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Endo Repro Exam > Reproductive Pharmacology 1 > Flashcards

Reproductive Pharmacology 1 Flashcards

1
Q

roles of endogenous estrogen

A

*development and regulation of female reproductive system and secondary sex characteristics:
1. development of endometrium
2. thin cervical mucus
3. prepare uterine lining for implantation (with progesterone)
4. surge (follicular phase) → release LH → ovulation
5. vaginal lubrication
*also reduces bone resorption & increases blood clotting (platelet adhesion & clotting factors)

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2
Q

exogenous estrogens - examples

A
  1. estradiol (PO, patch, cream, gel, lotion, IM)
  2. ethinyl estradiol (PO, patch, vaginal ring)
  3. mestranol (PO)
  4. conjugated estrogens (PO)
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3
Q

exogenous estrogens - MOA

A

*modulate the pituitary secretion of gonadotropins, LH, and FSH through a negative feedback system
*binds estrogen receptors

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4
Q

exogenous estrogens - ADEs

A

*N/V
*breast tenderness
*headaches
*cyclic weight gain
*dysmenorrhea
*hypertriglyceridemia
*HTN
*VTE
*CVA
*MI

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5
Q

exogenous estrogens - place in therapy

A

*hormonal contraception (estrogen + progesterone)
*menopausal hormone therapy (MHT)
*hormonal therapy for transgender females (male to female)
*amenorrhea
*hypogonadism
*abnormal uterine bleeding
*endometriosis
*osteoporosis - postmenopausal (fallen out of favor)

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6
Q

roles of endogenous progestin

A

*pro-pregnancy (pro-gestation) hormone
*development of endometrium
*thicken cervical mucous
*maintain uterine lining - secretory phase (with estrogen)
*breast developmet

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7
Q

exogenous progestins - examples

A

1st generation: medroxyprogesterone, norethindrone, ethynodiol diacetate, norgestrel
2nd generation: levonogestrel
3rd generation: desogestrel, norgestimate, norelgestromin, etonogestrel
4th generation: drospirenone

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8
Q

exogenous progestins - MOA

A

*modulate the pituitary secretion of gonadotropins, LH, and FSH through a negative feedback system
*bind progesterone receptors, decrease growth and increase vascularization of endometrium, thicken cervical mucus

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9
Q

exogenous progestins - ADEs

A

*increase appetite / weight gain, bloating, acne, oily skin, hirsutism, depression/fatigue (systemic worse), amenorrhea

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10
Q

exogenous progestins - place in therapy

A

*hormonal contraception
*abnormal uterine bleeding
*amenorrhea ?
*dysmenorrhea
*endometriosis-associated pain
*progesterone + estrogen for menopausal hormone therapy (MHT)

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11
Q

progestin activities

A

*1st generation and 2nd generation progestins also have ANDROGEN activity
*3rd and 4th generation progestins do not have androgen activity
*drosperinone has anti-androgen and anti-mineralocorticoid activities

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12
Q

estrogen: contraceptive considerations

A

*primary mechanism: inhibition of FSH → preventing maturation of follicles → preventing ovulation
*potential inhibition of implantation of fertilized egg
*most common uses of estrogen in contraception: ethinyl estradiol or mestranol
-low doses preferred
-low doses can result in decreased libido, early cycle breakthrough bleeding or amenorrhea

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13
Q

contraindications for estrogen use in hormonal contraception

A

*people > 35yo who smoke tobacco
*pts with increased risk of CVD (including hx of VTE, CAD, stroke)
*pts with migraines (esp. with aura)
*hx of breast cancer
*hx of liver disease

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14
Q

progestin: contraceptive considerations

A

*primary mechanism: inhibition of LH → no LH surge → prevention of ovulation
*also thickens cervical mucus
*without estrogen, consistent timing of dosing is extremely important for efficacy

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15
Q

contraindications for progestin use in hormonal contraception

A

*recommended against using in women with uncontrolled dyslipidemia or current breast cancer
*safe to use in pts with diabetes, if without other risk factors or complications

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16
Q

emergency contraception: levonorgestrel (PO) - MOA

A

*brand name = plan B
*MOA: delay ovulation/thicken cervical mucus → prevent fertilization, may impair implantation

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17
Q

emergency contraception: levonorgestrel (PO) - advantages

A

*up to 72 hours after unprotected sex
*over-the-counter
*94% effective at 24h
*89% effective at 72h

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18
Q

emergency contraception: levonorgestrel (PO) - disadvantages

A

*less effective for women with BMI > 25
*may not work for women with BMI > 30

19
Q

emergency contraception: ulipristol - MOA

A

*brand name = Ella
*MOA: progestin receptor modulator (anti-progestin) → prevent or delay ovulation, prevent fertilization, and may impair implantation

20
Q

emergency contraception: ulipristol - advantages

A

*up to 5 days after unprotected sex (equal efficacy)
*effective in overweight/obese women

21
Q

emergency contraception: ulipristol - disadvantages

A

*less effective for BMI over 35
*PRESCRIPTION REQUIRED
*affects efficacy of hormonal contraception
*category X (requires a negative pregnancy)

