Estrogens and Progestins- Burkin Flashcards

1
Q

What are the estrogen drugs?

A
  • estradiol
  • mestranol
  • estradiol esters
  • conjugated estrogens
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2
Q

What are the antiestrogen drugs?

A
  • clomiphene citrate
  • anastrozole
  • exemestane
  • letrozole
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3
Q

What are the SERMS drug?

A

Tamoxifen

Raloxifene

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4
Q

What are the progestins?

A
Medroxyprogesterone
Mestranol
Norethindrone
Norgestrel
Levonorgestrel
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5
Q

What are the anti-progestins?

A

Mifepristone

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6
Q

What is a combined oral contraceptive?

A

hormonal contraceptive administerd orally that contains estrogen and progestin

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7
Q

WHat is HRT? What is MHT?

A

Hormone replacement therapy

Menopausal hormone therapy

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8
Q

What are SERMs?

A

Selective estrogen receptor modulator

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9
Q

What does estrogen do to your brain?

A

maintain body temp
delay memory loss
prepare for sex and reproductive development

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10
Q

What does estrogen do to heart and liver?

A

liver production of cholesterol (redues plaque)

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11
Q

What does estrogen do to the ovary?

A

stimulates maturation of ovaries

starts womens cycle

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12
Q

What does estrogen do to the vagina?

A

maturation of the vagin

maintain lubricated and thick vaginal lining

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13
Q

What does estrogen do to the breast?

A

sitmulates development of breast at puberty and prepares the glands for future milk production

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14
Q

What does estrogen do to the uterus?

A

stimulates maturation of the uterus

prepare uterus to nourish a developing fetus

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15
Q

What does estrogen do to the bone?

A

estrogen helps to preserve a bone density

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16
Q

What do you use hormone replacement regimens for?

A
  • Menopause
  • hypogonadism
  • dysfunctional uterine bleeding
  • w. small doses of androgens to promote growth
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17
Q

What do you use antiestrogen regimens for?

A

infertility and breast cancer

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18
Q

What are teh three most important enzymes in steroid hormone biosynthesis?

A

3b-hydroxysteroid dehydrogenase

17b-hydroxysteroid dehydrogenase

Aromatase

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19
Q

What converts pregnenolone to progesterone?

A

3b-hydroxysteroid dehydrogenase

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20
Q

What converts estrone to estradiol and androstendione to testosterone?

A

17b-hydroxysteroid dehydrogenase

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21
Q

What converts androgens to estrogens?

aromatic hydroxylation of the A ring of C19 androgens to form estrogens

A

aromatase

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22
Q

What are the three classes of estrogen available?

A

natural
synthetic steroidal
synthetic non-steroidal estrogens

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23
Q

What are the three natural estrogen preparations?

What is essential for a natural estrogen prep?

A
  • estradiol (E2)
  • estrone (E1 1/12th)
  • estriol (E3 1/80th)

Phenolic A ring essential

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24
Q

Why cant you take natural estrogen preparations orally?

A

not orally active due to extensive first-pass hepatic metabolism

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25
Q

(blank) is a transdermal patch that provides slow, sustained release of estradiol; this route results in lower hepatic exposure and metabolism of the steroid and thus therapeutic levels of estradiol with lower circulating levels of estrone and estriol.

A

Estraderm

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26
Q

What are the estradiol esters?
What is the structure of these?
How are these taken?
What are the effects like?

A
  • estradiol valerate
  • estradiol cypionate
  • Short chain fatty acids at C17
  • w/ oil and injected intramuscularly
  • provides slow, but sustained effects (several weeks)
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27
Q

What are the conjugated estrogens?
What are the made up of?
How are they taken?
How is it absorbed?

A

estrone sulfate
equilin sulfate

sodium salts of the sulfate esters

orally, parenterally, topically

hydrolyzed in the intestine to remove sulfate groups and allow absorption

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28
Q

What are used orally for replacement therapy (e.g. in menopausal women)?

