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SoR > Lecture 6: Menstrual Cycle > Flashcards

Lecture 6: Menstrual Cycle Flashcards

1
Q

What axis controls the menstrual cycle?

A
  • HPO axis (Hypothalamic-Pituitary-Ovarian)
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2
Q

What are the key requirements to maintain the HPO axis?

A

Pulsatile release of both:

  • GnRH
  • Gonadotrophins
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3
Q

What are the gonadotrophins?

A
  • LH
  • FSH
    (-hCG)
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4
Q

Describe the HPO axis

A
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5
Q

What determines the length of a menstrual cycle?

A
  • number of days between first day of menstrual bleeding of one cycle to the onset of menses of the next cycle
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6
Q

What are the characteristics of the normal menstrual cycle (MC)

A
  • Median duration of MC is 28 days with most cycles between 25-30 days
  • Menstruation lasts 3-8 days, written as 7/28 or 5-6/27-32
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7
Q

What is the term when the MC is less than a certain number of days?

A
  • MC<21 days
  • polymenorrheic
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8
Q

What is the term when the MC is greater than a certain number of days?

A
  • MC>35 days
  • oligomenorrheic
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9
Q

When is MC most irregular typically?

A
  • around extremes of reproductive life
  • i.e menarche and menopause
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10
Q

Describe/Draw the levels of steroids and gonadotrophin during a normal MC

A
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11
Q

Describe the follicle and its size during a normal MC

A
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12
Q

What is the corpus luteum?

A

Mass of cells (leftovers of the follicle), secreting mainly P and some E2:

  • Granulosa cells
  • Theca cells
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13
Q

An increase in E2 levels leads to a …

A
  • decrease in FSH levels
  • negative feedback
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14
Q

Where do we get the Progesterone in MC?

A
  • Corpus luteum
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15
Q

Where do we get the E2 from in the MC?

A
  • Granulosa cells
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16
Q

What causes recruitment of early antral follicles?

A
  • intercycle rise of FSH
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17
Q

What is the 2 cell 2 gonadotrophin theory?

A

Different enzymes in different cellular compartments
- Theca: enzymes predominately responsible for P & Androgen families
- Granulosa: production of E2

  • LHR only - Theca
  • FSHR (& LHR) - Granulosa
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18
Q

Where and what drives androgen & progesterone production?

A
  • Theca cells
  • LH
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19
Q

Where is E produced?

A
  • Granulosa cells
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20
Q

When is E produced?

A
  • Follicular phase
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21
Q

What drives E production?

A
  • FSH
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22
Q

Which steroids are made where?

A
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23
Q

When is LHR acquired in the granulosa cell?

A
  • From mid-follicular phase onwards in DF only
  • After selection of dominant follicle; allows Dominant follicle to make P
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24
Q

What is the function of the LHR in the granulosa cell?

A
  • To produce Progesterone only
  • after MF phase, will drive P and E production as well
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25
Q

Between Theca and GC, where is aromatase only found?

A
  • Granulosa
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26
Q

What happens during the LL and EF phase of the MC?

A
  • P declines
    -> Selectively raises FSH (break from HPO axis is released due to decline in P)

= Inter-cycle rise in FSH

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27
Q

Why does P decline in the LL and EF phase?

A
  • CL dies if no pregnancy thus decline in P
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28
Q

What is the significance of the inter-cycle rise in FSH?

A
  • recruitment of the antral-follicles into the MC
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29
Q

What happens during the MF phase of the MC?

A
  • E2 increases
    -> Negative Feedback

= FSH falls -> Selection of dominant follicle

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30
Q

What causes the increase in E2?

A
  • Antral follicles grow (i.e. GC grow) -> release E2 -> E2 levels increase -> exerts negative feedback -> FSH levels decrease
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31
Q

When does the LH surge occur?

A
  • Mid-cycle
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32
Q

What requirements need to be fulfilled for the LH surge to occur?

A
  • 2 days of E2; >300 pmol
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33
Q

What does 2 days of E2 > 300 pmol cause?

A
  • Positive Feedback
  • Thus LH surge
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34
Q

What causes the high E2 levels mid cycle?

A
  • Dominant follicle
  • As it grows quickly and expansively it pumps out E2
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35
Q

What does the LH surge cause?

A
  • Ovulation
  • Formation of CL
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36
Q

What happens to the antral follicles when FSH decreases?

A
  • Die
  • EXCEPT for dominant follicle
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37
Q

What occurs during the ML phase?

A
  • High P due to High LH (LH surge)
    -> Negative feedback
  • P overcomes E2 (P always dominates of E2)

=Low FSH/LH

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38
Q

What is the cause of the high P in the ML stage?

A
  • CL
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39
Q

What is the Follicular Phase?

A
  • growth of follicles up to ovulation
  • dominated by E2 production from follicles
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40
Q

What is the luteal phase?

A
  • formation of CL from the empty follicle
  • dominated by P production from CL
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41
Q

Which phase has a set number of days?

A
  • Luteal phase
  • 14 days
  • Dominated by CL
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42
Q

What feedback occurs during Follicular Phase?