22
Q

emergency contraception: levonorgestrel IUD - MOA

A

*thicken cervical mucus → prevent fertilization, may impair implantation

23
Q

emergency contraception: levonorgestrel IUD - advantages

A

*up to 5 days after unprotected sex (equal efficacy)
*99.9% effective
*provides contraception for years
*effective for all weight patients

24
Q

emergency contraception: levonorgestrel IUD - disadvantages

A

*inserted by provider

25
Q

emergency contraception: copper IUD - MOA

A

*prevention of fertilization and implantation

26
Q

emergency contraception: copper IUD - advantages

A

*up to 5 days after unprotected sex (equal efficacy)
*99.9% effective
*provides contraception for up to 12 years
*effective for all weight patients

27
Q

emergency contraception: copper IUD - disadvantages

A

*inserted by provider
*cramping/bleeding

28
Q

menopausal hormone therapy (MHT) - overview

A

*conjugated estrogens preferred; lower equivalent dosing than required for contraception
*use with progestin in patients with a uterus to reduce risk of endometrial cancer

29
Q

menopausal hormone therapy (MHT) - recommendations

A

*recommended for:
-reduction of vasomotor symptoms (estrogen most effective)
-mood lability/depression (often combined with an antidepressant like SSRI)
-urogenital atrophy/vaginal dryness (local therapy preferred if without other menopause symptoms)

*no longer recommended for prevention of bone fractures of CHD

30
Q

menopausal hormone therapy (MHT) - contraindications

A

*not recommended for women with:
-breast cancer
-coronary heart disease
-previous VTE or stroke
-liver disease

31
Q

full estrogen receptor antagonist: fulvestrant

A

*MOA: competitively binds to estrogen receptors on tumors and other tissue targets → dose-related down-regulation of estrogen receptors → inhibition of tumor growth
*ADEs: fatigue, GI upset, hot flashes, hepatic dysfunction, arthralgia, headache (menopausal symptoms)
*place in therapy: **breast cancer (advanced, hormone-receptor POSITIVE, HER2 negative)

32
Q

selective estrogen receptor modulators (SERMS) - examples

A
  1. raloxifene
  2. tamoxifen
33
Q

selective estrogen receptor modulators (SERMS) - MOA

A

*competitively binds to estrogen receptors on tumors and other tissue targets and exerts selective agonistic / antagonistic activity

*recall: raloxifene & tamoxifen are examples of SERMs

34
Q

selective estrogen receptor modulators (SERMS) - ADEs

A

*peripheral edema, hot flashes, VTE, arthralgia, leg cramps, dyslipidemia, endometrial cancer (tamoxifen), mood changes

*recall: raloxifene & tamoxifen are examples of SERMs

35
Q

selective estrogen receptor modulators (SERMS) - place in therapy

A

*estrogen receptor-positive breast cancer (esp. tamoxifen)
*postmenopausal osteoporosis treatment and prevention (3rd line - raloxifene)

*recall: raloxifene & tamoxifen are examples of SERMs

36
Q

aromatase inhibitors - examples

A
  1. letrozole
  2. anastrozole
  3. exemestane
37
Q

aromatase inhibitors - MOA

A

*inhibition of the aromatase enzyme (ovaries) and reduction in conversion of androstenedione to estrone and testosterone to estradiol → reduction in plasma estrogen:
-in breast cancer: → decreased tumor mass and delayed progression
-in infertility: → decreased estrogen feedback → increases FSH to stimulate follicle maturation

38
Q

aromatase inhibitors - ADEs

A

*edema, HA, dyslipidemia, hot flashes, GI upset, arthralgia/arthritis/bone pain, osteoporosis, VTE, mood changes, ischemic heart disease / HTN

39
Q

aromatase inhibitors - place in therapy

A

*estrogen receptor-positive breast cancer (postmenopausal)
*delayed puberty
*short stature (males)
*anovulatory infertility

40
Q

SERM/ovulation stimulator: clomiphene - MOA

A

*occupies estrogen receptors at the hypothalamus → interferes with receptor recycling and inhibits negative feedback → hypothalamic release of GnRH → pituitary release of FSH/LH → ovarian follicle growth

41
Q

SERM/ovulation stimulator: clomiphene - ADEs

A

*hot flashes, breast discomfort, mood changes, vaginal dryness, headaches, GI upset, ovarian enlargement, visual disturbances
*INITIALLY, ANTIESTROGEN EFFECTS, followed by ESTROGEN EFFECTS

42
Q

SERM/ovulation stimulator: clomiphene - place in therapy

A

*ovulation induction in anovulatory infertility (normogonadotropic normoestrogenic)

43
Q

options for treating anovulatory infertility

A
  1. clomiphene:
    -most effective for WHO class 2 (normogonadotropic normoestrogenic)
    -use on start of 5th day of cycle for 5 days
  2. letrozole:
    -most effective for WHO class 2
    -take on days 3-7 of cycle
    -advantages: often works in women with fail clomiphene (esp. in pts with PCOS)

Endo Repro Exam (56 decks)

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