A

conjugated estrogens

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29
Q

What can you use IV for emergency tx of dysfunctional uterine bleeding?

A

conjugated estrogens

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30
Q

What are the alkyl estrogens?

What is the structure?

A

ethinyl estradiol
mestranol
-ethinyl sub at C17 inhibits first-pass hepatic metabolism.

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31
Q

What is the most potent steroidal estrogens?

What makes them so potent?What are they widely used in?

A

alkyl estrogens

  • increased affinity for ER contributes to higher potency
  • oral contraceptives
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32
Q

(blank) is a pro-drug of ethinyl estradiol that is activated by removal of the C3 methyl group.

A

Mestranol

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33
Q

What are no longer used clinically due to exposure associated with potentially toxic side effects?
What are the 2 drugs?

A

Synthetic non-steroidal estrogens

-Chlorotrianisene (Tace), and Methallenestril (Vallestril)

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34
Q

(blank) is a potent estrogen that is historically important as it provided a cheap, orally active estrogen to use in the development of endocrine therapies when natural products were unavailable

A

Diethylstilbestrol

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35
Q

Many synthetic agents-often polycyclic compounds with a phenolic ring resembing the steroid A ring- have estrogenic and antiestrogenic properites. What are these?

A
  • pesticides (DDT)
  • plasticizers (Bisphenol A)
  • industrial chemicals (polycholorinates biphenyls)
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36
Q

What are the natural progestins?

A
  • P4 (not orally active due to extensive first pass metabolism)
  • 17 alpha-hydroxyprogesterone (inactive)
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37
Q

Why do natural progestins bind to androgen, glucocorticoid and mineralcorticoid receptor?

A

C21 structure (favores progesterone receptor though)

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38
Q

How do you give P4?

A

oil solution intramuscularly (ma cause local irritation)

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39
Q

What are the synthetic C21 progestins and how do you take them?
Why are these better than C19 progestins as a progesterone supplement?

A
MPA (orally)
Hydroxyprogesterone caproate (intramuscular)

-Because they are more selective for PR

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40
Q

What derived from C19 nortestosterone and has more androgenic activity than C21 compounds? What do you use them for?

A

Synthetic C19 progestins

-oral and implanatable contraceptives

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41
Q

What are the major uses of progestins?

A

contraceptives and HRT

-> used in conjuction with estrogen in replacement therapy or in combo or alone as a female contraceptive

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42
Q

What are the minor uses of progestins?

A

dysmenorrhea
endometriosis
hirsuitism
uterine bleeding

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43
Q

What is this:
permanent end of menstruation and fertility. Defined as 12 months after last menstrual period. Average age is (blank) in the US>

A

Menopause

51

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44
Q

(blank) stabilizes the CNS thermoregulatory set point and leads to a normal thermoregulatory response. During menopausal transition, decreased estrogen levels lead to instability of the set point and an altered response to external thermal stimuli. Gradually overtime the set point becomes stable again. How can you fix the hot flashes?

A

Estrogen

exogenous estrogen or SSRIs

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45
Q

(blank) withdrawal or rapid fluctuation affects neurotransmitter level and/or function (beta endorphins) and module adrenergic receptors (norepinephrine) and causes sensitivity of the hypothalamic serotonin 5-HT2A receptor, What are the risk factors for hot flashes?

A

Estrogen

-surgical menopause, race/ethnicity, body mass, smoking

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46
Q

(blank) is a major indication for HRT

A

osteoporosis (estrogen prevents bone loss)

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47
Q

In premenopause, (blank) limits RANKL expression from osteoblasts and thus limits osteoclast formation.

A

E2

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48
Q

In postmenopausal women, decreased (blank) leads to increased RANKL expression. Result is increased (Blank) number, activity, and life span i.e bone loss

A

E2

osteoclast

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49
Q

(blank) helps maintain favorable lipoprotein profiles in women

A

estrogen

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50
Q

Osteoporosis is a major indication for (Blank) in postmenopausal women. What are other symptoms that will respond to estrogen treatment.

