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Urogynae and menopause > Menopause RANZCOG guideline > Flashcards

Menopause RANZCOG guideline Flashcards

1
Q

Definition of menopause

A

The last menstrual period a woman will ever have

A woman is ‘post menopausal’ 12 months after LMP

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2
Q

Age of ‘early’ menopause?

A

<45

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3
Q

Age of premature menopause?

A

<40

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4
Q

Definition perimenopause

A

the time from the onset of menstrual cycle changes until one year after the final menstrual period

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5
Q

Signs of early menopause transition?

A

marked by a persistent difference of at least 7 days in length of consecutive cycles

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6
Q

Signs of late menopause transition

A

marked by periods of amenorrhoea of 60-days or more, frequent anovulation and the onset of perimenopausal symptoms

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7
Q

Average age of menopause?

A

51

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8
Q

How to diagnose the menopause?

A

Clinical diagnosis: cessation of menstruation for a period of 12
months.

Younger women/ if the diagnosis is uncertain:
- elevated gonadotrophins (FSH) +
and a low oestradiol

on 2 occasions can confirm menopause.

AMH is not currently recommended to predict or diagnose menopause.

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9
Q

What advice/assessment to give women who are approaching menopause? (e.g. from age 45)

A
  • offer information and
    advice about normal menopausal changes and symptoms
  • if required, individualised discussion of management options for troublesome symptoms.
  • routine health assessment,
    education and primary prevention including cardiovascular, bone and mental health.
  • National breast and cervical screening guidelines should be
    followed.
  • Bone density should be measured using DXA in those at increased risk of osteoporosis and fracture.
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10
Q

How to assess women at risk of osteoporosis?

A

FRAX assessment + BMD by DEXA scan (included in FRAX)

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11
Q

How to determine cardiovascular risk?

A

CVD calculator

Takes into account:

  • Age
  • Gender
  • BP
  • Smoking status
  • Cholesterol levels
  • LVH on ECG
  • Diabetes
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12
Q

How long do vasomotor symptoms persist for?

A

most women 4-5 years

10% for 10 years

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13
Q

Which women are at an increased risk of anxiety/depression?

A

Women with a history of affective disorders and those with premature/surgical menopause or following a cancer diagnosis

Consider mental health referral

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14
Q

Women of which ethnicity are more likely to have joint genitourinary/vasomotor symptoms?

A

Asian

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15
Q

What are the management options for symptoms of the menopause?

A

non-pharmacological
nonhormonal
hormonal treatments

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16
Q

What risks should be assessed when considering HRT?

A

Risks of:

  • developing osteoporosis,
  • cardiovascular disease,
  • thromboembolism
  • dementia
Lifestyle factors should be addressed and focused on as part of primary prevention and education including:
- weight bearing exercise, 
- calcium/ vitamin D intake,
- avoidance of smoking, excessive
alcohol and caffeine intake, 
- optimal weight maintenance 
- reduction of stress.

Sexual counselling should be considered for the woman, either on her own or with her partner.

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17
Q

Indications for HRT?

A

relief of troublesome VMS impacting on quality of life

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18
Q

Which other menopausal symptoms may improve with oestrogen?

A

vaginal dryness/dyspareunia, sexual dysfunction, sleep
disturbance, mood swings and joint or muscle pains

However, treatment of low mood and libido is not a primary indication for MHT.

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19
Q

How long/until when should women with premature menopause be offered HRT?

A

Women with premature (less than 40 years) or early (less than 45-years)
menopause should be offered MHT at least until aged 50 years unless
otherwise contraindicated

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20
Q

After what age should MHT not be commenced?

A

Commencement of MHT after the age of 60 is generally not

recommended as benefits are less likely to outweigh risks.

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21
Q

What dose of MHT should women be started on?

A

Dose is generally titrated to symptom relief and side effects, but most clinical guidelines advise starting with low dose therapy

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22
Q

How long can MHT be prescribed for?

A

There are no fixed guidelines on duration. Many would recommend less than 5-7 years.

VMS may persist in around 40% of women age 60-65, but the risks of treatment may increase with longer duration of use.

Annual follow up is recommended, to review general health status and need for continued MHT.

Starting MHT over the age of 60, or more than 10 years beyond menopause, is generally not
recommended although, in the presence of persistent troublesome symptoms, continuation of existing therapy can be considered.

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23
Q

Association between MHT and fracture risk/bone density?

A

MHT increases bone density and reduces fracture risk.

