L8 and 9 Flashcards

1
Q

What are female primary sex organs?

A

Ovaries i.e. those responsible for GAMETE PRODUCTION

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2
Q

What are female accessory sex organs?

A

Vaginal, uterus, clitoris

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3
Q

Examples of secondary sex characteristics? How are they developed and when?

A
  • breast and mammary gland development, wide pelvic structure, bone density, fat deposition pattern
  • mediated by ESTROGEN
  • develop during PUBERTY
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4
Q

What are the OVERALL 5 fxns of female sex organs?

A
  1. Oogenesis
  2. Facilitating syngamy (fertilization)
  3. Providing a site for implantation of embryo (uterus - endometrium)
  4. Provide a physical environment and nutritional needs for developing fetus
  5. Provide pathway for parturition and nourish the neonate
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5
Q

Fxn of the following sex organs:

1) Uterine/fallopian tubes
2) Breasts
3) Uterus
4) Cervix
5) Vagina
6) Ampulla
7) Infundibulum
8) Fimbrae
9) Endometrium

A

1) Uterine/fallopian tubes: contractile and ciliated (isthmus)
2) Breasts: lactation
3) Uterus: suspended by supporting ligaments
4) Cervix: dense fibrous connective tissue and smooth muscle
5) Vagina: epithelium and muscle
6) Ampulla: outswelling
7) Infundibulum: lined w/cilia
8) Fimbrae:
- cilia/peg cells (peg cells secrete fluids/nutrients to nourish ovum and sperm)
- produce wave movement to draw ovum into uterine tube
9) Endometrium: complex glandular tissue

The uterus has 3 layers, which together form the uterine wall. From innermost to outermost, these layers are the endometrium, myometrium (muscle), and perimetrium (connective tissue)

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6
Q

What is an ectopic pregnancy

A
  • occurs in fallopian tube
  • not viable
  • zygote much be implanted in uterine wall
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7
Q

Describe the clitoris both internal and external structure, and its fxn

A

EXTERNAL: Visible clitoris (glans): small cylindrical mass of erectile tissue
- Covered externally by the
prepuce

INTERNAL:

  • Most of the organ is internal
  • Only human organ with sole purpose of pleasure; ~8000 nerve endings
  • develops from the same embryonic tissue as the male glans penis
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8
Q

What are the 2 cycles in the ovarian cycle? What days do each encompass

A
  1. Follicular phase (0-14 days)

2. Luteal phase (14-28 days)

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9
Q

What are the phases in the uterine/endometrial cycle?

A
  1. Menses (0-4 days)
  2. Proliferative phase (4-14 days)
  3. Secretory phase (14-28 days)
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10
Q

Describe the follicular phase in the ovarian cycle

A

During the follicular phase, the primary follicle will develop into a mature follicle that will leave the ovary. Pathway goes primordial follicle -> primary follicle -> pre antral follicle -> antral follicle -> preovulatory (mature) follicle -> graafian follicle

  1. Begins with onset of menstruation
  2. FSH and LH stimulate growth of a cohort (~10) of primary follicles (all produce E)
  3. E stimulates rapid growth of endometrium
  4. ONE single dominant primary follicle develops (source of E)
  5. Theca cells on the antral follicle have LH receptors. LH surge (onday 14) causes rupture
  6. Ovulation (release of egg from ovary)
  7. Rupture followed by repair of ovary stigma
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11
Q

How are the ovarian cycles and endometrial cycles aligned?

A

During the follicular phase of the ovarian cycle, FSH and LH will stimulate growth of a cohort (~10) of primary follicles. These follicles will produce E, which in turns act on the endometrium and cause rapid build up of the endometrium lining. So as the follicle matures, the endometrial layer thickens.

