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Pharm blk4- HRT

Hormone tx

what is between premenopause and menopause (+characteristic of that period) Perimenopause, wacky E levels
When does perimenopause start Mid 30s
What can lead to instant menopause: Bilateral removal of ovaries
What is an easy way to assess menopause Level of FSH >100 (normal less than 10)
Menopause is due to Ovaries are not making hormones anymore
After menopause the primary E is Estrone
How come men have more E than menopausal women Testosterone can become Estrogen thanks to aromatase
Progesterone levels in menopause: Low (like in follicular phase)
Estrone vs Estradiol: Estrone has 1/10th potency
Fraction of women life spent during menopause: 3-Jan
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
Definition of menopause: 1yr w/o period
How can menopause lead to sleep disturbance Low E, leads to low serotonin that leads to sleep disturbance (and probably depression too)
HRT alleviates what Sx of menopause (+ one) ALL the Sx of menopause + cardiovascular help (remember LDL:HDL changes)
What is the most common HRT E + P called EPT (EP Tx)
Why is P added in EPT Decrease the risk associated btw E and endometrial cancer
What patients only get ET (w/o P) If they don’t have a uterus (hysterectomies)
what Es are used in ET or EPT CEE (premarin) or 17beta-estradiol-micronized (minimizes 1st pass)
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)
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
How can P be given (route of entry) Oral, Vaginal cream
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
What regimen was used in the WHI (include amounts) 0.625 CEE, 2.5 MPA
Since the WHI, what amounts are used Minimum that relieve Sx (0.3 CEE)
HRT doses and Contraceptive doses of E: Contraceptive are much higher
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)
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
What is the #1 reason to try HRT Hot flashes
% of women that experience hot flashes 80% (go away with time)
% of women with urogential atrophy 40% (gets worse with time)
When is the greastest decline in bone mass 1-3 year after menopause
Does E restore bone Not prevents worsening
Can E be recommended for osteoporosis No
If a woman has hot flashes and no vaginal atrophy, what alternate tx can be considered SSRIs (only EPT/ET will tx vaginal atrophy)
What kind of study was the Harvard nurse study: Observational
What kind of study was the WHI: Clinical trial
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
Created by: mcafej02