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Therapeutics > Exam 1 Sex Hormones > Flashcards

Exam 1 Sex Hormones Flashcards

1
Q

What is testosterone?

A
  1. the most important androgen secreted by the testis
  2. binds to the androgen receptor and alters the rate of transcription
  3. men produce 8 mg of testosterone a day → 95% by Leydig cells in testis and 5% by the adrenal glands
  4. men have 0.6 mcg/dL after puberty in the blood but decreases after 50 while women have 0.03 mcg/dL
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2
Q

Circulating testosterone is bound to what?

A

65% is bound to sex hormone binding globulin (SHBG), 33% is bound to albumin, and 2% is free

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3
Q

How is testosterone synthesis regulated?

A

hypothalamus secretes GnRH that goes to the anterior pituitary that secretes LH for the Leydig cells that produce testosterone to develop sex organs but anterior pituitary also secretes FSH for sertoli cells that function in spermatogenesis

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4
Q

How does testosterone negatively feedback in its synthesis?

A

can negatively feedback to the Sertoli cells and to the anterior pituitary and hypothalamus

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5
Q

How is testosterone metabolized?

A
  1. aromatase in some tissues changes it to 17beta-estradiol
  2. 5alpha reductase in target tissues transforms it to 5alpha-dihydrotestosterone → more potent and active that has stronger binding to testosterone receptors
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6
Q

How is testosterone excreted?

A
  1. occurs in the liver
  2. inactivated and conjugated and then excreted to the urine → oxidized to androsterone and etiocholanolone that have a ketone instead of OH group
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7
Q

What are adrenal androgens?

A
  1. intermediates of the testosterone pathway
  2. produced in significant amounts, mainly in adrenal glands
  3. weak androgen effects
  4. examples → androstenedione, DHEA, DHEAS
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8
Q

What are the physiological effects of testosterone?

A
  1. responsible for many changes at puberty
  2. has growth promoting properties → penile/scrotal growth, change in hair (oilier/thicker), pubic/axillary/beard hair, voice deepening, skeletal growth followed by epiphyseal closure, increased lean body mass (positive nitrogen balance)
  3. stimulation and maintenance of sexual function → without testosterone, no libido and be infertile
  4. stimulation of erythrocyte production → why athletes use steroids for more O2
  5. decrease in HDL levels → men have higher risk of cardiovascular events
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9
Q

What are the clinical uses of testosterone?

A
  1. androgen replacement therapy in men → male hypogonadism (testosterone deficiency) and hypopituitarism
  2. gynecologic disorders → endometriosis (danazol), in combo with estrogens for replacement therapy in postmenopausal period to eliminate endometrial bleeding and enhances libido
  3. protein anabolic agents → reverse protein loss after trauma, surgery, or prolonged immobilization with diet and exercise
  4. andropause → male menopause
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10
Q

Why are synthetic androgens used?

A
  1. when administered orally, testosterone is readily absorbed but inactivated
  2. 17-alkyl forms are more active orally
  3. ester forms (cypionate) have prolonged absorption time and greater activity for IM injection
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11
Q

What are the role of anabolic steroids in sports?

A
  1. used in doses 10-200 times than daily normal production to increase strength and aggressiveness → effects in women
  2. have risks with long term use → harmful changes in cholesterol levels (low HDL and high LDL), acne, high blood pressure, hepatic dysfunction with 17-alkyl steroids (since liver has to work harder to metabolize the drug)
  3. large doses suppress the secretion of gonadotropins → lead to testicular atrophy (testicles become tiny)
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12
Q

What are the adverse effects of testosterone?

A
  1. not be used in infants or pregnant women → disturbances in sexual development may occur
  2. in women → hirsutism (excessive hair growth), acne, amenorrhea (missing periods), clitoral enlargement, voice deepening
  3. in men → acne, sleep apnea, gynecomastia (female like breast development), azoospermia and testicular atrophy, increased aggressiveness and psychotic symptoms
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13
Q

What are some antagonists of androgens?

A
  1. 5alpha reductase inhibitors → blocks the conversion from testosterone to 5alpha-dihydrotestosterone
  2. androgen receptor inhibitors → blocks the binding of endogenous androgens to the receptor or inhibit the activation of the receptors → includes steroidal inhibitors and non-steroidal inhibitors
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14
Q

What are the 2 5alpha reductase inhibitors?