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12
Q

What is the zona pellucida

A

Secondary layer inside follicle, when ovum released, it becomes the exterior surface of ovum. Thus is the sperm binding site (has receptors sperm recognize and bind to)

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13
Q

Describe oogenesis

A

Differentiation of ovum

  1. By the time female hits puberty (menarche), our ovarian reserve contains 300,000 primordial follicles. 270,000 of these will undergo atresia (apoptosis).
  2. Over the course of ~40-50 years, ~450 will grow to become dominant follicles and undergo ovulation. Majority of the 30,000 left (primary, secondary, tertiary) will undergo atresia.
  3. In terms of the follicles that do become dominant follicles, they must undergo meiosis.
  4. In the primordial follicle state, they are 4N. They are arrested in the end of meiosis I. In the presence of FSH and LH, some primordial follicles will develop into primary follicles and then pre antral follicles and so on. Process from pre antral to antral is ~25 days. Antral follicle lasts ~45 days. Throughout the follicular phase, the follicle has been producing E, which negatively feedbacks onto the H and AP (already have dominant follicle so don’t need anymore FSH/LH to stimulate growth)
  5. Just before ovulation, when E lvls are highest for an extended period, we get a neg to pos feedback switch. This causes LH surge which leads to ovulation.
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14
Q

Describe steroidogenesis in dominant follicle

A
  • Dominant follicle contains both THECAL and GRANULOSA cells
  • Granulosa cells contain FSH and LH receptors while thecal cells contain LH receptors
  • Thecal cells main fxn is to convert cholesterol to (eventually) androstenedione (androgen precursor). Androstenedione can then be converted into T, or go to granulosa cells to be used as a precursor. T made can leave the cell and into circulation.
  • Granulosa cells main fxn is to convert androstenedione into estradiol. So they use the androstenedione given by neighbouring thecal cells to convert it into T. Then T can be converted into estradiol by CYP19 aka aromatase. Estradiol can then leave into circulation
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15
Q

Using a flow chart describe the ovarian cycle leading to ovulation

A

Move from ovarian cycle into uterine cycle. During follicular phase an increase in FSH, selection and development of one dominant follicle, marketed inc in LH 2 days before ovulation. Why do u get market inc in LH surge? Neg feedback to pos feedback! Estrogen mediated switch from neg feedback to pos feedback on hypothalamus and AP. Granulosa cells will start to secrete P, important for maintenance of endometriulBlood vessel growth to feed to dominant follicle as glandocrine gland. Prostaglandins are important for inflammation. Inflammtory response mediated by prostaglandin.
Thecal will release colaginase. Outer stigma (region surrounding outer portion of ovaries) will weaken. Collagenase will weaken stoma of the stigma. Prostaglandin important for inflammation. Follicle swells and fluid builds up in antrum, at the same time the stigma outer surface weakens. Bursting of ovum thru wall. Follicular rupture an evagination of ovum. Free ovum can be taken up by fimbre of uterine tubes.

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16
Q

Using a flow chart describe oogenesis

A
  1. Oogonium
    - Meisosis begins but lvls of proteins required for completion of meiosis too low so oocyte arrests at prophase I
  2. Primary oocyte arrested at prophase I
    - As oocyte grows, it synthesizes enough proteins to complete meiosis, but high cAMP lvls maintain arrest
  3. Primary oocyte arrested at prophase I
    - A few hrs b4 ovulation, oocyte completes meiosis I and extrudes 1st polar body. Synthesized enough MAPK pathway proteins to arrest at metaphase II
  4. Secondary oocyte arrested at metaphase II
    - Secondary ooycyte completes meiosis at fertilization n extrudes second polar body
  5. Haploid ovum

Oogonium = pre primary site exists during fetal development, during gestation. Meioisis begins so going from 1 4N to 1N ovum.Won’t be tested on diff stages of meiosis I and II. Arrested in meiosis one cause don’t have cell cycle proteins to complete meisosis. Primary oocyte arrested at meiosis I until few hours before ovulation, when the cell will has what it needs to complete meiosis I. Will finish meiossi 1 2N and polar body. Polar body also diploid but disintegrate. Unlike spermatogensis where we go from one 4N to one 4N cells. Here, we go from 1 4N to 1 haploid cell; everything else will disintegrate. Prior to ovulation, will complete meiosis I. Meiosis II does not complete until fertilization.
Upon fertilization a diploid zygote.

