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11-8-06

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11-8-06. For next time: read thoroughly the sections on labor & delivery; Lactation; Contraception Ch 15 Gall Bladder case study. Quick survey: Approx score last exam (nearest 10 pts) Did you study in a group? Did you study at least 6 hrs/week every week b/t exams (not average)? - PowerPoint PPT Presentation
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11-8-06 For next time: read thoroughly the sections on labor & delivery; Lactation; Contraception Ch 15 Gall Bladder case study. Quick survey: Approx score last exam (nearest 10 pts) Did you study in a group? Did you study at least 6 hrs/week every week b/t exams (not average)? Did you ensure that you could fulfill all objectives?
Transcript

11-8-06• For next time: read thoroughly the sections on

labor & delivery; Lactation; Contraception

• Ch 15

• Gall Bladder case study.

• Quick survey:

─ Approx score last exam (nearest 10 pts)

─ Did you study in a group?

─ Did you study at least 6 hrs/week every week b/t exams (not average)?

─ Did you ensure that you could fulfill all objectives?

Female Reproductive System

Before we get going, take 1 min and compare and contrast M & F systems:

• M: continuous Sperm Prod. Vs F – 1 egg/month

• M: releases gamete vs. F: retains & nurtures fertilized gamete

─ F: regulates environment over cycle

─ F: Hormones control release of egg

─ F: Egg cell cycle control complex (long) & 1 ovum / oogonia

Path for spermatozoa ejaculated into the female reproductive tract:

Vagina cervix uterus fallopian tube

Path for egg:

ovaries fallopian tube (combined actions of fimbrial contractions and the oviduct’s “ciliary escalator.”)

Figure 17-13

Question #2: Describe the various stages from oogonium to mature ovum

• Oogonia Mitosis & Differentiation Primary oocyte; meiotic arrest

• Follicles (1 egg & supporting tissue)─ Primordial follicle = egg +

granulosa

─ 1˚ = larger egg + zona pelucida (layer of material), proliferation of ganulosa

─ Pre-antral follicle multiple granulosa layers,

─ Antral follicle antrum (fluid-filled space) forms

Female Hormonal Control

• Menstrual Cycles─ As W/males, HPA control

GnRH FSH, LH release sex hormones

Long and short loop feedback

─ Resulting in

Cyclical gamete release

Preparation of uterus for implantation, nurturing

If not, then menstruation

Note: Fig 17-18 Summarizes the “BIG PICTURE” tying everything together between HPA, Ovaries and Uterus

The 1st portion of the questions covers ovarian events of the menstrual cycle;

The later questions, cover uterine events linking them to ovarian cycle

Q # 4: Name 3 hormones produced by the ovaries and name the cells that produce them

• Estrogen (s) --- Granulosa Cells (follicular phase); Corpus luteum (luteal phase)

• Progesterone --- granulosa and theca (little) before ovulation; corpus luteum (luteal phase)

• Inhibin --- Granulosa Cells & Corpus luteum

Q #6: What are the analogies between the granulosa cells and the sertoli cells and between the theca cells and the Leydig cells?• Sertoli and granulosa

─ support gametes

─ Respond to FSH

─ secrete chemicals that directly stimulate gamete development

─ Inhibin

• Leydig and Theca─ Both secrete androgens

─ Both respond to LH

─ Secretions of both feed back to hyp and AP

Q #7: List the effects of FSH on the follicle

• 1st wk: levels of FSH,LH low, but enough that

─ FSH stimulates follicle dev.; granulosa cells to divide and produce estrogen; Estrogen acts as an auto-/paracrine agent more estrogen secretion

─ LH stimulates theca cells to release androgens needed by granulosa cells for estrogen production

New edition has error in this figure... FSH & LH switched (17-19)

Q #8: Describe the effects of estrogen and inhibin on gonadotropin secretion ...

• Early & Mid:

─ Estrogen short loop to AP inhibits FSH & LH release

Decrease in FSH & LH at this time causes atresia of non-dominant follicles

─ Estrogen long loop to hyp: inhibits GnRH releases

─ Inhibin: inhibits mainly FSH

• Late: everything changes!!!

