menopause Flashcards
what are the treatment options for mood symptoms during menopause
non-pharmacological
1. CBT
pharmacological - OTC and prescription
OTC -
1. St John’s wart - enzyme inducer in P450 system
Prescription medicines:-
1. SSRIs e.g. fluoxetine, paroxetine (reduce efficacy of tamoxifen so CI if breast cancer currently on tamoxifen - only these SSRIs)
2. SNRIs e..g venlafaxine, duloxetine
what are the OTC treatment options for vasomotor symptoms e.g. hot flushes
OTC
- Black Cohosh
- Isoflavones
what symptoms can evening primrose oil help with?
breast tenderness, hot flushes, night sweats
what are the interactions associated with evening primrose oil
SERMs, anticoagulants, anti-epileptics and asthma
what is tibolone and when can it be used
tibolone is a synthetic form of HRT (oestrogen and progestogen) can only be used when a patient is postmenopausal (i.e. >12 months since last bleed)
how is tibolone taken
oral tablet, taken once a day
how does tibolone work?
broken down into two types of oestrogen and one type of progesterone which is strongly androgenic.
It lowers SHBG, increasing free testosterone == androgenic
(as testosterone is bound to SHBG to if we reduce SHBG this means less for testosterone to bind to, increasing free amount of testosterone as bound testosterone has decreased)
what are the main CI to a person taking tibolone
past or current breast cancer (can increase risk of relapse of breast cancer)
caution when using in over 60 year olds as could increase risk of stroke
what menopausal symptoms is tibolone found to be effective at treating?
is it effective in improving BMD?
vasomotor symptoms (hot flushes and night sweats) and libido
yes - beneficial in preventing decrease in BMD
what are the management options for vasomotor symptoms in terms of
1st line
second line
herbal meds
1st line - HRT
second line - SSRIs, SNRIs and clonidine
herbal- black cohosh and isoflavones
what can be added as an addition to HRT if patients struggling with low libido
testosterone (off licence), measure total tesosterone before starting at 3 months, 9 months and then annually
what is the first gonadotrophin to increase during peri-menopause stage?
FSH
what is the last sex steroid to decrease in menopause
oestradiol
what happens to inhibin A and B during peri-menopause and when?
Inhibin A and B decrease these are the first serological markers to decrease and it starts 2-3 years before the menopause
if a patients FSH is >50 and oestradiol is <20 what does this imply?
cessation of ovarian function
If a patient is age 47 years and still having periods albeit a little irregular what type of HRT would you recommend if wanting to start?
combined sequential HRT
i.e. oestrogen and progesterone/gen
take oestrogen on its own first half cycle and then combined E&P for at least 12-14 days of the cycle. This should give the patient a regular withdrawal bleed
if someone is taking combined sequential HRT at what point do you switch them to continuous combined
if amenorrhoeic or if been on sequential HRT for about 5 years
if a patient attends asking for HRT, they have a uterus and no CI. They tell you that their last period was about 18 months ago. What type of HRT would you start
continuous combined HRT (i.e. E&P together all the time) = should be bleed free!
when can you prescribe continuous combined HRT rather than sequential?
if a patient is postmenopausal i.e. bleed free for >12 months
if taking continuous combined HRT how long can it take for irregular bleeding to settle
up to 6 months
what % of patients taking continuous combined HRT can experience irregular bleeding in the first 6 months
irregular bleeding is common occurrence during the first 6 months (regardless of route of HRT i.e. oral or transdermal), occurs up to 77% of patients, often don’t know why!
what % of patients taking CC HRT after 9 months experience irregular bleeding
3-10%
what proportion of patients discontinue HRT due to irregular bleeding SE
up to 25% of patients
Aileen is taking CC combined HRT. She has been taking it for 3 months and comes to see you as she is worried about some irregular bleeding. Prior to starting HRT she hadn’t had a bleed for > 2 years. She has no risk factors for endometrial cancer. What would you advise?
no need to investigate, reassure if no risk factors can take up to 6 months for bleeding to settle down when just starting on CC HRT.