17
Q

Describe the role of corpus luteum during ovulation

A
  1. Ovulation is triggered by LH dependant surge
  2. Corpus luteum is whats leftover after ovulation; it is maintained by moderate lvls of LH after ovulation and secretes P and E.
  3. P maintains endometrial lining and prepares it for implantation and feedsback negatively on AP. It degenerates w/in 2 weeks unless rescued by HUMAN CHORIONIC GONADOTROPH
  4. CL of pregnancy (rescued by human chorionic gonadotroph) will produce P/E and inhibit LSH/FH (so no ovulation occurs) as well as maintains endometrial lining and prepare mammary glands
18
Q

Describe the hormone production in corpus luteum

A

Still thecal and granulosa cells but inside corpus luteum they’re groupwed as luteal cells

  1. Luteal cells dedicated to production of androgens (thecal cells)
  2. Luteal cells dedicated to production of estradiol and P (maintains endometrial lining)
19
Q

Using a flow chart describe luteal phase of ovarian cycle

A
  1. Expulsion of ovum
  2. Granulosa and theca interna become lutein cells
  3. Leutinization: enlarge and fill with lipid inclusions
  4. Corpus luteum
    Secretes P and E (granulosa cells)
    Secretes androgens (theca cells)
  5. Corpus albicans
    Degenerates and looses secretory fxns - involution
  6. Reabsorption (in absence of hCG)
20
Q

Describe the layers of the endometrium and how it changes with uterine cyccle

A

Uterine cycle.
Innermost layer of uterus is endometrium. Muscle layer that is immediate most superficial is myometrium. Conenctive tissue surroiund uterus is perimetrium. If we go day 0 to day 28, there’s build up, maintenance, and then shedding of endometium lining. Loss of endometrial linigng is ~25-35 mL (fluid, blood, tissue). 4-5 days. Onset of menstration is day 0 of both uterine and ovarian cycle. Day 1 shedding, build up, shedding again. E builds up the endometrial lining up and P maintains it. P also inc adhesiveness.
Another fxn of progesterone is inc/upregulate sticky receptors that zygote can bind to in prep for implantation.

21
Q

Connect endometrial/uterine cycle with basil body temp

A

Menstrual, proliferative, secretory (secretory has a early, middle, late). Mentrsual and proliferate together is ~14 days. How much when building up? 3-5 mm of tissue. Endometrial stoma is whats left behind after endometrial layer has shed. Stroma is connective tissue onto which endometrial lining has build up.
- Change in cervical mucus. Cervical cells secrete sugar rich mucus that nourish sperm cells. Also act as barrier for substances moving from vaginal canal into uterus. Thought that Cervical mucus formed a plug and while. Vaginal canal populated with microflora, it thought uterus sterile cause of cervical plug-. But its not sterile its contains yeast and flora. Cervix does form barrier but not absolute plug. Changes in cervical muscus and change in basil body temp can be used as indicators of fertility. Prior to ovulation, basil body temp tend to dip and cervical mucus tend to thicken. If one monitors cervial mucus and basil body, under when best for pregnancy.
Just before ovulation there’s a dip in basil temp, after ovulation there’s a rise. Most fertile days are not before but after ovulation (elevation in basil body temp will occur).

22
Q

How can women plan pregnancy

A

Changes in cervical muscus and change in basil body temp can be used as indicators of fertility. Prior to ovulation, basil body temp tend to dip and cervical mucus tend to thicken. If one monitors cervial mucus and basil body, under when best for pregnancy.
Just before ovulation there’s a dip in basil temp, after ovulation there’s a rise. Most fertile days are not before but after ovulation (elevation in basil body temp will occur).

