wk 12, lec 2 Flashcards by Claire Jamieson

two types of menopause

physiologic and artificial

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physiologic menopause

natural process via depletion of ovarian follicles

oocyte depletion (gradually lost over years via ovulation and atresia)

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2 key processes in menopuase

loss of gonadotropin responsive oocytes

remaining oocytes become unresponsive to gonadotropins

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gonadotropin levels (FSH, LH) in menopause

high (bc of ovarian failure)

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what factor accelerate menopause

smoking

(not age, childbearing, weight, OCP)

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premature menopause (primary ovarian insufficiency)

cessation of menstruation before age 40

-genees, autoimmune, radiation, chemo, tumor, infection

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artificial menopuase

cessation of ovarian function bc of medical intervention

chemo, radiation, oophorectomy (remove ovaries)

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indications for artificial menopause

-endometriosis
-estrogen sensitive cancers
-intra-ab disease (i.e fibroids)
-prophylactic oophorectomy (BRCA gene)

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androstenedione and testosterone and DHEAS changes in menopause

A: drops a lot
T: stable
DHEA: decrease a lot (adrenopause)

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estrogen changes in menopause

estradiol drops a lot (comes from estrone conversion and ovarian secretion)

estrone more stable bc of peripheral conversion (from aromatization of androstenedione in fat, muscle, liver)

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progesterone changes in menopuase

source: corpus luteum in premenopausal, and adrenal secrete post menopause

drops lots

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gonadotropins (LH and FSH) post menopuase

increase lots becasue lack of ovarian feedback from estradiol

pulsatile release remains but with greater amplitutde

FSH levels rise earlier and are higher than LH

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2 criteria for diagnosis of menopause

FSH > 40 IU/L and estradiol < 75 pmol/L.

No need to measure LH clinically for menopause confirmation.

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androgen, estrogen, progesterone, gonadotropin changes in menopause

Androgens: Decrease in androstenedione, mild decrease in
testosterone.
Estrogens: Major drop in estradiol, moderate decrease in estrone.
Progesterone: Significant decline; adrenal source only.
Gonadotropins: Large increase in LH & FSH due to loss of ovarian
feedback.

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clinical implications of homrone changes in menopause

decrease estrogne= osteoporosis, CVD, vasomotor sx

persistent androgens: hirsutism, defeminization

high LH and FSH: ovarian failure and also stimulate androgen secretion

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perimenopuase

over aging the mean cycle length shortens

** Shortening of follicular phase; luteal phase remains constant

hormonal changes after age 45 in perimenopause

shorten follicular phase

lower estradiol

elevated FSH

LH unchanged

perimenopause; role of inhibin in FSH regulation

inhibin via granulosa cells; negative feedback on FSH

ovarian reserve declines –> inhibin level drop

leads to increased FSH

transition to menopause changes

Marked by menstrual irregularity
Variability in cycle length increases
Shorter transition in women with early menopause
Longer transition in women with later menopause

perimenopause and estrogen and impacts

not a state of estrogen deficiency!

can have higher estradiol levels (irregular secretion)

Occasional corpus luteum formation with limited progesterone
secretion

Increased risk of endometrial hyperplasia due to unopposed estrogen

sx: irregular bleed, hot flash, mood swing

hromones in perimenopause

Elevated FSH and irregular estradiol secretion

pros and cons of uterine atrophy in menopause

shrink endometrium and myometrium

pro: reduce fibroids, adenomyosos, endometriosis

risk: Postmenopausal bleeding from atrophic or hyperplastic
endometrium.

ovarian and oviduct changes in menopuase

decrease in size

palpable ovaries in post menopause –> possible ovarian neoplasm

reproductive tract changes in menopusae

pelvic floor weak; prolapse

vaginal atrophy; flatten rugae and thin epithelium

vaginal pH increase- predispose to infections (staph, strep, dip.)

cervical atrophy- vaginal dryness and dyspareunia

libido in menopause

* Decline in estrogen → vaginal dryness, discomfort with sex * Decrease in testosterone → reduced sexual desire * Changes in progesterone → mood changes that may indirectly affect libido psychological and social: sleep, mood, stress, self image, relationships

urinary tract changes in menopause

* Atrophic Cystitis: Urgency, frequency, incontinence, dysuria. * Recurrent UTIs: Due to thinning of bladder & urethral epithelium. * Urethral Caruncle: Pouting meatus, possible dysuria & hematuria.

mammary gland changes in menopause

breast regression resolve breast pain and cysts and cyclic sx

CVD system and estrogen and menopause

estrogen decerases CVD risk (decrease in menopause) benefits: * Improves lipoprotein profile * Promotes vasodilation * Inhibits vascular injury response * Reduces atherosclerosis risks: * Promotes coagulation * Increases thromboembolic events

bone metabolism and impacts of menopause of which type of bone

cortical bone: dense, in appendicular skeleton (i.e. legs, arms) trabecular bone: porous, metabolically active, in axial skleleton (i.e. spine, pelvis, femur) --> respond to hormones; loss of estrogen

RANK/RANKL/OPG pathway

osteoblasts express RANKL (ligand) RANKL bind RANk receptors on osteoclast precursors --> promote osteoclast formation and activity osteoprotegerin (OPG), secreted by osteoblasts, inhibits RANKL by binding it = regulate bone turnover

impacts of estrogen on bone remodelling and the RANK/OPG system

* Suppresses RANKL expression * Stimulates OPG production * Inhibits osteoclast formation and activity --> so in postmenopause: a decrease in estrogen causes more RANKL and less OPG --> excess osteoclast; and bone resorption and bone loss; postmenopausal osteoporosis RANK + RANKL= osteoclast make OPG + RANKL = inhibit osteoclast

mood changes in menopause from hormones

* Estrogen fluctuations affect serotonin and other mood-related neurotransmitters. * Progesterone changes may influence GABA pathways (calming effect). * Lower hormone levels may heighten emotional sensitivity.

sleep in menopuase

bad especially in late menopausal transition night wakings and hot flashes sleep disordered breathing homrone therapy may help with sleep and hot flashes

condition in menopause

memory decline is age related; some show more so in menopuase estrogen neuroprotective high progesterone for mood and cognition risks: alcohol, smoke, TIA, hypertension

vasomotor sx in menopause

hot flash usually 4.5 yrs begin with pressure in head --> increase to physiologyc flush palpitation, hot face neck and chest, sweat moments to 10 mins

experience of hot flush

* cutaneous vasodilation and increased perspiration * ↓ Core body temperature * ↑ Pulse rate * No significant changes in heart rhythm or BP

thermoregulatory dysfunction in menopuase causing hot flashes

defect in central thermoregulation set point narrows; so minor temp changes trigger heat-loss mechanisms --> sweat, vasodilate thermoregulatory center: rostral hypothalamus

estrogen withdrawal hypothesis of hot flashes in menopause

not triggered by low estrogen alone (ie.. prepubertal kids dont have) occur after estrogen exposure is withdrawn (i.e. menopause, oophorectomy)

neurochemical factors in hot flashes

NE increases post-flush (narrows thermo-neutral zone) serotonin; thermostimulus increase serotonin receptor --> hot flush SSRIs can improve VMS associated with LH surges but not caused by * Kallmann’s syndrome (no GnRH) → still experience flushes * Hypothalamic amenorrhea (low estrogen, no flushing) suggests: * Dopamine & opioid suppression of GnRH → protective?