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443-SRH and MSK > Menopause > Flashcards

Menopause Flashcards

1
Q

what is the average age and range of menopause

A

~51yrs
45-55yrs

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2
Q

what is the menopause transition

A

when you start seeing changes i ncycle

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3
Q

what is perimenopause

A

menopausal transition + 1yr post menopause

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4
Q

what is considered early and premature menopause

A

early <45yrs
premature <40yrs

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5
Q

what happens biologically during the menopause transition
- FSH and LH
- E and P
- flow regularity and amount
- E types

A

↓ number and function of follicles + ↓ response to FSH and LH
No progesterone release = irregular + heavy (may also be lighter)
increased FSH and LH
prev more estradiol -. more estrone
increasing and fluctuating E and decreasing P in perimenopause

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6
Q

what happens to E and P in postmenopause

A

both plumet

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7
Q

what is estrone

A

⅓ potency of estradiol
Conversion in liver, androstenedione in peripheral tissue

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8
Q

what is estradiol

A

Most potent
Main endogenous hormone
Produced in ovaries

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9
Q

what is estriol

A

Least potent
Metabolite from estradiol and estrone
Highest levels in pregnancy as also produced by placenta

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10
Q

after menopause, where is estrogen made

A

androstenedione stored in body fat is converted into estrone which can be conv into estradiol

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11
Q

where is T made in women

A

25% ovaries, 25% adrenals, 50% peripheral conversion from androstenedione

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12
Q

T or F: T declines drastically after menopause

A

F- gradually as we age
unless surgical menopause- then decreases 50%

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13
Q

what is a dx of menopause

A

cessation of periods F12mths + elevated FSH (≥30mIU/ml)

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14
Q

is perimenopause dx with FSH levels

A

no

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15
Q

how long do VMS last

A

7-8yrs, median duration after last period ~4.5yrs
1/3 pts have it for 10yrs

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16
Q

what are VMS

A

hot flashes, night sweats

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17
Q

T or F: E levels predict severity of VMS

A

F

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18
Q

how does E changes in menopause cause hot flashes

A

↓E = ↓ endorphin conc in hypothalamus = ↑NE, ↓5HT levels = narrow thermoregulatory zone in hypothalamus (narrowed thermoneutral zone)
KNDy neurons in hypothalamus- control of thermoregulatory centers are stimulated by neurokinin B + inhibited by estrogen
↓ estrogen = hypertrophy of KNDy neurons = ↑activity = hot flashes
Target of new tx approaches for VMS (neurokinin 3 receptor antagonists)

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19
Q

when do VMS tend to peak

A

early in the evening

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20
Q

what is GSM

A

genitourinary sx of menopause

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21
Q

describe GSM sx and physiology

A

Degeneration of connective tissue (collagen, elastin, smooth muscle) = vaginal shortening + narrowing
Reduced vaginal blood flow and secretions
↓ Glycogen production = △ vaginal pH from acidic to alkaline (↑pH)
Thinning mucosa + ↓ blood flow = ↓ secretions
Sx: vaginal atrophy (dryness, irritation/ itch, dyspareunia, post coital spotting), lower urinary tract (recurrent UTI, LUTS), sexual fx (low libido)

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22
Q

what are some menopausal sx that are more common in perimenopause

A

breast tenderness, headaches

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23
Q

estrogens have a_______ effect on arteries

A

protective- prevents atherosclerosis

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24
Q

rapid effects of E on arteries

A

dilation and NO release

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25
Q

rapid effects of E on arteries

A

dilation and NO releasel

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26
Q

long term effects of E on CV health

A

↓atherosclerosis, vascular injury, smooth muscle cell growth ↑ endothelial cell growth

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27
Q

midlife changes on bone health

A

bone loss occurs at faster rate with loss of estrogens = always assess for osteoporosis RFs

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28
Q

midlife changes on cognition

A

estrogens modulate aspects of brain function (hippocampus) → NT (ie 5HT, NE, dopamine, ACh)
Loss of estrogens = may affect concentration, memory (esp verbal memory- what was that word?)
Eff on cognition LT unknown- is it the loss of estrogens or is it aging

