth.

Question 7

Primary oocytes?

Answer 7

Diploid cells, 46 chromosomes.

Start meiosis - stop at prophase I…become dormant and are halted at this stage of development.

Question 8

Can primary oocytes be generated after birth?

Answer 8

NO!

Question 9

Explain primordial follicles.

Answer 9

Immature dormant oocyte.
Surrounded by flat granulosa cells.
Can remain dormant for up to 50 years until inital recruitment.
~40micrometers.

Question 10

Explain primary follicles.

Answer 10

Oocyte genome is activated - gene transcription and signalling between oocyte and follicle.
Granulosa cells are now cuboidal.
Zona pellucida forms around oocyte.
Follicle develops FSH receptors - although FSH is not yet required.

Question 11

Explain secondary/antral follicles.

Answer 11

Theca cells form basal lamina - theca externa, theca interna - provides blood supply to the follicle.
Antrum forms – a fluid filled cavity next to the oocyte.
300 days have passed since initial recruitment.

Question 12

Explain the follicular phase of the ovarian cycle.

Answer 12

[FSH] and [LH] are high from end of previous cycle.
Antral follicles become dependant on FSH - continue growing, enter the oestus cycle.
LH stimulates theca cells to produce androgens.
Granulosa cells convert androgens to oestradiol.
As follicle cells grow, oestradiol levels increase.

FSH stimulates growth of follicle and release INHIBIN from granulosa cells.
Follicles compete for FSH.
Competition for FSH causes weaker follicles to be destroyed - atresis.
CONTINUES UNTIL 1 FOLLICLE REMAINS.

Question 13

Explain the ovulatory phase of the ovarian cycle.

Answer 13

Normally oestradiol has a -ve feedback on LH release. But at high concentrations = +ve feedback.
= LH surge!
OVULATION.
oocyte completes meiosis I and is released from follicle to fallopian tube as a secondary oocyte.
Polar body of DNA degenerates.
Secondary oocyte starts meiosis II but stops at metaphase II.

Question 14

Explain the luteal phase of the ovarian cycle.

Answer 14

Theca cells become small luteal cells….produce progesterone and androgens.
Granulosa cells become large luteal cells produce oestrogen and progesterone.

Follicle collapses become corpus luteum.
Corpus luteum releases oestrogem and progesterone.
After 14 days - corpus luteum degenerates - falling oestrogen and progesterone levels…removes negative feedback on FHS - which increases. Cycle starts again.

Question 15

Explain the menstrual phase.

Answer 15

Uterus lining sloughs off and is removed from the body.

Once the uterine lining is removed - the endometrium starts to proliferate again.

Question 16

Explain the proliferative phase.

Answer 16

Endometrium, the lining of the uterus, begins to proliferate and thicken, tubullar glands and arteries form.

Stimulation of progesterone receptor synthesis in endometrial cells.

Question 17

Explain the later proliferative phase.

Answer 17

The glands are long and tortuous due to active growth. Stroma gradually becomes oedemus.

Question 18

Explain the secretory phase.

Answer 18

The growing endometrium becomes dependant on progesterone released from the corpus leutum. Enlargement of tubular glands which begin secreting mucus and glycogen in prepration for implantation of fertilised ovum.

Question 19

Explain the late secretory phase.

Answer 19

If fertilisation doesn’t occur - the corpus luteum degenerates, [progesterone] decreases and the endometrium degenerates. Uterine glands are wide. Arteries begin contracting and capillary beds begin leaking blood to the endometrium and uterus.

Question 20

Explain fertilisation.

Answer 20

Causes secondary oocytes to finally complete meiosis II.
Another polar body is formed and degenerates.
The sperm chromosomes fuse with the remaining oocyte chromosomes to form a diploid zygote (46chr). The zygote starts to divide and moves along the fallopian tube, After 5 days, zygote has reached the uterus and becomes a blastocyst. Inner cell mast becomes embryo.
Outer cell mass becomes placenta.

Question 21

Explain implantation.

Answer 21

The trophoblast layer attaches to the surface of the endometrium.
The blastocyst invades the endometrium.
Trophoblast cells release human chorionic gonadotropin which maintains the corpus luteum during early pregnancy.

Question 22

Triple X syndrome?

Answer 22

47XXX
Effects vary - many symptoms
Can result in inder developed ovaries and reduced fertility.
1/1000.

Question 23

Turner syndrome?

Answer 23

Only 1 X.
Majority of embryos spontaneously abort/still born,
Health problems - non functional ovaries, lack of reproductive function.

Question 24

Kallman Syndrome.

Answer 24

Hypothalamic level.

Question 25

Hyperprolactinemia.

Answer 25

Pituitary level.

Question 26

Poly cystic ovary syndrome.

Answer 26

Ovary level.
Some follicles at early antral stage, halt development and release excess androgens.
Severity varies…irregular cycles, infertility, hirsutism, susceptible to other disease eg diabetes.
5-10% of women.

Question 27

Congenital adrenal hyperplasia

Answer 27

Mutation leading to inactivation of 21-hydroxylase responsible for cortisol release.
Adrenal glands - no cortisol produced…produce excess androgens.
Excess androgens in females - male physical development.
Development of external male genitalia/ambiguous genitalia.
Can still have normal uterus and ovaries.