A
  1. finasteride → treats benign prostatic hyperplasia (Proscar), male pattern baldness (Propecia), hirsutism in women
  2. dutasteride → treats benign prostatic hyperplasia and male pattern baldness
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15
Q

What are examples of steroidal androgen receptor inhibitors?

A
  1. cyproterone and cyproterone ester → treats hirsutism in women and excessive sex drive in men
  2. spironolactone → treats acne and hirsutism in women
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16
Q

What are examples of non-steroidal androgen receptor inhibitors?

A
  1. flutamide → is a non-steroidal antiandrogen that treats prostate cancer
  2. enzalutamide → is a non-steroidal antiandrogen that treats metastatic castration-resistant prostate cancer
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17
Q

What is the importance of estrogens?

A
  1. development and maintenance of female reproductive tissues (ovaries, uterus, breast, vagina)
  2. regulation in CNS (temp, mood)
  3. effects in peripheral tissues (bone cardiovascular, liver)
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18
Q

What is the importance of progesterone?

A
  1. development and maintenance of female reproductive tissues (uterus and breast)
  2. maintenance of pregnancy
  3. effects in other tissues (brain)
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19
Q

What is 17-beta estradiol?

A
  1. most potent estrogen
  2. binds to estrogen receptor and alters rate of transcription
  3. produced mostly in the ovaries in premenopausal women and synthesized in placenta during pregnancy
  4. plasma levels are 5-85 ng/dL which varies during menstrual cycle
  5. mostly bound to sex hormone binding globulin (SHBG) and albumin and only 2% is free in circulation
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20
Q

How is estrogen synthesis regulated?

A

hypothalamus secreted GnRH that activates anterior pituitary to release FSH and LH that go to the ovaries to produce estrogens and progesterone → can be negative or positive feedback loop in which estrogens and progesterone can feedback to inhibit the anterior pituitary and hypothalamus

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21
Q

What do granulosa cells produce?

A

estrogen

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22
Q

What does the corpus luteum produce?

A

both estrogen and progesterone

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23
Q

How is the menstrual cycle broken down?

A
  1. in the ovaries → follicular phase and luteal phase (starts on day 14 and ends on day 28) of the follicle
  2. in uterus → endometrium decreases during menstruation phase then slowly increases during proliferative phase and secretory phase (ready for implantation)
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24
Q

What are the different phases of the menstrual cycle?

A
  1. early follicular phase → estrogen suppresses production of FSH
  2. late follicular phase → estrogen stimulates surge of LH and FSH → ovulation and formation of corpus luteum
  3. luteal phase → estrogen and progesterone suppresses the production of LH and FSH
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25
Q

What happens if pregnancy does not occur?

A
  1. corpus luteum degenerates

2. production of estrogen and progesterone by corpus luteum declines → menstruation

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26
Q

What happens if pregnancy does occur?

A
  1. fertilized egg/embryo secreted human chorionic gonadotropin (hCG)
  2. hCG acts like LH to stimulate corpus luteum to produce progesterone during first trimester
  3. higher progesterone levels support the maintenance of the endometrium
  4. assays of hCG in the urine are used as pregnancy tests → hcG is present only if pregnant
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27
Q

Where are estrone and estriol produced?

A

synthesized in the liver and peripheral tissues

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28
Q

Where is 17-beta estradiol produced?

A

synthesized in the ovaries mostly

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29
Q

How are estrogens produced?

A
  1. androstenedione → testosterone → 17-beta estradiol via aromatase
  2. androstenedione → estrone (via aromatase) → 17 beta estradiol or estriol
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30
Q

What are the different types of estrogens?

A
  1. natural estrogens
  2. synthetic estrogens
  3. phytoestrogens
  4. environmental estrogens
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31
Q

What are natural estrogens?

A
  1. 17 beta estradiol → most potent
  2. estrone → less potent
  3. estriol → less potent, dominant form during pregnancy (synthesized in placenta)
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32
Q

What are synthetic estrogens?

A

drugs with estrogenic activities (steroidal and non-steroidal)

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33
Q

What are phytoestrogens?

A

estrogen mimetic compounds in plants (flavonoids) → use in menopausal women to relieve their symptoms like soy and miso

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34
Q

What are environmental estrogens?