23
Q

Describe the complex hormone interactions

A

5 hormones/molecules (FSH, LH, E, P, & Inhibin), plus multiple feedback loops make these cycles complex

Complex hormone interactions:

  1. Low/moderate E+P (at end of cycle) promotes FSH production
  2. High E only (late follicular phase) promotes LH production
  3. High P + E (luteal phase) prevents positive feedback by E on LH/FSH
  4. Plus inhibin (produced by follicle and corpus luteum and inhibits FSH/LH)
  5. hCG maintains corpus luteum

Hormonal interaction. Summary size. Rising and falling levels of hormones thruout both cycles. Coincident events w/in endometrium and ovaries.
Development of primary follicle is dependent on FSH and a bit on LH. In Early development is high lvls of FSH and inc lvls of LH. FSH lvls fall off once we have dominant follicle cause of neg feedback throut most of follicle cycle. Then domiannt follicle becomes E producer so we have inc lvls of estrogen for a 2-3 day period. Once hypothalamus exposed to elevated estrogen lvls for 2-3 day period, causes switch from neg to postive feedback. Thus we see LH surge and then see ovulation. After ovulation we have corpus luteum, which secetes some estrogen (so elevated E) and lots of progesterone. Elevated lvls of progestone during luteal phase, leading to maintenance of endometrium lining until CL degenerates (lvls of E and P fall off) endometrium lining shed, and back to where we started.

24
Q

Hypothalamic-pituitary-gonadal axis

A
  1. E + P feedback onto the H-P axis
  2. Whether feedback is negative or positive depends on [hormone] and duration of exposure (i.e. timepoint in the cycle)
  3. Activins and inhibits also feedback onto AP
  4. Through most of the cycle, E and P feedback neg on the hypothalamus and AP = ↓ in FSH and LH production
  5. E inhibits preoptic area indirectly via GABAergic interneurons
  6. E + P have opposite effect near end of follicular phase
  7. With elevated [E] for ~2 days, H-P reverses sensitivity
    ↑ sensitivity of gonadotrophs in the AP to GnRH
  8. Elevated E+P promote LH surge that precedes ovulation
  9. FSH causes Granulosa cells to produce inhibins -> inhibit FSH production by AP
  10. Activins ↑ synthesis of FSH
25
Q

What is a somatic, affective, educational activity, and interpersonal relationship of premenstrual syndrome?

A
  1. somatic
    - breast tenderness
  2. affective
    - angry outbursts
  3. educational activity
    - lack of concentration
  4. interpersonal relationship of premenstrual syndrome?
    - social withdrawn
26
Q

Describe leptins role in HPG-axis

A
  1. Leptin is produced by adipocytes and regulates nrg balance
  2. [Leptin] in circulation reflects abundance of nrg stores
  3. Leptin promotes release of GnRH
  4. Normal levels of leptin are required for onset of puberty (in both F and M)
  5. Normal levels also required to maintain menstrual cycle… Extreme exercise (e.g. gymnastics) is associated with amenorrhea; cause nrg stores n circulating leptin lvls too low to maintain cycle.
27
Q

Describe 5 reasons for IMPORTANCE of pusatility of GnRH

A
  1. FSH and LH produced by the same gonadotrope
  2. Pulsatile release of GnRH important for development of sexual function
  3. GnRH pulsatility involve NE and kisspeptin
  4. Increase in GnRH -> puberty
  5. Pulsatile regulation prevents downregulation of receptor in AP
  6. Pulsatility seems to be autonomous (i.e. like a pacemaker)
28
Q

Summary connecting ovarian and uterine cycles

A
  1. Corpus luteum dies, thus E and P lvls fall
  2. AP responds to falling E and P by inc FSH secretion
  3. FSH recruits a cohort of large antral follicles to enter rapid growth phase. Follicles secrete low amts of E and inhibin.
  4. E and inhibin negatively feedback on FSH
  5. Declining FSH lvls progressively cause atresia of all but 1 follicle – leading to selection of dominant follicle, which produces high lvls of E
  6. High E has pos feedback on gonadotropes– LH (and some FSH) surge
  7. LH surge induces meiotic maturation, ovulation, and lutenization. The CL produces high P, along with E and inhibin.
  8. High P, E, and inhibin negatively feedback on LH and FSH, returning them to basal levels.