Module 8 Hormone Flashcards

1
Q

what is the major estrogen produced in women

A

estradiol

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2
Q

estradiiol is formed from the precurosrs what

A

androstenedione and testosterone

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3
Q

the formation of estrogens is catalyzed by what

A

the araomatase enzyme

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4
Q

the anterior pituitary produces what 2 gonadotrophins

A

folicle stimualting hormone and leutenzing hormone

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5
Q

what does fsh do in women

A

causes folicular development

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6
Q

what does lh do in women

A

stimulates ovulation

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7
Q

fsh/gonadotrophins act to incrase the activity of the aromatase enzyme thus what

A

agumenting estradiol production

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8
Q

gonadotrphin release is under control by what

A

gonadotrophin releasing hormone which is produced in the hypothalamus

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9
Q

once formed, estradiol actshow to inhibti fsh and lh release

A

negative feed back

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10
Q

when estradiol is given clinically, it does whatq

A

prevents ovulation

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11
Q

estradiol in the oral contraceptive does what

A

inhibits lh and fsh release
also will bind to estrogen recetpors and peripheral tissues

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12
Q

the selective estrogen receptor modulars (serms) are a class of drug that act as waht

A

as either estrogen receptor antagonist or agonist depending on the tissue

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13
Q

estradiol undergoes waht

A

extenstive first pass metabolism so not effective given orally

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14
Q

what has oral bioavailability

A

ethinyl estradiol
this is the estrogen component of teh combination oral contraceptive

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15
Q

what was previously used in postmenopausal replacement therapy but is no longer used in the us

A

diiethylstibestrol

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16
Q

what is now used in post menopausal therapy

A

premarin which is estrone and equilin in one formulation

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17
Q

what are the orally effective synthetic progestins

A

medrocyprogestrone, norethindrone, levonorgestrel and desogrestrel
these are synthetic progresterone analogues that are effective orally

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18
Q

what are the progestin components of combination oral contraceptives

A

norethindrone, levonorgestrel and desogestrel

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19
Q

what is used as an injectable contraveptive

A

meddroxyprogesterone (depo-provera)

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20
Q

progestins have esterogenic and androgenic activity meaning what

A

some bind to androgen and estreogen receptors so they have more than one binding spot

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21
Q

levonorgestrel has relative what androegenic action

A

high androgenic action

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22
Q

desogestrel ahs relativelt what androgenic action

A

low

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23
Q

oral contraceptives containing ethinyl estradiol and progestein in form of levonorgestrel and destogestrl etc have what kind of preparations