A

compounds used in the manufacture of plastics (bisphenols, alkylphenols, phthalate phenols) → additives or byproducts → example is BPA which can leak into food

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35
Q

How is estrogen metabolized and excreted?

A
  1. metabolized in the liver mostly and excreted into the bile and urine
  2. conjugated estrogens in the bile can be hydrolyzed in the intestine and reabsorbed (enterohepatic circulation)
  3. orally administered estrogens have a high ratio of hepatic to peripheral effects → can be avoided by using routes that avoid first pass liver exposure
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36
Q

How can estrogen be reabsorbed?

A

bacteria can cleave the conjugation group and can then be reabsorbed

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37
Q

How is estrogen made to be more soluble?

A

hydroxylation in the A ring and conjugation

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38
Q

What are the physiologic effects of estrogen?

A
  1. female maturation
  2. endometrial effects
  3. metabolic and cardiovascular effects
  4. blood coagulation → enhanced blood coagulability (can lead to stroke or heart attack)
  5. CNS effects → mood
39
Q

What are the female maturation effects of estrogen?

A
  1. development of the vagina, uterus, and uterine tubes
  2. stromal development and ductal growth in the breast
  3. accelerated growth phase and the epiphyseal closure
  4. growth of axillary and pubic hair
  5. alteration in distribution of body fat to produce body contours
  6. pigmentation in the skin (nipples, areolae, genital region)
40
Q

What are the endometrial effects of estrogen?

A
  1. development of endometrial lining during menstrual cycles

2. prolonged exposure leads to hyperplasia (too much growth) of the endometrium and abnormal bleeding

41
Q

What are the metabolic and cardiovascular effects of estrogen?

A
  1. decrease in the rate of resorption of bone → estrogen deficiency can lead to osteoporosis
  2. stimulation of synthesis of transcortin and SHBG
  3. alteration in composition of plasma lipids → increase HDL, decrease LDL
42
Q

Estrogen is relatively a safe drug can it could possibly increase the likeliness of what?

A

breast cancer

43
Q

What are the clinical uses of estrogens?

A
  1. hormone replacement therapy in postmenopausal women
  2. osteoporosis
  3. hormonal contraception
  4. replacement therapy in patients with primary hypogonadism
44
Q

How is estrogen used as a hormone replacement therapy in postmenopausal women?

A
  1. relief of CNS disturbances → hot flashes, sweating, flushing
  2. relief of symptoms resulting from urogenital atrophy → vaginal dryness, increased risk of infections
  3. relief of psychological effects → mood swings, insomnia, depression, nervousness
44
Q

How is estrogen used as a hormone replacement therapy in postmenopausal women?

A
  1. relief of CNS disturbances → hot flashes, sweating, flushing
  2. relief of symptoms resulting from urogenital atrophy → vaginal dryness, increased risk of infections
  3. relief of psychological effects → mood swings, insomnia, depression, nervousness
45
Q

How is estrogen used to treat osteoporosis?

A
  1. only for post menopausal osteoporosis

2. estrogens decrease the rate of bone resorption

46
Q

How is estrogen used in replacement therapy in patients with primary hypogonadism?

A
  1. failure of development of the ovaries
  2. chromosomal disorders like Turner syndrome which the absence of one or all sex chromosomes
  3. castration (oophorectomy) → like ovarian cancer/tumor
47
Q

What are the adverse effects of estrogen?

A
  1. uterine bleeding → estrogen therapy is a major cause of postmenopausal uterine bleeding, endometrial hyperplasia (too much endometrial growth), estrogen should be given cyclically to mimic body cycle, can be given progestin in each cycle to prevent bleeding
  2. endometrial carcinoma → concomitant use of progestin reduces risk
  3. breast cancer → long term use but progestin does not have a protective effect
  4. nausea, headache, fluid retention, weight gain
48
Q

What is the SAR of estrogen?

A
  1. aromaticity in A ring is required
  2. hydroxyl at C3 is essential for activity → can be masked as ether that is readily hydrolyzed in vivo
  3. unsaturation in B ring is tolerated
  4. 16-OH decreases activity
  5. 17-alpha-ethynyl substituent blocks metabolism (increase half life) and allows oral activity
  6. 17-beta OH group is required for activity but can be temporarily blocked by ester for drug delivery
49
Q

What are 17-alpha-alkylated estrogens?