A

estrogen therapy

atrophic vaginits, irritabiliy, anxiety, fatigue

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51
Q

Hormone replacement regimens usually include low doses of an (blan) and a (blank) in women with a uterus

A

estrogen

progestin

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52
Q

What are oral contraceptives made up of?

How does it help?

A

static doses of E and P (ex. ethinyl estradiol and norethindrone acetate)
-eliminates vasomotor symptoms and restores regular cyclicity

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53
Q

What are the contraindications for oral contraceptives?

A

cigarette smoking, liver disease, history of thromboembolism or cardiovascular disease, breast cancer, unexplained vaginal bleeding

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54
Q

What kind of medical hormone therapy do you give to postmenopausal women? Does it work?

A

lower doses of estrogen and progestin are used

Those choosing HT tended to be healthier, have greater access to medical care, more compliant, and maintain a more health promoting lifestyle

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55
Q

Researchers studied estrogen-progestin (Prempro) combo and found out what?

A
  • increase stroke
  • increase heart attack
  • increase breast cancer
  • doubling of blood clots
  • increased dementia
  • increase ovarian cancer in estrogen only HRT
  • made tumors hard to detect
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56
Q

What are the current guidlines of medical hormone therapy?

A

prescribe hormone therapy to treat symptoms for the shortest period of time possible

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57
Q

What are problems that are reduced with medical hormone therapy?

A

hip fractures and colorectal cancer

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58
Q

Where do you find alpha estrogen receptors?

A

uterus, testes, pituitary, ovary, kidney, epididymis, and adrenal gland

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59
Q

Where do you find beta estrogen receptors?

A

prostate, ovary, lung, bladder, brain, uterus, and testes.

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60
Q

How do SERMs work on the breast?

How do they work on the uterus?

A

breast-> stops cell proliferation

uterus-> cause uterine proliferation

61
Q

What type of drug is Raloxifene? What is its half-life like? What does it bind to? Where in the body does it work as an agonist? Where in the body does it work as an antagonist?

A
SERM
Long half life
Binds to ERalpha and ERbeta.
-Bone and CV system
-breast and uterus
62
Q

What does raloxifene improve?

A

bone density, decreases fractures, decreases total cholesterol
AND causes a 50% decrease in overall cancer incidence

63
Q

Raloxifene is an FDA approved treatment for (Blank)

A
osteoporosis
Breast cancer (in postmenopausal women at high risk for invasive breast cancer)
64
Q

Why is raloxifene better than estrogen supplementation for improving bone density and lipoprotein profiles?

A

It provides the same beenfit without its adverse effects on endometrial and breast tissue and doesnt increase risk of breast cancer or uterine cancer (i.e increases estrogen in bone and decreases it is breast)

65
Q

What are the SEs of raloxifene?

What are the contraindications?

A

Hot flashes
Leg cramps
Blood clots

Women who are pregnant, breastfeeding, premenopausal, History of thromboembolic events, history of stroke, smoking

66
Q

What is used to treat dyspareunia (painful intercourse) and what type of drug is it? How do you take it?

A

Ospemifene-SERM

-orally

67
Q

Where does Ospemifene have its estrogenic effects?

What are the risks of taking this?

A

vaginal epithelium

-stroke, coronary heart disease, venous thromboembolism

68
Q

What are the SEs of ospemifene? What are the contraindications?

A

Side effects: vaginal discharge, hot flashes, diaphoresis, endometrial cancer

Contraindications: undiagnosed vaginal bleeding; estrogen-dependent neoplasia; history of thrombosis; pulmonary embolism, pregnancy, hepatic impairment

69
Q

What would be the perfect SERM?

A
  • prevents fractures
  • reduce menopausal symptoms
  • treat vaginal atrophy
  • neutral or protective uterus, breast and CV system
70
Q

What is used in anovulation and works as an antagonist at the hypothalamus?