If bleeding persists > 6 months on CC HRT then investigate with TV USS initially
when would you investigate irregular bleeding on CC HRT earlier than 6 months?
if significant risk factors for endometrial cancer
e.g. BMI, family history
at what timeframe would you start to investigate irregular bleeding on CC HRT
if irregular bleeding for > 6 months on CC HRT
start with TV USS
you do a TV USS for Aileen as she has come back with irregular bleeding > 6 months on CC HRT. The ET is 6 mm what would you do next?
If ET >=5 mm –> endometrial biopsy or hyst & biopsy
If on CC HRT and irregular bleeding for > 6 months and you organise a TV USS what is the ET cut off for organising further investigations?
If ET>= 5mm –> need biopsy +/- hyst
if ET < 5mm –> atrophic endometrium
if taking sequential HRT and irregular bleeding when do you investigate
if irregular bleeding for >2 cycles
what is the ET cut off in patients taking sequential HRT for further investigations i.e. pipelle
ET is allowed to be slightly thicker in patients taking sequential HRT. Therefore if ET >=7mm then need pipette or hyst +pipelle.
if the ET is <7mm in a patient who is experiencing IMB on sequential HRT do you need to do any further investigations
no - just observe, can change HRT regime to help eliminate the bleeding.
what % of focal endometrial lesions can a pipelle miss
up to 20% e.g. polyps
what is the pipelle endometrial detection rate
up to 99.9% i.e it is very good as a first line investigation
what are the criteria for hysteroscopy when experiencing unscheduled bleeding on HRT
- multiple episodes/ prolonged
- ET >5mm if on CC HRT, or ET >7mm if on - sequential HRT
- risk factors e.g. raised BMI, FH of HNPCC
- focal endometrial lesions on scan e.g, endometrial polyps
- incomplete visualisation of the ET on TV Scan
what is the gold standard investigation for irregular bleeding on HRT
hysteroscopy
what would you suggest if bleeding on sequential HRT, ET <5mm and bleeding is occurring early in progesterone/ progestogen phase? (used for >2 cycles)
increase dose of progestogen or change it
what would you suggest if bleeding on sequential HRT, ET <5mm and spotting before progesterone/ progestogen withdrawal bleed? (i.e bleeding when just taking oestrogen aspect of sequential) (used for > 2 cycles)
increase oestrogen dose
what would you suggest if bleeding on sequential HRT, ET <5mm and irregular bleeding? (used for > 2 cycles)
increase dose of progestogen or change regime
what would you suggest if bleeding on sequential HRT, ET <5mm and painful bleeding? (used for > 2 cycles)
change progestogen
what would you suggest if bleeding on sequential HRT, ET <5mm and heavy or prolonged withdrawal bleed? (used for > 2 cycles)
increase or change progestogen or decrease oestrogen
what are the general principles in PMW having bleeding on CC HRT and investigations have all come back normal?
bleeding outcomes are best on lowest possible dose of oestrogen in PMW.
Increase or change type progestogen or fitting IUS
if this doesn’t settle may be better switching back to sequential HRT
what happens to CVD risk once you are post-menopausal?
CVD risk increases in post-menopausal women
In the first 10 years after the menopause e.g. 51-61, CVD increases by four folds
why does your CVD risk increase when you are postmenopausal?
lack of oestrogen:-
- increase LDL to HDL ratio (remember LDL is your lazy cholesterol, whereas HDL is your ‘good cholesterol’)
- increase in triglycerides
-insulin resistance/ t2dm
what role does oestrogen play on your HDL and LDL cholesterol ratio
HDL = absorbs cholesterol in the blood and takes it to the liver to be broken down and excreted
LDL = lazy cholesterol, clogs up arteries think atherosclerosis
oestrogen increases the ratio of HDL:LDL therefore reducing risk of atherosclerosis.
