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Pharmacology > EXAM #5: ESTROGENS & PROGESTINS > Flashcards

EXAM #5: ESTROGENS & PROGESTINS Flashcards

1
Q

What regulates steroidogenesis in the ovary?

A

Gonadotropins (LH and FSH)

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2
Q

What cells are required for estrogen synthesis in the ovary?

A

Theca and granulosa cells

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3
Q

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

A

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

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

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4
Q

How will estrogen and progesterone alter GnRH release?

A

Negative feedback

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5
Q

When does positive feedback occur with estrogen and progesterone ?

A

Mid-ovarian cycle i.e. day 14

*Positive feedback= increased LH necessary for ovulation

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6
Q

What are the three phases of the menstrual cycle?

A

1) Follicular
2) Ovulation
3) Luteal

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7
Q

What happens during the follicular phase of the menstrual cycle?

A
  • ESTROGEN rises

- Endometrial cell proliferation occurs

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8
Q

What happens during ovulation?

A

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

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9
Q

What happens during the luteal phase of the menstrual cycle?

A
  • Rise in estrogen and progesterone, but MOSTLY PROGESTERONE

- Progesterone control differentiation of the endometrial lining for implantation

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10
Q

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

A

Steroidogenesis is NOT maintained and endometrial lining is shed

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11
Q

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

A

Bind intracellular receptors and modulate trascriptional activity

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12
Q

Where do endogenous steroid agonists and antagonists compete?

A

Steroid binding sites

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13
Q

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

A

Estrogen= proliferation
- Follicular phase

Progesterone= differentiation to prepare for implantation
- Luteal phase

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14
Q

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

A

Lipids= decrease LDL and increase HDL

Bone= antiresorptive

Liver= increased plasma proteins

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

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15
Q

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

A

Lipids= increase LDL and fat deposition

Glucose= increased fasting glucose

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16
Q

What effect does progesterone have on uterine contraction?

A

Progesterone DECREASES uterine contraction

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17
Q

How does progesterone decrease uterine contraction?

A

1) Decreased prostaglandin production

2) Maintenance of relaxin

18
Q

What effect does progesterone have on cervical glands?

A

Increased cervical mucous viscosity

*This impairs the sperm ability to swim

19
Q

What is the primary natural estrogen?

A

Estradiol

20
Q

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

A

Ethinyl estradiol

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

21
Q

What is diethylstilbestrol?

A

Non-steroid synthetic estrogen-mimic

*Not used in clinically practice but important for boards

22
Q

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

A

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

This is advantageous from a compliance standpoint

23
Q

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

A

Natural water-soluble estrogen sulfates

  • Higher dose vs. synthetics
  • Used for hormone replacement therapy
24
Q

What are the clinical indications for estrogen therapy?

A

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

25
Q

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

A

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

*Often done in post-menopausal women

26
Q

What risks are associated with estrogen/hormone replacement therapy?

A

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

27
Q

What can hormone/ estrogen replacement be protective against?

A

1) Colorectal cancer

2) Hip fracture

28
Q

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

A

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

29
Q

What is the MOA of estrogen as an acne treatment?

A

1) Suppress steroidogenesis

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

30
Q

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

A

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

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

31
Q

What is the relationship between combined HRT and cancer?

A

Increased risk of invasive breast cancer

*May be related to progestin not estrogen

32
Q

What is the relationship between HRT estrogen monotherapy and cancer?

A

Increased risk of endometrial cancer

33
Q

What is the relationship between estrogen contraceptive therapy and cancer?

A

REDUCED ovarian and endometrial cancer

34
Q

How can estrogen lead to the development of cancer?

A

1) Trophic effects of the hormone (proliferation promotion)

2) ROS production during metabolism

35
Q

What are the two parent steroids for the progestins?

A

Progesterone and 19-nortestosterone

36
Q

List the progestins.

A
  • Medroxyprogesterone (MPA)
  • Norethindrone
  • Norgestrel
37
Q

What are the clinical uses for progestins

A

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

38
Q

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

A

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

Contraception= equal b/c of effect on cervical mucous

39
Q

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

A

Decreased risk of endometrial hyperplasia

40
Q

What is the MOA of progestins to treat dysmenorrhea?

A
  • Decreased endometrial mass

- Decreased prostaglandin production/ uterine contraction

41
Q

What is the MOA of progestins to treat endometriosis?

A

Decreased endometrial proliferation

42
Q

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

A

Continued growth

*Progestins inhibit growth/ proiferation mediated by estrogen

Pharmacology (64 decks)

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