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Life Cycle > Menopause > Flashcards

Menopause Flashcards

1
Q

What is the menopausal transition?

A

period of time from changes in menstrual pattern to menopause

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2
Q

What is menopause?

A

permanent cessation of menstruation due to loss of ovarian follicular function

must have amenorrhoea for 12 months - retrospective Dx

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3
Q

What is perimenopause?

A

no consistent definition

period of changing ovarian function which preceded the menopause by 2-8 yrs

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4
Q

What is premature ovarian failure?

A

menopause < 40

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5
Q

What are the Sx of the menopause?

A

VARIABLE

  • initially reduced menstrual cycle (reduced follicular phase)
  • mean = 4yrs before final menstrual period
  • irregular periods, with amenorrhea episodes
  • hot flushes, disturbed sleep (occurs 1year before menopause, due to reducing E2 levels)
  • dry vagina
  • no menstrual irregularity
  • impaired fertility
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6
Q

Why does menopause occur?

A
  • number of granulosa cells in pre-antral follicles reduces with age
  • ability to synthesise E2 also decreases
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7
Q

What is the mechanism behind menopause?

A
  • active follicles become inefficient in E2, Inhibin B and AMH synthesis
  • high levels of serum FSH
  • GnRH secretion impaired -> impaired LH surge -> anovulation
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8
Q

What pathophysiogical observations are noted with menopause?

A
  • reduced follicle count - none or few at menopause
  • reduced granulosa cell number
  • reduced granulosa cell function
  • increased aneuploidy in oocyte
    (higher miscarriage rate, increased T21 risk)
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9
Q

What is the ‘critical threshold’ of ova numbers?

A

point at which there is an accelerated decline in the number of ova (due to follicular atresia)

occurs at ~37yr

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10
Q

Why is there an acceleration in follicular loss?

A
  • follicular depeletion

- decline in granulosa cell/function

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11
Q

What are the main mechanisms in follicular depletion?

A
  • increased follicular atresia (pro-apoptotic environment e.g. smoking)
  • accelerated follicular loss (AMH declines, FSH increases, increased follicular recruitment)
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12
Q

What are the mechanisms underlying decreased granulosa cells/function?

A
  • 30% decrease in granulosa cells in oder women
  • reduced Inhibin B production leads to high FSH levels [follicular phase]
  • anovulatory cycle: reduced inhibin A [no luteal phase] so higher FSH
  • reduced FSH receptors so impaired follicle recruitment
  • impaired GF secretion, E and P
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13
Q

What are the main consequences of granuolosa cell dysfunction?

A

SHORTENED CYCLE

  • decline in inhibin B production (from granulosa cells)
  • elevated FSH in follicular phase
  • earlier E2 production and earlier LH surge

DELAYED/ABSENT OVULATION

  • E2 production stimulates earlier in cycle (elevated FSH)
  • however not high enough [E2] to induce GnRH-mediated LH surge (dysfunctional granulosa cells)
  • ovulation is delayed or doesn’t occur
  • FSH insensitivity
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14
Q

How does FSH insensitivity result in heavier periods in peri-menopause ?

A

Fewer FSH-R in granulosa cells -> FSH insensitivity

fewer follicles recruited, no inhibin A -> FSH rises

longer E2 stimulation with higher [E2] -> rich, thick endometrium

sloughs off due to weight of lining -> menorrhagia

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15
Q

What causes breast tenderness in peri-menopause?

A

transitory increases in E2

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16
Q

What causes hot flushes in peri-menopause?

A

reduced E2 levels -> disturbed serotonin levels

resets thermoregulatory nucleus -> excessive heat loss

N.B. SSRIs can be an effective Rx (in place of HRT)

17
Q

What are the hormonal consequences of menopause?

A
  • AMH levels: first sign of declining ovarian function
  • declining inhibin B: ~2yr before final menstrual period
  • FSH levels generally variable, but will increase towards menopause
  • LH increases later in menopause
  • E2 levels fall near the menopause
  • Androgen levels decline (ovarian and adrenal) NOT RELATED TO MENOPAUSE
  • no progesterone production post-menopause
18
Q

Why is there a decline in oocyte function and development during menopause?

A
  • consequence of impaired production of GFs from granulosa cells
  • increased aneuploidy
  • increased oocyte abnormality -> impaired follicle recruitment (even with clomiphene)

= anovulatory cycles
= increased miscarriage rate

19
Q

What is clomiphene?

A

used to treat infertility for women who do not ovulate

it is selectively modulate the ER by acting like an oestrogen analogue

20
Q

What is the variation in age of menopause attributed to?

A
  • smoking status
  • geographical location
  • maternal age at menopause
  • (polygenic) risk loci
    surgery/chemo
21
Q

What markers can be used to indicate declining fertility?

A
  • ovarian volume = antral follicle count
  • ovarian stimulation = antral follicle count
  • AMH

not very reliable for menopause prediction

22
Q

Why considerations should be taken when prescribing HRT?

A
  • oestrogen has 80% efficacy at reducing hot flushes (lower doses also effective)
  • patient centred
  • consider baseline risks
  • always use P for women with uterus
  • need contraception if <1yr amenorrhea
  • minimise side effects: mastalgia, nausea
  • risks are lower for short term use: transdermal oestrogen (patch) = low VTE risk
23
Q

What is oestrogen-induced endometrial hyperplasia?

A

found in 56% of women who use unopposed oestrogen
~3% develop carcinoma

protection obtained by 10-13 days of P

cyclical P: pre-menopausal with periods

continuous P: menopausal women with amenorrhoea

24
Q

Which kinds of oestrogen preparations have VTE risk?

A

transdermal and gel: no increased risk

oral oestrogen: increased VTE risk

25
Q

How is HRT usually given?

A

COCP: continuous E2, cyclical P

oestrogen alone: continuous E2 for women w/o uterus

topical oestrogen: vaginal creams or rings for dryness (reduced endometrial risk as no systemic absorption)

26
Q

What alternatives to HRT can be used to treat osteoporosis in menopausal women?

A
  • bisphosponates
  • ? raloxifene (Selective ER modulator - SERM)
  • calcium and vitamin D
  • Strontium

Other (currently under Ix)

  • teriparatide (PTH peptide fragment)
  • simvastatin
  • leptin
  • photo-oestrogens
  • manipulation of RANK-L gene
  • anti-oxidants
27
Q

What techniques have modern medicine come up with for premature ovarian failure?

A
  • ovaries removed (earlier in disease)
  • re-implanted ovarian fragments near fallopian tube
  • stimulated follicular development
  • removed eggs

results: 27 women, 1 live birth

Life Cycle (29 decks)

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