A

clomifene

71
Q

What is used in managing menopause symptoms and osteoporosis, and works as an agonist at brain and bone?

A

femarelle

72
Q

What is used as contraception and works as an agonist at the bone and an antagonist at breast and uterus?

A

Ormeloxifene

73
Q

What is used for osteoporosis and breast cancer, it is an agonist at the bone and an antagonist at breast and uterus?

A

Raloxifene

74
Q

What is used for breast cancer and works as an agonist at bone and uterus, and an antagonist at breast?

A

tamoxifen

75
Q

What is used for breast cancer and and is SERM and its effects and locations are unknow?

A

Toremifene

76
Q

What is used for osteoporosis, breast cancer, vaginal atrophy and works as an agonist at the bone and an antagonist at breast and uterus?

A

Lasofoxifene

77
Q

What is used for vaginal atrophy, dysparunia and works as an agonist at the bone and an antagonist at breast and uterus?

A

-Ospemifene

78
Q

What is this:
third gen SERM
Not approved in US
Part of A TSEC (tissue selective estrogen complex; pairs a SERM with estrogen)

A

Bazedoxifene

79
Q

What is aprela?

What does this do?

A

Bazedoxifene plus conjugated estrogens (results form phase III clinical trials)
protects endometrium, relieves hot flashes, maintains bone mass

80
Q

Which is perferred, conventional hormone therapy or compounded hormone therapy?

A

Conventional

81
Q

What are phytoestrogens and what do they do?
What is black cohosh and what does it do?
Do they work?

A

substances found in plant-based food that have weak estrogenic effects-> helps lower cholesterol, relieve hot flashes
Black cohosh-helsp with short term tx of hot flashes and vaginal dryness

Most are untested, more studies needed

82
Q

What is Genistein is a natural (blank). It is a weak (blank) with a high affinity for (blank) receptors. How does it affect bone formation? May help relieve (blank).
Lower doses inhibit (blank X 5) cancers

High doses can increase rate of growth of some (blank) dependent breast cancer

What shouldnt you use this with?

A
phytoestrogen
estrogen
ERBeta
-stimulates bone formation, inhibits bone resorption, and prevents bone loss
-hot flashes
  • Prostate, cervical, brain, colon and breast cancers
  • Estrogen
  • tamoxifen and aromatase inhibitors because it reduces the efficacy of these drugs
83
Q

Genistein depresses (blank) function and causes (blank)

A

thyroid function

infertility

84
Q

What are lifestyle factors that can help with menopause systems?

A

Obtain adequate sleep every night
Exercise regularly to reduce stress
Avoid long work hours and maintain your personal schedule
Limit stress
Limit intake of alcohol, drugs, and nicotine
Eat a healthy and well-balanced diet
Sunlight, vitamin D, calcium increase bone formation.
Drink adequate amounts water during the early part of the day

85
Q

what are competitive antagonists for the estrogen receptors? what do they do?

A

Antiestrogen

inhibitors of estrogen synthesis

86
Q

(blank) and (Blank) are chemically similar drugs that act as partial estrogen agonists or antagonists depending on tissue examined

A

clomiphene and tamoxifen

87
Q

How do you give clomiphene citrate (clomid)?
What does it do?
Increases (blank) and (blank) production by inhibitory actions of (blank) (in women with a functioning HPA axi)

A

Orally
induces ovulation (given for female infertility)
FSH and LH
E2

88
Q

What is the half life like in clomiphene and why is it this length? It is less active as an antiestrogen in the (blank). What are the side effects?

A

long half life (~5-7 days)
due to plasma protein binding, hepatic recycling and accumulation in fatty tissue.
-periphery
-hot flashes, ovarian cysts, multiple births

89
Q

Tamoxifen is an (Blank) provided as the trans isomer. WHat is the half life like?

A

antiestrogen

long half life (4-11 days) and may require weeks to reach steady state

90
Q

What is the treatment of choice in postmenopausal women with breast cancer?
How does it effect lipids? How does it affect bones?