In PMW who aren’t on HRT their LDL:HDL ratio increases - increased risk of CVD and stroke
what menopausal symptoms have the majority of alternative therapies been evaluated for?
vasomotor symptoms
what cohort of patients does the evidence for alternative therapies come from
breast cancer survivor patients
what treatment is the most effective in treating menopausal symptoms
oestrogen! (HRT)
what non-hormonal treatments have been evaluated in RCTs vs placebo and found to be effective
SSRIs, SNRIs
Gabapentin, pregabalin
clonodine
What is clonidine? what is its licenced indication?
Clonidine is an anti-hypertensive. It is a centrally acting alpha 2 adrenergic agonist. It is the only licenced non-hormonal drug in the UK to treat hot flushes.
what is the only licenced non-hormonal drug in the UK to treat hot flushes
A) SSRIs
B) SNRIs
C) Tibolone
D) Clonidine
D = clonidine
what are the side effects a/s with clonidine
hypotension, sleep disturbance
what do you need to be careful when stopping clonidine
withdraw gradually to prevent rebound hypotension
why do get hot flushes during peri-menopause?
decreased oestrogen –> increased noradrenaline and serotonin ==> narrows thermoregulation zone ==> small changes in core temp triggers heat dissipation mechanisms
what SSRIs and SNRIs could you consider using to help treat vasomotor symptoms in women who don’t want hormonal treatment?
Which ones should you avoid if on tamoxifen?
SSRI: fluoxetine, paroxetine, citalopram, sertraline
SNRI: venlafaxine, desvenlafaxine
avoid fluoxeteine, paroxetine and sertraline if on tamoxifen as reduces efficacy of Tamoxifen therefore increases risk of breast cancer recurrence
note no studies have compared SSRI vs SSRI or clonidine)
what symptoms are SSRIs and SNRIs predominantly utilised for in menopause treatment
vasomotor symptoms (but can be used for mood as well)
what are the top three most effective SSRIs or SNRIs to use to help treat menopausal symptoms
paroxetine, citalopram, venlafaxine,
what is the most effective SSRI for treating menopausal symptoms
Paroxetine, good at low doses 10mg OD
what is the least effective SSRI for treating menopausal symptoms
sertraline
what are common SE of SSRIs that are important to discuss if initiating
nausea
dry mouth
constipation
decreased libido
what would be the first line SSRI or SNRI in breast cancer survivors to use to help with vasomotor symptoms
venlafaxine 75 micrograms OD (can increase to 150mcg/day, max dose)
avoid F and P as inhibit metabolism of tamoxifen –. endoxifen (decrease serum endoxifen, increase risk of cancer relapse)
gabapentin and pregablin are controlled drugs. Which schedule of controlled drugs do they belong to?
A) Schedule 1
B) schedule 2
C) schedule 3
D) schedule 4
B - schedule 3
what can gabapentin and pregablin be used to treat in menopausal symptoms
vasomotor symptoms
(gabapentin 300mg OD –> increase up to TDS max dose)
(pregabalin 75-150mcg BD)
what are the SE associated with pregablin and gabapentin
dry mouth
somnolence
dizzyness
weight gain
what is BMS position of phytoestrogens in terms of helping vasomotor symptoms?
phytoestrogens are plant derived oestrogens - can’t be used in BC survivors or anyone on tamoxifen
BMS state evidence is limited, no evidence to show they reduce vasomotor symptoms
can you name some examples of phytoestrogens
red cohosh
soy
isoflavones
? black cohosh
what stamp should patients look for on the bottle of a herbal remedy to ensure it has been checked/regulated
THR = traditional herbal remedy - validates strength and quality/quantity
what can black cohosh be used to treat in menopausal symptoms? who should avoid it
avoid in tamoxifen users and probably breast cancer patients
? is a phytoestrogen
possibly helps reduce vasomotor symptoms but evidence limited
what does NICE state St John’s wart can be used for in menopausal patients
NICE state can help with vasomotor symptoms
obv most people use it for mood benefits
lots of interactions, unsure re dose, safety
what would your advice be to a patient on tamoxifen and has researched st johns wart
we don’t know if it decreases levels of tamoxifen, advice is to avoid
interferes with chemo
what complementary therapies have been found to reduce hot flushes
acupuncture - decreases hot flushes and improves sleep patterns
which behavioural therapies have been shown to improve mood and hot flushes
CBT, hypnosis, sleep hygiene & relaxation techniques
what does NICE think in regards to SSRIs, SNRIs, gabapentin and pregablin for treatment of vasomotor symptoms (how does this differ to BMS position statement)
NICE suggest that none of them are any better than placebo, whereas BMS recommend them as alternatives to HRT.