A
  1. examples are ethynyl estradiol, mestranol, quinestrol
  2. the 17 alpha alkylation prevents conversion to estrone → enhanced oral bioavailability and increased half life (prodrug!)
  3. 3-alkylated ether is quickly dealkylated in vivo
50
Q

What are estrogenic esters?

A
  1. esterification (OH group replaced by ester) decreases solubility and slows absorption
  2. slow absorption from injection site (depot) prolongs action so need less frequent injections
  3. examples → estradiol valerate and estradiol cypionate
51
Q

What are conjugated estrogens?

A
  1. usually collected from pregnant mares’ urine (Premarin)
  2. mixture of estrogens → 50-60% estrone sulfate, 20-30% equilin sulfate, other estrogenic substances
  3. since conjugated, it can be reabsorbed and utilized
52
Q

What is the SAR in nonsteroidal estrogens?

A
  1. amine substituted side chain blocks helix-12 and leads to antagonist/SERM activity
  2. hydroxyl enhances activities (tamoxifen oxidized in vivo)
  3. aromatic ring interferes with helix 12 conformation and leads to antagonist/SERM activity
  4. OG group required for agonist activity and should be 10-12 angstroms from other OH group (diagonal from each other)
  5. rigid core (double bond) is required to maintain proper space between the aromatic rings
53
Q

What is the structural basis of SERM activity?

A
  1. ligand binding domain with agonist (diethyl stilbestrol) bound → helix 12 conformation allows coactivator binding
  2. ligand binding domain with selective estrogen receptor modulator (tamoxifen) bound → helix 12 conformation blocks coactivator binding
54
Q

What are examples of non-steroidal estrogens?

A
  1. diethyl stilestrol → used in 1940-70 to prevent miscarriage, increased risk of vaginal adenocarcinoma in women exposed in utero, used in advanced prostate cancer
  2. chlorotrianisene → postpartum breast engorgement, menopause symptoms, prostate cancer
    BOTH NOT SERM has no nitrogen substitution
55
Q

What are SERM?

A
  1. designer estrogens
  2. partial estrogen agonists that block the action of stronger estrogens
  3. estrogenic in some tissues and antiestrogenic in others
  4. mostly non-steroidal estrogens
  5. hold promise as the alternative for estrogen replacement therapy
56
Q

What is the first clinically available SERM?

A

tamoxifen

57
Q

What is tamoxifen?

A
  1. brand name is Novaldex
  2. is a prodrug that is oxidized in vivo
  3. partial estrogen agonist
  4. has antiestrogen actions → treat breast cancer and prevents breast cancer in high risk women
  5. has estrogenic actions → weak estrogen agonist at endometrial cells (can cause bleeding), increases risk of thromboembolic events, prevents osteoporosis
58
Q

What is toremifene?

A
  1. structurally similar to tamoxifen
  2. SERM
  3. used to treat advanced breast cancer
59
Q

What is ospemifene?

A
  1. structurally similar to toremifene
  2. SERM
  3. estrogenic effects on the vaginal epithelium
  4. used to treat dyspareunia in post menopausal women
60
Q

What is raloxifene?

A
  1. brand name is Evista
  2. SERM, partial estrogen agonist
  3. has tissue specific activities
  4. estrogen actions → prevents osteoporosis in postmenopausal women, decreases LDL levels in blood, increases risk of blood clots
  5. antiestrogen effects → decreases risk for breast cancer, does not stimulate endometrial cells, may cause hot flashes
61
Q

What is an analog that has similar activities to raloxifene?

A

bazedoxifene

62
Q

What is clomiphene?

A
  1. brand name is Clomid
  2. SERM, partial estrogen agonist
  3. unique feature: increases secretion of FSH and LH by inhibiting negative estradiol feedback
  4. used to stimulate ovulation in women with oligomenorrhea or amenorrhea and ovulatory dysfunction (from polycystic ovary syndrome)
  5. PCOS (affects 7% of women in reproductive age) → is gonadotropin dependent ovarian hyperandrogenism and leads to anovulation (ovulation stimulated too much, can get twins) and infertility
63
Q

What is fulvestrant?

A
  1. brand name is Faslodex
  2. selective estrogen receptor downregulator (SERD)
  3. pure estrogen receptor antagonist for the treatment of breast cancer
  4. somewhat more effective than SERM in patients who have become resistant to tamoxifen
64
Q

What are aromatase inhibitors?

