Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RGU 1 > Estrogens and Progestogens > Flashcards

Estrogens and Progestogens Flashcards

1
Q

What do steroid hormones (estrogens and progetins) look like chemically?

A

tetracyclic (4 ringed) structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the most common naturally occurring estrogen and progestin?

A
  • estrogen= 17B-estradiol (aka estradiol; E2)
  • progestin= progesterone
  • primary steroid hormones produced in the ovaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the weaker estrogens?

A
  • estrone (E1) and estriol (E3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are estrogens made again?

A
  • from circulating cholesterol (in ovaries, testes, and adrenal glands) to progesterone, to androgens, and finally via AROMATASE to estrogen!
  • remember mineralocorticoids and glucocorticoids are also made from progesterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where are both estradiol and progesterone broken down?

A

in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are phytoestrogens?

A

phytoestrogens= from plants in our diet:

  • polyphenols (reservatrol in red wine)
  • flavonoids (citrus, chocolate, and green tea)
  • isoflavonoids (soy)
  • bind to ER-beta receptor more than ER-alpha, which makes these GOOD for you :)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are environmental estrogens?

A

mostly BAD; endocrine disruptions:

  • bisphenol A (BPA; released as plastics degrade)
  • bind to ERs stronger than metabolic estrogens.
  • polychlorinated hydroxybiphenyls (PCBs; banned in 1979 but some are still found in children’s toys, plastic bottles, and aluminum cans).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

*** What is the main synthetic estrogen?

A
  • ETHINYL ESTRADIOL= most common in birth control

* ETHINYL GROUP (C triple bonded to CH) allows it to pass through stomach and liver; aka allows it to be taken ORALLY.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

*** What are the main synthetic progestins?

A
  • 19-NORESTOSTERONES and are classified as either:
    1. ESTRANES= first-generation progestins.
    2. GONANES= greater progestational activity, so you can use a lower dose.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are the synthetic progestins made?

A
  • by removing the 19 carbon from ethisterone (a derivative of testosterone).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 specific GONANE progestins?

A
  1. Desogestrel
  2. Norgestrel
  3. Levonorgestrel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 5 specific ESTRANE progestins?

A
  1. Norethynodrel
  2. Lynestrenol
  3. Norethindrone
  4. Norethindrone acetate
  5. Ethynodiol diacetate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the “classical/direct” (genomic) steroid signaling pathway?

A
  1. hormone passes through the lipid membrane and bind to steroid receptor in the cytoplasm.
  2. translocation of hormone-receptor complex to nucleus.
  3. binding of complex to DNA regulatory site
  4. transcription of mRNA
  5. translocation of mRNA to cytoplasm to be translated to protein.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

** What is the “rapid action” (non-genomic) steroid signaling pathway? (newly discovered pathway)

A
  1. hormone binds to plasma membrane receptor.
  2. MAP kinase or cAMP, PKC, Ca2+ activation
  3. activation of biological responses (or to a lesser degree gene expression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

*** How does the ESTROGEN GENOMIC signaling pathway work?

A
  1. Estrogen enters the cytosol and binds to the ER (receptor, which is already bound to a HEAT SHOCK PROTEIN).
  2. upon binding hormone-receptor complex forms a DIMER.
  3. move into the nucles and binds to ESTROGEN RESPONSE ELEMENT (ERE) activating gene transcription.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

*** How does the ESTROGEN NON-genomic signaling pathway work?

A
  1. activation of a cell surface receptor (TKR or other) activates ER through PHOSPHORYLATION.
  2. activation of intracellular signaling pathways.
  3. rapid changes including Ca2+ and NOS release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 2 types of estrogen receptors (ERs)?

A
  1. ER-alpha (NR3A1)= endometrium, hypothalamus, breast tissue (often BREAST CANCER), and stromal cells of ovary.
  2. ER-beta (NR3A2)= hippocampus, cortex, thalamus, granulosa cells of ovary, bone, heart, lungs, prostate, andendothelial cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is important to know about the G-protein coupled estrogen receptor 1?