what treatments does NICE recommend for vasomotor symptoms in breast cancer survivors
Clonidine/ venlafaxine/ gabapentin
advise that St John’s wart may help but avoid due to concerns over interactions with tamoxifen
why is it not advisable to use FSH as a diagnostic tool in menopausal women aged >45 years?
a) its expensive
b) it fluctuates and does not corelate to menopausal symptoms or duration
c) it should be offered routinely as helps in guiding management
b)
FSH fluctuates, levels don’t correlate with menopausal symptoms or duration and won’t change management. Treat symptoms and patient not tests
if a patient is considering stopping or trialling stopping HRT what is the best method to stop? abruptly stop or gradual decrease?
is either better in preventing onset of symptom recurrence
either abruptly stop or gradual decrease, makes no difference to whether or not symptoms will return
advise re HRT and VTE risk
no increased risk of VTE with transdermal HRT
small increased risk of VTE with oral HRT
what type of HRT should be offered to a patient seeking HRT who has a BMI > 30 but no other risk factors?
a) oral
b) transdermal
c) oestrogen only
b) transdermal (as BMI >30 is a risk factor for VTE)
which of the following statements are correct regarding risk of CVD and HRT
a) increased risk of CVD when starting HRT regardless of age
b) no increased risk of CVD if started before age 60 but risk increases after age 60
c) HRT started within 10 years the menopause or before age 60 is cardio protective and no increased risk after this time
c)
HRT started before age 60 (or in 10 years after menopause) is thought to be cardio protective. After this time risk is neutral. I.e. no increase or decrease in background risk.
cohrane analysis found reduction in progression of atherosclerosis, CHD and death from CVD as well as all cause mortality if HRT started within 10 year window of opportunity or < 60 years old.
risk of stroke with HRT?
small increased risk with tablets compared to transdermal, but baseline risk is small in patients under 60.
risk of stroke increases with age.
risk of stroke is dose and duration dependent with oral E and therefore lowest effective dose should be used.
The type of P MAY effect risk of stroke so those with RF consider using micronised P or dydrogesterone.
diabetes and HRT (SBA)
a) oral HRT increases glycaemic control
b) HRT can increase risk of developing diabetes
c) HRT does not increase risk of developing diabetes and is unlikely to affect glycaemic control in patients already known to have diabetes
d) transdermal HRT has no effect on glycaemic control
c) c) HRT does not increase risk of developing diabetes and is unlikely to affect glycaemic control in patients already known to have diabetes
counselling someone about risk of breast cancer and HRT
HRT does not increase risk of dying from breast cancer.
oestrogen only HRT is a/s with little or NO increased risk of breast cancer
E&P HRT is a/s with a small increased risk of breast cancer that is a/s with duration of HRT and reduces after stopping. It is thought that HRT promotes cancer cells in the breast growing, rather than causing a breast cancer to develop.
It is unclear whether different types of Progestogen are associated with different risks. However french cohort study found decreased risks of breast cancer if using micronised P or dydrogesterone.
It should be noted that being overweight and drinking more than 14 units of alcohol per week is associated with greater risks of breast cancer than HRT.
