PHYSIOLOGY OF MENOPAUSE

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PHYSIOLOGY OF MENOPAUSE

• DR MOUSUMI DAS GHOSH
• TATA MAIN HOSPITAL
• JAMSHEDPUR

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MENOPAUSE

• MENOPAUSE comes from the greek word ' menos'(
  month) and 'pausis'(cessation).
• Diagnosis is made retrospectively after a minimum
  of one year amenorrhoea.
• PERIMENOPAUSAL TRANSITION--
• The years prior to menopause that encompass the
  change from normal ovulatory cycles to cessation
  of menses.

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THE DECLINING OOCYTE POOL

• Accelerated follicular depletion begin at age
  37-38, and menopause follows 13 years
• later.
• menopause occurs when the number of follicles
  falls below a critical threshold, about 1000
  ,regardless of age.

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COMPENSATED FAILURE

• Initially ovarian failure is compensated by
  rising Gn levels, about the age of 30yrs
• inhibin production from granulosa cells fall
  leading to a reduced INHIBIN FSH ratio.

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DECOMPENSATED FAILURE

• Critical decline in oocyte pool leads to further
  rise in FSH.(10-20 FOLD)
• LH rises only 3-fold due to its shorter half
  life.
• OESTROGEN levels drop due to reduction in
  follicle number and granulosa cell ageing.
• Permanent cessation of progesterone production.

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OTHER HORMONAL CHANGES

• Both adrenal and ovarian androgen levels fall.the
  drop in androgen levels is profound in premature
  ovarian failure.
• OESTROGEN therapy increase SHBG LEVELS
  ---further fall in free androgen levels.
• Main postmenopausal oestrogen is
  oestrone-produced mainly by adipose tissue and
• postmenopausal ovary by aromatization of adrenal
  androstenedione.
• insulin resistance and rise in central
  adiposity.

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PREDICTION OF OVARIAN RESERVE

• FSH levelgt30 is diagnostic of menopause.
• combination of FSH, INHIBIN WITH ANTI-MULLERIAN
  HORMONE.
• Measurement of ovarian volume.

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PREMATURE OVARIAN FAILURE

• Defined as cessation of menstruation before the
  age of 40 years.
• CAUSES
• spontaneous or idiopathic
• turner syndrome
• fragile X syndrome
• FSH receptor polymorphism
• INCIDENCE IS RISING.

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CONSEQUENCES OF MENOPAUSE

• IMMEDIATE
• INTERMEDIATE
• LONG TERM

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IMMEDIATE

• HOT FLUSHES---
• Thought to arise due to loss of
  oestrogenic induced opioid activity in the
  hypothalamus.
• NA and serotonin mediate this activity.
• Obese women are protected due to large
  amounts of oestrone and low SHBG.

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• INSOMNIA, ANXIETY, IRRITABILITY
• POOR CONCENTRATION
• MOOD DISTURBANCES
• REDUCTION IN SEXUALITY AND LIBIDO
• MEMORY LOSS

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INTERMEDIATE CONSEQUENCES

• Oestrogen deficiency leads to rapid loss of
  collagen
• dyspareunia and vaginal bleeding
• urethral syndrome(dysuria, urgency and
  frequency)
• increased bruising
• generalized aches and pains

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Long term health problems

• Osteoporosis
• Disorder of bone matrix resulting in
  reduction in bone strength to the extent that
  there is increased risk of fractures.
• Women lose 50 of their skeleton by
  the age of 70 years, but men only lose 25 by the
  age of 90 years.
• Predisposing factors-
• genetic predisposition, use of
  corticosteroids, pre-menopausal amenorrhea,
  smoking, premature ovarian failure

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Cardiovascular

• Protective effect of oestrogen
• increase in HDL
• decrease in LDL
• NO mediated vasodilatation
• antioxidant effect
• direct effect on aorta decreasing
  atheroma

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• Risk factors include high BMI and a decrease in
  oestradiol levels.
• Women with day3FSH gt 7 IU/ml compared to those
  with day3 FSH lt 7 IU/ ml were found to have
  higher lipid levels.

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C N S

• Oestrogen has a direct effect on the vasculature
  of the CNS and promotes neuronal growth and
  neurotransmission. Also improves cerebral
  perfusion and cognition in women.
• Causes alzheimers disease, dementia. (intervenes
  at the level of amyloid precursor protein).

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Diagnosis

• Characteristic history of hot flushes and night
  sweats with prolonged periods of amenorrhoea.
  Measurement of plasma hormone level is not
  necessary.
• However in a young patient or in a woman after
  hysterectomy, where the diagnosis is more
  difficult, measurement of FSH is helpful.
• (gt 15 iu/ml).

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• Thank you