A

monophasic and triphasic

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24
Q

what were phasic contraceptives develoepd

A

to reduce side effects

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25
minipills are waht
progestin alone containing deosgestrel
26
why are minipillls good
side effects of estradiol such as nausea and breast tenderness are eliminated
27
morning after pills are made of what
levonorgestrel only including plan b and next choice emergency situation effective in preventing pregncy if given within 48-72 hours after intercourse
28
implanon and nexplanon are good for how long and made of what
etonogestrel implants good for 3 years (a progestin implant in the arm)
29
norelgestromin and EE patch good for how long
weekly transdermal patch
30
devo provera im injections are done when
every 3 months
31
in a triphasic combinationn waht happens to progesterone
progestin increases as the days go on
32
what is the pharmacology of combination oral contraceptives
inhibit fsh and lh secretion and this inhibit follicular development and ovulation (primary mechanism of action) primarily estrogen action inhibit sperm transport or embryo implantation by altering endometrela linging progestins cause thickening of lining
33
what are the mild adverse effects of oral contraceptives
mild side effects include nausea, edema, breast swelling and headahce (usually only problem in first few months) this is primarily from the estrogen part of the pill
34
what are moderate sdie effects of oral contraceptives
breakthrough bleeidng, weight gain, hypertension
35
what is breakthrough bleeding
bleeding that occurs during the 21 days taht the oral contraceptive is used
36
why is weight gain a problem with combination pills
contain angrofen like progestinve levo to deso gets rid of this problem
37
what are severe side effects of oral contraceptives
venous thrombosis and pulmonary embolism ( especially 30 or older and smoker)
38
in less than 30 year old and non smoke what kind of cardiovascular disease or breat cancer risk si there with low dose ethinyl estradiol
no overall increase
39
why does oc increase reisk of venous thrombosis
estrogens increase the activity of blood clotting factors antithrombin which is major palsma inhibitor of thombin is reduced
40
estradiol binds to estroegen recepotrs where
in the perihpheral tissues such as breast bone and uterus
41
what are the selective estrogen receptor modulators
tamoxifen and faloxifene
42
what is the pharmacology of the serms
competative estrogen antagonist in breast and agonist in bone act as antagonists on bone for treating osteroproosis and breast cancer
43
when is tamoxifen and raloxifene most effective
in the first 5 years of therapy
44
what are the therapeutic uses of serms
first line therapy in ER positive breast cancer prevention of breast cancer in high risk individuals such as if mom or sister ahs breast cancer treatment of osteoporosis in reloxifene
45
what are the side effects of serms
hot flashes and vaginal dryness dvt (both tam and ral) endometrial proliferation is a risk in tamoxifen can lead to endometrial cancer
46
what is the pharmacology of mifepristone (RU 486)
progestin antagonist glucocorticoid antagonist (no clinical relevance) inhibits progesin binding (progestin needed for maintenance of pregnancy) so termination of pregnancy
47
mifepristone is given with what
misoprostol which is a prostaglandin antalog which causes strong uterine contractions
48
what are the therapeutic uses of mifepristone
approved as an abortifacient given with misoprostol which contracts uterine smooth muscle
49
what are side effects of mifeprisotone
cramping and excessive bleeding
50
what is the action of finasteride
inhibits 5 alpha reductase that converts testosterone to dihydrogen testosterone decreases dht in various tissues (skin, prostate)
51
what does anaztrazole do
inhibtis the aromatase enzyme that converts testosteronne to estradiol
52
what is dihydrogen testotsroen
the active androgen in many tissues including prostate, skin and liver
53
what does dihydrogen testosterone do in the prostate
incrases prostate size
54
what are the therapeutic uses of finasteride
used in treatment of benging prostatic hyperplasia to increase urine flow as it decreases size of prostate treatment of male pattern baldness since it decrases DHt in hair follicle
55
what does prazosin do in BPH
increaes urinary flow by decreaseing the tone of prostate does not shirnk size of prostate
56
what are the side effects of finasteride
teratogenic action form crushed pills and during sex - warning to pregnat women
57
what is the pharmacology of anastrozole
decreases estradiol formation by inhibiting the aromatase enzyme this is usefil in the treatment of estrogen receptor positive breast cancer more effective in breast over ovary
58
what is the therapetic use of anastrozole
first line therapy for ER positive breast cancner not appropirate for premanopausal patient who have estorgen production from the ovary
59
what are the side effects of anazstole
low levls of estradiol resuling in hot flahes, difficulty sleeeping etc
60
why is hormonr therapy used
to treat symptons of menopause sucha s hot flashes and night sweats
61
hormone therapy is generally appropriate for treatmethn of vasomotor symptoms if
women less tahn 60 years old less than 10 years since menopause without high risk for cardiovasucalr disease
62
what is general practice for hormone replacement therpy
to use the lowest effective dose to treat menopausal symptoms and to attempt to taper hormone therpy 3-5 years after use
63
when deciding to do hormone replacement what should be concidered
comprehendive cardiovasuclar risk factor assessmetn standard or converional cvd risk factors sex specific or predominant risk facotrs in women calculat risk scores (pooled cohort equationns or framinham risk calculator)
64
what are contraindicatiosn to systemic hormone therapy
estasblished atherosclerotic cardiovascualr disease venous thromboemnolic disease
65
may consider hormone replacement therapy if waht
ascvd risk less than 5% and 1 or less cvd risk factor
66
may consider hormonr therapy transdermal formilation if
ascvd risj 5-10% or less than 5 but 2 or less cvd risk factors
67
not receommended to use ht if what
if greater than 60 or greaster than 10 years since menopause onsent or ascvd risk greater than 10
68