Endo - Ovary & Female Reproductive Tract

Question 1

Describe 2 kinds of long loop negative feedback from 17-b-estradiol (what it is acted on, what happens to GnRH/LHRH).

Answer 1

1) . Acts on Arcuate Nucleus – decreases manufacture and release of GnRH/LHRH.
2) . Acts on Anterior Pituitary – down regulates the receptors on gonadotropes.

Question 2

Describe the long loop positive feedback from 17-b-estradiol (what it is acted on, what happens to GnRH/LHRH).

Answer 2

Acts on Medial Preoptic Area (MPOA) to cause increase release of LH after >200 pg/mL for >36 hrs of 17-b-estradiol release.

Question 3

What stimulates GnRH/LHRH release? What suppresses it?

Answer 3

Epinephrine / Norepinephrine - stimulates GnRH/LHRH release.

B-endorphins and negative feedbacks - inhibit GnRH/LHRH release.

Question 4

What is the importance of the pulsatile release of FSH & LH?

Answer 4

Prevents down regulation / desensitization of LHRH gonadotropes.

Question 5

Describe the - and + feedback control of the menstrual cycle.

Answer 5

Follicular Phase – Estrogen causes negative feedback on anterior pituitary

Midcycle – Estrogen causes positive feedback on anterior pituitary (>200 pg/mL for >36 hrs)

Luteal Phase – Estrogen & Progesterone causes negative feedback on anterior pituitary

Menses – no negative feedback because estrogen and progesterone suddenly drop after corpus luteum regresses to become corpus albicans

Question 6

Describe the steroid precursors of androgens & estrogens.

Answer 6

LH binds to LH receptors on theca cells to produce androgens (androstenedione & testosterone).

FSH binds to FSH receptors on granulosa cells and stimulate aromatase enzyme to convert androgens to estradiol.

Question 7

What is inhibin? Where is it synthesized and what does it do?

Answer 7

Granulosa cells of ovarian corpus luteum.

Inhibits secretion of FSH and LH by anterior pituitary gland.

Question 8

Discuss the selection of the dominant follicle.

Answer 8

One of the primarily follicles grow more rapidly than others and secrete more local inhibitor factors which suppress the growth of the other follicles. This one follicle proceeds to become the secondary follicle.

Question 9

Describe the Follicular Phase (Day 0 - 14) of the menstrual cycle.

Answer 9

Increase FSH & LH (more FSH than LH) – causes primordial follicle growth to mature Graffian follicle.

Estradiol levels increase = causes growth of uterus. Progesterone is low.

Estrogen causes negative feedback of anterior pituitary, decrease FSH & LH secretion.

Question 10

Describe the Ovulation Phase (Day 14) of the menstrual cycle.

Answer 10

Burst of estradiol causes LH surge.

Ovulation occurs due to LH surge.

Estrogen levels decrease just after ovulation.

Ovum goes to peritoneal cavity, picked up by fimbria, brought to the fallopian tubes, awaiting fertilization.

Cervical mucus increases and become less viscous and more penetrable by sperm.

Question 11

Describe the Luteal / Progesterone Phase (Day 14 - 28) of the menstrual cycle.

Answer 11

Vascularity and secretory activity of endometrium increase to prepare for receipt of a fertilized egg.

Corpus luteum (from left over granulosa cells) secrete progesterone and some estrogen.

Negative feedback on ant. pit. because of progesterone / estrogen.

Lutein cells - secrete inhibin which inhibits ant. pit secretion especially FSH.

Increase progesterone cause increase basal body temperature.

If no fertilization, corpus luteum becomes corpus albicans.

Abrupt drop in estradiol and progesterone levels.

Question 12

Describe the Menses (Day 0 - 4) and the beginning of the new menstrual cycle.

Answer 12

Endometrium is sloughed because of abrupt withdrawal of estradiol and progesterone.

