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Reproductive > Female Reproductive Hormones > Flashcards

Female Reproductive Hormones Flashcards

1
Q

Disruptions to the Hypothalamic-Pituitary Reproductive Axis in Females (2)

A
  1. PCOS

2. Prolactinomas

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2
Q

PCOS (polycystic ovarian syndrome) Pathophysiology and Treatment

A

Pathophysiology:

  • Increase in LH secretion
  • Increased androgen secretion (compared to estrogen)
  • Results in masculine characteristics: male-pattern baldness and inappropriate facial hair growth
  • Suppression of normal ovulatory cycles

Treatment:

  1. Lifestyle modification – diet and exercise in overweight women to reduce diabetes mellitus risk and restore ovulatory cycles
  2. Hormonal contraceptives treat anovulation
  3. Insulin-sensitizing agents, e.g. metformin, are associated with improved ovulation rate
  4. Estrogen-modulating medications are used to INDUCE ovulation such as letrozole or clomiphene citrate
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3
Q

Female Reproductive Agent - Clomiphene Citrate (MOA, PK, Pregnancy, Indications)

A

MOA: Nonsteroidal ovulatory stimulant that acts as a competitive estrogen receptor antagonist and these anti-estrogenic properties may contribute to initiation of ovulation

PK: Dosed orally QD

Pregnancy: X

Indications: Female infertility due to ovulation disorder, male hypogonadism

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4
Q

Female Reproductive Agent - Clomiphene Citrate (ADRs and Considerations)

A

ADRs:
Common - Nausea, vomiting, flushing, breast pain, visual disturbance
Serious - hyperstimulation of ovaries, acute pancreatitis, loss of vision

Considerations: Pregnancy test should be preformed prior to treatment to avoid inadvertent administration during early pregnancy. A pelvic examine should be done before treatments to check for ovarian enlargement or ovarian cyst formation. Check plasma triglycerides prior to treatment because drug can raise these levels.

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5
Q

Prolactinomas Pathophysiology and Treatment

A

Pathophysiology: Tumors of lactotrophs of anterior pituitary gland.

  • Increases prolactin levels which suppress estrogen synthesis
  • Antagonizes GnRH release
  • Decreasing gonadotroph sensitivity to GnRH
  • Decrease in LH and FSH release
  • Crowding-out effect: Lactotroph proliferation in anterior pituitary gland leads to crowding and inhibits gonadotroph cell function

Treatment:

  • Lower prolactin levels by using a dopamine agonist, e.g. cabergoline, bromocriptine
  • Surgery, Radiation, Chemotherapy
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6
Q

Dopamine Receptor Agonists - Cabergoline, Bromocriptine (MOA, PK, Pregnancy, Indications, ADRs, and Considerations)

A

MOA: Inhibits prolactin release from the pituitary

PK: Carbergoline 2x per week. Bromocriptine 2x per day.

Pregnancy: B

Indications: Hyperprolactinemia

ADRs:
Common - nausea, dizziness, headache
Serious - heart failure, heart valve disorder, pulmonary fibrosis

Considerations: Bromocriptine causes a FIRST-DOSE phenomenon in 1% of patients and may result in SYNCOPE. Cabergoline should be used with CAUTION in patients with ARRHYTHMIAS and with underlying psychiatric disorders.

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7
Q

GnRH Agonists (pulsatile)/Antagonists (continuous): Leuprolide + —relins

A

*See Male Reproductive Hormones!

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8
Q

GnRH Receptor Antagonists: —relixs

A

*See Male Reproductive Hormones!

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9
Q

Which enzyme converts androgens to estrogens?

A

Aromatase

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10
Q

Aromatase Inhibitors: Anastrozole, Letrozole, Exemestane, Formestane (—trozole/—mestane) - MOA, PK, Pregnancy, Indications

A

MOA: Anastrozole and letrozole are competitive inhibitors of aromatase, the enzyme that catalyzes the formation of estrogens from androgen precursors. Exemestane and formestane are irreversible inhibitors of aromatase.

PK: Administered orally once daily

Pregnancy: X

Indications: Treatment and prevention of ER-positive breast cancer, polycystic ovary syndrome (PCOS)

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11
Q

Aromatase Inhibitors: Anastrozole, Letrozole, Exemestane, Formestane (—trozole/—mestane) - ADRs and Considerations

A

ADRs:
Common - Hypertension, peripheral edema, rash, nausea, diarrhea, arthralgia, bone pain, headache, depression
Serious - Thromboembolic disorders (DVT, PE), osteoporotic fractures, hepatitis, profuse vaginal bleeding, increased risk of neoplasm

Considerations: Elevated serum cholesterol has been reported; consider monitoring. May increase risk for ischemic cardiovascular events; consider risk verse benefit. Should not be taken with tamoxifen or estrogen-containing therapies.