However, due to the remainder of the risk/benefit profile, prevention of osteoporosis or fracture is not a primary indication for MHT use.

It may be used in asymptomatic women for whom other treatments are considered inappropriate.

MHT should be considered for women with menopausal symptoms who have reduced bone
density but have not sustained a fracture

First line treatment for osteoporosis is 1g calcium and 400IU vitamin D replacement +/- bisphosphonates

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23
Q

Which MHT increases breast ca risk?

A

Breast cancer risk appears greater with combined MHT compared to oestrogen alone, and greater exposure to progestogen (continuous vs intermittent, longer treatment duration) may lead to greater breast cancer risk

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24
Q

MHT and VTE risk?

A

Oral MHT is contraindicated in women with a personal history of VTE.

Compared with oral MHT, transdermal MHT does not appear to increase VTE risk in women at
low risk for this condition

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25
Q

How much does oral oestogen + P increase VTE risk?

A

2 fold

Oral estrogen therapy also increases risk, but to a lesser extent

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26
Q

Factors that increase the risk of VTE with MHT?

A
  • increasing age
  • hormone dose, routine and combined vs oestrogen only MHT,
  • obesity,
  • smoking,
  • immobility,
  • thrombophilia
  • previous VTE
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27
Q

Risk of recurrent VTE in 1st year of using MHT with hx of previous VTE?

A

10%

28
Q

MHT and stroke risk

A

An increased risk of stroke has been reported amongst women over the age of 60 or >10 years
from the menopause using either oral oestrogen or combined therapy.

The increased risk is
confined to ischaemic stroke and is probably related to thromboembolic risk. A large
observational study found that whilst oral oestrogen and high doses of transdermal therapy
increased stroke risk, no increase was seen when transdermal doses of 50ug or less were used

29
Q

MHT and CVD?

A

MHT should not be used for the primary prevention of CVD.

Overall it has no effect on CVD risk or overall survival.

In women within 10 years of the menopause MHT reduces CVD risk and mortality, with no increased risk of stroke.

(Cochrane 2015)

30
Q

What is the ‘window of opportunity’ hypothesis relating to MHT and CVD risk?

A
  • Follow up of The Women’s Health Initiative RCT CHD was not significantly different during the intervention or post intervention phase for either estrogen
    only or combined therapy, compared with placebo.
  • When stratified for women aged 50-59 in cumulative follow up, the risk was significantly reduced for users of estrogen only therapy (HR
    0. 65, 95%CI 0.44-0.96) and not increased for users of combined MHT.

A recent cochrane systematic review concluded that, overall, MHT conferred no protective effect on all-cause mortality, cardiovascular death, non-fatal infarction, angina or revascularisation but did increase risk of stroke and VTE.
- However, in women who started MHT less than 10 years after the menopause there was lower mortality (RR0.70, 95%CI 0.52-0.95) and a lower incidence of coronary heart disease. There was no evidence of increased risk of stroke in this group.

These findings are
supportive of the ‘window of opportunity’ hypothesis that initiation of MHT in women within 10 years of their last period is associated with maximum benefit and minimal risk

31
Q

MHT and breast cancer risk

A

MHT should be avoided in women with a personal history of breast
cancer

MHT increases breast density and combined oestrogen-progestogen increases the risk of breast
cancer.

The use of daily progesterone appears to increase risk above cyclic progesterone use and risk increases with duration of use.

It is uncertain whether oestrogen alone increases breast cancer risk. Large RCT’s suggest no increase in risk but observational studies indicate that oestrogen alone may increase breast cancer
risk but to a lesser extent than combined MHT.

Whether 5 years of combined MHT use is safe for the breast is uncertain, it seems there is minimal increased risk with <5 years use. For 7.5 years use there is a 35% increased risk (30/1000 vs 22/1000).

HOWEVER the increased risk associated with MHT is comparable to the risk from lifestyle factors like obesity, smoking and sedentiary lifestyle.

Breast cancer risk may persist after discontinuation of MHT.

For women with no personal hx but family hx: data very limited, MHT may be safe

32
Q

MHT and endometrial cancer risk

A

In women who have an intact uterus, unopposed oestrogen increases the risk of endometrial
hyperplasia and cancer.

Combined continuous MHT reduces the risk of endometrial cancer compared to untreated women.

Sequential MHT confers a slight increase risk of endometrial
cancer

33
Q

Which ovarian cancers are users of MHT at an increased risk of?

A

serous and endometrioid subtypes

There is a reduction in risk of clear cell and mucinous subtypes

34
Q

What is the increased risk of ovarian cancer in women using MHT?

