Menopause Flashcards

1
Q

Define Natural Menopause

A

The permanent cessation of menses of 1 year’s duration secondary to lack of estrogen production by the ovaries

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2
Q

Define perimenopause

A

(menopause transition) – the time period prior to menopause which is characterized by menstrual cycle irregularity, frequency of anovulatory cycles, & symptoms similar to menopause

Perimenopause – Endocrine changes, irregular menstruation

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3
Q

Describe the age relating to menopause

A

Early menopause: before age 45
Premature menopause: before age 40

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4
Q

Describe the briefly what Early Natural Menopause / Primary ovarian insufficiency is and when it occurs?

A

Loss of ovarian function at a young age

POI (Primary Ovary Insufficiency): before 40yo, but can still have irregular or transient menstruation

Premature menopause: before 40yo

Early menopause: 40-45yo

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5
Q

Presentation of Early natural menopause / Primary ovarian insufficiency. Management?

A

These people are at risk of symptoms from estrogen deficiency (CA have low estrogen but cycle regularily)

Restoring estrogen levels until natural age of menopause is recommended to help prevent some complications – may require higher doses of estrogen

Also, calcium, Vit. D, exercise, follow-ups

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6
Q

Natural age menopause and average age

A

(Natural age of menopause: 40-65 years old) – Average of menopause: 51 years of age in North America

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7
Q

What are some risk factors that may precipitate earlier onset of menopause?

A

Smoking
Exposure to toxins
Chemotherapy
Hysterectomy

Show mixed results when studied
Toxins – Arsenic exposure
Lower SES as well

Conflicting evidence for some of these risk factors

BMI, having children – Possible risk factors; variable results in studies

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8
Q

Describe the hormonal changes that occur in menopause

A

Estradiol is produced in ovaries – When low, hypothalamus does not get stimulation

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9
Q

Describe the hormonal changes in pre-menopause

A

Estrogen is mainly produced by the ovaries (as 17-estradiol)

However, other sites can produce smaller amounts of estrogen through the conversion of androgens

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10
Q

Describe the hormonal changes in post-menopause

A

Estrogen production decreases to ~10% of premenopausal levels

The primary estrogen is estrone, which has ~ 1/3 estrogenic potency of estradiol

It is produced in adipose tissue via conversion of androstenedione

Androstenedione -> estrone –> estradiol

Estrone is less potent than estradiol

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11
Q

Describe the symptoms of menoapuse. What can occur as a result of these sx?

A

Vasomotor symptoms (Hot flashes, night sweats) – Changes in body temp. that occur rapidly
Sleep pattern changes
Mood and cognition changes
Genitourinary changes (Vagina, urethra) – Sometimes incontinence can happen
Bleeding changes (Changes in menstrual bleeding patterns)

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12
Q

Describe the perceptions of menoapuse regarding mneoapuse sx

A

Some women will experience menopause as a normal event w/o significant difficulty

54% of women still think talking about menopause is taboo

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13
Q

How does vasomotor sx occur in menopause

A

Decline in estrogen – altered neuronal activity in hypothalamus – Temperature regulation in the brain

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14
Q

What is the most common vasomator symptom(s)? Descrobe it. Prevalence?

A

Hot flashes and Night sweats

Hot flashes: the classic sign & major complaint of menopause

VMS affects up to 80% of women

Begin pre-menopause, max prevalence in 1st 2 years post-menopause

On average, VMS persist for 7-8 years

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15
Q

Define Hot Flashes. What are they accompanied with? Duration?

