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Menopause Flashcards

1
Q

Define menopause

A

After 1 year has passed since a woman’s last period

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2
Q

What is the average age of menopause?

A

51

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3
Q

What is perimenopause?

A

5 years or so before menopause where the woman undergoes hormonal and psychological changes and are experiencing symptoms

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4
Q

Define premature menopause

A

Menopause at 40 or before 40

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5
Q

Why does menopause occur?

A

Ovarian insufficiency
Reduced no. of functional follicles/reduced sensitivity of remaining follicles to FSH and LH –> oestradiol falls, GnRH, FSH and LH rise (but their secretion becomes very erratic) –> symptoms of perimenopause

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6
Q

Where can some oestradiol still come from in the body?

A

Peripheral conversion of adrenal androgens in fat

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7
Q

Menopause can occur naturally, how else may it occur?

A

After oophorectomy, chemo or radiotherapy

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8
Q

What are the symptoms of menopause?

A 
Muscle/joint aches
Hot flushes
Vaginal dryness
Low libido 
Mood changes/memory problems 
Osteoporosis
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9
Q

Define osteoporosis

A

Reduced in bone mineral density

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10
Q

How do you monitor osteoporosis?

A

DEXA scan, T score, FRAX score

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11
Q

What is the issue with osteoporosis?

A

Woman at increased risk of fractures

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12
Q

What things would lead to a high FRAX score?

A

Thin, Caucasian, smoker, alcohol use, +ve FH, steroids, malabsorption, hyperthyroidism

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13
Q

How can prevent/treat osteoporosis?

A

Exercise, vit D/calcium supplements, bisphosphonates, denosumab (monoclonal Ab against osteoclasts), teriparatide

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14
Q

How can you treat menopause?

A 
HRT 
Selective oestrogen receptor modulators
SSRI/SNRI antidepressants
Natural methods
Non-hormonal vaginal lubricants
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15
Q

What are the two forms of HRT you can use?

A
  1. SYSTEMIC
    Patch (avoids first pass met –> less VTE risk), oral, gel
    Oestrogen only if no uterus
    Oestrogen and progesterone if uterus
  2. LOCAL
    Vaginal oestrogen only (pessary/ring/cream)
    Minimal absorption so no increased VTE/breast ca risk
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16
Q

Why must you give progesterone to someone in systemic HRT who has a uterus?

A

Unopposed oestrogen has a proliferative effect on the endometrium so may lead to endometrial hyperplasia

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17
Q

What are the different ways you can give progesterone as HRT?

A

LNG IUD, transdermal patch, POP

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18
Q

What are the contraindications to HRT?

A

Current hormone dependent cancer of breast/endometrium, current active liver disease, uninvestigated abnormal vaginal bleeding

Seek advice about prev. VTE, thrombophilia, FH VTE, prev. breast ca/BRCAn carrier

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19
Q

Why might we not do continuous combined HRT?

What is the alternative?

A

Despite it being assoc. w lower endometrial cancer risk, may lead to inconvenient breakthrough bleeding if still some ovarian function

Can do cyclical combined - 14 days oestrogen 14 days oestrogen and progesterone (withdrawal bleed after stopping progesterone)

NB any age can use mirena and daily oestrogen

20
Q

What are SERMs?

A

Have oestrogen effect on selective organs

Used to treat vasomotor symptoms assoc. with menopause

21
Q

What natural methods can you use for menopause symptom treatment?

A

Phytooestrogen (red clover, soy, black cohosh)

Hypnotherapy, CBT, exercise

22
Q

What are the benefits of HRT?

A

Improves vasomotor and local genital symptoms

Reduces risk of osteoporosis and bowel cancer

23
Q

What are the risks of HRT?

A

Breast Ca if combined HRT (and BMI >30, or >14u EtOH/wk & returns to normal after 5y of cessation), ovarian cancer
VTE and CVA if oral route

24
Q

What are the HRT use NICE guidelines?

A

Rx of severe vasomotor symptoms - review annually
For woman with premature ovarian insufficiency - HRT benefits outweigh risks until 50
Not first line Rx for osteoporosis - use bisphosphonates
Vaginal oestrogen for vaginal symptoms

25
Q

What is andropause?