─ High levels of estrogen enhance AP sensitivity to GnRH (mainly LH-releasing cells) LH surge ovulation

Q # 9: List the effects of the LH surge on the egg and the follicle

He he he... Couldn’t have said it better myself:

Q #10: What are the effects of the sex steroids and inhibin on gonadotropin secretion during the luteal phase

• IN THE PRESENCE OF ESTROGEN high progesterone suppresses GnRH and gonadotropin release

• Inhibin: feeds back to AP and inhibits FSH release

• (Fig 17-18)

Q #11: Describe the hormonal control of the CL in a non-pregnant and in a cycle when pregnancy occurs

• No pregnancy: low LH keeps CL going for ca. 2 weeks; sensitivity drops off over time and CL degenerates lower estrogen/progesterone menstruation & releases feedback suppression of gonadotropin release

• W/ /pregnancy: hCG from placenta sustains CL for about 2 mos. So that it secretes estrogen and progesterone for the uterus.

Q # 12: What happens to the sex steroids and the gonadotropins as the CL degenerates?

• Sex steroid levels drop off (uterine effects?)

• Alleviates negative feedback inhibition of gonadotropin release which increases a bit, thus triggering the development of a new set of follicles

Q # 13: Compare the phases of the menstrual cycle according to uterine and ovarian events• This is part of figure 17-22

Q #14: Describe the effects of estrogen and progesterone on the endometrium, cervical mucous, and myometrium

• Estrogen (follicular phase): proliferation of endometrium; development of myometrium; receptors for progesterone (endometrial cells)

• Estrogen & Progesterone (luteal phase): ─ Progesterone inhibits myometrial contractions

─ Increase glandular activity of endometrium

─ Increase glycogen content of endometrium

─ Increase vascularization of endometrium

─ Changes cervical mucous from watery and abundant to sticky viscous plug (bacterial blockade)

Q #15: Describe the uterine events associated with menstruation

• Drop in estrogen and progesterone prostaglandins vasoconstriction lack of oxygen/nutrients leads to degeneration of endometrium

• Myometrium begins undergoing contractions

• Later vasodilation bleeding

Pregnancy

• Fertilization of Egg = Zygote Formation

• Cleavage turns zygote into Conceptus

─For now, composed of all totipotent cells

─For 3-4 d, conceptus stuck in fallopian tube b/c of estrogen mediated contraction of opening to uterus

Pregnancy

• ~ d 17: ─progesterone relaxes opening to uterus

─conceptus released floats freely for ~ 3 d.

─differentiates; by the end its cells are no longer totipotent

─Becomes a Blastocyst Outer layer = trophoblast

Inner Cell mass --> eventually becomes embryo

@ 2 months embryo = fetus

Pregnancy

• ~ d 21: implantation occurs

─Sticky Trophoblast cells

Proliferative when in contact w/ endometrium

Secrete proteolytic enzymes, paracrine agents: facilitate entry of blastocyst into endometrium

Secrete Chorionic Gonadotropin (CG)

• Remember CG Maintains CL until the placenta is formed

─Estrogen and Progesterone to maintain endometrium

Pregnancy

• Initially, endometrial cells directly nourish bastocysts

• After the first few weeks the Placenta takes over nutrition, environmental control

Q # 24: State the sources of estrogen and progesterone during the different stages of pregnancy. What is the dominant estrogen of pregnancy and how is it produced?

• Estrogen

─ 1st Corpus luteum, after ca. 60-80 d, Placenta becomes main source; promotes myometrial development

─ Main estrogen = Estriol

• Progesterone

─ 1st Corpus luteum, after ca. 60-80 d, Placenta becomes main source

─ Inhibits contractions

Q #25: What is the state of gonadotropin secretion during pregnancy and what is the cause?• CG

─ High for 2-3 months when it stimulates est. & prog. from CL

─ Then placenta takes over

• LH/FSH levels

─ Low throughout pregnancy

─ B/c GnRH secretion is inhibited by high levels of progesterone in presence of estrogen

─ Prevents development of additional follicles/eggs


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