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Pharm Exam 5 > Estrogens and Progestins > Flashcards

Estrogens and Progestins Flashcards

1
Q

Steroidogenesis in the ovary

-what cell types and what do they produce and do?

A

1) theca cell:
- Stimulated by LH to produce testosterone and androstenedione from cholesterol
2) Granulosa cell
- stimulated by FSH to convert testosterone and androstenedione to estrenone and estradiol by aromatase

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2
Q

Hypothalamic-Pituitary gonadal axis - feedback regulation:

  • what hormones
  • how?
A

-estrogen and progesterone have both pos and neg effect

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3
Q

Menstrual cycle:

  • phases?
  • which hormonses involved?
A

1) Follicular phase
- high frequency, low amplitude LH secretion
- ESTROGEN rises-controls endometrial proliferation
2) Ovulation (day 14)
- estrogen induced gonaotropin surge (Surge of FSH and LH due to high estrogen) LH IS REQUIRED FOR OVULATION
3) Luteal Phase
- FSH AND LH DROP
- INHIBIN A and B RISE
- rise in estrogens and progesterone
* *-endometrial differentiation under control of progesterone**
4) No implantation-steroidogenesis is not maintained and endometrial lining is shed

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4
Q

Rise in body temp due to what hormone?

A

progesterone

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5
Q

Steroid-Estrogen MOA?

A

-endogenous steroid bind intracellular receptors and modulate transcriptional activity

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6
Q

Estrogen vs progesterone:

-effect on endometrium?

A

E=proliferation

P=differentiation/prepare for implantation, decrease uterine contractions

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7
Q

Estrogen vs progesterone:

Metabolic effects:

A

E=LIPIDS- dec LDL, Inc HDL inc triglyc (CARDIO PROTECTIVE); BONE-antiresorptive (MAINTAIN BONE DENSITY); LIVER-inc plasma proteins; BLOOD-inc coa factor, dec antithrombin

P=LIPIDS-inc LDL, in fat deposition; GLUCOSE-inc fasting glucose levels

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8
Q

Estrogen vs progesterone:

development:

A

E&P=ovaries, fall tubes, uterus, vagina, breasts

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9
Q

Estrogen vs progesterone:

menstrual cycle-

A

E=key regulator during follicular phase

P=key regulator during luteal chase

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10
Q

Estrogen vs progesterone:

uterus smooth muscle

A

E=NONE

P=dec uterine contractions, dec prostaglandin production, maintina relaxin secretion

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11
Q

Estrogen vs progesterone:

cervical glands

A

E=NONE

P=inc cervical mucous viscosity

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12
Q

Which hormone appears to be cardio protective?

A

estrogen

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13
Q

Inc in blood glucose with which hormone?

A

progesterone

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14
Q

Which hormone decreases prostaglandin production? What does this mean for the uterus?

A
  • Progesterone

- Prostaglandins CONTRACT muscle so by dec levels we are relaxing the uterus muscles

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15
Q

steroidal naturals:

A
  • estradiol
  • estrone
  • estriol
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16
Q

steroidal synthetics:

A
  • ethinyl estradiol

- mestranol

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17
Q

Nonsteroidal synthetic:

A

diethylstilbestrol

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18
Q

benefit of steroidal synthetics compared to naturals?

A

naturals have t.5 of minutes while the synthetics have t.5 of 13-27 hrs.

sturctural alteration = SIGNIFICANTLY LESS LIVER METABOLISM

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19
Q

Conjugated equine estrogen

  • type?
  • solubility?
  • benefit to use?
A
  • estrogen prep
  • natural water-soluble estrogen sulfates
  • need mcuh LESS equine than ethinyl estradiol
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20
Q

Ethinyl estradiol

  • type?
  • -use?
A
  • synthetic steroid estrogen
  • contraception
  • need much less of these synthetics than the naturals
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21
Q

Mestranol

  • type?
  • use?
A
  • synthetic steroid estrogen
  • contraception
  • need much less of these synthetics than the naturals
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22
Q

Diethylstilbestrol (DES)

  • type
  • use?
A
  • first synthetic non-steroidal estrogen

- not used much

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23
Q

Uses of estrogen:

A

1) hypogonadism-promote dev of female sex organs
2) hormone replacement therapy (HRT) - maintain bone density, suppress hot flashes, suppress urogenital atrophy (NEGATIVE FEEDBACK ON PIT AND HYPOTHAL
3) contraception - negative feedback on HPG axis = prevent LH surge = inh ovulation
4) Acne treatment-suppress steroidogenesis which cause acne produced by theca cells - so we are blocking LH hormone which stimuates theca cells; INC sex hormone binding globulin (SHBG) production by the liver=less free testosterone concentrations

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24
Q

*Key results of womens health initiative studies (estrogen + progestin)?