SBA : breast cancer and HRT
a) oestrogen alone HRT is associated with an increased risk of breast cancer
b) confident evidence shows risk of breast cancer increases dependent upon the type of progestogen
c) risk of breast cancer on E&P HRT increases after 4 years of use
d) E & P HRT is associated with small increased risk of breast cancer that increases with duration and reduces after stopping
d - true
a) false - E alone a/s with little or no increase
b) false - we don’t have enough evidence to support this (BMS consensus suggests micronised P and dydrogesterone are likely to be associated with reduced risk- french cohort study)
c) false - risk of breast cancer increases with duration of combined HRT but we don’t have a specific time frame specified. although a lot of studies measure from 5 years of use
what happens to risk of osteoporosis fractures on HRT
risk of OP fractures reduces whilst on HRT, benefit only maintained whilst on HRT and is dose related.
what happens to dementia risk whist on HRT
unclear - BMS say it is unlikely HRT causes a risk of dementia or detrimental effect on cognition if starting before age 60 but we don’t really know. However HRT should not be started for the sole purpose of preserving cognition or reducing risk of dementia.
what happens to risk of sarcopenia whilst on HRT
sarcopenia - is gradual loss of muscle mass strength and function. HRT could potentially improve muscle strength and mass but this is not certain.
in a patient with POI which of the methods has more benefit for blood pressure control
a) COCP
b) combined HRT
b) combined HRT
(both can be used as HRT and both have bone protection benefit, for HRT may have better blood pressure control than CHC)
what do the acronyms cBHRT and rBHRT mean?
cBHRT = custom ‘compounded’ bioidential HRT
rBHRT = regulated bioidentical HRT
what does the BMS suggest we should call rBHRT when referring to it with patients?
rBHRT = regulated bioidentical HRT best to call it ‘body identical’
what is the difference between rBHRT and cBHRT?
what we usually prescribe/ prescribed by regulated BMS specialists is body identical (regulated bioidentical HRT) - body identical synthetic production of oestrogens and progestogens to match what we naturally produce. These types of HRT are regluated, have gone through clinical drug trials to be approved and evaluated in RCTs.
Whereas cBHRT (custom, compounded bioidentical HRT) is not regulated, not undergone clinical trials and is not evidence based. They are not licenced and often produced by ‘specialist pharmacies’
what are some of the concerns regarding cBHRT
- concerns over safety - combine different types of E 1/E2 and E3 ? safety profile .. unsure if too much or too little
- no data on amounts of progesterone combined with ? too much or too little to provide endometrial protection
- not regulated
- unknown quantities of the amounts of E& P contained as not regulated
- no clinical trials, no evidence for this type of HRT
-data for the use has been extrapolated from studies on regulated HRT - insufficient evidence for their expensive and labour intensive tests that suggest can predict the exact amount of hormones a patient requires. (salvia and serum testing)
- often prescribed by HCP who are not menopause specialists
BMS, NICE does not advocate their usage
what are the first line treatment options for urogenital atrophy
vaginal moisturisers and lubricants
e.g. yes or replens (ideally use ones whose pH match that of the vagina)
what symptoms are suggestive or urogenital atrophy
vaginal dryness, itching, burning, pain with sexual intercourse.
urinary symptoms - frequency, nocturia, dysuria, (some women do get positive UTI cultures)
can affect the urogenital tissue of the vulva, vagina, bladder and urethra. urogenital atrophy used to be called genitourinary syndrome of menopause and vulvovaginal atrophy.
what causes urogenital atrophy, describe pathophysiology
low oestrogen levels cause a rise in vaginal pH and can lead to reduction in healthy bacteria (lactobacilli) and changes in microbiome - increase vaginal discharge. pH rises to >5, reduced lactobacilli allows for vaginal commensals like e.coli to predominate.
low oestrogen causes vaginal thinning due to dormant fibrocytes and collagen fibres fuse leading to reduced elasticity.
