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Human Reproduction > Week 4: Reproductive pharmacology: Estrogens and Progestins > Flashcards

Week 4: Reproductive pharmacology: Estrogens and Progestins Flashcards

1
Q

Antiestrogens: Receptor antagonists

A
  • fulvestrant (full antagonist)
  • Tamoxifen (SERMs)
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2
Q

Antiestrogens: aromatase inhibitors

A

Anastrozole

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3
Q

Antiestrogens: GnRH agonists

A

Danazol

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4
Q

Antiandrogens: receptor antagonists

A

Flutamide

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5
Q

Antiandrogens: 5α-reductase inhibitors

A

Finasteride

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6
Q

Antiandrogens: Synthesis inhibitors

A

Ketoconazole

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7
Q

Antiandrogens: GnRH agonists

A

Combined oral contraceptives

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8
Q

Hypogonadism in girls and women Drugs

A

Estrogen component:

  • Conjugated estrogens
  • Ethinyl estradiol
  • Estrone
  • Estriol

Progestin component:

  • Progesterone
  • Medroxyprogesterone acetate
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9
Q

Drugs for oral hormonal contraceptive

A

Combined

  • Ethinyl estradiol or mestranol + a progestin

Progestin-only

  • Norethindrone or Norgestrel
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10
Q

Drugs for parenteral contraceptive

A
  • Medroxyprogesterone as a depot IM injection
  • Ethinyl estradiol and norelgestromin as a weekly patch
  • Ethinyl estradiol and etonogestrel as a monthly vaginal ring
  • 1-Norgestrel as an intrauterine device (IUD)
  • Etonogestrel as a subcutaneous implant
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11
Q

Drugs for Postcoital contraceptive

A
  • 1-Norgestrel
  • combined oral contraceptive
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12
Q

Drugs for Intractable dysmenorrhea or uterine bleeding

A
  • Conjugated estrogens
  • ethinyl estradiol
  • oral contraceptive
  • GnRH agonist
  • Depot injection of medroxypreogesterone acetate
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13
Q

Drugs for infertility

A
  • Clomiphene
  • hMG and hCG
  • GnRH analogs
  • Progesterone
  • Bromocriptine
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14
Q

Drugs for Abortifacient

A
  • Mifepristone (RU 486) and misoprostol
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15
Q

Drugs for endometriosis

A
  • Oral contraceptive
  • depot injection of medroxyprogesterone acetate
  • GnRH agonist
  • Danazol
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16
Q

Drugs for breast cancer

A
  • Tamoxifen
  • aromatase inhibitors (eg anastrozole)
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17
Q

Drugs for osteoporosis in postmenopausal women

A
  • Conjugated estrogens
  • estradiol
  • raloxifene
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18
Q

Drugs for hypogonadism in boys, men or used as replacement therapy

A
  • Testosterone enanthate or cypionate
  • methyltestosterone
  • Fluoxymesterone
  • Testosterone (patch)
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19
Q

Drugs for Anabolic Protein Synthesis

A
  • Oxandrolene
  • Stanozolol
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20
Q

Drugs for Prostate hyperplasia (benign)

A

Finasteride

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21
Q

Drugs for prostate carcinoma

A
  • GnRH agonist
  • GnRH receptor antagonist
  • Androgen receptor antagonist (eg flutamide)
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22
Q

Drugs for Hirsutism

A
  • Combined oral contraceptive
  • Spironolactone
  • Flutamide
  • GnRH agonist
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23
Q

Clinical uses of estrogens

A
  • Primary hypogonadism in young females
  • Hormone replacement therapy (HRT)
    • Premature ovarian failure
    • Postmenopausal
    • Post-surgical removal of ovaries
  • Suppress ovulation in patients with intractable dysmenorrhea
  • Suppression of ovarian function is used in the treatment of hirsutism and amenorrhea due to excesive secretion of androgens by the ovary
  • Components of hormonal contraceptives
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24
Q

Specific estrogen toxicity in primary hypogonasim

A

in hypogonadal girls, dosage must be adjusted carefully to prevent premature closure of epiphyses of the long bones resulting in short stature

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25
Q

Specific estrogen toxicities when used as HRT

A
  • Estrogen increases the risk of endometrial cancer
    • this effect is prevented by combining estrogen with a progestin
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26
Q

How is the risk of endometrial cancer through estrogen HRT reduced?