At end of cycle, small increase in FSH which stimulates recruitment of next 6 - 10 primordial follicles.

Question 13

Describe the effects of estrogen.

Answer 13

Increase size of uterus, ovaries, fallopian tubes, and vagina.

Increase endometrial glands to provide nutrition to implanted ovum.

Increase glandular tissue of lining of fallopian tubes.

Breasts – 1). develop stromal tissues on breast, 2). growth of ductile system, 3). deposition of fat in breasts.

Increase growth of bones but fuse epiphysis faster.

Increase protein / body metabolism / fat deposition.

Stimulates increased water content and a thinner mucous to help sperm pass into cervix.

Question 14

Describe the effects of progesterone.

Answer 14

“Pro-gestation” = prepare for gestation.

Blood – increase growth of spiral arteries to provide blood, O2, and nutrients to surface of developing uterine layers.

Prepare uterus – increase secretion by mucosal lining of fallopian tubes (nutrition); secretory changes in uterine endometrium to prepare for implantation.

Breasts – promotes development of lobules & alveolar cells to proliferate, enlarge, & become secretory.

Contractions – inhibits myoepithelium of uterus from contracting.

Increase mucus content to prevent introduction of pathogens.

Question 15

What are the mechanisms of action of oral contraceptives?

Answer 15

Chemical compound of estrogen & progesterone.

Provide continuous negative feedback to suppress GnRH/LHRH secretion.

Question 16

Describe the pathophysiology of Polycystic Ovarian Syndrome.

Answer 16

SHORT ANSWER:

Too much estrone causes increase LH and decrease FSH –> too much androgen. Infertility, insulin resistance, male characteristics (broad shoulders with cliteromegaly, patent vagina)

Can be due to tumor

LONG ANSWER:

Obesity (body fat) –> increased insulin secretion. Insulin binds to insulin receptors on ovarian theca cells –> produce excess androgens.

Fat cell aromatases change androgens –> ESTRONE.

Estrone acts on hypothalamus / pit. to disrupt GnRH/LHRH.

Increase LH and decrease FSH.

Increase LH causes theca cells to produce excess androgens.

Decreased FSH produces chronic anovulation (amenorrhea), cannot convert androgens to estrogen.

This produces male characteristics, insulin resistance, and infertility.

Question 17

What is the treatment of Polycystic Ovarian Syndrome?

Answer 17

Estrone antagonist (“Clomid” or “Clomiphrene”). Blocks estrone effect on hypothalamus and drives successful ovulation.

Can also do Ovarian Wedge Resection – removes barrier of thickened tissue of ovary, & removes excess androgen.

Question 18

What are the stress hormones that affect the female reproductive tract? How?

Answer 18

Increase B-endorphins
Increase corticotropic releasing hormone (CRH) - anorexia nervosa.

Both inhibit GnRH/LHRH – no ovulation

Question 19

Describe the pathophysiology of Precocious Puberty in females. Why does it occur? What is the treatment?

Answer 19

Premature activation increase GnRH, FSH, LH, estrogen / progesterone. Occurs due to infection, tumor, or trauma to hypothalamus or pituitary.

Treatment – GnRH/LHRH super agonist analogues – bombardment desensitive and down regulate gonadotrope receptors.

Question 20

What is the role of GABA and Glutamate prepuberty and after puberty?

Answer 20

Before puberty – Increase GABA inhibits GnRH/LHRH. Decreased glutamate.

After puberty – Increase in glutamate stimulates GnRH/LHRH. Decreased GABA.

Question 21

Describe the resetting of gonadostatin.

Answer 21

Children – extremely sensitive to sex hormones.

Adolescents – threshold for sex hormones is higher – allows higher pulsatile release.

Question 22

What happens during menopause?

Answer 22

1) . Follicles become weak – secrete less estrogen / progesterone.
2) . Hypothalamus tries to compensate by increasing GnRH/LHRH.
3) . Eventually follicles fail – follicular atresia.