if no improvement or not much with vaginal moisturisers and lubricants what would you prescribe next? can you name any options
vaginal oestrogen
Pessaries:-
e.g. vaginal pessaries - estradiol e.g. vagifem or vagirux (10mcg daily for 2 weeks then twice weekly for a long as needed)
Creams:-
e.g. estriol 0.01% or 0.1% - applied daily for 2 weeks then twice weekly using an applicator
ring:-
estring impregnated with estradiol releases 7.5mcg estradiol daily, keep in for 12 weeks
what type of oestrogen does estring contain
estradiol 7.5mcg released daily, keep in for 12 weeks
what type of oestrogen is found in the vaginal creams
estriol 0.1 or 0.01%
apply daily for two weeks using an applicator then twice weekly
what type of oestrogen is found in pessaries
estradiol e.g. vagifem or vagirux
apply daily for two weeks, then twice weekly for as long as needed
what lifestyle modifications can help in reducing symptoms of urogenital atrophy
smoking cessation and regular sexual function
smoking increases metabolism of oestrogen and regular sexual activity improves blood supply to vaginal mucosa.
beyond lubricants, vaginal oestrogen what other treatments could you suggest to help with urogenital atrophy symptoms
pelvic floor physio (if struggling with vaginismus, or increased vaginal tone)
DHEA pessaries e.g. prasterone 6.5mg is broken down into oestrogen and androgens, CI in previous breast cancer
Ospemifeme - SERM (60mg OD): increases oestrogen receptors (agonist) in the vagina but antagonist effect on endometrium and breast. BMS state can use in someone completed Rx for breast or endometrial CA? but NO clinical trial data for patients with current breast cancer. CI if currently having Rx for breast cancer.
laser - more studies needed though
can you name the different types of oestrogen produced by the human body and list them in order of potency
estradiol (e2) made in ovarian granulosa cells (most potent)
estrONE (e1), PMW, adrenal glands and adipose tissue
estriol (e3), placenta,
estetrol (e4), produced by fetal liver in pregnancy (least potent, note not avaliable in any HRT formulation but is in drovelis COCP!)
why is it important to monitor serum estradiol levels in patients using oestrogen implants
to avoid tachyphylaxis (decrease in response to oestrogen when previously was good despite adequate serum estradiol levels)
high levels of estradiol levels beyond physiological levels can lead to anxiety and low mood.
what is the recommended dose of calcium and vitamin D for PMW for bone protection
1000mg (1g) calcium
1000 IU vitamin D
daily
also- Smoking cessation, exercise, healthy diet and alcohol reduction
what is considered first line treatment in the prevention of OP in POI and menopausal women aged < 60 years old with menopausal symptoms?
a) calcium and vitamin D
b) Raloxifene
c) HRT
d) diet and lifestyle advice
c) HRT
risk of endometrial cancer and HRT
increased risk of endometrial cancer with unopposed E (but this risk is mitigated by using combined E&P)
small increased risk after 5 years of use with sequential combined HRT (hence advice to move it to continuous combined after 5 years use)
combined HRT has a neutral effect on risk of endometrial cancer during its use but significant reduction noted with combined HRT in long term follow up
risk of ovarian cancer and HRT
very small increased risk of serous and endometroid ovarian cancer
risk of cervical cancer and HRT
no associated between cervical cancer and HRT (unlike with CHC)
risk of colorectal cancer and HRT
reduction in risk with HRT
risk of breast cancer recurrence if using HRT?
How would you counsel someone
evidence is too limited to be able to advise fully. Evidence is inconclusive as number of breast cancer events in published studies is too small.
Of the studies started a lot have been stopped as they have found increased numbers of breast cancer recurrences in HRT arms of the trials.
It is not recommended first line to use HRT in patients with past or current breast cancer due to risk of recurrence. Non hormonal options should be considered first and if these fail to improve symptoms then referral to a specialist with individualised care plan together with their oncologists should be made. Risk and benefit discussion.
if a patient with previous history of breast cancer wants to use vaginal oestrogen and is on aromatase inhibitor what would the advice be
evidence is inconclusive - small amount of data suggest risk of recurrence of breast cancer is higher for women using AI compare to tamoxifen - advice would be try and switch to tamoxifen then use but this would need discussion with their oncology team and we can’t specify the actual risk of recurrence of breast cancer.
what is ospemifeme?