A
  1. blocks the biosynthesis of estrogens
  2. effective in patients whose breast cancer becomes resistant to tamoxifen
  3. ovulation induction (off label use) → chance of having increased ovulation that results in multiple births is less
  4. gynecomastia
  5. examples → anastrozole, letrozole, exemestane
65
Q

What is progesterone?

A
  1. most important progestin
  2. functions as a hormone and a precursor to the estrogens, androgens, and corticosteroids
  3. binds to the progesterone receptor and alters rate of transcription
  4. synthesized in the ovary, testis, and adrenal glands
  5. a large quantity of progesterone is synthesized by the corpus luteum in the ovary in the luteal phase and by the placenta during pregnancy
66
Q

How is progesterone metabolized?

A
  1. rapidly absorbed following administration of any route
  2. half life in plasma is 5 minutes → not useful as a drug so synthetics are used
  3. almost completely metabolized in one passage through the liver
  4. converted to pregnanediol and conjugated with glucuronic acid
  5. excreted in the urine
67
Q

What are the physiological effects of progesterone?

A
  1. menstrual cycle → causes the maturation and secretory changes in the endometrium following ovulation
  2. metabolic effects → increases basal insulin levels and insulin response to glucose AND promotes glycogen storage in the liver
  3. interferes with aldosterone → competes with aldosterone for the mineralocorticoid receptor, causes decrease in Na+ reabsorption, increase in aldosterone secretion by adrenal cortex during pregnancy
  4. depressant and hypnotic effects on the brain
  5. can increase appetite at higher levels → make you fat
68
Q

What are the clinical uses of progesterone?

A
  1. hormonal contraception
  2. hormone replacement therapy in combo with estrogens → prevents some adverse effects of estrogens (uterine bleeding and endometrial carcinoma)
  3. endometriosis (growth of endometrial cells outside uterine cavity in which cells respond to hormonal changes and cause severe pain from inflammation during menstruation) → progestins suppress growth of endometrial cells
  4. dysmenorrhea (painful menstruation)
  5. bleeding disorders
69
Q

What is the SAR in progestins?

A
  1. C19 methyl group can be replaced by H or double bond
  2. ketone at C3 is essential for activity → can be introduced in vivo by oxidation
  3. unsaturation or cyclopropyl ring is tolerated, C6 methyl group enhances activity
  4. unsaturation or cyclopropyl ring is tolerated (the 5 membered ring)
  5. 17-alpha ethynyl moiety leads to oral activity
  6. native acetyl moiety has highest activity but poor oral bioavailability
  7. 17 beta OH or esters are used in oral preparations
  8. C18 methyl group or ethyl group is required for activity
  9. aromatic/amine substituent leads to antagonist on third ring
70
Q

What are the 19-nor, 17-ethnyl steroids?

A
  1. first generation progestins → norethindrone, ethynodiol diacetate
  2. 17-ethynyl group increases oral bioavailability
  3. 19 methyl group is not necessary for progestenic activity
  4. replacement of 19 methyl with H enhances activity
  5. replacement of 17-acetyl with OH increases oral bioavailability
  6. ester groups are rapidly hydrolyzed in vivo
71
Q

What is levonorgestrel?

A
  1. second generation progestin
  2. levo isomer of norgestrel which is a racemic mixture
  3. only levo form is active
  4. high oral bioavailability
  5. used in intrauterine devices (IUDs) and Mirena
  6. has ethyl group on C18
72
Q

What is norgestimate?

A
  1. prodrug (has N-OH group)

2. converted to levonorgestrel oxime and then to levonorgestrel in vivo

73
Q

What is desogestrel?

A
  1. third generation progestin
  2. prodrug
  3. rapidly metabolized to etonogestrel
  4. high oral bioavailability
74
Q

What is etonogestrel?

A
  1. active form of desogestrel (has ketone added)
  2. structurally analogous to levonorgestrel
  3. used in subdermal implant Nexplanon or the vaginal ring (NuvaRing) which releases the hormone slowly
75
Q

What is drospirenone?

A
  1. fourth generation progestin
  2. relatively weak progestogenic activity (10% of levonorgestrel)
  3. antimineralocorticoid activity → increase water release to regulate effects of ethynyl estradiol
  4. negates side effects of ethynyl estradiol in combo therapy
76
Q

What is medroxyprogesterone acetate?

A
  1. first generation progestin

2. used for depot injection (Depo-Provera) as a long acting progesterone only contraception

77
Q

What are the hormonal activities of progestins?

A
  1. progestins frequently have hormonal activities other than progestonic effects due to their interaction with other steroid receptors
  2. want to minimize androgenic and antiestrogenic activities!
78
Q

Which progestin is antiandrogenic?

A

drospirenone

79
Q

Which progestin has the highest androgen activity?

A

levonorgestrel

80
Q

Which progestins have strongest progestin effect?

A

levonorgestrel, norgestimate, desogestrel

81
Q

Which progestins have strongest antiestrogen effects?

A

norgestimate, desogestrel

82
Q

What are the types of hormonal contraception?

A
  1. combo of estrogens and progestins → typically 21 days on active tablet and 7 days on placebo (to have withdrawal bleeding), can be monophasic, biphasic, triphasic
  2. continuous progestin therapy without estrogen (minipill, norethindrone)
83
Q

What is the delivery of hormonal contraception?

A
  1. mostly oral administration → adherence on administration schedule is more critical for progestin only therapies
  2. implantable (etonogestrel), IUD (levonorgestrel), or depot injection (medroxyprogesterone acetate)
84
Q

What are the effects of oral contraceptives?

A
  1. inhibition of ovulation → combos selectively inhibit pituitary function but progestin only compounds do not always inhibit ovulation
  2. effects of ovaries → ovarian function is suppressed and when discontinued, majority of patients return to normal cycle in 1-2 months
  3. uterus effects → change in cervical mucus and uterine endometrium to decrease the likelihood of contraception and implantation
  4. breast effects (COMBO ONLY) → enlargement and lactation suppression
85
Q

What are the mild effects of oral contraceptives?

A

due to estrogens → nausea, hypertension, edema, breast fullness
due to progestins → increased appetite, fatigue, breast regression

86
Q

What are moderate effects of oral contraceptives?

A
  1. irregularities in menstruation (breakthrough bleeding) → more common in progestin only
  2. weight gain, acne, hirsutism → more common in combo containing androgen like progestins
  3. amenorrhea
87
Q

What are the severe effects of oral contraceptives?

A
  1. venous thromboembolic disease → due to estrogens
  2. myocardial infarction → due to androgenic activity of progestins
  3. can be dangerous in women over 35 who smoke
88
Q

What are drug interactions with contraceptives?

A
  1. other steroids → oral contraceptives may increase blood levels of other steroids by interfering with their metabolism like glucocorticoids
  2. anticonvulsants → induce drug metabolizing enzymes in the liver (ex phenytoin)
  3. antibiotics → induce drug metabolizing enzymes in the liver and increases the rate of metabolism of many other drugs (ex rifampin) + suppress gut flora that participate in enterohepatic recycling (ex tetracyclines)
89
Q

What are emergency contraceptives?

A
  1. effective 99% of time as long as within 72 hours, like OC but stronger dose
  2. types: combination (Ovral, Preven), progestin only (Plan B)
  3. side effects → nausea, vomiting (more common in the combos)
90
Q

What is ulipristal acetate?

A
  1. brand name is Ella
  2. selective progesterone receptor modulator (SPRM)
  3. used as an emergency contraceptive
  4. can be effective up to 5 days of unprotected sex
  5. side effects → nausea, abdominal pain
91
Q

What is mifepristone?

A
  1. RU-486
  2. progesterone antagonist → can terminate pregnancy
  3. abortifacient → used in combo with misoprostol (PGE derivative) for up to 70 days
  4. side effects → nausea, vomiting, bleeding (5%) → requires intervention and administered only by physicians
92
Q

What is danazol?

A
  1. doesn’t belong to a single class → weak androgen, weak antiestrogen, weak progestin
  2. effective for endometriosis → inhibits surges of LH and FSH and suppress ovarian function and causes atrophy of the endometrium
  3. adverse effects → mostly from weak androgenic activity, weight gain, decreased breast size, acne, oily skin, hirsutism
  4. contraindications → hepatic dysfunction, pregnancy and breast feeding

Therapeutics (15 decks)

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