A

By combining the estrogen with a progestin

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27
Q

What are the dose-dependent toxicities of estrogen?

A
  • nausea
  • breast tenderness
  • increased risk of migraine headache
  • thromboembolic events (eg deep vein thrombosis (DVT))
  • Gallbladder disease
  • Hypertriglyceridemia
  • hypertension
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28
Q

Antiestrogens: Receptor antagonists

A

Full antagonists

  • Fulvestrant

Selective-estrogen receptor antagonists

  • Tamoxifen
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29
Q

Antiestrogens: Aromatase inhibitors

A

Anastrozole

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30
Q

Antiestrogens: others

A
  • GnRH agonists
  • Danazol
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31
Q

What is Fulvestrant?

A

A pure full estrogen receptor antagonist (in all tissues)

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32
Q

Fulvestrant clinical uses

A

used in the treatment of women with breast cancer that have developed resistance to tamoxifen

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33
Q

SERM AKA

A

Selective Estrogen Receptor Modulators (SERMs)

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34
Q

What are SERMs?

A
  • SERMs are mixed estrogen agonists that have estrogen agonist effects in some tissues and act as partial agonists or antagonists of estrogen in other tissues
  • Interactions of the estrogen receptor with various coregulators appear to be responsible for some of the tissue-specific effects of SERMs
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35
Q

What is Tamoxifen?

A

a Selective Estrogen Receptor Modulator (SERM)

has mixed agonist and antagnoist effects in various tissues

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36
Q

Tamoxifen clinical uses

A
  • effective in the treatment of hormone-responsive breast cancer where it acts as an antagonist
  • Prophylactic treatment of tamoxifen reduces the incidence of breast cancer in women who are at very high risk
  • Has greater agonist effect in bone and thus prevents osteoporosis in postmenopausal women
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37
Q

Tamoxifen side effects

A
  • Works as an agonist on endometrial receptors and thus promotes endometrial hyperplasia and increases the risk of endometrial cancer (agonist effect)
  • Causes hot flushes (antagonist effect)
  • increases the risk of venous thrombosis (agonist effect)
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38
Q

What is Clomiphene?

A

A Selective Estrogen Receptor Modulator (SERM) + is a nonsteroidal compound with tissue-specific actions

has mixed agonist and antagonist effects on the estrogen receptors of various tissues (tissue-dependent)

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39
Q

Clomiphene clinical uses & mechanism

A
  • used to induce ovulation in anovulatory women who wish to become pregnant
    • By selectively blocking estrogen receptors in the pituitary, clomiphene reduces negative-feedback and increases FSH and LH output
    • This increase in gonadotropins stimulates ovulation
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40
Q

Antiestrogens: Aromatase inhibitors

A

Anastrozole

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41
Q

What is anastrozole?

A

A non-steroidal competitive aromatase inhibitor

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42
Q

Anastrozole related compounds

A

Letrozole

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43
Q

What is Letrozole

A

related to anastrozole

A non-steroidal competitive aromatase inhibitor

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44
Q

Anastrozole clinical uses

A

used in the treatment of breast cancer

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45
Q

What is Exemestane?

A

an irreversible aromatase inhibitor unlike Anastrozole which is a competitive inhibitor

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46
Q

Anastrozole & related compounds MOA

A
  • nonsteroidal competitive inhibitors of Aromatase
    • Aromatase is the enzyme required for the last step in estrogen synthesis
  • Exemestane is an irreversible aromatase inhibitor
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47
Q

What is Danazol?

A

Danazol inhibits several cytochrome P450 enzymes involved in gonadal steroid synthesis and is a weak partial agonist of progestin, androgen and glucocorticoid receptors

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48
Q

Danazol clinical uses

A

Sometimes used in the treatment of endometriosis and fibrocystic disease of the breast

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49
Q

What are GnRH analogs?

A

The cotinuous administration of GnRH agonists (eg Leuprolide) suppresses and thereby inhibits ovarian production of estrogens and progesterone

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50
Q

Examples of GnRH analogs

A

Leuprolide

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51
Q

Clinical uses in women of GnRH analogs

what is an example of a GnRH analog?

A

*eg Leuprolide*

GnRH agonists are used in combination with other agents in controlled ovarian hyperstimulation and are also used for treatment of precocious puberty in children and short term (<6 months) treatment of endometriosis and uterine fibroids in women

52
Q

Clinical uses of Progestins

A
  • Hormonal contraception, either alone or in combination with an estrogen
    • the presence of progestin reduces estrogen-induced endometrial cancer
  • Postmenopausal hormone replacement therapy, in combination with Estrogen
  • Progesterone is used in assisted reproductive technology methods to promote and maintain pregnancy
  • Long-term ovarian suppression for other purposes
53
Q

What is the toxicity of Progestins?

A

toxicity of progestins is low, but, they may;

  • increase blood pressure
  • decrease HDL
  • Long-term use of high doses in premenopausal women is associated with a reversible decrease in bone density (a secondary effect of ovarian suppression and decreased ovarian production of Estrogen)
  • delayed resumption of ovulation after termination of therapy
54
Q

What is Mifepristone?

A

an orally active steroid antagonist of progesterone and glucocorticoids

55
Q

Mifepristone clinical uses

A
  • Major use is as an abortifacient in early pregnancy (up to 49 days after the last menstrual period)
  • used with the PGE analog Misoprostol to increase uterine contractions
  • The combination of Mifepristone and Misoprostol achieves a complete abortion in >90% of early pregnancies
56
Q

Pure Mifepristone toxicities

A
  • The most common complication is failure to induce a complete abortion
  • Contraindicated during chronic glucocorticoid therapy due to anti-glucocorticoid activity
57
Q

Mifepristone + Misoprostol side effects

A
  • Most common complication is failure to induce a complete abortion
  • Primarily due to misoprostol = NVD
  • Rarely, patients who use Mifepristone + Misoprostol for medical abortion have experienced serious infection, sepsis and even death due to unusual infection (eg Clostridium sordelli)
  • Contraindicated during chronic glucocorticoid therapy due to anti-glucocorticoid therapy due to synergystic anti-glucocorticoid activity
58
Q

Mifeprestone + Misoprostol contraindications

A
  • Contraindicated during chronic glucocorticoid therapy due to anti-glucocorticoid therapy due to synergystic anti-glucocorticoid activity
  • Rarely, patients who use Mifepristone + Misoprostol for medical abortion have experienced serious infection, sepsis and even death due to unusual infection (eg Clostridium sordelli)
59
Q

Mifepristone MOA in Pregnancy Termination

A
  • Causes decidual breakdown, blastocyst detachment and decreased hCG production
  • Decreased hCG results in decreased progesterone secretion from the corpus luteum, causing futher decidual breakdown
  • Decreased progesterone production and receptor blockade leads to increased prostaglandin levels
    • causes
      • myometrial contractions
      • Cervical softening
60
Q

Describe the menstrual cycle and the hormone levels during the cycle

A
61
Q

What are the various preparations of Oral Contraceptives?

A

two types of preparations

  • Estrogen + Progestin combination
  • continuous progestin w/o co-administration of an estrogen
62
Q

What is the MOA of Oral contraceptives?

A

Primary

  • Prevent ovulation by suppressing LH and FSH secretion by the anterior pituitary: *Negative feedback*
  • Estrogen acts directly on the anterior pituitary on the anterior pituitary to decrease FSH and LH secretion
  • Progestins act on the hypothalamus to decrease GnRH release, which reduces FSH and LH secretion by the anterior pituitary

Secondary

  • Progesterone thickens cervical mucus, acting as a barrier to sperm
  • Reduction in endometrial growth interferes with implantation
  • Slowed uterine tubal motility and ova transport reduce fertilization
63
Q

How do the MOAs of Estrogens and Progestins differ as an Oral Contraceptive?

A
  • Estrogen acts directly on the anterior pituitary on the anterior pituitary to decrease FSH and LH secretion
  • Progestins act on the hypothalamus to decrease GnRH release, which reduces FSH and LH secretion by the anterior pituitary
    Progesterone also thickens the cervical mucus to act as a sperm barrier and also inhibits the endometrium growth and slowed tubal motility resulting in reduced implantation and fertilization respectively but in the wrong order fertiliization would occur first
64
Q

What are the types of combination agents?

A
  • Monophasic
  • Biphasic
  • Triphasic

These attempt to lower total steroid dose and mimic the menstrual cycle

21 vs 28 day packs (inert pills during withdrawal bleed)

Estrogen: Ethinyl estradiol 20-35 ug

Progestin dose varies due to differences in potency

“perfect use” has an effectiveness of 99%

65
Q

What is the effectiveness in preventing pregnancy for “perfect use” of Combination Oral Contraceptives?

A

“perfect use” effectiveness is 99%

66
Q

Adverse effects of Combination Oral contraceptives?

A
  • Incidence of serious adverse effects associated w/ COCs is lower than the incidence of complications associated with pregnancy

Major adverse effects

  • VTE (3-4 fold ↑ compared to those not taking OCs)
  • HTN
  • Lipid effects (↑TG, ↑ cholesterol, ↑ or no change HDL, ↓ LDL)
  • MI
  • CV risks are greatest in smoker > 35 years old

Minor-to-moderate side effects

  • nausea
  • edema
  • HA
  • worsening migraines
  • breakthrough bleeding
  • increased skin pigmentation
  • ↑ skin pigmentation
  • increased incidence of vaginal infections
  • amenorrhea
67
Q

Describe the risk of cancer associated with COCs

A
68
Q

Non-contraceptive benefits of COCs

A
  • 50% ↓ in endometrial cancer risk, benefit lasting 15 years after the COCs are stopped
  • ↓ risk of ovarian cancer
  • ↓ ovarian cysts and fibrocystic disease
  • ↓ iron-deficiency anemia
  • ↓ dysmenorrhea and endometriosis side effects
  • ↓ ectopic pregnancies and pelvic inflammatory disease
69
Q

COCs effect on breast feeding

A
  • Estrogens suppress lactation
  • low dose OCs produce minimal effects on milk production, Low concentrations of OCs are found in breast milk
  • existing low-quality evidence suggests that combined oral contraceptives may reduce the volume of breastmilk but not affect the growth of infants
70
Q

Drug interactions of COCs

A
  • Antibiotics may alter enterohepatic cycling of oral contraceptive metabolites
  • Multiple pharmacokinetic interactions CYP- and uridine 5’-diphosphate glucuronosyltransferase (UGT) catalyzed reactions
  • Ethinyl estradiol is metabolized by CYP3A4 and CYP2C9
  • UGT1A1 is the predominant UGT for Ethinyl Estradiol
  • Most progestogens are substrated for CYP3A4 and some metabolites require glucuronidation
71
Q

Progestin-only OCs AKA

A

often called “minipill”

72
Q

Progestin-only OCs MOA

A
  • GnRH suppression through negative feedback on the hypothalamus is the major mechanism
  • increases the viscosity of cervical mucus, acting as a physical barrier to sperm penetration
  • Rapid first-pass metabolism
  • Same dose taken daily (no inert pills)
73
Q

Progestin-only OCs “perfect use” effectiveness

A

“perfect use” effectiveness for Progestin-only OCs is less than COCs

74
Q

Progestin-only OCs Adverse effects

A
  • Breakthrough bleeding is the most common adverse effect (up to 25% of patients)
  • No evidence of increased VTE
  • May cause more acne
75
Q

Properties of progestational agents

A
76
Q

What are the failure rates for Oral contraceptives vs condoms?

