Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology Test 2 > Estrogens, Progestins, & Their Antagonist > Flashcards

Estrogens, Progestins, & Their Antagonist Flashcards

1
Q

Estrogens

A
  • critical for sexual development and 2nd characteristics

- stimulate growth of uterine muscle & endometrial lining

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

3 human nature estrogens

A

E1: estrone
E2: estradiol
E3: estriol

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

Strongest most potent estrogen

A

E2 (80x) > E1 (8x) > E3 (1x)

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

Metabolic & Cardiovascular Effects of Estrogen

Blood, Lipid, Bone

A

(good) Bone: increase formation, decrease resorption, increase height, decrease muscle mass
(good) Lipid: increase HDL, VLDL, TG; decrease LDL, total cholesterol, fat deposition; increase fat metabolism
(bad) Blood: increase coagulation factors, increase coagulability of blood, increase risk of blood clots

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

Estrogen Receptors

ERa ERb

A

made from two different genes
ERa: endometrium
ERb: kidney, brain

E2 binds both receptors; E1 prefers ERa; E3 prefers ERb

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

Estrogen is expressed mainly in

A

bone, heart, breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ERa

A

endometrium; over expressed in breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Estrogen Mechanism of Action

A
  • estrogen cross cell membrane and bind ERa/b
  • conformational change
  • interacts with coregulators
  • coregulators may affect tissue-specific effects of selective estrogen receptor modulators (SERM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ERb vs ERa

A

ERb has its own separate action, and may have a dominant negative effect on ERa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ERa/b are made from

A

two different genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Biosynthesis of Estrogens

Premenopausal

A

producing mainly E2 upon FSH stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Biosynthesis of Estrogens

Postmenopausal

A

producing mainly E1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Biosynthesis of Estrogens

Pregnancy

A

producing mainly E3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Biosynthesis of Estrogens

Men

A

producing small amounts of E1 & E2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Main target for drug therapy

A

Aromatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ethinyl Estradiol EE

A

Synthetic Estrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diethylstilbestrol DES

A

no longer used; hurt babies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Commonly used Estrogens

A 
Ethinyl Estradiol
Micronized estradiol
Estradiol cypionate
Estradiol valerate
Estropipate

ESTRADIOL & ESTROPIPATE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

17a-ethinylestradiol

A

as active as E2

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

Mestranol

A
  • converted into 17aEE by liver

- chemical alterations increase oral bioavailability

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

Estrogen modifications

A

delay metabolism, increasing oral bioavailability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical Uses of Estrogens

Primary Hypogonadism

A
  • replacement therapy in estrogen-deficient patients
  • attempts to mimic the physiology of puberty
  • chronic maintenance therapy consists of both estrogens and progestins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical Uses of Estrogens
HRT
Postmenopausal Hormone Therapy

A
  • use estrogen/progestin to make up for declines after menopause

relieving symptoms including:

  • hot flashes
  • drying itchiness
  • sleep disturbances

USE SHOREST AND LOWEST POSSIBLE because potential risks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Estrogens for HRT

A

E1, E2, E3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Estrogens for HRT

E1

A
  • estropipate

- CCE, PREMARIN (conjugated equine estrogens)

26
Q

Estrogens for HRT

E2

A
  • attached to acetate, valerate, and cypionate groups that are hydrolyzed away in the body to produce estradiol
27
Q

Estrogens for HRT

E3

A
  • weak natural estrogen elevated during pregnancy

- ISNT converted into estrone; DOESNT INCREASE RISK OF BREAST OR ENDOMETRIAL CANCERS; higher dosage needed

28
Q

ERa cancer

A

over expressed in breast cancer

29
Q

Estrogen + Progestin for HRT

A

NEVER USE PROGESTIN ALONE; can use estrogen alone

  • CEE + MPA (medroxyprogesteron acetate)
  • indicated in women with a uterus
  • progesterone added to prevent endometrial hyperplasia from estrogen
  • added risks
30
Q

Progestins

A
  • need lots during pregnancy
31
Q

Progesterone

A
  • natural progestin in human
  • controls menstrual cycle, pregnancy
  • C21 steroid; precursor to other steroids
32
Q