A
  • VARIES
  1. Release of -ive feedback from CL
  2. -ive feedback then reinstated, then
  3. Switch from -ive to +ive feedback
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43
Q

What feedback occurs during Luteal phase?

A
  • Negative feedback

-> Progesterone

44
Q

When does ovulation occur?

A
  • end of Follicular phase
45
Q

What becomes of the reminent of the follicle after ovulation?

A
  • Becomes CL
46
Q

What occurs at the end of Luteal Phase if no pregnancy?

A
  • CL dies
    -> Increase in FSH & MC restarts
47
Q

What happens during the rise and fall of FSH during the follicular phase?

A

Rise:
- “window of opportunity”: Recruitment of the growing follicles into the follicular stage

Fall:
- Increase in E2 -> Selection of one of these follicles (others die) -> DOMINANT FOLLICLE -> PREOVULATORY FOLLICLE -> OVULATES

48
Q

Do all animals have the MC?

A

No, only:

  • Humans
  • Primates (apes and monkeys)
49
Q

What do all mammals have in common?

A
  • cyclical ovarian function
  • Same reproductive system when it comes to HPG axis
  • Produce mature egg and necessary sex steroids
50
Q

What is the oestrus cycle?

A
  • cyclic appearance of behavioural sexual activity (heat or oestrus)
51
Q

Do animals that undergo oestrus menstruate?

A

No - endometrium reabsorbed if no fertilisation

52
Q

What is day 0 of the oestrus cycle?

A
  • First day of sexual receptivity
53
Q

When does ovulation occur in animals that undergo oestrus?

A
  • Early in cycle
  • High E2 levels = stimulation of sexual behaviour & +ive feedback
54
Q

Do all species that undergo oestrus have the same cycle length?

A
  • No
55
Q

What is poly-oestrus?

A
  • In heat several times/year
  • cats, cows, pigs
56
Q

What is di-oestrus?

A
  • Twice/year
57
Q

What is mono-oestrus?

A
  • One breeding season/year
  • usually in spring (daylight)
  • Bears, foxes, wolves
58
Q

Which animal has no oestrus cycle?

A
  • Rabbits
  • Induced ovulates
  • Induced to ovulate by mating & can conceive at any moment
59
Q

HPO axis

A
60
Q

What gonadal protein inhibits FSH directly? Where is it produced?

A
  • Inhibin
  • Sertoli cells in testes
  • Granulosa cells in ovary
61
Q

What is the structure of inhibin?

A
  • Disulphide-linked protein dimers
  • Common α-subunit with different β-subunits giving two forms of Inhibin
  • Both forms suppress FSH secretion by pituitary
  • Not affecting LH secretion
62
Q

What gonadal protein stimulates FSH secretion?

A
  • Activins
  • Isolated from follicular fluid
63
Q

What gonadal protein indirectly suppresses FSH secretion?

A
  • Follistatin
  • FSH-suppressing protein
  • From follicular fluid
64
Q

How does Follistatin work?

A
  • binds activin with high affinity » neutralizes FSH-stimulating ability of activin
65
Q

How do we know inhibin only works on FSH and not LH?

A
  • Experiment: Using ovariectomized (ovx) sheep, GnRH agonist was injected in the presence and absence of inhibin
66
Q

Why did they use ovx sheep?

A
  • Mono-ovulators
  • similar to humans
  • Sheep are a good model for reproduction
  • otherwise mice due to limitations when it comes to sheep (expense/storage etc.)
67
Q

What does overiectomised (ovx) mean?

A
  • Removal of ovaries
68
Q

Why were ovx sheep used?

A
  • Prevent the endogenous feedback effects interfering
69
Q

Why did the experiment inject GnRH agonist?

A
  • stimulate gonadotrophin production
70
Q

Biosynthesis of inhibins and activins occurs from how many genes?

A
  • 3
71
Q

What are the TGFβ- superfamily of precursor proteins involved in?

A

3 genes encoding for:

  • α- protein (specific for inhibin)
  • βA- protein,
  • βB- protein,

These alpha and beta subunits are all members of TGF-beta superfamily of proteins.

72
Q

The genes encode for larger precursor proteins which are then processed… (activin/inhibin genes)

A

proteolytically

73
Q

What are the isoforms of inhibin?

A
  • Inhibin A
  • Inhibin B
74
Q

What are the isoforms of activin?

A
  • Activin A (βA-homodimer),
  • Activin B (βB-homodimer)
  • Activin AB (βAβB-heterodimer)
75
Q

How are inhibin and activin produced?

A
  • The gene products are the sub-units which will combine at the time of release from the cell.
76
Q

How is the amount of activin and inhibin determined during MC and folliculogenesis?

A
  • Ratio of Activin:Inhibin
77
Q

Where is inhibin and activin produced in females?

A
  • Granulosa cells
78
Q

When do activins dominate in the MC?

A
  • EFP
  • Correlates with high FSH
79
Q

When do inhibins dominate in the MC?