A

tamoxifen.

not thought to alter lipid profiles or accelerate osteoporosis

91
Q

Tamoxifen increases the risk of (blank) cancer. What are the side effects of tamoxifen?

A

endometrial

-Hot flashes, nausea, vomiting

92
Q

Is tamoxifen also effective in premenopausal women?

A

yes but oophorectomy or tx with GnRH analogs (leuprolide) are used to decrease ovarian estrogen synthesis

93
Q

Tamoxifen is also used for the (blank) of breast cancer and tx is effective for only (blank) years before it begins decreasing efficacy to drug-resistant tumors.

A

5

94
Q

What are the estrogen synthesis (aromatase) inhibitors?
What is their MOA?
What is it used for?

A
  • aminogutethimide, anastrozole (arimidx), exemestane, letrozole
  • Binds reversibly to the aromatase, blocks estrogen production by competitive inhibition
  • adjuvant tx (following surgery w/ or w/out radiation) for postmenopausal women with localized or metastatic ER+ breast cancer
95
Q

(blank) is an oral steroidal inhibitor that binds aromatase irreversibly. What is it indicated for?

A

Exemestane (aromasin)

tx: of ER+ breast cancer in postmenopausal women whose disease has progressed following 2-3 years on tamoxifen

96
Q

What is the ideal way to give exemestane?

A

with mTOR inhibitor everolimus

97
Q

(blank) prevents aromatase from producing estrogens by competitive, reversible binding to heme of its cytochrome p450 subunit

A

Letrozole (femara)

98
Q

What are the approved uses of letrozole?

What are the off label uses?

A

tx of local and metastatic breast cancer that is ER+ or of uknown hormonal status in postmenopausal women

-ovarian stimulation, gynecomastia, endometriosis

99
Q

Who are aromatase inhibitors contraindicated in?

What are the adverse effects?

A

Premenopausal women during pregnancy and lactation

-Hot flashes, arthalgia, fatigue, long term use leads to osteoporosis

100
Q

Aromatase inhibitors cause osteoporosis, what shoud you give with them to prevent this?

A

bisphosphonates

101
Q

A 54 year old woman was found to have node-positive breast cancer. Following surgery she was treated with a drug that blocks conversion of testosterone to estrogen (aromatase). The drug used for her treatment was most likely?

A. Anastrozole
B. Ethinyl estradiol
C. Tamoxifen

A

A. Anastrozole

102
Q

What are all the hormonal BC methods?

A
pills
injections
skin patches
subdermal implants
vaginal rings
Intrauterine Devices
103
Q

What is the most efficacious contraceptive (99.9%) and what are the common types?

A

Oral contraceptives

  • Ethinyl estradiol
  • Mestranol Plus a 19-Nortestosterone

Available as mono, bi, or tri phasic

104
Q

What are the formulations for hormonal contraceptives?

A
  • Combination: containing an estrogen and progestin

- Progestin only: progestin only pills or implants

105
Q

What is the primary action of combination oral contraceptives?

A

-suppress the secretion of FSH and LH through negative feedback

106
Q

Since combo oral contraeptives block both FSH and LH, what effect with this have on your body?

A

prevents follicle development (FSH)
Prevents ovulation (LH)
Inhibits GnRH sensitivity
Progestin makes cervix mucousy and impenetrable by sperm
Endometrium is not susceptible to implantation

107
Q

What is the monophasic way to take BC?

A

fixed amount of hormones 21 days and 7 days off

108
Q

What is the biphasic/triphasic way to take BC?

A

reduces total amount of steroids administered, more closely approximates the menstrual cycle.

109
Q

What are extend cycle pills of BC?

A

allows women to have fewer menstrual periods

110
Q

What are the extended cycle pills? Do you get a period?

A

ethyinyl estradiol and levanorgestrel combos

yes but it isnt a true period and has no medical function other than to let a girl know shes not pregnant.