A

The effect of MHT on ovarian cancer is unclear.

The absolute increase in risk was 2.4 per 10,000 women per year in one met analysis of observational studies - the clinical significance of this area outcome is unclear.

The only large randomised trial examining MHT and ovarian cancer risk found no increase after 5 years of therapy, though was insufficiently powered for this rare outcome for the results to be definitive.

35
Q

MHT and gallbladder disease

A

Large RCT’s have shown an increased risk of cholecystitis with oral MHT.

The effect is reduced in transdermal MHT; women with deranged LFTs should be started on transdermal MHT.

36
Q

Other considerations prior to commencing MHT

A

MHT should not be commenced in women with undiagnosed vaginal bleeding.

Combined MHT may be associated with unscheduled bleeding during the first six months of therapy. Persistent, or new onset, bleeding beyond that time requires investigation.

In women with abnormal liver function tests transdermal therapy should be preferred.

Migraine is not a contraindication to MHT use however low dose transdermal therapy may be
preferable.

37
Q

Common side effects of MHT?

A

nausea, headache and breast tenderness.

Initiating therapy with low doses should minimise these side effects whilst transdermal therapy is also less likely to induce nausea

38
Q

Options for perimenopausal women?

A

The combined oral contraceptive pill provides contraception, cycle control, relief from VMS and
other symptoms. It will also prevent bone loss. Each woman’s risks must be assessed, including
smoking status, blood pressure, lipid profile and VTE risk. Eliminating placebo tablets can prevent
VMS developing in the pill free week.
The levonorgestrel releasing intrauterine system (LNG-IUS) provides contraception and reduces
uterine bleeding. LNG-IUS can provide endometrial protection from systemic oestrogen.
Cyclical (sequential) MHT may be initiated during the peri-menopause for alleviation of VMS
however it is not contraceptive and will not regulate menstrual cycles

39
Q

MHT options for postmenopausal women?

A

For women with an intact uterus MHT may be
prescribed as oestrogen plus a progestogen for 14 days per month (cyclical therapy) or every day
(continuous combined therapy). Cyclical therapy results in scheduled progestogen withdrawal
bleeds. Continuous combined therapy results in amenorrhoea in 90% of women after 12 months
although spotting and breakthrough is common in the first 3-4 months of therapy

40
Q

Oestrogen options for MHT?

A

Oral oestrogen is available as oral conjugated oestrogens, micronised 17B oestradiol, oestradiol
valerate or oestrone sulphate. Transdermal oestradiol patches, gel or implants may also be used
for systemic MHT.

41
Q

Use of topical vaginal oestrogen?

A

Local vaginal therapy is preferred for women with isolated GU symptoms of menopause.
Treatment is available in the form of pessary, tablet, cream and ring, with no significant differences
between these formulations noted for effectiveness or development of endometrial hyperplasia.28
Data on safety is primarily based on short-term trials, however for use over 1-2 years, there has
been no evidence of an associated increase in risk of endometrial hyperplasia or cancer, DVT,
breast cancer or cardiovascular disease.29,30,31 Use of topical vaginal oestrogen therapy does not
require additional use of a progestin in women with a uterus

42
Q

Progestogen therapy and MHT?

A

Progestogen therapy is required for systemic MHT in all women with an intact uterus and may be
cyclical or continuous. Progestogens include micronized progesterone and synthetic progestins. It
is uncertain whether micronised progesterone is safer than synthetic progestogen.
32 Progestogens
are usually taken orally in a fixed dose combination with oestrogen or separately. Fixed dose
combined transdermal patches are also available and the LNG-IUS may also be used for
endometrial protection

43
Q

What follow up should women on MHT have? and what should be reviewed at each appointment?

A

All women using MHT should be reviewed after 6 months therapy.

This should include a general health check, a breast check and a mammogram every two years.

Bone densitometry should be performed where indicated

any unexpected vaginal bleeding after 6 months therapy requires appropriate investigation

44
Q

Testosterone therapy?

A

May be beneficial for postmenopausal women with hypoactive sexual desire disorders.

This diagnosis requires a full assessment.

Testosterone should not be routinely added to MHT in the treatment of menopausal symptoms

45
Q

What is Tibolone?

A

A synthetic steroid with oestrogenic, progestogenic and weak androgenic effects.

It is effective for vasomotor and urogenital symptoms in post-menopausal women

46
Q

Who shouldn’t use Tibolone?