A

1) INC risk of coronary heart disease
2) INC risk of stroke
3) INC risk of pulmonary embolism
4) INC risk of invasive breast cancer
5) DEC risk of colorectal cancer
6) DEC risk of hip fracture

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25
Q

Key physiological effects of estrogens:

A
  • breast tenderness
  • endometrial hyperplasia
  • inc blood coagulation
  • nausea
  • cholestasis-changes in cholesterol secretion into bile, bile canaliculi function
  • migraine-sign of altered blood coag
  • cancer- beast or endometrial
  • bloating-loss of intravascular fluid
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26
Q

Adverse effects of HRT combo therapy:

A

1) inc risk of invasive breast cancer

2) likely due to progestin not estrogen

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27
Q

Adverse effects of HRT estrogen monotherapy:

A

1) inc risk for endometrial cancer

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28
Q

Adverse effects of contrceptive therapy;

A

1) reduced risk of ovarian and endometrial cancer

2) breast cancer (dose has changed so its hard to tell- low dose seems to show no risk but high dose shows risk)

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29
Q

Estrogen and cancer MOA

A

1) trophic effects of hormones

2) reactive oxygen species production during metabolism

30
Q

When can you give estrogen therapy monotherapy?

A

-ONLY if woman has had a total hysterectomy

31
Q

Progestins

-what is the parent steroid and what progestin is made from it?

A
  • Progesterone–> medroxyprogesterone acetate (MPA)

- 19-nortestosterone –> nerethindrone

32
Q

Medryoxyprogesterone (MPA)

  • what type?
  • how used?
  • used for what purpose?
A
  • progesterone family
  • combined with estrogen for HRT
  • long acting contraceptive
33
Q

Norethindrone

  • what type?
  • how used?
  • used for what purpose?
A
  • 19-nortestosterone deriv

- combined OR progestin only horomone contraceptive

34
Q

Norgestrel

  • what type?
  • how used?
  • used for what purpose?
A
  • 19-nortestosterone deriv

- combo or progestin only hormone contraceptive

35
Q

What is the problem with 19-nor compounds?

A

-they also have affinity for androgen receptors

36
Q

Uses of progestins

A

1) contraceptive - ALONE or combo with estrogen (inh ovulation and inc cervical mucous viscosisty)
2) Hormone replacement therapy - dec risk of endometrial hyperplasia caused by estrogens
3) Dysmenorrhea -
- dec endometrial mass
- dec prostaglandin production
4) endometriosis
- dec endometrial proliferation by regulating ER expression and stimulaing differentiation of endometrial cells

37
Q

why dont we usually give progestins alone for contraception even though we could?

A

-progestins alone have a lower success rate of preventing contraception compared to progestins +estrogens

38
Q

Adverse effects of progestins:

A
  • breakthrough bleeding-changes in endometrial vasculature
  • impaired glucose tolerance (hyperglycemia)
  • changes in lipid metabolism (atherosclerosis)
39
Q

Important AE of 19-Nor compounds:

A

Acne

hirsutism

40
Q

Oral pill birth control

  • which hormones?
  • treatment duration?
  • MOA?
A

1) -estrogens & progesterone
- progestins alone
2) Monthly, quarterly, yearly
3) -suppress LH and FSH surge
- alter cervical mucus
- alter endometrium

41
Q

Injectable birth control

  • which hormones?
  • treatment duration?
  • MOA?
A

1) -estrogens & progesterone
- progestins alone
2) monthly or quarterly
3) -suppress LH and FSH surge
- alter cervical mucus
- alter endometrium

42
Q

Implantable birth control

  • which hormones?
  • treatment duration?
  • MOA?
A

1) progestins alone
2) 5 years or 3 years
3) -suppress LH and FSH surge
- alter cervical mucus
- alter endometrium

43
Q

Intrauterine device (IUD) birth control

  • which hormones?
  • treatment duration?
  • MOA?
A

1) Progestins alone
- COPPER
2) 5 years
3) -suppress LH and FSH surge
- alter cervical mucus
- alter endometrium

44
Q

transdermal birth control

  • which hormones?
  • treatment duration?
  • MOA?
A

1) Estrogens & progestins
2) monthly
3) -suppress LH and FSH surge
- alter cervical mucus
- alter endometrium

45
Q

Vaginal ring birth control

  • which hormones?
  • treatment duration?
  • MOA?
A

1) estrogens and progestins
2) monthyl
3) -suppress LH and FSH surge
- alter cervical mucus
- alter endometrium

46
Q

What drug is depo-provera?

A

medroxyprogesterone - IM injection

47
Q

Oral contraceptives are what drugs?

A

-combo estrogen and progestin
OR
-progestin only

48
Q

Injectable contraceptives are what drugs?

A

-progestin only

49
Q

What is the key to success with emergency contraceptives?

A

HIGH DOSE but MOA is unknown

50
Q

Hormone contraceptive- MILD adverse effects:

A
  • nausea
  • mastalgia
  • breakthrough bleeding (estrogen)
  • edema
  • headache
  • withdrawal bleed failure
  • serum protein changes
51
Q

Hormone contraceptive- MODERATE adverse effects:

A
  • breakthrough bleeding (Progestin) - fragile vasculature
  • weight gain
  • inc skin pigmentation
  • acne
  • hirsutism (19-nor effects)
  • vaginal infections
  • amenorrhea
52
Q

Hormone contraceptive- SEVERE adverse effects:

A
  • thromboembolic disease
  • MI
  • cerebrovascular disease
  • GI disorders (cholestasis)
  • depression
  • cancer (high dose issue)
53
Q

Non-contraceptive benefits to using hormone birth control:

A

1) reduced risk of ovarian and endometrial cancer
2) reduction in dysmenorrhea, endometriosis
3) dec incidence of ectopic pregnancy
4) dec incidence of benign breast disease
5) inc hemoglobin concentrations
6) suppress acne and hirsutism

54
Q

Contraindications of estrogen containing contraceptives:

A

1) known or suspected breast cancer or cancer of reproductive tract
2) thromboembolic disorders
3) liver disease
4) Hx of MI, CAD, hyperlipidemia (CV disease)
5) smokers 35 yr old +

55
Q

Interactions of birth control:

A

1) inc metabolism=
- HIV agents -
- anticonvulsants
- St johns wort
2) antibiotics lower contraceptive effectiveness-knock out gut flora=inc estrogen excretion

56
Q

Clomiphene

  • type?
  • MOA?
  • use?
  • AE?
A
  • estrogen receptor partial agonist (reduce inhibitor effects of estrogen with partial agonist)
  • fertility drug - if its due to low levels of FSH and LH -used 5 days prior to day 14 ovulation
  • multiple births
  • hot flashes
  • ovary enlargement
  • blurred vision
57
Q

SERMS-selective estrogen receptor modulators

-Actions in tissues?

A

depends on the tissue- either agonist (inc estrogenic transcription), partial agonist, or antagonist (complete transcriptional block of estrogen)

58
Q

SERMS - effect on bone?

A

-agonist activity = suppress resorption

59
Q

SERMS - effect on endometrium?

A

-partial agonist - proliferation but not to same extent as estrogen would

60
Q

SERMS - effect on Pituitary and breast?

A
  • antagonist -
  • pit=hot flashes
  • breast=inh proliferation
61
Q

SERMS - name the drugs:

A
  • tamoxifen

- raloxifene

62
Q

Tamoxifen

1) MOA?
2) USE?
3) AE?

A

1) -agonist- bone
- partial agonist - endometrium
- antagonist-breast/ HPG axis
2) Estrogen Receptor positive BREAST CA
3) -hot flashes
- endometrial CA
- nausea
- vomting

63
Q

Raloxifene

1) MOA?
2) USE?
3) AE?

A

1) -agonist- bone
- partial agonist - none really (lower risk for endometrial cancer)
- antagonist-breast/uterus/HPG axis
2) -CA
- postmenopausal bone loss
3) -Hot flashes
- nausea
- vomit

64
Q

Which SERMS drug has lower risk for endometrial cancer?

A

Raloxifene lower risk

Tamoxifen has more risk

65
Q

Which SERMS drug is good for postmenopausal bone loss?

A

raloxifene

66
Q

Danazol

  • type?
  • MOA?
  • uses?
  • AE?
A

1&2) inhibition of estrogen - inh gonadal function (displacing steroids from plasma proteins = inc clearance)

3) -endometriosis
- breast fibrocystic disease
4) -WG
- edema
- oily skin
- acne
- hirsutism
- hot flashes

67
Q

Anastrozole and letrozole

1) type
2) mOA?
3) use?
4) AE?s

A

1) inh of estrogen
2) aromatase inh
3) breast cancer
4) -GI disturbances
- hot flashes
- lethargy

68
Q

Anti-progesterone drugs:

A
  • abortifacient - Mifepristone

- emergency contraceptive - Ulipristal

69
Q

Mifepristone

1) type?
2) MOA?
3) Dosing?

A

1) ant-progesterone or progesterone receptor modulators or abortifacient
2) Antagonist
3) less than 7 weeks= 1 dose and dose of misoprostol 48hrs later

70
Q

Ulipristal

1) type?
2) MOA?
3) Dosing?

A

1) ant-progesterone or progesterone receptor modulators or emergency contraceptive
2) Partial agonist
3) longer acting up to 5 days after sex

71
Q

Anti-progesterone MOA?

A

1) inh progesterone receptors
2) induce uterine contractions
3) shed lining of uterus
4) open cervix

72
Q

Anti-progesterone other uses:

A
  • contraceptive=distrupt ovulation
  • anticancer - breast or endometrial
  • induce delivery after fetal death
  • induce labor at end of 3rd trimester

Pharm Exam 5 (10 decks)

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