A

The sudden onset of intense warmth that begins in the chest and may progress to the neck and face

Often accompanied by visible red flushing
May also be accompanied by anxiety, palpitations, and profuse sweating

Are typically episodic and last, on average, for 4 minutes

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16
Q

Describe the repurcussions of VMS in menopause for women

A

Sweating – embarrassment
Overheating – uncomfortable
Night sweats – terrible sleep – terrible next day

VMS associated with diminished sleep quality, irritability, difficulty concentrating, decreased QOL (Can effect relationships)

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17
Q

Descroibe the pathophysiology of hot falshes in menopause

A

Appears to be due to a narrowing of the thermoregulatory system caused by changes in estrogen levels
Postmenopausal women are thought to have narrowing of their “thermoneutral zone” - small changes in temp can stimulate the regulatory response of sweating or shivering

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18
Q

Risk FActors of Hot Flashes

A

Less physical activity (sedentary lifestyle)
Family history/genetics (Maternal hx)
Age of onset (increased risk < 52 years old)
Induced menopause

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19
Q

Describe the management of VMS

A
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20
Q

Lifestyle Modification of VSM in Menopause

A
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21
Q

What is another non-Rx option for management of VSM in menopause?

A

May improve sleep
Access is a barrier here

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22
Q

Describe the indication of estrogen in menopause

A

Estrogen therapy (ET) is used alone for VMS if women have had a hysterectomy

In those who have a uterus, it is used in combination with a progestogen (EPT) (Avoid endometrial hyperplasia – cancer)

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23
Q

Efficacy of estrogen in menopause

A

ET and EPT are the most effective treatment options for vasomotor symptoms

Cochrane review: ↓’s hot flash frequency by 77% & severity by 87% vs. placebo
WHI study: 77.6% ↓ in night sweats

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24
Q

Why must estrogen be combined with progesterone in women who have a uterus?

A

Unopposed ET (0.625mg CE) for 3 years is associated with a 5-fold increase in risk of endometrial hyperplasia or cancer

Risk is related to dose and duration of ET

Systemic progestogens ↓ this risk in a dose and duration fashion

Use P for a minimum of 12-14 days/month, & match the dose of the P to the dose of the E

E.g. high dose E requires high dose P

Taken together, the risk of endometrial hyperplasia is no higher than in untreated women

It appears low-dose unopposed estrogen carries a low risk of endometrial neoplasia, but only very limited data exists to support this (and it is generally not recommended)

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25
Q

Describe the estrogen formulations for use in menopause? Effectiveness of the options?

A
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26
Q

Describe when a transdermal estrogen may be sued for menopause?

A

Guidelines – Recommend transdermal estrogen for individuals with CV risks – Lower VTE risk (studies

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27
Q

What is the dose of estrogen for menopause?

A

Use the most appropriate, often lowest, effective dose

E.g. 0.3mg Premarin or 0.5mg Estrace or 25ug 17β-estradiol

Titrate dose based upon symptom relief

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28
Q

How should someone be inoitiated on estrogen tjherapy for menopause? When should effect be seen?

A

Generally, start with low doses and titrate up based on symptom response

Lower doses may take longer to see a response – may take as long as 12 weeks

For standard doses check for a response after 4 weeks.

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29
Q

Describe the onset of Sx relief for Estrogen in Menopause

A

As little as 2 weeks for some, up to 8 weeks for others

Assess for response at 4 weeks at standard dose and 6-12 weeks for lower doses

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30
Q

What are the formulatiosn avilable for systemic estrogen products?

A

Estrace – Generics available

Premarin – Only brand name

Patch – Differnece in dosing frequency

Estardot, Oesclim - Twice Weekly
Climara - weekly

Application Site s- Clean, dry, intact skin – Butt is preferred place, lower abdomen, lower back, or hip

  • Rotate from left to right side each time

Gels are used daily

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31
Q

Describe systemic estrogen combination products?

A
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32
Q

Describe the difference in efficcay between transdermal and oral estrogen for menopause

A

Are similarly effective for vasomotor sx’s
Appear to provide same protection on BMD

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33
Q

Benefits of transdermal estrogen

A

Avoids the FPE, so less nausea, less h/a, less of an effect on TG’s
↑ sex drive? (some studies)
↓ risk of DVT
↓ risk of gallbladder dx

** BAsed on observational data**

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34
Q

Progestogen Products. Considerations?