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29
Q

early or premature menopause is associated with increased risk of

A

osteoporosis, CV disease, cog impairment/ memory, early mortality

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30
Q

lifestyle management of menopausal sx include

A

cooling techniques (layers, fan), avoid triggers (excessive alcohol, spicy foods), maintain healthy body weight, smoking cessation, exercise

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31
Q

what are phytoestrogens

A

plant compounds with estrogen like activity but 500-1000x weaker than estradiol

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32
Q

3 types of phytoestrogens

A

isoflavones
lignans
coumestans

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33
Q

3 isoflavones of soy

A

daidzein, genistein, glycetin

34
Q

isoflavone supplement efficacy, how long to work, cautions

A

Marginal effect with hot flashes, inconsistent results
Takes 8-12wks to work
Food is a better source
Caution with hormone sensitive cancers and supplements

35
Q

femarelle efficacy

A

RCT showed ↓in vasomotor sx, no adverse △ in breast or endometrium

36
Q

black cohosh sus mech + AEs + efficacy

A

may act as a SERM, exact mech unknown
most studies have found no effect, but generally well tolerated
rare liver damage

37
Q

what hormone replacement to use if pt has had a hysterectomy

A

E alone - no endometrial protection from systemic E required

38
Q

systemic MHT is safe and effective for

A

healthy pts <60yrs of age or <10yrs after last menstrual period
For early or premature menopause, consider MHT until average age of menopause

39
Q

why is P added in MHT

A

endometrial protection from systemic estrogen (prevents endometrial cancer)

40
Q

what is E used for in MHT

A

sx management such as VMS + doses can be adjusted for sx management

41
Q

vaginal estrogen is used for
1. GSM
2. VMS

A

1

42
Q

what is the most common MHT regimen

A

EPT continuous

43
Q

what is EPT cyclic

A

estrogen continuous, progestogen x12-14d

44
Q

what is the timing hyp9othesis

A

: increased risk of atherosclerosis with age/ time after menopause (E is usually protective and prevents plaque formation)
If start E >10yrs after menopause = is actually harmful as it can dislodge the plaques that have already formed due to prothrombotic and proinflamamtory effects of estrogen
Primary benefit of MHT is <10yrs after menopause

45
Q

what was the women’s health initiative

A

designed as an RCT to assess if MHT reduced CV morbidity and mortality (CEE and medroxyprogesterone were used)

46
Q

describe the relationship between MHT and VTE

A

E has a dose dependent procoagulant effect
Increased risk of VTE with both WHI-EPT and ET with greatest risk in first year, with familial thrombophilia or other RFs
Transdermal E may have lower VTE risk, but are based on obs studies only (may just be d/t lower dose)

47
Q

describe the relationship between MHT and CV risk

A

Age and time since menopause matter- those at high risk of CVD should avoid MHT (hx VTE, stroke, CHd event)
Mod risk with comorbidities may use transdermal or lower dose of E
Comorbidities: HPTN, smoking, obesity, DM

48
Q

describe the relationship between MHT and breast cancer

A

EPT in WHI showed ↑ after 5yrs of use
ET alone did not show increase of breast cancer in WHI
May be differences in risk with type of progestogens - progesterone may have lower risk compared to synthetic progestins
Avoid MHT if personal hx of breast cancer
Caution if strong family hx

49
Q

oral estrogen effects (TG, SHBG, TBG, CRP, hormones, lipids)

A

High first pass eff: ↑TG, SHBG, TBG, CRP
Some △ in hormones
Improve lipids ↑HDL, ↓LDL

50
Q

when should you choose TD over PO estrogens

A

Avoid first pass effect: smokers, high TG, HPTN, ↓libido, gallbladder disease, RF for VTE/ CVD
For consistent lvls: migraine, shift workers, malabsorption issues