111
Q

Extended cycle pill, how are they taken:
seasonale?
Seasonique?
Lybrel?

A
Seasonale:
taken continuously for 84 days
4 periods a year
Seasonique: 
taken continuously for 77 days
4 periods a year
Lybrel: 
taken all 365 days of the year
no monthly period at all
112
Q

Oral contraceptive preparations mainly contain (blank) or (blank)

A

ethinylestradiol or mestranol

113
Q

What happens to estrogens in the liver? Then where do these go?

A

undergoes sulfation or glucornidation

The conjugates are eliminated, go to the tissues or go to the small intestine via the bile duct.

114
Q

If your oral contraceptive preparation are in the intestine, what happens

A

intestina bacteria breaks the conjugates down, releasing free, active estrogenic hormone

115
Q

(blank) is responsible for plasma estrogen levels necessary for contraception. What can disrupt this and thus diminish OC efficacy?

A

Enterohepatic cycling

-antibiotics

116
Q

What is the patch?
How is it applied and where?
What kind of contraceptive is it?

A

ortho evra-> transfermal and applied WEEKLY to upper outer arm, buttocks, abdomen or thigh.
Combined hormonal contraceptive of ethinyl estradiol and norelgestromin

117
Q

What are the side effects of estrogenic affects?

A

hypertension, thromboembolic disorders, gall bladder disease
nausea, headache, vomiting, breast tenderness, edema

118
Q

What are the side effects of progestional agents?

A
weight gain
hirsutism
depression
acne
irregular bleeding
119
Q

What are the potential benefits of contraceptives?

A

include decreased incidence of endometrial and ovarian cancers

120
Q

What are the risks of combined agents?

A
  • Increased risk of MI or stroke in smokers older than 35
  • venous thromboembolism
  • minimal HTN
  • no effects on serum lipids
  • 50% decrease in endometrial cancer (effects last 15 years after tx stopped), decreased ovarian cancer, small increase in hepatic adenoma (rare)
  • NOT ASSOCIATED with breast cancer
  • increasd incidence of gallbladder disease
  • increase incidence of cervical carcinoma
121
Q

What are the contraindications for combo BC?

A

hepatic disease
suspected pregnancy
undiagnosed vaginal bleeding
smokers> 35

122
Q

What is the nuvaring?
What does it release?
How do you use it?
Why is it scary?

A

Combined hormonal vaginal contraceptive

  • flexible plastic ring that release low dose of ethinyl estradiol and progestin (etonogestrel) over three weeks
  • insert ring for 3 weeks and remove for 1 week
  • increases blood clots by 56% (increased 5x more than other BCs)
123
Q

What are the serious side effets of nuva ring?

A
aggravate pre-existing conditions
strokes and heart attacks
increased risks of breast cancer
organ damage
increased risk of cervical cancer 
blood clots
124
Q

What is marketed as a “newer progestin” closer to the natural progesterone?
What is it approved to treat? What does it do to your weight? What is its MOA?

A

Drosperinone

  • moderate acne and premenstrual dysmorphic disorder
  • decreases it
  • Aldosterone antagonist
125
Q

What are the adverse side effects of drosperinone?

A

Increases developing thromboembolism 6-7x, and 2x compared to women on pills containing levonorgestrel

Risk of hyperkalemia- dangerous or fatal for patients taking other drugs that increase potassium

126
Q

What is Yaz?

A

drosperinone with estrogen (ethinylestradiol)

127
Q

Progestin only contraceptives are taken as (blank) dose pills. How does this effect your estrogen levels?

A
low dose (mini pills)
they remain normal
128
Q

What kind of BC can a breastfeeding woman take? Do they work?

A

progestin only

highly efficacious but block ovulation in only 60-80% of cycles. (due to different thickening of cervical mucosa)

129
Q

What BC can you take with antibiotics without a negative effect?