A

Food allergies Prometrium - Some generics made with peanut oil and sunflower oil – Allergy Concerns

Mirena IUD – Off label when used for menopause - good option for those wanting contraception, convenience of IUD, irregular menses still – Useful for any doses of estrogen

  • Used for up to 5 years
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35
Q

Micornized Progesterone Adverse Effecrs, Advatages, Cocnerns, Cousnelling Tip

A

May cause drowsiness, especially when taken with food

Advantages vs. MPA:
Observational data shows it has a lower risk of VTE and breast cancer

Of note…
Prometrium made with sunflower oil, some generics made with peanut oil, some with sunflower oil

Educate to take at bedtime – IMPORTANT

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36
Q

What is an alternative to progestogen?

A

Duavive® (0.45mg CE and 20mg bazedoxifene)

Conjugated Estrogen and SERM

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37
Q

Describe Duavive® (0.45mg CE and 20mg bazedoxifene) and the Bazedoxifene component

A

Bazedoxifene:
is a selective estrogen receptor modulator (SERM) that acts as an antagonist of estrogen receptors on endometrial and breast tissue and an agonist at receptors in bone

CE + bazedoxifene is called a tissue selective estrogen complex (TSEC)
provides endometrial protection without the need for a progestogen

–> Protection of BMD – Avoids side effects of progestin (do not need to take a progestin here)

avoids bothersome adverse effects of progestogens such as breast tenderness and uterine bleeding

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38
Q

How is Duavive taken?

A

Take 1 tablet daily

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39
Q

Describe therapy with Bijuva. Evidence and dose?

A

(17β estradiol (estradiol hemihydrate) and progesterone (micronized)

A bioidentical formulation of HRT in combination format

Evidence shows ↓ in moderate-to-severe VMS, ↑ QOL and sleep quality

Dose: 0.5 mg/100 mg and 1 mg/100 mg capsules once daily with food

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40
Q

Describe Tibolone Therapy Indication

A

Indicated for short-term tx of VMS in menopausal women with an intact uterus

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41
Q

What is Tibolone therapy?

A

A synthetic steroid analogue of norethynodrel (a progestogen), which is metabolized in the body to make 3 substances that act like E, P, and A (androgen) – it has weak activity

Weak activity compared to natural hormones - DOES NOT CONTAIN ACTUAL HORMONES

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42
Q

Tibolone Efficacy

A

Cochrane review: more effective than placebo, but slightly less effective than EPT

Similar to EPT products, consider risks before using
Has the same CI’s and AE’s as E and P

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43
Q

Tibolone Dose and Duration

A

Dose: 2.5mg tab (po) once daily

Tx of VMS in menopause – atleast 1 2months from last menstrual people

  • Indicated for short term use – Studied for 3 years (not much real world data)
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44
Q

Cocnern with all estrogen Therapy Options

A

Black Box Warning:

Endometrial cancer risk, breast cancer risk

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45
Q

Tibolone Black Box Warning

A

– Endometrial cancer. Risk, breast cancer risk – Does not contain actual estrogen, but leads to asubstance that mimics estrogen

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46
Q

Describne teh dosing admin of any produyct containing mirconized progestogen

A

HS DROWSINESSSSS

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47
Q

Can preganancy occur in menopause?

A

Pregnancy can still occur in perimenopause

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48
Q

What if contraception is desired in women experiencing VMS?

A

If date of last menses was <1yr ago, contraception may be desired

Options to provide VMS relief and contraception:

Low dose CHC (pill, patch, or ring)
Estrogen + LNG-IUS (contraception)
MHT + barrier
Nonhormonal tx option + progestogen-only contraceptive

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49
Q

Are cHC’s safe to use in perimenopause? Menopause? WHy or why not?

A

Safe to use in the perimenopausal period when contraception is required, but do not use once in menopause as the daily dose of ethinyl estradiol (e.g. 20 µg) is 4-5x times higher than the low-standard dose of estradiol required for symptom relief and bone benefit (e.g. 1mg estradiol)

50
Q

Perimenopause and contraception Risks

A

“Perimenopausal women with contraindications to OCP shoulod not nuse them

51
Q

When should CHC’s be stopped in menopause?

A

Taking CHC’s can mask signs of VMS & menstrual irregularities. This can make it difficult to know when ‘it is safe to stop taking’

If ≥50yo, stop and use non-hormonal contraceptive until amenorrhea for >12 months

If ≥55yo, stop. Spontaneous conception very rare (to be conservative the menopause society recently suggested >58yo)

52
Q

What are bio-identical hormones? What is compounded bio-identical hormone therapy?

A

What are bioidentical hormones?
Plant-derived hormones structurally identical to what is naturally produced in the body

Compounded products may contain a mix of estradiol, estrone, estriol, DHEA, testosterone, progesterone
–> Whether from pharma or compounded pharmacist – contain the same ingredients

Neither is more ‘natural’ than the other– they still need to be converted through a synthetic process to mimic body’s hormones

53
Q

Arguments in favour of compounded BHT

A

‘Safe and natural’ (generally a marketing advantage)
‘Custom-made’ based on salivary, serum, urine hormone level testing
Can compound in many different delivery routes (e.g. troches, subdermal implants)
Still require a written Rx…

54
Q

Arguments against compounded BHT

A

Individualized testing not necessary as not narrow TI meds. Hormone testing is unreliable

The desired levels of hormones have not been established and may not correlate with symptoms

Products have variable potency which could result in under/over-dosing – don’t adhere to strict FDA-mandated potency tests that Rx products do (PK/PD testing)

Lack safety / efficacy data

55
Q

Describe the ET and EPT dosing regimens

56
Q

What is continous combined EPT?

A

Patient takes both E and P daily

57
Q

Main Advatages of Combined Continous EPT

A

easy to remember
avoids the withdrawal bleeding
Decreases risk the most for endometrial hyperplasia

58
Q

Diadvatages of continous combined EPT

A

However, unpredictable bleeding may occur: 40% have irregular breakthrough bleeding in 1st 6 months; 20% by 1 yr

If bleeding continues after first 6 months – see Dr.

AUB after 6 months may indicate a need for a higher dose or something more serious

59
Q

describe continous E and cyclic P Therapy

A

The E is taken daily and the P is taken for 12-14
continuous days per cycle

Withdrawal bleeding typically begins after last P dose (within 1-2 days)

Recommended starting dose differs for continuous vs cyclic dosing

60
Q

When is continous E and cyclic P preferred?

A

Prefer fewer pills

Recent menopausal who do not want breakthrough bleeding (predictable bleeding vs breakthorough)

61
Q

Common Adverse EFfects of Estrogen and MAnagement

A

Nausea
Breast tenderness
Headache
Bloating

Management:
Often dose related
Change products

62
Q

Progestins Adverse Effects

A

Irritability
Breast tenderness
Bloating
Headache
“PMS-like symptoms”: mood swings, bloating, fluid retention, sleep disturbance, decreased libido, weight gain

63
Q

Adverse Effects simialr between estrogen and progestins? Management?

A

Vaginal bleeding is common in 1st 3-6 months

Different HT’s can have different effects; individualize tx and periodically reassess

64
Q

Contraindications of MHT

A

Unexplained vaginal bleeding
Active liver dx
Estrogen-dependent cancer (breast, endometrial, cervical)
Pregnancy
Active thromboembolic dx (e.g. DVT, PE, stroke, MI)
Untreated / uncontrolled CVD

65
Q

Caution of MHT

A

High cancer risk

66
Q

Non-oral Estrogen should be considered for:

A

Hypertriglyceridemia
Hepatobiliary disease
Migraine
Established CVD
Past VTE
Diabetes
Advanced age and no previous MHT

67
Q

What are some other agents that can be used for the management of VMS?

A

SSRIs and SNRIs

Veozah (fezolinetant)

Clonidine

Oxybutynin

gabapentin

pregabalin

68
Q

Sertonergic Antidepressants for VMS Indication and effeicacy

A

Alternatives to tx vasomotor sx’s when HT is CI or not desired
Less effective than HT, but still efficacious (reduce VMS 25-69%) – Varibale response

69
Q

Which serotenergic antoidepressnats can be sued for VMS?