51
Q

0.625mg CEE = ____ 17b-estradiol (oral) = __ug patch = ___pumps estrogel = ___ug EE

A

1mg
50ug patch
1-2 pumps
5ug EE

52
Q

progesterone doses for systemic HT- continuous and micronized

A

P: continuous MPA 2.5mg or micronized progesterone 100mg daily// cyclic MPA 5mg or micronized progesterone 200mg F12-14d/mth

53
Q

continuous EPT BTB is expected __________

A

up to 6-9mths after starting, if >!2 mths = investigate

54
Q

cyclic EPT will lead to bleed when

A

withdrawal bleed when progesterone is stopped at the end of the 12-14d cycle

55
Q

what is tibolone

A

Selective tissue estrogenic activity regulator (STEAR)- usually not 1st line
Synthetic steroid analogue of the progestin, norethynodrel

56
Q

tibolone is converted into

A

3 active metabolites with estrogenic, progestogenic, and androgenic activity (doesn’t need + P)

57
Q

androgenic eff of tibolone may help with

A

libido

58
Q

AEs of tibolone

A

fatigue, breast tenderness, fluid retention, stomach upset/ nausea, increased appetite
Same risk profile as other MHTs

59
Q

advantages of tibolone

A

less BTB compared to EPT, less mood effects b/c no progesterone

60
Q

tissue selective estrogen complexes combined _____

A

E with a SERM

61
Q

duavive is

A

bazedoxifen + CE

62
Q

duavive effects

A

↓BTB and breast tenderness comp EPT
No increase in breast density (cancer)

63
Q

bazedoxifen is a

A

SERM with antagonistic ER eff on uterus and breast- agonist eff on bones
Inhibits endometrial hypertrophy as an antagonist

64
Q

bioidentical hormones are

A

chemically identical in molecular structure to human hormones

65
Q

most MHT products come from

A

plant sources

66
Q

biest =

A

estriol (80%) + estradiol (20%) or estriol (50%) + estradiol (50%)

67
Q

triest =

A

estriol (80%), estradiol (10%), estrone (10%)

68
Q

T or F:Natural progesterone creams (compounded) should not be used with estrogen for endometrial protection

A

T- lacks evidence that it will prevent endometrial hyperplasia

69
Q

hormone customization for bioidentical hormones are made based on

A

blood levels or saliva testing

70
Q

when to d/c MHT

A

Individualized decision on when to discontinue- decision to continue should be reassessed at regular intervals (ex- annually)
No age limit to continue MHT- can be continued as long as individual is getting benefit, even into 60s
Baseline risk changes over time

71
Q

nonhormonal options for VMS

A

SNRIs/SSRIs
oxybutynin
gabapentinoids
clonidine

72
Q

SSRI MOA in VMS

A

increase 5HT lvls in thermoreg zone

73
Q

gabapentinoids MOA in VMS

A

for VMS unknown, may have direct eff on hypothalamic thermoreg center

74
Q

clonidine MOA in VMS

A

centrally acting a2 adrenergic agonist, may decrease vascular reactivity
Not as effective as other nonhormonal rx options

75
Q

nonpharm tx for GSM

A

regular sexual activity/ partner/ solo, dilators, pelvic floor physio, laser

76
Q

nonhormonal GSM options

A

moisturizers and lubricants

77
Q

what moisturizers can be used in GSM

A

polycarbophil
hyluronic acid

78
Q

what hormonal therapies are available for GSM

A

vaginal E therapies
intarvaginal DHEA
ospemifene
systemic E therapies

79
Q

ospemifene is an _______ for _____

A

oral SERM for vaginal dryness and dyspareunia

80
Q

intravaginal DHEA AEs

A

vaginal discharge from melting of hard fat excipient in ovules

81
Q

what is an Inactive sex steroid precursor converted to estroge and androgen in vaginal cell wall

A

intravaginal DHEA

82
Q

waht are some vaginal estrogen therapies for GSM

A

estragyn
Estring
vagifem

443-SRH and MSK (24 decks)

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