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12
Q

SERM (selective estrogen receptor modulators) Agents (3)

A

MOAs: Compounds that bind to the estrogen receptor and have tissue-selective effects. Depending on tissue, a SERM acts as an estrogen agonist or an antagonist: retain estrogen beneficial effects and eliminate undesirable effects

  1. Tamoxifen - AGONIST of the brain, vasculature, bone, and uterus; ANTAGONIST of at the breast
  2. Raloxifene - AGONIST of the vasculature and bone; ANTAGONIST of the breast and uterus; no data on the brain
  3. Bazedoxifene - AGONIST of the vasculature and bone; ANTAGONIST of the breast and uterus; no data on the brain
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13
Q

SERMs (Tamoxifen, Raloxifene, Bazedoxifene, Ospemifene, Clomiphene) - MOA, PK, Pregnancy, Indications

A

MOA: Estrogen antagonist is some tissues and estrogen agonist in other tissues. The basis for tissue selectivity may be related to tissue-specific expression of estrogen receptor subtypes and the differential ability of the ligand-receptor complex to recruit transcriptional coactivators and corepressors.

PK: Administered orally once daily, tamoxifen is a prodrug activated by CYP2D6.

Pregnancy: D

Indications: Prevention of breast cancer, menopausal hot flashes, prevention of postmenopausal osteoporosis, induction of ovulation (clomiphene)

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14
Q

SERMs (Tamoxifen, Raloxifene, Bazedoxifene, Ospemifene, Clomiphene) - ADRs and Considerations

A

ADRs:
Common - Vaginal discharge headaches, flushing, breast pain, visual disturbances, multiple births, ovarian enlargement
Serious - Thromboembolic disorders (DVT, PE), increased risk of neoplasm

Considerations: Refer to chart to determine agonist/antagonist estrogen effects for agents.

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15
Q

Androgen Receptor Antagonists: Ketoconazole and Spironolactone - MOA, PK, Pregnancy, Indications, ADRs

A

MOA: Competitively inhibit binding of androgen to androgen receptor. Blocks the action of testosterone and dihydrotestosterone (DHT) on target tissues

PK: Food increases spironolactone bioavailability

Pregnancy: C

Indications: polycystic ovarian syndrome (PCOS), hirsutism, acne

ADRs: amenorrhea, gynecomastia, liver toxicity

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16
Q

2 Classes of Female Contraception and MOA

A
  1. Estrogen/progestin combinations
  2. Progestin-only contraception

MOA: Inhibit ovulation

  • Suppressing GnRH, LH, FSH release
  • Inhibit follicular development
17
Q

Pathophysiology of Ovulation

A

Ovulation: Rupture of mature follicle

  • Ovarian follicles mature when stimulated by FSH and LH
  • Decrease in estrogen before LH surge
  • LH surge causes ovulation to occur
18
Q

Estrogen-Progestin Combination Contraception MOA and Effects (4)

A
  1. Taken together >99% effective
  2. Primary MOA
    - Suppress GnRH, LH, FSH release
    - Inhibit follicular development
  3. Secondary MOA: Inhibit pregnancy
    - Decreased tubal peristalsis
    - Endometrial receptivity is decreased due to low endometrial layer development
    - Cervical mucus secretions are thicker which impedes sperm transport
  4. Do not protect from sexual transmitted infections
    - Patients need to use barrier methods for STI protection
19
Q

Estrogen-Progestin Combination Formulations (3)

A
  1. Monophasic pills – same amount of estrogen and progestin for 21 days, followed by a 7-day placebo phase
  2. Multiphasic pills – variable amounts of estrogen and progestin for 21 days, followed by a 7-day placebo phase
    - Biphasic pills – Same amount of estrogen each day, but the level of progestin is increased about halfway through the pill cycle
    - Triphasic pills – Three different doses of hormones so the hormone combination changes approximately every seen days throughout the pill pack. Depending on the brand the amount of estrogen may change as well as the amount of progestin.
  3. Extended-cycle pills – same amount of estrogen and progestin for 84 days, followed by a 7-day placebo phase, resulting in four menstrual cycle per year
20
Q

Estrogen-Progestin Combination Agonist Contraception (Estrogens: Ethinyl estradiol, Mestranol; Progestins: Norgestrel, Levonorgestrel, Norethindrone, Ethynodiol, Norgestimate, Gestodene, Desogestrel, Drospirenone) MOA, PK, Pregnancy, Indications

A

MOA: Suppress GnRH, LH and FSH secretion and follicular development, thereby inhibiting ovulation. Secondary mechanisms of pregnancy prevention include alterations in tubal peristalsis, endometrial receptivity, and cervical mucus secretions.

PK: Oral preparations are taken once daily

Pregnancy: Little or no increased risk of birth defects when combination oral contraceptives were inadvertently used during early pregnancy. Use should be stopped during pregnancy.

Indications: Contraception, dysfunctional uterine bleeding, endometriosis

21
Q

Estrogen-Progestin Combination Agonist Contraception (Estrogens: Ethinyl estradiol, Mestranol; Progestins: Norgestrel, Levonorgestrel, Norethindrone, Ethynodiol, Norgestimate, Gestodene, Desogestrel, Drospirenone) ADRs and Considerations

A

ADRs:
Common - Nausea, abnormal menstruation, break through bleeding, breast tenderness, bloating symptoms, migraine, weight gain
Serious - Thromboembolic disorders (DVT, PE), increased risk of neoplasm, ectopic pregnancy

Considerations: Adherence is important to maintain efficacy and patients who have difficulty taking oral medications daily may benefit from a vaginal ring or a transdermal patch. Combination oral contraception can increase: (1) Blood pressure, (2) Risk of MI, stroke, breast cancer, (3) LDL levels, and (4) Blood clots. Consider risk verse benefit. Postpartum use of combination hormone contraception should be avoided because of mother’s hypercoagulability and the effects on lactation; if contraception is required, then progestin-only contraceptive methods may be acceptable alternatives.

22
Q

Progestin-only Contraception MOA and Effects (6)

A
  1. “Mini-pill”
  2. 96% to 98% effective
  3. Primary MOA
    - Alters the frequency of GnRH release
    - Decrease pituitary gland response to GnRH
  4. Secondary MOA: Inhibit pregnancy
    - Decreased tubal peristalsis
    - Endometrial receptivity is decreased due to low endometrial layer development
    - Cervical mucus secretions are thicker which impedes sperm transport
  5. Do not protect from sexual transmitted infections
    - Patients need to use barrier methods for STI protection
  6. Can be used in postpartum women
23
Q

Progestin Contraception (Norethindrone, Desogestrel, Medroxyprogesterone acetate [injectable], Etonogestrel [silastic implant]) - MOA, PK, Pregnancy, Indications

A

MOA: Alter frequency of GnRH pulsing and decrease anterior pituitary gland responsiveness to GnRH. Secondary mechanisms of pregnancy prevention include alterations in tubal peristalsis, endometrial receptivity, and cervical mucus secretions, which together prevent the proper transport of both egg and sperm.

PK: Oral preparations are taken once daily

Pregnancy: Little or no increased risk of birth defects when combination oral contraceptives were inadvertently used during early pregnancy. Use should be stopped during pregnancy.

Indications: Contraception, dysfunctional uterine bleeding, endometriosis

24
Q

Progestin Contraception (Norethindrone, Desogestrel, Medroxyprogesterone acetate [injectable], Etonogestrel [silastic implant]) - ADRs and Considerations

A

ADRs:
Common - Nausea, abnormal menstruation, breast tenderness, weight gain, depression, decreased bone mineral density, acne, fluid retention
Serious - Thromboembolic disorders (DVT, PE), hypertension, increased risk of neoplasm, ectopic pregnancy

Considerations: Progestin-only oral contraceptives must be taken every day at approximately the same time to maintain efficacy. If the dose is more than 3 hours late, patients should use a backup method of contraception for 48 hours. Progestin-only therapy is associated with irregular and unpredictable menstrual bleeding. Increased risk of ectopic pregnancy because mini-pill may not block ovulation. Can increase: (1) Blood pressure, (2) Risk of MI, stroke, breast cancer, (3) liver disease, and (4) Blood clots. Consider risk verse benefit. If contraception is required postpartum, then progestin-only contraceptive methods may be acceptable alternatives.

25
Q

Emergency (“Morning-after”) Contraception (2)

A
  1. Levonorgestrel – over the counter
    - Take between 3 to 5 days after having unprotected sex
    - Potent progestin: Blocks LH surge, disrupts normal ovulation, changes endometrial tissue to prevent implantation
    - ADRs: nausea, abnormal menstruation, breast tenderness
  2. Ulipristal acetate — by prescription
    - Take up to 5 days after having unprotected sex
    - Synthetic progesterone antagonist: Disrupts normal ovulation, changes endometrial tissue to prevent implantation
    - ADRs: abdominal pain, nausea, headache
26
Q

Menopausal Hormone Replacement Therapy (3)

A
  1. Most effective for alleviating moderate to severe vasomotor symptoms (hot flashes)
    - Women with intact uterus use estrogen plus progestogen or SERM to prevent endometrial hyperplasia
    - Women who have undergone a hysterectomy use estrogen only therapy
  2. Mild vulvovaginal symptoms can be managed with lubricants and moisturizers, but severe symptoms may require vaginal estrogen therapy (cream, suppository, or ring)
  3. For each patient need to weigh risk verses benefit because Women’s Health Initiative trial discovered HRT increased the incidence of coronary heart disease, invasive breast cancer, stroke, pulmonary embolism, endometrial cancer, and hip fracture
    - Recommend the lowest dose for the shortest duration of time to adequately manage menopausal symptoms

Reproductive (6 decks)

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