A

Paroxetine 10-20mg od or 12.5mgCR to 25mgCR od
Citalopram 10-20mg od
Escitalopram 10-20mg od

Venlafaxine 37.5 – 75mg od
Desvenlafaxine 100mg od

70
Q

How shoukd one be initiated on a serotenergiuc antidepressnat for VMS? Onset?

A

Low dose often effective.

Quicker onset vs. depression: allow 2-4 weeks for effect

71
Q

Which antidepressnat should be choosen for VMS? Who should they be cosnidered in?

A

Must be cognizant of their associated AE’s and DI’s

Consider use in those with co-morbidities

72
Q

Which anti-depressnat is not listed for management of VMS?

A

Duloxetine

73
Q

Veozah (Fezolinetant) Indictaiion

A

Indicated for treatment of moderate to severe VMS associated with menopause

74
Q

Veozoah MOA

A

MOA: nonhormonal selective neurokinin 3 receptor antagonist

75
Q

Veozah Dose

A

Dose: 45mg po once daily (do not crush/chew tablets)

76
Q

Veozah Adverse Effects

A

Common adverse effects – headache (9.7%), liver enzyme elevation (5.4%) [MONITOR], abdominal pain (4.4%), diarrhea (3.9%), insomnia (3.9%), nausea (3.1%)

77
Q

Veozah Drug Interactions

A

CYP metabolism – watch for interactions

78
Q

Clonidine VMS

A

Clonidine 0.05mg bid
Modestly effective: 38% ↓ sx’s vs. 30% placebo
SE’s: orthostasis, drowsiness, dry mouth, constipation
D/c if no benefits after 2-4 weeks

79
Q

Oxybutynin VMS

A

Oxybutynin 2.5-5mg bid
Can reduce hot flash frequency by up to 77%
SE: anticholinergic side effects

80
Q

Gabapentin VMS

A

Gabapentin 300mg hs up to 900mg hs
Meta analysis: ↓ hot flashes by 20-30%
SE’s: dizziness, light-headed, fatigue

81
Q

Pregabalin VMS

A

Pregabalin 75mg BID up to 300mg hs
Limited data; one study showed ↓hot flashes by 65% vs. 50% placebo
SE’s: dizziness, somnolence

82
Q

Herbal Products and VMS

83
Q

What can occur after Menopause?

A

Bone Loss After Menopause

Incraesed risk of bone fracture

84
Q

Osteoprosis and Menopause Relationship

A

Post-menopause, estrogen deficiency causes accelerated bone loss by increasing ’ing bone turnover & resorption

Estrogen enhances osteoblasts to produce more OPG, which binds to RANKL. This blocks the RANKL-RANK interaction, thereby preventing osteoclast activation and bone resorption.

85
Q

Estrogen Therapy for Bone Loss in Menopause. Indication?

A

Estrogen therapy can reduce fracture risk at various sites by 24% to 39% in postmenopausal women

Indicated for prevention of osteoporosis only – not treatment – Ca2+, Vit D, exercise

Effects on bone protection are dose-related

** Shoud not be on HT for osteoporosis if not othe rindications for it (e.g. VMS)*

86
Q

Describe the efficacy of MHT for osteoprosis in menopause:
a) Standard Dose
b) Low Dose
c) Discontinuation
d) Indication

A

Standard dose HT reduces the risk of osteoporotic fracture–> hip & vertebral

Low dose HT beneficially increases BMD (less data for reducing fracture risk)

The benefits on fracture risk dissipate upon d/c of HT – return to pre-treatment levels in 1-2yrs

“In the absence of CI, systemic HT is an appropriate therapy to protect against bone loss in women <60yo or within 10yrs of menopause onset”

87
Q

Describe the CV effects of MHT

88
Q

Describe estrogens effects on the CV system

A

It causes vasodilation with short-term use

With long-term use it:
↓ LDL, ↑ HDL
Lowers fibrinogen
Lowers plasminogen-activator inhibitor type 1

Countering this is its effect on inflammation (measured by C-reactive protein) and on markers of thrombosis

89
Q

Womens health Initiative Study

A

Found negative CV outcomes.

More recent studies found that the use of
estrogen in women under 60 and within 10 years of menopause actually have a neutral to decreased CVD risk.

Older women starting HT and women who are further away from their final menstrual period appear to be at greater risk of a cardiac event vs. those who are younger and those who initiate HT closer to their menopause

90
Q

Stroke risk with MHT

A

No increased risk with MHT if initiated <10yrs since menstrual cycles and <60yo

Higher incidence if initiated later

91
Q

VTE Risk and MHT

A

Cochrane review: increased risk regardless of <10yrs or >10yrs (although higher in older starters)

Address risk factors for stroke and DVT before deciding to initiate HT:

  • Those at high risk should avoid HT and use non-hormonal
  • Those at medium risk may want to consider lower dose E, transdermal products, or non-hormonal
  • Low dose HT may confer less stroke & DVT risk (observational studies)
  • Transdermal ET may confer less DVT risk (observational)
    Micronized Progesterone may be less thrombogenic than MPA
92
Q

MHT and Breast Cancer Risk

A

Risk ↑ with longer duration

Risk persists for those on EPT but no effect on breast cancer mortality

Trends persist for those on ET

Studies are lacking with regard to breast cancer risk with long term use

Observational data is mixed; risk may depend on a variety of factors

93
Q

previous history of breast cancer and MHT

A

In women with prior breast cancer history, systemic HT is not is generally not advised – joint decision with oncologist

Low dose vaginal therapy provides minimal systemic absorption for GSM symptoms in breast cancer survivors – joint decision with oncologist

94
Q

Duration of tx for MHT

A

Duration of treatment: (unknown)

Individualized – used to say 5 years. Now, the safest regimen at the appropriate dose to control symptoms

  • periodically (~yearly) assess to see if still require treatment

e.g. no sx for the last year – taper or come off altogether

95
Q

What are some otehr sx seen in menopause?

96
Q

Describe insomnia and sleep disorders in menopause. Consequence?

A

Sleep difficulty is a hallmark symptom of the menopause transition

Both sleep onset and maintenance insomnia are ↑’ed during (peri-)menopause

Can interfere with QOL, and
cause daytime fatigue, irritability, and impaired cognition

97
Q

Management tof Insomnia/Sleep Disorders in Menopause

A

General insomnia recommendations: CBT, valerian, hypnotics, antidepressants

MHT may help in those also experiencing VMS

Hormone tx may improve night sweats – Only used if VMS

98
Q

Describe mood changes in menopause. Cause?

A

Some women may be more vulnerable to depressive symptoms during menopause transition, or experience anxiety & irritability

May be due to estrogen depletion, deficiency, or changing levels

99
Q

Estrogen Role in Mood Regualtion

A

Estrogen has multiple effects on brain function:

Positive effect on serotonergic activity
Increases the activity of NA
E receptors located in regions of brain responsible for learning and memory
Increases cerebral blood flow

100
Q

Estrogen Therapy for Mood

A

Women with moderate to severe VMS up to 3x more likely to have moderate-severe depressive sx’s

Some studies show ET improving depressive sx’s in perimenopausal women (but not late menopausal) , and it may augment the clinical response to SSRI’s

The use of antidepressants and psychotherapy (CBT) remains the mainstay of treatment for mood disorders and anxiety

Depressive Sx – Should still be treated with antidepressants

If have VMS and mood sx – Hormone therapy and then add on antidepressants if continued

101
Q

Menopause and Cogniotion/Dementia

A

Anecdotally, women often report experiencing memory changes, ↓in concentration with menopause transition

Limited data suggests early use of HT in menopause may be associated with diminished risk of later dementia, whereas later initiation of no benefit or perhaps even harmful

Where we stand today: HT is not recommended to preserve cognitive function or prevent/tx dementia. Further, initiation >65yo may ↑ the risk

102
Q

Pathophysiology or Urogenital Aginig

A

There are many E receptors located in:
vagina, vulva, urethra and bladder

A decraese in E levels causes many changes such as:

tissue atrophy
reduced secretions
reduced blood flow
vaginal pH increase 6-8 (premenopause 4.5 - 5)
A decraese in E in addition to normal tissue aging can result in vaginal symptoms