A

Testosterone decreases by 1% every year after 20

Fertility remains and no sudden change

26
Q

What is primary amenorrhoea?

A

Never having had a period
>14y + no secondary sexual characteristics
>16y + secondary sexual characteristics

27
Q

Define secondary amenorrhoea

A

Has had periods in past but none for last 6m

28
Q

What are the causes of secondary amenorrhoea?

A 
Pregnancy/breast feeding
Contraception related
Polycystic ovaries
Early menopause 
Thyroid/cushings dx/any serious illness
Raised prolactin - prolactinoma/medication related 
Hypothalamic - wt change/stress/exercise
Androgenic secreting tumour 
Sheenan's syndrome
Asherman's syndrome
29
Q

What is sheenan’s syndrome?

A

Pituitary failure

30
Q

What is asherman’s syndrome?

A

Intrauterine adhesions

31
Q

What tests would you do/signs would you look for in examination of someone with secondary amenorrhoea?

A

BMI/Cushingoid
Androgenic signs - hirtuism, enlarged clitoris, deep voices, acne
Pregnancy test/dipstick for glucose
FSH, oestradiol, thyroid function tests, prolactin, testosterone
Pelvic USS to check for polycystic ovaries

32
Q

How do you treat secondary amenorrhoea?

A

Direct at cause
Aim for BMI 20-25
Check for fragile X
If premature ovarian insufficiency offer HRT until 50, emotional support, daisy network

33
Q

Can someone still be fertile if they have secondary amenorrhoea?

A

Assume fertile and need contraception until 2 years after confirmed menopause

34
Q

How do you diagnose PCOS?

A

2/3 are present:
PCO morphology on USS (x10 small peripheral follicles/volume >12ml)
Clinical/biochemical hyperandrogenism - hirtuism/acne
Oligo/anovulation - amenorrhoea/infertility

35
Q

What are people with PCOS at risk of if they are not on hormones?

A

Endometrial hyperplasia if <4 periods a year and not on hormones

36
Q

What do half of PCOS patients have?

A

Metabolic syndrome (obesity, insulin resistance and hypercholesterolaemia)

37
Q

What is the underlying aetiology of PCOS?

A

Reduced insulin sensitivity –> hyperinsulinaemia (insulin receptors on theca cells - this is thought to lead to increased LH secretion)
Increased LH leads to increased production of androgens which the granulosa cells can’t convert all of into oestrogen –> imbalance between androgen precursors and oestrogen produced by granulosa cells
–> low FSH and improper follicle maturation, LH so high there is no surge –> anovulation

Increased circulating androgens –> virilization and increase in oestrogen production in adipose tissue

Inhibited production of sex hormone binding globulin in liver –> increased free androgens and oestrogens

38
Q

What does hyperinsulinaemia result in (apart from increased androgens)?

A

Obesity, acanthosis nigricans

39
Q

What would the blood tests of someone with PCOS show?

A

Increased testosterone, LH increased LH:FSH ratio

Oestrogen normal/raised

40
Q

What is involved in the management of PCOS?

A

Wt loss/exercise
Increase SHBG so reduced free androgens
Antiandrogens - COCP, spironolactone, elfornithine cream
Endometrial protection - COCP, POP, mirena
Fertility Rx - clomiphene/metformin

41
Q

How does metformin work in treating PCOS?

A

Helps ovulation

42
Q

How does clomiphene work in treating PCOS?

A

Inhibits hypothalamic oestrogen receptors –> increased production of GnRH and therefore FSH/LH which stimulates ovulation

43
Q

What can cause premature ovarian insufficiency?

A

Idiopathic or genetic causes, e.g. Turner’s syndrome, or post-chemo

44
Q

What is the mechanism behind premature ovarian insufficiency?

A

Impaired follicular development –> reduced oestrogen –> loss of feedback inhibition of oestrogen on FSH and LH –> FSH and LH rise

45
Q

What age is a woman required to be for it to be considered premature ovarian insufficiency?

A

Before age or 40

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