Name the Active Progesterone

A

P4

33
Q

Biosynthesis of Progesterone

Non-pregnant women

A
  • by granulosa lutein cells in corpus luteum

- LH stimulation

34
Q

Biosynthesis of Progesterone

Pregnant women

A
  • from corpus luteum

- hCG stimulation

35
Q

Biosynthesis of Progesterone

2nd month of pregnancy

A
  • placenta secretes estriol and progesterone under delivery

- peaks third trimester

36
Q

Progesterone Receptor A&B made by

A

ONE gene; different due to splicing

37
Q

Need estrogen and progestin or

A

nada will happen (pregnancy wise)

38
Q

MPA

Medroxyprogesterone Acetate

A

mixed with CEE estrogen for HRT

39
Q

6 Progestational Agents

A
  • progesterone
  • hydroxyprogesterone
  • medroxyprogesterone
  • dimethisterone
  • norethindrone
  • desogestrel
40
Q

Most Important use of Progestins

A

Hormonal Contraception

- can use just progestin but usually with estrogen

41
Q

Therapeutic Applications of Progestins

A
  • HRT (w/ estrogen, never alone)
  • Long-term ovarian suppression
  • diagnostic uses: test estrogen secretion
  • hormonal contraception
42
Q

Norgestrel

aka Norethindrone

A

Progestin-ONLY Pills
- taken daily
ectopic pregnancy risk
- less effective than combination pills

43
Q

Levonorgestrel

A

Plan B

  • ONLY progestin
  • use within 3 days; sooner = better
44
Q

Ulipristal Acetate

A

SPRM
Selective PR modulator
Emergency Contraceptive

45
Q

Mechanism of Hormonal Contraceptives

A

1) suppress ovulation
2) affects viscosity of mucus fluid and mobility and secretion of the uterine tubes (sperm can’t reach egg)
3) interfere with implantation

46
Q

Tamoxifen

A

Selective Estrogen Receptor Modulator (SERM)

  • nonsteroidal, antagoinst on the breast, and partial agonist on uterine and bone
  • palliative care for ER+ breast cancer
  • decreases total cholesterol
  • – does not increase HDL and triglyceride
47
Q

Rolaxifene

A

Selective Estrogen Receptor Modulator

  • nonsteroidal partial agonist on bone and antagonist on uterus and breast
  • ** same as tamoxifen EXCEPT less uterine cancer risk ***
48
Q

Fulvestrant

A

Anti-estrogen

  • estrogen receptor
  • analog of estradiol with no known estrogenic activity
  • indicated for ER-positive metastatic breast cancer when resistant to Tamoxifen
  • degrades ERa receptor
  • affects fetus
49
Q

Mifepristone

A

Anti-progestin

  • progestin receptor
  • PR and GR antagonist with luteolytic properties
  • medical abortion
50
Q

Selective Estrogen Receptor Modulator

SERM

A
  • tissue-selective estrogenic actions
  • Agonist: bone & CVS
  • Antagoinst: Breast & uterus
51
Q

Toremifene

A

similar to Tamoxifen

52
Q

Aromatase Inhibitors

Type 1

A
  • Irreversible

- Steroidal

53
Q

Exemestane

A

Aromatase Type I Inhibitor

  • binds irreversibly to aromatase
  • for postmenopausal women with ER+ early breast cancer
  • MORE EFFECTIVE than tamoxifen
54
Q

Aromatase

Type 2

A
  • reversible

- nonsteroidal

55
Q

Anastrozole

A

Aromatase Type II Inhibitor

  • for ER+ breast cancer; first line treatment or following tamoxifen
  • sometimes helps ER-
  • NO RISK OF UTERINE CANCER OR DVT
56
Q

Letrozole

A

Aromatase Type II Inhibitor

  • ER+ breast cancer
  • block estrogen production, increase FSH, stimulate follicle growth
57
Q

Formestane

A

Aromatase Type I Inhibitor

  • irreversible
  • steroidal
  • similar to exemestane
  • weak androgen, mild AI; poor oral availability; no longer popular
58
Q

Bazedoxifene

A

SERM

- in combination with conjugated estrogens, approved as HRT and osteoporosis

59
Q

Clomiphene

A

SERM

  • older partial agonist
  • ovulation-inducing agent
60
Q

Progestins without androgenic activity include

A
  • desogestrel
  • norgestimate
  • gestodene

Pharmacology Test 2 (8 decks)

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