A
  • LFP
  • Correlates with decreased FSH
80
Q

Which hormone aids the inter-cycle rise in FSH?

A
  • Activin
81
Q

What does the inter-cycle rise in FSH cause?

A
  • recruits early antral follicles
82
Q

What is the significance of inhibin on the MC?

A
  • Rise in E2
  • Fall in FSH
83
Q

What happens to the levels of activin and inhibin as we go through folliculogenesis?

A
  • Inhibin production increases
  • Activin produced decreases
84
Q

Describe the experimental procedure that questioned what happens when inhibin is blocked?

A
  • (Red) Inject rats in the late antral phase with Inhibin anti-serum
  • = blocks inhibin from working as it has antibodies that bind to and prevent it from working
  • Red = increase in FSH
  • (Green) Inject with normal serum = no peak of FSH (as you’d expect at this stage of MC)

= thus showed that in Late Antral phase, inhibin needed for fall in FSH; NOT ONLY E2!!

85
Q

? + ? = Fall in FSH

A

E2 + Inhibin = Fall in FSH

86
Q

What are the main hormones in the TGFBeta superfamily?

A
  • Inhibin
  • Activin
  • AMH
87
Q

What is AMH?

A
  • Anti-Mullerian Hormone
  • glycoprotein
  • member of TGFBeta superfamily
88
Q

What is the importance of AMH in males?

A
  • expressed from week 8 of development
  • causes regression of Müllerian ducts by a wave of apoptosis.
89
Q

Do females express AMH?

A

Yes

90
Q

Where is AMH expressed in females?

A
  • ovarian granulosa cells
91
Q

Do AMH levels peak in females, and if so, where?

A
  • levels peaking in selectable follicles (large preantral & small antral follicles)
    –> then decreases
92
Q

Has AMH been detected elsewhere? (other than preantral and small antral follicles)

A

Yes

  • Prenatal follicles
  • However variable and may be species variable
93
Q

What is the role of AMH in the MC?

A
  • regulator of normal follicle growth and development
94
Q

What is the function of AMH?

A
  • Inhibits transition from primordial to primary follicles
  • Inhibits FSH-dependent cyclical recruitment of follicles
    -> by inhibiting FSH-stimulated aromatase & FSHr expression → in normal MC, prevents over-recruitment of growing follicles
95
Q

What is the function of FSH?

A
  • To drive follicle growth
  • Recruiment of antral follicles into MC
  • stimulates aromatase
96
Q

What does AMH inhibit?

A
  • The function of FSH
97
Q

What does AMH prevent in the normal MC?

A
  • over-recruitment of growing follicles

= AMH maintains a balance

98
Q

What is the problem with over-recruitment of follicles?

A
  • Depletion of follicles quicker
    -> early menopause
99
Q

Where do inhibins and alctivins act on?

A
  • Anterior Pituitary ONLY
100
Q

Where to E2 and P act on?

A
  • Hypothalamus
  • A. Pituitary
101
Q

What is the ‘window of opportunity’ & follicle selection?

A
  • Raised FSH present a “window” of opportunity
  • FSH threshold hypothesis
  • One follicle from the group of antral follicles in ovary is just at the right stage at the right time….
  • Becomes DOMINANT follicle -> survives fall in FSH & goes onto ovulate
  • Known as “selection”
  • Can be in either ovary
  • E2 levels rise reinstating -ive feedback at pituitary -> FSH levels fall = prevents further follicle growth
102
Q

How does the dominant follicle survive the fall in FSH?

A
  • As FSH falls, LH increases.
  • Dominant follicle acquires LH receptors on granulosa cells.
  • Other follicles do not, so they loose their stimulant and die.
103
Q

How are the gonadotrophin receptors distributed in follicles? Thus, what steroids are produced?

A

Granulosa:
- FSHr
- LHr from mid-follicular phase onwards in DF
- FSH drives E2 production in FP; LH drives P ONLY (no androgens) in LP

Theca:
- LHr ONLY
- P and androgen production

104
Q
A
  • Inhibin B: highest in early-mid FP (ratio of activin: inhibin) and declines in LFP (small peak at LH surge), zero in luteal phase.
  • decline in Inhibin A at end of L phase allows for increase in FSH.

Inhibin A: increases in late FP with highest levels in L phase (being made by CL) – contributes to inhibition of FSH in this phase.
- Decline in Inhibin A at end of L phase allows for increase in FSH.

  • Activin High = FSH High
  • E2 rises via -ive feedback = inhibit B which contrinbutes to this -ive feedback
105
Q

Are E2 and P the only factors affecting the HPO axis?

A

No!!

106
Q

Are the gonadal steroid hormones only acting on the follicles?

A

NO!!

  • Acting elsewhere in the female reproductive tract - everything has to be ready for both transport of fertilised egg and sperm!
107
Q

Other than the follicles, what else are the steroid hormones acting on?

A

E2, P and (Androgens?) are acting on:

  • Endometrium
  • Oviduct/Fallopian tubes
  • Cervix
  • Vagina - changes in vaginal epithelial cells

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