A
  • responds only to estradiol and functions via the rapid (non-genomic) signaling pathway.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Is the progesterone signaling pathway similar to the estrogen signaling pathways?

A

YES and has both classic (genomic) and rapid (non-genomic) pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 2 types of progesterone receptors?

A
  1. PRA (short)= more rapid pathway.

2. PRB (long)= more classic (genomic) pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

** What are the physiologic functions of estrogens?

A
  • female reproductive development= reproductive organ development, secondary sexual characteristics, and regulates menstrual cycle.
  • metabolic= REDUCES BONE RESORPTION; aka strengthens bones, increases plasma triglycerides, but lowers LDL and increases HDL.
  • cognitive= protects against neurodegenerative disorders, and helps learning and memory through synaptic remodeling.
22
Q

** What are the physiologic functions of progestins?

A
  • progesterone= induces secretory changes in endometrium and maintains pregnancy.
  • progestins= fat deposition, block ovulation and GnRH secretion, may increase BP, decrease HDL, increase LDL, increase insulin and response to glucose.
23
Q

What are the clinical uses of ESTROGENS?

A
  • ORAL CONTRACEPTIVES (always with progestins).
  • hormone replacement therapy (HRT) for premature ovarian failure, menopause, or ovariectomy.
  • HYPOGONADISM in females.
  • prevention of OSTEOPOROSIS.
24
Q

What are the clinical uses of PROGESTINS?

A
  • ORAL CONTRACEPTIVES (with or without estrogen).
  • HRT (with estrogen)
  • Progesterone= MAINTENANCE of PREGNANCY (prematurity risk…) or assisted reproductive technology.
25
Q

What are the 2 different mechanisms of action of oral contraceptives (OCs)?

A
  1. BLOCK OVULATION at the level of the PITUITARY= suppress FSH, LH, and GnRH pulses, lowering their levels and thus suppressing the mid-cycle LH SURGE.
  2. BLOCK OVULATION at level of OVARY and UTERUS= alters cervical mucus, tubal transport of of ovum, and endometrial development.
26
Q

*** What are the 2 roles of ESTROGEN (produced by the ovaries) during the FOLLICULAR phase of the ovarian cycle?

A
  1. provides NEGATIVE FEEDBACK to the hypothalamus and anterior pituitary to keep FSH and LH levels low.
  2. stimulates the endometrium of the uterus to grow.
27
Q

*** What are the 2 roles of ESTROGEN (produced by the ovaries) during OVULATION of the ovarian cycle?

A
  1. STIMULATES the hypothalamus to increase GnRH and thus LH and FSH from the anterior pituitary; this LH surge is what causes ovulation
  2. continued stimulation of the endometrium of the uterus to grow.
28
Q

*** What are the roles of ESTROGEN (produced by the ovaries), and PROGESTERONE (produced by the corpus luteum) during the LUTEAL phase of the ovarian cycle?

A
  • BOTH provide NEGATIVE FEEDBACK to the hypothalamus and anterior pituitary to decrease GnRH, LH, and FSH.
  • PROGESTERONE will maintain the endometrium until the corpus luteum degrades, causing the endometrium to slough off.
29
Q

So how do OCs work at the hormonal level?

A
  • stop the estradiol flux, thus preventing the LH surge and subsequent ovulation.
30
Q

What are the 3 types of OCs?

A
  1. combination (estrogen-progestin pills)= 99% of women.
  2. progestin only
  3. postcoital contraceptives (plan B)
31
Q

*** What are the combination (estrogen-progestin) OC pills?

A
  • can be used as monthly or extended dosing

- mono-, bi-, tri- or 4-phasic (aka how many times the estrogen-progestin dose changes throughout the cycle).

32
Q

Do monophasic combination OC pills have the same efficacy as multiphasic?

A

YES, however skipping any pills in a multi-phasic course causes more disruption than skipping a monophasic

33
Q

What is one thing that is different about the 4-phasic combination pill?