103
Q

What is genitourinary sydrome of menopause (GSm)

A

GSM refers to the signs/sx’s resulting from E deficiency on the genitourinary tract

104
Q

GSM Sx

A

Vaginal dryness
Vaginal itching / irritation
Burning
Painful intercourse
Lower urinary tract sx’s: (urinary frequency, urgency, UTI’s)
Nocturia, dysuria

105
Q

GSm Onset

A

Onset varies; may begin perimenopause or commonly a couple years after menopause

106
Q

GSM Tx Options

A

If OTC agents are ineffective → vaginal estrogen / prasterone / ospemifene

  • Vaginal Estrogen preparations
107
Q

Describe vaginal estrogen preparations in the tx of GSM

A

Effective: ↓ GSM sx’s by 60-80%

Safety: minimal systemic absorption, hence less concerns with use

At recommended doses (low), an accompanying progestogen is not needed
Risk of VTE, CVD does not seem to be increased

Rates of endometrial cancer appear to be consistent with general population

Does not appear to be associated with increased breast cancer risk

There is no clinical data beyond 1 year but continue using as long as necessary. Long term observational data supports safety

108
Q

What are some local vaginal estrogen products? What can they be sued for?

A

In addition to helping with GSM sx’s such as dryness and dyspareunia, intravaginal ET may also be useful in preventing recurrent UTIs and managing incontinence

1) VAgoinal Creams
2) Vaginal RIng
3) Vaginal Tablets
Vaginal Softgel Inserts

109
Q

Vaginal Creams

110
Q

Vaginal Ring `

A

17-beta estradiol (Estring vaginal ring)
Insert 1 ring vaginally q 3 months (delivers 7.5ug/24h)

111
Q

Vaginal Tablets

A

17-beta estradiol 10 ug tablets (Vagifem 10)
Insert 1 tab qd x 2 weeks, then 1 tab 2x/week (with days between)

112
Q

Vaginal Softgel Inserts

A

17-beta estradiol 4ug and 10ug (Imvexxy)
For the treatment of moderate to severe dyspareunia due to menopause
Insert 1 vaginal insert daily x 2 weeks, then 1 insert twice weekly.
Start at 4 mcg dose & adjustment is guided by the clinical response

113
Q

Local VAginal products: Monitroing and FOllow Up

114
Q

Systemic Estrogen Therapy for GSM ROle

A

If someone is also experiencing VMS, then oral MHT would be trialed as in addition to helping the VMS sx’s, it will also help with the GSM sx’s as well

∼10-15% of women will still experience GSM sx’s while on systemic MHT, so systemic and intravaginal ET may be used together

115
Q

What are some additional agents to treat GSM?

A

Prasterone (Intrarosa®)
Ospemifene (Osphena®)

116
Q

Describe Prasterone Therapy

117
Q

Describe ospemifene therapy for GSM

118
Q

What are some otehr sx experienced with menopause? Management?

A

Weight gain:
During menopause transition: avg. weight gain of 1.5lbs/yr– this is due to a decraesed resting metabolic rate that occurs with aging (change in fat-to-lean body mass ratio) – not MHT

Skin changes
Soon after menopause, skin collagen content, thickness, and elasticity decline

Abnormal Uterine Bleeding (AUB)

119
Q

What is AUB?

A

AUB (irregular menstrual cycles) is common during the menopause transition period
Prolonged cycle intervals as well as variable bleeding patterns precede eventual amenorrhea and menopause

120
Q

Potnetial causes of AUB?

A

Dysfunctional uterine bleeding (DUB) which results from anovulation
Endometrial hyperplasia and cancer
Benign lesions (endometrial polyps)

121
Q

DUB Diagnosis and Cocnerns

A

Since DUB is a diagnosis of exclusion, evaluation of DUB in a perimenopausal woman is warranted
Any bleeding after 12 months of amenorrhea is considered post-menopausal bleeding and should also be investigated

122
Q

Tx of AUB