Hormone tx
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| what is between premenopause and menopause (+characteristic of that period) | Perimenopause, wacky E levels
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| When does perimenopause start | Mid 30s
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| What can lead to instant menopause: | Bilateral removal of ovaries
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| What is an easy way to assess menopause | Level of FSH >100 (normal less than 10)
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| Menopause is due to | Ovaries are not making hormones anymore
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| After menopause the primary E is | Estrone
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| How come men have more E than menopausal women | Testosterone can become Estrogen thanks to aromatase
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| Progesterone levels in menopause: | Low (like in follicular phase)
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| Estrone vs Estradiol: | Estrone has 1/10th potency
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| Fraction of women life spent during menopause: | 3-Jan
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| Sx of perimenopause and menopause (6) | 1.Hot flashes, 2.Sleep disturbances, 3.Osteoporosis, 4.Uro-gential atrophy, 5.Mood swings/depression/anxiety, 6.memory problems
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| Definition of menopause: | 1yr w/o period
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| How can menopause lead to sleep disturbance | Low E, leads to low serotonin that leads to sleep disturbance (and probably depression too)
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| HRT alleviates what Sx of menopause (+ one) | ALL the Sx of menopause + cardiovascular help (remember LDL:HDL changes)
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| What is the most common HRT | E + P called EPT (EP Tx)
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| Why is P added in EPT | Decrease the risk associated btw E and endometrial cancer
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| What patients only get ET (w/o P) | If they don’t have a uterus (hysterectomies)
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| what Es are used in ET or EPT | CEE (premarin) or 17beta-estradiol-micronized (minimizes 1st pass)
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| How can E be given (route of entry) (Pros and Cons of each) | 1.oral (good for lipid profile, bad for clots), 2.transdermal-17beta only (good for clots, bad for lipid profile), 3.vaginal ring/cream (only affects vagina not systemic effect)
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| What Ps are used in EPT, Which one is better (why) | 1.medroxyprogesterone acetate, 2.micronized progesterone (mini 1st pass effect), 2 is better cuz it does not reduce the lipid profile advantages like 1 does
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| How can P be given (route of entry) | Oral, Vaginal cream
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| What is difference btw oral sequential and oral continuous and transdermal patches (include content of each) | Sequential: CEE +MPA (MPA 14/14), Continuous:daily CEE + MPA, Transderma: 17beta + norethinedrone or levonorgestrel
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| What regimen was used in the WHI (include amounts) | 0.625 CEE, 2.5 MPA
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| Since the WHI, what amounts are used | Minimum that relieve Sx (0.3 CEE)
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| HRT doses and Contraceptive doses of E: | Contraceptive are much higher
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| Explain hot flashes (include other name, location) | Vasomotor changes are due to increase NE (due to low E). Increase NE in the hypothalamus decrease the threshold for hot and cold feelings and lowers the thermostat (you feel hot easily, you feel cold easily)
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| Other than postmenopausal women, who gets hot flashes | 1.women with oophorectomy, 2.women w/ breast cancer on anti-estrogen tx, 3.men on anti-androgen tx for prostate cancer
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| What is the #1 reason to try HRT | Hot flashes
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| % of women that experience hot flashes | 80% (go away with time)
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| % of women with urogential atrophy | 40% (gets worse with time)
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| When is the greastest decline in bone mass | 1-3 year after menopause
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| Does E restore bone | Not prevents worsening
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| Can E be recommended for osteoporosis | No
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| If a woman has hot flashes and no vaginal atrophy, what alternate tx can be considered | SSRIs (only EPT/ET will tx vaginal atrophy)
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| What kind of study was the Harvard nurse study: | Observational
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| What kind of study was the WHI: | Clinical trial
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| Conclusion of the clinical trials: | 1.use HRT shortly after menopause and for a limited amount of time, and only enough to prevent Sx 2.only 2Sx can be txed with HRT (hot flashes and vaginal atrophy
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