A
  • uses a bioidentical estrogen (estradiol valerate) instead of ethinyl estradiol.
34
Q

Why are there so many types of combination pills?

A
  • lower doses of E2 (estradiol)= fewer adverse side effects. but amenorrhea.
  • Higher doses of E2 (estradiol)= treat excessive menstrual pain and bleeding.
  • progestins can be tailored to gain or avoid different side effects.
35
Q

Do the progestin-only pills have inactive pills like the combo pills?

A

NO

36
Q

Why would you take the progestin-only pill (Norethindrone) over the combo pill?

A
  • useful for women sensitive to estrogen (smokers, cardio risk).
  • safe for breastfeeding mothers.
37
Q

What must you be wary of in progestin-only pills?

A
  • will not always block ovulation.

- cannot miss any pills (must take at same time every day).

38
Q

What are the 2 oral postcoital/ “emergency contraceptives”/ “morning-after pills”?

A
  1. LEVONORGESTREL (Plan B)= best within 3 days, but the sooner the better; however, won’t affect an attached embryo.
  2. ULIPRISTAL ACETATE= selective progesterone receptor modulator (SPRM; Ella). Must use within 5 days. This one will be just as effective on day 5 as day 1. Thus, more effective than levonorgestrel.
39
Q

What postcoital contraceptive is also used to treat uterine fibroids?

A
  • ulipristal acetate
40
Q

What is Mifepristone?

A
  • another rarely used form of postcoital contraceptive that is a Norethindrone derivative acting as a progestin antagonist. This is known as the abortive pill because it will cause abortion up to day 49.
41
Q

What are some beneficial effects of the combo pill?

A
  • decreases incidence of amenorrhea, irregular periods, intermenstrual bleeding, and reduces blood loss/anemia.
  • decrease pain in endometriosis.
  • reduce benign breast disease, uterine fibroids, and ovarian cysts.
  • reduces risk of ovarian, endometrial, and colorectal cancer.
  • preserves bone density
  • treats severe acne
42
Q

What are some ADRs of the combo pill?

A
  • weight gain, libido changes (usually decrease), nausea, dizziness, headache, iritability and increased risk of breast cancer.
  • VENOUS THROMBOEMBOLISM.
43
Q

What are some ADRs of the progestin-only pill?

A
  • irregular bleeding

- acne, hirsutism (RARE)

44
Q

What are the major drug interactions with OCs?

A
  • EPILEPSY MEDICATIONS
  • certain antibiotics (RIFAMPIN).
  • some antifungals have a slight risk of decreasing efficacy.
  • CYTOCHROM P450 INDUCERS (St. john’s wort is an herbal supplements).
45
Q

What are some other uses for estrogen/progesterone modulators?

A
  • ER-positive breast cancers= SERMs (agonist and antagonist properties depending on tissue) and AROMATASE INHIBITORS to decrease estrogen.
  • osteoporosis
  • infertility
46
Q

What are the main SERMs used for cancer treatment? (PICMONIC)

A
  • TAMOXIFEN= ER antagonist in breast tissue :) but agonist in uterus, bone, and liver.
  • FULVESTRANT= antagonist ONLY (so technically SERD; selective estrogen receptor down-regulator). Used in POSTmenopausal women only after failure with Tamoxifen.
47
Q

What are aromatase inhibitors? (PICMONIC)

A
  • Anastrozole and Letrozole= inhibit estrogen synthesis from androgens.
  • indicated for breast cancer following treatment with Tamoxifen.
48
Q

Can you use aromatase inhibitors in pregnancy?

A

NO

49
Q

What drug is used to treat osteoporosis? (PICMONIC)

A
  • RALOXIFENE= SERM similar to Tamoxifen, but with STRONGER AGONIST activity in BONE.
50
Q

What drug is used to treat infertility?

A
  • CLOMIPHENE= SERM that can induce ovulation by inhibiting estradiol’s negative feedback.
  • Letrozole (aromatase inhibitor) can also be used to induce ovulation.

RGU 1 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions