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Physiology 3 > Week 9 (Repro) physiology > Flashcards

Week 9 (Repro) physiology Flashcards

1
Q

Where are primordial follicles formed?

A

cortex of the ovary

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2
Q

Are primordial follicles diploid or haploid?

A

diploid

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3
Q

What happens to form primordial oocytes?

A

(diploid) oogonia undergoes mitosis and become primoridal oocytes

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4
Q

primordial follicle growth initiation

A
  1. Oocyte will grow in size
  2. the granulosa cells undergo mitosis and increase in number
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5
Q

resting state and primordial follicle growth initiation

A

- Majority of them will undergo atresia

Once growth initiates the oocyte cannot stop and return to resting state.
- majority will undergo atresia (follicle death)
-

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6
Q

1st meiotic arrest (when?)

A

At birth

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7
Q

2nd meiotic arrest (when?)

A

ovulatory follicles (oocytes) - before fertilisation

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8
Q

Primary follicle is also?

A

pre-antral

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9
Q

p

primary follicle layers

A
  1. an oocyte
  2. layers of granulosa cells
  3. basement membrane
  4. thecal cells
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10
Q

antral follicle

A

the antral cavity forms

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11
Q

last follicle before ovulation

A

Graafian/pre-ovulatory

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12
Q

How is an ovulation of one oocyte regulated?

A

There’s competition between follicles of all stages, this ensures that only one follicle matures to become the Graafian follicle.
- the rest undergoes atresia

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13
Q

step-wise development of follicles

A
  1. independent primordial follicle - NO meiotic divisions
  2. primary oocyte - can undergo 1 meiotic division
  3. early antral oocyte - can be fertilised, 1 cell division
  4. mid antral oocyte - can undergo multiple cell divisions
  5. pre-ovulatory oocyte- can grow to a baby
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14
Q

Which step of folliculogenesis - can start cell division

A

antral follicle

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15
Q

Which step of folliculogenesis - mature enough to grow to a baby

A

Graafian follicle
- fully support post-fertilisation development

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16
Q

What releases GnRH?

A

hypothalamus

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17
Q

What does the pituitary release in response to GnRH

A

FSH and LH

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18
Q

When is FSH required?

A

antral follicle growth

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19
Q

When is LH required?

A

stimulate final stage of follicle growth (late-antral)
required for ovulation

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20
Q

early stage of follicle development - endocrine feedbacks

A
  1. early follicles produce low levels of oestrogen
  2. low oestrogen +ve feedback —-> Hypth. and Pit.
  3. INCREASE FSH
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21
Q

later stage of follicle development - endocrine feedbacks

A
  1. As follicles are more developed, they release more oestrogen
  2. high oestrogen will have negative feedback to H. and P.
  3. P. will release less FSH, LH is unaffected
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22
Q

what does high oestrogen affect?

A

lower FSH but unaffected LH

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23
Q

how does more developed follicles gain competitive advantage?

A
  1. Initially: Ahead follicle will get more sensitive to FSH - more receptors
  2. The ahead follicle will undergo rapid growth - produce more oestrogen
  3. FSH levels will fall
  4. Since the follicle is developed its growth can depend on LH.
  5. Other follicles will undergo atresia due to low FSH.
24
Q

Follicles moving through antral stage increasingly release….

A

oestrogen
- stimulate the uterus and support pregnancy

25
Q

oestrogen production dependent on?

A

both LH and FSH

26
Q

LH contribution to oestrogen production

A

outlayer - thecal cells
binds to LH receptor and activate PKA via ATP-cAMP pathway
PKA stimulates conversion from cholesterol to androgen

27
Q

FSH contribution to oestrogen production

A

androgen will move from outer layer - thecal cells
to granulosa cells.
FSH binds to FSH receptor stimulate cAMP pathway
stimulates gonadal aromatase - androgen to oestrogen

28
Q

androgen example

A

androstenedione

29
Q

oestrogen example

A

oestradiol

30
Q

PCOS apparent symptom on imaging

A

many follicles seem to mature, but are all very small

31
Q

PCOS criteria

A
  1. appearance of polycystic ovaries
  2. ovulation is abnormal or absent
  3. high levels of androgen - hyperandrogenaemia
32
Q

PCOS criteria if no apparent polycystic ovaries

A

hyperandrogenaemia and abnormal ovulation

33
Q

what’s the FSH endocrine issue with PCOS

A

Early stage follicles respond improperly to FSH
- problem with competition
- follicles do not mature properly
- multiple follicles that are not fully developed
- lack of dominant follicle

34
Q

What could be a kind of treatment to deal with refractory response to FSH in PCOS

A

stimulate the system with excess FSH

35
Q

LH issue in PCOS

A

Anovulatory patients have abnormally high LH
- excess LH will act on early-mid antral follicles

36
Q

PCOS - LH lead to twins?

A

issue with development and selection - multiple follicles that mature

37
Q

Severe cases of LH in PCOS

A
  1. The eggs do not mature properly, thus cannot fully support post-fertilisation development.
  2. anovulation - no ovulation
38
Q

Why does anovulation occur in PCOS

A

severe case of PCOS where follicles cannot ovulate properly
- the oocyte is retained in the corpus luteum after improper ovulation.

39
Q

abnormal corpus luteum in PCOS

A

since the follicles are underdeveloped
the CL formed are not fully functional.

40
Q

Corpus luteum effect on LH and FSH

A

normal CL will secrete mainly progesterone and oestrogen:
- high progesterone level will have negative feedback to H. and P.
- lowers FSH and LH levels

41
Q

why high LH in PCOS (abnormal corpus luteum)?

A

immature CL will lead to lower progesterone production
- reduced negative feedback
- HIGH FSH and LH.

42
Q

increased androgen production in PCOS (where?)

A

mainly in thecal cells.
more androgen is produced due to:
1. high LH
2. thecal cells become more

43
Q

High androgen affects progesterone effects

A

High androgen will antagonise progesterone’s negative feedback to hypothalamus.
- androgen will desensitive H. and P. to progesterone feedback.
- Thus GnRH level is not regulated properly.

44
Q

metabolic disorder in PCOS patients

A

PCOS patients are more prone to weight gain
Obese PCOS patients have lower post-prandial energy thermogenesis, reduced energy expenditure.
There will be insulin resistance: hyperinsulinaemia as a consequence.

45
Q

A potential in treating insulin resistance in PCOS (sheep)

A
  • administering insulin
  • increased PPT and energy expenditure
46
Q

PCOS effect on obesity, obesity effect on PCOS

A

PCOS patients gain weight easier and insulin resistance.
obese patients often have worse PCOS outcomes - more likely to have anovulation.

47
Q

how does obesity and IR affect PCOS

A
  • sensitise thecal cells to LH
  • upregulating androgen production
48
Q

PCOS cause - genetic predisposition

A

Statistics: 20-40% of offsprings of PCOS parents develop PCOS
Case: PCOS Pregnant mother
- high androgen in circulation
- predisposes her daughter to PCOS

49
Q

GWAS usage in finding genetic causes of PCOS

A

Genome-wide association study:
some genes show strong association with PCOS symptoms:
- FSH receptors
- insuline receptors

50
Q

epigenetics significance in PCOS

A

genome involved in: LH and insulin signalling
more methylation - more gene suppression
This means that some PCOS symptoms are reversible through epigenetic therapy.

51
Q

Further therapy to anovulatory infertility (refractory to FSH)

A

Raise FSH levels by reducing oestrogen negative feedback:
1. clomiphene citrate: oestrogen antagonist (bind to oestrogen receptor)
2. letrozole - inhibit aromatase

52
Q

clomiphene citrate effect

A

inhibit oestrogen feedback/signalling

53
Q

letrozole effect

A

reduce oestrogen synthesis

54
Q

further therapy to IR in PCOS

A

metformin: decrease plasma glucose
sensitises insulin signalling

55
Q

evolutionary benefits of PCOS?

A

1.PCOS amplifies metabolic outcome - eg. prone to weight gain:
Obesity could help survival in times of privation?
2.PCOS leads to Less fertility - help in childbearing -> better survival?
3.hyperandrogenism leads to increased muscle and bone mass.

Physiology 3 (11 decks)

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