SERM - agonist for ER in the vagina but antagonist in the uterus and breast.
can be used for urogenital atrophy in patients with past breast cancer apparently but data is limited so probably needs discussion with oncology and specialist, CI if active Rx.
what type of previous endometrial cancer is a CI to use HRT in the future
endometrial sarcomas (as oestrogen sensitive), CI to use HRT in the future even if Rx complete
Diane presents for discussion regarding HRT for management of vasomotor symptoms following Rx 5 years ago for endometrial cancer (was not a sarcoma). What would your advice be?
studies assessing use of HRT following Rx for endometrial cancer showed either a reduction in recurrence or neutral effect (i.e no increase or decrease)
what types of ovarian cancer should we avoid using HRT in future in?
ovarian granulosa cell tumours
ovarian germ cell tumours
what would your advice be re previously Rx ovarian cancer and using HRT to manage menopausal symptoms
HRT CI in granulosa cell and germ cell tumours
however studies have found no change in survival time if HRT initiated following Rx. Can’t find anything on risk of recurrence ? and we know that HRT increases risk albeit small of serous and endometroid ovarian cancer
previous cervical cancer can they use HRT
yes - not CI after squamous cell or adenocarcinoma of the cervix
previous vaginal and vulval cancer can they use HRT
yes - most vulval and vaginal cancers are squamous cell carcinomas and behave similar to squamous cell carcinoma of cervix and thus not contraindicated to use systemic HRT or topical HRT.
when is risk of VTE highest if starting oral HRT
risk is highest in first year of use.
risk of VTE with oral compared to transdermal HRT is 2-4 times higher
can you name some risk factors for VTE that you should consider prior to starting HRT and at annual reviews
raised BMI >30
smoking
previous VTE
family history of VTE
thrombophillia
increasing age
what does the risk of VTE depend upon if using oral oestrogen HRT
VTE risk is dependent upon the dose and type of oral oestrogen
conjugated equine oestrogen are more pro thrombotic than estradiol.
does the type of progestogen/ progesterone affect VTE risk
yes - micronised P and dydrogesterone are associated with reduced risk of VTE (also reduced risk of breast cancer)
prior to starting HRT is recommended to do routine thrombophillia testing on all patients?
false
a patient is taking transdermal HRT and is having elective hip replacement - the orthopaedic reg rings to ask for advice re stopping HRT. What would your advice be?
no need to stop as transdermal HRT does not increase risk of VTE. Therefore would advise to do VTE risk assessment like normal and dependent upon this then give thromboprophylaxis.
a patient is taking oral HRT and is having elective hip replacement - the orthopaedic reg rings to ask for advice re stopping HRT. What would your advice be?
oral HRT is associated with increased risk of VTE 2-4 times increased risk, but risk is greatest in first year.
Hard to 100% know as probably no studies but could advise patient to switch to transdermal at time of surgery to reduce risk or can carry on oral HRT. As long as VTE risk assessment and thromboprohylaxis given if required.
what % of women with POI will achieve spontaneous pregnancy
a) 1-2%
b) 2-5%
c) 5-10%
d) > 10%
c) 5-10%
Sally is 49 years old. She started sequential combined HRT 13 months ago and has found it beneficial in management of her menopausal symptoms. She has attended for her annual review with her GP. She is getting some withdrawal bleeds but they are sporadic, no IMB and wonders if she can be switched to CC as doesn’t want a bleed?
yes can be switched after a minimum of 1 year of sequential combined HRT or one year from last menstural bleed for women who wish to avoid monthly bleed. (two years for women with POI/early menopause 40-45).
why were testosterone implants and patches withdrawn by pharmaceutical companies
commercial reasons not safety reasons
what is the purpose of measuring total testosterone prior to commencing testosterone therapy in patients will low libido/lack of sexual desire and during treatment?
to confirm safety - want to ensure testosterone levels remain within female physiological ranges
not monitoring to assess effectiveness
acupuncture for vasomotor symptoms?
more studies needed didn’t compare it to placebo so hard to say if it works
CBT for vasomotor symptoms
good evidence it works for vasomotor and menopausal symptoms