A

peri-menopausal women due to the potential for irregular bleeding

47
Q

Benefits of Tibolone?

A

In randomised trials, Tibolone has been shown to:
- alleviate VMS,
- improve bone density
- reduce fracture risk,
- to have a modest
effect on some domains of female sexual function
- and to stimulate breasts less than combined
MHT.
- doesn’t increase the risk of endometrial hyperplasia or cancer, and is also
associated with less bleeding in the first 3 months of treatment.

48
Q

Disadvantages of Tibolone?

A

Relative efficacy compared to MHT not well established

increases the risk of
breast cancer recurrence and increases risk of stroke in women >65 years

49
Q

Use of bioidentical hormone therapies?

A

Bioidentical hormonal therapies are not recommended as composition is not standardised, and efficacy and safety data is lacking.

50
Q

Non hormonal therapies proven to be effective for VMS?

A

Hypnosis

CBT

51
Q

Non hormonal therapies NOT proven to be effective for VMS?

A 
Yoga, 
exercise, 
diet, 
supplements 
other lifestyle changes 
including weight loss

— but likely have other health beneftis

Over the counter complementary/ alternative medications, such as black cohosh and phytoestrogens, have not consistently been shown to be effective for VMS

52
Q

Non-hormonal pharmacological medications shown to be superior to placebo in some
randomised controlled trials

A

SSRIs
SNRIs
centrally acting medications including gabapentin, pregabalin and clonidine

Long term data lacking

53
Q

Which drugs can interact with tamoxifen and should be avoided?

A

Paroxetine and Fluoxetine

54
Q

Non-hormonal therapies for vaginal dryness

A

Lubricants and moisturisers:
- Little evidence supporting effectiveness
- RCT of water- and silicone- based lubricants found that the siliconebased lubricant was more effective at reducing pain during sexual activity in patients with breast cancer. A pilot study of olive oil (as a lubricant), vaginal moisturiser and pelvic floor muscle
relaxation significantly improved dyspareunia, sexual function and quality of life after breast
cancer.

Vaginal lidocaine
- Topical vulvar lidocaine (4%) applied for 3 minutes prior to penetration reduces pain during intercourse after breast cancer.

Vaginal Laser
- use of vaginal laser
therapy outside of clinical trials is not currently recommended
- Variable results, some trials found reduced dyspareunia and dryness + improved urinary sx but small trials and evidence conflicting

55
Q

MHT and cancer:

- Cervical (SCC and adenocarcinoma)

A

Acceptable

Not considered hormonally responsive. No
correlation between ER or PR status and survival

56
Q

MHT and cancer:

- Endometrial stage 1 & 2

A

May be considered

Limited data available suggests no additional harm

57
Q

MHT and Cancer:

Endometrial Ca -
Stage III & IV

A

Not recommended

No data to inform use.

58
Q

MHT and Cancer:

Uterine Sarcoma

A

Not recommended

Some are ER and PR positive, and respond to anti-E therapy. No data to demonstrate safety of MHT use in women with ER/PR negative tumours.

59
Q

MHT and cancer:

Ovarian Ca - high
grade serous, clear cell,
mucinous

A

Acceptable

Limited data suggests no harm with E therapy.

60
Q

MHT and Cancer:

Ovarian Ca - low
grade serous &
endometrioid

A

Not recommended

61
Q

MHT and Cancer:

Vulval & Vaginal Ca

A

Acceptable

Not considered hormonally responsive

62
Q

MHT and Cancer:

Breast ca

A

Avoid MHT and Tibolone

No consensus on use of vaginal oestrogens. Consult
with breast surgeon or oncologist to optimise
treatment options for individual patients.

63
Q

MHT and cancer:

Colorectal Ca

A

Acceptable

64
Q

MHT and cancer:

Lung Ca ER+ve

A

No consensus

65
Q

MHT and cancer:

Haematological ca

A

Acceptable

66
Q

MHT and cancer:

Malignant melanoma

A

No consensus

67
Q

By what mechanism does oestrogen affect bone density?

A

In low oestrogen states there’s an increase in cytokines signalling an increase in apoptosis of osteoblasts, and promoting osteoclast activity and lifespan. The overall effect is an increase in bone resorption.

68
Q

Why is transdermal oestrogen beneficial in women at higher risk of VTE?

A

It avoids the first pass effect, thus a lower dose can often be used to obtain symptoms control.

It dose not induce increased secretion of coagulation factors by the liver.

Urogynae and menopause (6 decks)

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