A

Progestin only pills (not affected by gut bacteria)

130
Q

What is Depo-provera?
What is it used for?
How long does it take to work? How often do you give if?

A

Depot medtroxyprogesteron acetate (DMPA)

  • contraception and ndometriosis pain managament
  • instantly (long acting)
  • every 3 months
131
Q

What is the MOA of depo-provera? Why should you only use this drug for 2 years?

A

Thickening of cervical mucus and endoemtrial lining becomes thin and atrophic
-due to concerns over bone loss

132
Q

What is this:
silicone capsule filled with levonorgestrel?
Where do you put it?
How long does it work for?

A

Levonorgestrel
implanted subdermally in upper arm
5 years but is not longer used

133
Q

What are the IUDs used and what is the hormone they utilize? How long do they work?
What all are they used to treat?

A

Mirena and Skyla
-Levonorgestrel
5 years and are reversible
-prevent or treat endometriosis and dysmennhorea and DECREases risk of cervical cancer

134
Q

What are the SEs of IUds?

A

side effects include bleeding pattern alterations, vulvovaginitis, abdominal/pelvic pain, acne/seborrhea, ovarian cyst and headache.

135
Q

Can you use oral contraceptives with pregnancy?

A

no

136
Q

What are post-coital contraceptives?

A

emergency contraceptives or morning after pills

-high dose estrogen or pregoestins alone or in comb (99% effective)

137
Q

What is plan B?

What are the side effects?

A

L-norgestrel

nausea, vomiting, abdominal pain, fatigue, headache, dizziness, breast tenderness, cycle disruption

138
Q

What is this:
Mifepristone; derivative of norethindrone
progesterone and glucocorticoid receptor antagonist
Antagonizes progesterone’s effects in early pregnancy
Causes decidual breakdown and detachment of the blastocyst
subsequent decreased hCG lowers P4 production by the CL.
lead to increased sensitivity of the uterus to prostaglandin F2, contraction and expulsion of the embryo.
can be employed as a post-coital contraceptive

A

RU-486

139
Q

(blank) infertility: no prior pregnancies

(blank) infertility: infertility following at least one prior conception

A

Primary

Secondary

140
Q

What is the most common way to become infertile?

A

female amenorrhea or ovulatory dysfunction due to hypothalamic pituitary causes

141
Q

What are all the ways you can assess ovulation?

A
  • menstrual pattern
  • basal temp
  • sonography
  • ovulation prediction kits
  • midluteal serum progesterone levels (7 days after ovulation~10 ng/ml or higher)
142
Q

WHat are the inherited anatomical disorders that can cause infertility?

A

distal outflow tract obstruction
-imperforate hymen, transverese vaginal septum
-isolated atresia of vagina
-increase in retrograde menstruation-> leading to endometriosis
Mullerian defects

143
Q

What did Diethylstilbestrol cause?

A

in utero exposure linked to malformation of uterine development-> small T shaped uterus, and increased risk for vaginal adenosis

144
Q

idiopathic hypogonadotropic hypogonadism

subset have associated defects in the ability to smell (anosmia) and are said to have (blank)

A

Kallmann syndrome

145
Q

How do you treat hyperprolactinemia?

A

Dopamine agonists

Surgical therapies when prolactin-secreting adenomas are resistant to medical therapy.

146
Q

How do you treat hypothyroidism (associated with oligomenorrhea and amenorrhea)?

A

T4

147
Q

How do you induce ovulation?

A

clomiphene citrate

148
Q
How do you give clomiphene citrate?
What is it used for?
How does it work?
What hormones will it increase?
What will these hormones lead to?
What is the half life like?
What are the side effects (X3)?
A

-Given orally for female infertility
-induces ovulation
-binds to the estrogen receptor in the pituitary and hypothalamus
-estrogen’s negative feedback is interrupted
-Increases FSH and LH production
-This leads to maturation of multiple follicles.
-long half- life (~5 to 7 days)
Side effects: hot flashes, ovarian cysts, multiple births