A
77
Q

Transdermal contraception Examples

A

Ortho Evra patch

78
Q

MOA of Transdermal contraception

A
  • Ortho Evra patch
  • Combination estrogen and progestin
  • Ethinyl estradiol and norelgestromin
  • apply to buttock, abdomen, upper arm or torso
  • Changed weekly x3 weeks, then 1 week off for withdrawal bleed
79
Q

Transdermal contraception side effects

A
  • some sensitivites to adhesive have been reported
  • concerns for higher estrogen levels due to no first-pass effect, ↑ risk of VTE
80
Q

Examples of the Contraceptive ring

A

Nuvaring

81
Q

MOA of Contraceptive ring

A

Combination of estrogen and progestin

  • Ethinyl estradiol and etonogestrel
  • 3 weeks in place followed by 1 week off for withdrawal bleed
  • transmucosal absorption
82
Q

Contraceptive ring side effects

A
  • issues with expulsion during sexual intercourse
  • safety profile appears to be the same as with other combined hormonal contraceptives
83
Q

Examples of Contraceptive Subcutaneous implant

A

Etonogestrel (Nexplanon)

84
Q

MOA of Contraceptive Subcutaneous implant

A

Progesterone-only

  • Etonogestrel is a progestin
  • Lasts 3 years
85
Q

Contraceptive Subcutaneous implant side effects

A

possible side effects

  • HA
  • weight gain
  • mood changes
  • acne
  • local infection
  • difficult removal

Irregular vaginal bleeding is the norm and pattern is unpredictable

Use with caution in those w/ history or predisposition to VTE

86
Q

Contraceptive Subcutaneous implant

A
87
Q

Examples of Contraceptive injection

A

Medroxyprogesterone acetate (Depo-Provera)

88
Q

MOA of Contraceptive injection

A
  • Medroxyprogesterone acetate (Depo-Provera)
  • Given IM
  • Lasts 12 weeks
89
Q

Contraceptive injection side effects

A
  • Causes irregular vaginal bleeding and eventual amenorrhea

Other possible side effects

  • HA
  • Mood changes
  • Weight gain
  • ↓ HDL
  • ↑LDL
  • ↓ bone density
  • return to fertility can be delayed

Contraindicated in those w/ history or predispotion to VTE

90
Q

Contraceptive injection Contraindications

A

Contraindicated in those w/ history or predisposition to VTE

91
Q

Examples of hormone-containing intrauterine devices

A

Levonorgestrel (Mirena)

92
Q

MOA hormone-containing intrauterine devices

A
  • Levonorgestrel (Mirena)
  • 5 year effectiveness
  • Local progestin concentration ~1000x higher than systemic levels
  • Thickening of cervical mucus to prevent sperm penetration
  • Inhibits ovulation in some cases
  • Reduced endometrial growth
  • expect spotting for up to 3 months, then light and irregular menses or amenorrhea
93
Q

What is Emergency Contraception?

