EXAM #5: ESTROGENS & PROGESTINS Flashcards Preview

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Flashcards in EXAM #5: ESTROGENS & PROGESTINS Deck (42):

What regulates steroidogenesis in the ovary?

Gonadotropins (LH and FSH)


What cells are required for estrogen synthesis in the ovary?

Theca and granulosa cells


What is the two-cell hypothesis in steroidogenesis in the ovary?

LH= increased androstenedione synthesis in Theca cells
- andorstenedione is then made into testosterone

FSH= stimulates testosterone-->estradiol conversion in the granulosa cells


How will estrogen and progesterone alter GnRH release?

Negative feedback


When does positive feedback occur with estrogen and progesterone ?

Mid-ovarian cycle i.e. day 14

*Positive feedback= increased LH necessary for ovulation


What are the three phases of the menstrual cycle?

1) Follicular
2) Ovulation
3) Luteal


What happens during the follicular phase of the menstrual cycle?

- ESTROGEN rises
- Endometrial cell proliferation occurs


What happens during ovulation?

Estrogen-mediated positive feedback on LH leads to a LH spike that causes ovulation


What happens during the luteal phase of the menstrual cycle?

- Rise in estrogen and progesterone, but MOSTLY PROGESTERONE
- Progesterone control differentiation of the endometrial lining for implantation


What happens if implantation does not occur during the menstrual cycle?

Steroidogenesis is NOT maintained and endometrial lining is shed


What is the MOA of endogenous steroids to produce a physiologic effect?

Bind intracellular receptors and modulate trascriptional activity


Where do endogenous steroid agonists and antagonists compete?

Steroid binding sites


How do progesterone and estrogen differ in regards to their effect on the endometrium?

Estrogen= proliferation
- Follicular phase

Progesterone= differentiation to prepare for implantation
- Luteal phase


What are the metabolic effects associated with estrogen in regards to lipids, bone, liver, and blood?

Lipids= decrease LDL and increase HDL

Bone= antiresorptive

Liver= increased plasma proteins

Blood= increased coagulation factors and decrease antithrombin i.e. PROCOAGULANT


What are the metabolic effects associated with progesterone in regards to lipid and glucose?

Lipids= increase LDL and fat deposition

Glucose= increased fasting glucose


What effect does progesterone have on uterine contraction?

Progesterone DECREASES uterine contraction


How does progesterone decrease uterine contraction?

1) Decreased prostaglandin production
2) Maintenance of relaxin


What effect does progesterone have on cervical glands?

Increased cervical mucous viscosity

*This impairs the sperm ability to swim


What is the primary natural estrogen?



What is the primary synthetic estrogen? What are these drugs used for?

Ethinyl estradiol

*Also, Mestranol both of which are used for birth control


What is diethylstilbestrol?

Non-steroid synthetic estrogen-mimic

*Not used in clinically practice but important for boards


What advantages are seen with synthetic estrogen vs. endogenous estrogen?

1) Increased half-life
2) Decreased first pass effect

*This is advantageous from a compliance standpoint*


What are conjugated equine estrogens? How are these used clinically?

Natural water-soluble estrogen sulfates
- Higher dose vs. synthetics
- Used for hormone replacement therapy


What are the clinical indications for estrogen therapy?

1) Hypogonadism
2) Hormone replacement therapy
3) Contraception
4) Acne


Specifically, what are the goals of estrogen used in hormone replacement therapy?

1) Maintain bone density
2) Suppress hot flashes
3) Suppress urogenital atrophy

*Often done in post-menopausal women


What risks are associated with estrogen/hormone replacement therapy?

1) CAD
2) CVA
3) PE
4) Invasive breast cancer

*Note that this is seen with 4-5 years of therapy; thus, estrogen is NOT a good choice for long-term HRT*


What can hormone/ estrogen replacement be protective against?

1) Colorectal cancer
2) Hip fracture


What is the MOA of estrogen therapy as a means of contraception?

Negative feedback on the HPG axis that prevents the LH surge necessary for ovulation


What is the MOA of estrogen as an acne treatment?

1) Suppress steroidogenesis
2) Increase Sex Hormone Binding Globulin (SHBG) to decrease free testosterone


What are the key adverse effects of estrogen therapy (not HRT)?

1) Breast tenderness
2) Endometrial hyperplasia
3) Increased blood coagulation

Also, nausea, cholestasis, migraines, cancer, and bloating


What is the relationship between combined HRT and cancer?

Increased risk of invasive breast cancer

*May be related to progestin not estrogen


What is the relationship between HRT estrogen monotherapy and cancer?

Increased risk of endometrial cancer


What is the relationship between estrogen contraceptive therapy and cancer?

REDUCED ovarian and endometrial cancer


How can estrogen lead to the development of cancer?

1) Trophic effects of the hormone (proliferation promotion)
2) ROS production during metabolism


What are the two parent steroids for the progestins?

Progesterone and 19-nortestosterone


List the progestins.

- Medroxyprogesterone (MPA)
- Norethindrone
- Norgestrel


What are the clinical uses for progestins

1) Contraceptive agents
2) HRT
3) Dysmenorrhea
4) Endometriosis


How does the efficacy of estrogen and progestins compare in prevention of ovulation? Contraception?

Ovulation= progestins only suppress LH surge/ ovulation 80% of the time

Contraception= equal b/c of effect on cervical mucous


What is the effect of progestins used in HRT with estrogen?

Decreased risk of endometrial hyperplasia


What is the MOA of progestins to treat dysmenorrhea?

- Decreased endometrial mass
- Decreased prostaglandin production/ uterine contraction


What is the MOA of progestins to treat endometriosis?

Decreased endometrial proliferation


In theory, what would happen to the endometrial lining with estrogen only? What is the role of progestin?

Continued growth

*Progestins inhibit growth/ proiferation mediated by estrogen

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