A

Refers to the use of any drug or device to prevent pregnancy after unprotected intercourse or when contraception has failed

94
Q

Types of progestin-only Emergency contraception

A

Levonorgestrel as Plan B or Plan B one-step

95
Q
A
96
Q

progestin-only Emergency contraception MOA

A

Levonorgestrel plan B

  • Most effective within 72 hours of unprotected sex
  • prevention of ovulation, blocking implantation, increased cervical mucus viscosity
  • available without prescription
97
Q

MOA of Selective progesterone receptor modulators as emergency contraception

A
  • 30 mg single dose
  • inhibits ovulation via inhibition of LH release
  • May block implantation of fertilized egg (uncertain)
  • Effective up to 120 hours after unprotected sex
  • Available by perscription only
  • May be more efficacious than levonorgestrel for overweight (BMI >25 kg/m2) women
98
Q

Selective progesterone receptor modulators as emergency contraception adverse effects

A

self-limited HA and abdominal pain

99
Q

Types of Selective progesterone receptor modulators as emergency contraception

A

Ulipristal acetate (Ella)

100
Q

Considerations of pericoital use of levonorgestrel

A

reasonably efficacious and safe

101
Q

Considerations of Combination estrogen-progesterone Emergency contraception

A
  • Less effective
  • More NV
  • Theoretical concerns of VTE
102
Q

Emergency Contraception hormone-free

A

Copper IUD (Paragard)

  • Most effective: 1% failure rate when inserted up to 5 days after unprotected sex
  • Provides 10 years of contraception
  • Copper is toxic to sperm
  • Copper increases inflammation in the uterus, which reduces sperm viability and reduces endometrial receptivity
103
Q

CDC Contraception guidelines

A
104
Q

Continued CDC Contraception guidelines

A
105
Q

Effectiveness of family plannning methods

A
106
Q

Question 1

A
107
Q

Question 2

A
108
Q

Question 3

A
109
Q

Question 4

A
110
Q

Question 5

A
111
Q

Additional info on the effects of estrogens on LDL and HDL

A
112
Q

The effects of OCs on serum lipid values

A
113
Q

Question 6

A
114
Q

Question 7

A
115
Q

Question 8

A
116
Q

Question 9

A
117
Q

Question 10

A
118
Q

Drugs for Ovulation induction for infertility

A
  • Clomiphene citrate
  • Gonadotropins
  • Human chorionic gonadotropin
  • Progesterone replacement in progesterone deficient women
  • Insulin sensitizers (metformin)
119
Q

Clomiphene citrate clinical uses

A

Ovulation induction for infertility

120
Q

MOA of Clomiphene citrate

A
  • Estrogen antagonist, blocking inhibitory effect on gonadotropin release from pituitary
  • Increases gonadotropin secretion (FSH>LH), stimulating ovulation
121
Q

Adverse effects of Clomiphene citrate

A
  • Ovarian hyperstimulation
  • multiple gestation
  • ovarian cysts
  • HA
  • hot flushes
  • blurry vision
  • luteal phase defect due to inadequate progesterone production
  • increased ovarian cancer risk with prolonged use
122
Q

Drugs for o

A
123
Q

Drugs for ectopic pregnancy management

A
  • Methotrexate
124
Q

MOA of methotrexate for ectopic pregnancy management

A
  • as antimetabolite: folic acid antagonist
  • Disrupts rapidly proliferating trophoblast
  • Used to treat certain types of cancer (for example gestational trophoblastic disease - choriocarcinoma) Psoriasis, RA
  • Can be used to terminate an intrauterine pregnancy, followed by misoprostol to induce uterine contractions, but mostly replaced by mifepristone now
125
Q

Methotrexate clinical uses

A
  • as antimetabolite: Folic acid antagonist
  • Used in medical management of ectopic pregnancy < 3.5 cm, no cardiac activity, hemodynamically stable, can adhere to f/u
    • Management is generally outpatient with frequent follow-up of labs and physical exam
  • Used to treat certain types of cancer (for example gestational trophoblastic disease = choriocarcinoma), psoriasis, RA
126
Q

Adverse effects of methotrexate for ectopic pregnancy management

A
  • Liver damage
  • lung damage
  • damage to the lining of the mouth, stomach or intestines
  • Increased risk of lymphoma
  • serious or life-threatening skin reactions
  • immunosuppression

Human Reproduction (40 decks)

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