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ENDO 2 > Hormone Contraception > Flashcards

Hormone Contraception Flashcards

1
Q

Describe the Mechanism of estrogen and progestin-induced gene transcription.

A

Both of these hormones will bind two their receptors in the nucleus of a target cell. Binding causes a conformational change leading to the dissociation of deactivating-heat shock proteins. Afterwards, the homodimerized receptors are free to bind DNA or other transcription factors.

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2
Q

What are the clinical uses of estrogens?

A

HRT of primary hypogonadism - given at 11-13 y/o and progestin follows first uterine bleed

Postmenopausal HRT - reduces hot flashes, fractures, and urogenital atrophy

Suppression of ovarian function in hirsutism and acne

Contraception and dysmenorrhea

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3
Q

What are the clinical uses of progestins?

A

Postmenopausal HRT and contraception

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4
Q

Describe the MOA of hormonal contraceptives

A

Prevent ovulation via feedback inhibition of the hypothalamic-pituitary axis.

Note: In combination, progestins and estrogens are more successful at suppression of LH and FSH and ovulation than either alone.

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5
Q

Describe the MOA of progestin-only contraceptives

A

Block ovulation in only 60-80% of cycles

Effectiveness - thickening of cervical mucus and endometrial alterations that impair implantation

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6
Q

What are the non-contraceptive benefits of oral contraceptives?

A

Reduced risk of epithelial ovarian and endometrial carcinoma

Reduced ectopic pregnancy and benign breast disease

Reduced Dysmenorrhea, hirsutism, and acne

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7
Q

What are the mild ADRs of oral contraceptives?

A

Nausea, mastalgia, breakthrough bleeding, edema, and migraines (indication to discontinue)

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8
Q

What are the moderate ADRs of oral contraceptives?

A

Breakthrough bleeding (avoided in combination therapies)

Androgenic effects (avoided with higher estrogen and anti-androgenic progestins)

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9
Q

What are the severe ADRs of oral contraceptives?

A

Vascular disease - thromboembolism (estrogens), myocardial infarction and CVA (elevated risk in smokers)

GI disease - cholestati jaundice and hepatic AD

Depression

Slightly increased risk of breast cancer

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10
Q

What are CIs for the use of estrogen-containing contraceptives?

A 
Smokers > 35 y/o
Cardiovascular disease
Migraines
Incomplete epiphysial closure
Estrogen-dependent neoplasms
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11
Q

What are the CIs for the use of progestin-only contraceptives?

A

liver disease and breast cancer

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12
Q

Describe the androgenic and estrogenic profiles of progestins

A

Progestins vary in their estrogenic and androgenic potencies:

More androgenic activity (e.g., L-Norgestrel, Norethindrone) leads to acne, hirsutism, weight gain, etc.

Progestins with lower (Norgestimate) or anti-androgenic (Drospirenone) potency actually treat acne

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13
Q

What are the different metabolic effects of L-Norgestrel?

A

Androgenic, anti-estrogenic, and anabolic

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14
Q

What are the different metabolic effects of Norethindrone?

A

Androgenic, anti-estrogenic, and anabolic

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15
Q

What are the different metabolic effects of Drospirenone?

A

Anti-androgenic

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16
Q

Rank the methods of contraception (Oral, transdermal, vaginal ring, injections, IUDs, and implants) with respect to failure rate.

A

Oral > transdermal > vaginal ring > injections > IUDs > implants

17
Q

Which oral contraceptives allow rapid return to fertility?

A

Oral, transdermal, vaginal ring, IUDs, and implantations

Note: Injections do not

18
Q

Rank the methods of contraception (Oral, transdermal, vaginal ring, injections, IUDs, and implants) with respect to duration of effectivity.

A

IUD > Implant > Injection > vaginal ring > transdermal patch, and pills

19
Q

Describe injectable progestin-only contraceptive

A

Medroxyprogesterone acetate
Injected intramuscularly every 3 months
The return of fertility can be delayed for 6-18 months after the last injection in some patients

20
Q

Describe IUD, progestin-only contraceptive

A

L-norgestrel

Effective for 5-7 years

21
Q

Describe the implantable progestin-only contraceptive

A

Etonogestrel
Placed under the skin of the upper arm and is effective for 3 years
Bleeding abnormalities are common

22
Q

Describe the transdermal combo contraceptive

A

Ethinyl estradiol and norelgestromin
A new patch is applied each week for three weeks, followed by one patch-free week

More frequent breast discomfort, dysmenorrhea, nausea, vomiting, and skin irritation

23
Q

Descibe the vaginal ring combo contraceptive

A

Ethinyl estradiol and etonogestrel

The ring is inserted and left in place for 3 weeks followed by one ring-free week

24
Q

What are the risks and benefits of estrogen-only HRT?

A

Decreased osteoporosis

Increased thromboembolism and ischemic stroke

25
Q

What are the risks and benefits of estrogen-progestin HRT?

A

Decreased osteoporosis and colorectal cancer

Increased breast cancer, MI, thromboembolism, and CVA

26
Q

What is the MOA of tamoxifen and toremifene?

A

Partial competitive agonist inhibitor of ER

27
Q

What are the uses of tamoxife and toremifene?

A

ER (+) breast cancer and chemoprevention of breast cancer

28
Q

What are the risks and benefits of tamoxifen and toremifene?

A

Reduced risk of osteoporosis and atherosclerosis

Slightly increased risk of endometrial cancer

29
Q

What is the MOA of Raloxifene?

A

Agonistic to ER in lipids and bone

Antagonistic at endometrium and breast

30
Q

What are the clinical uses of raloxifene?

A

Prevention of post-menopausal osteoporosis and chemoprevention of breast cancer

31
Q

What is the MOA and use of Mifepristone?

A

MOA - Progesterone receptor antagonist

Use - terminate early pregnancy and emergency contraceptive

Note: used with misoprostol (synthetic PGE-1)

32
Q

What is the MOA and use of levonorgestrel

A

MOA - progesterone receptor agonist; unknown how emergency contraception is implemented

Use - Plan B; CAN’T reverse an established pregnancy

33
Q

What is the MOA of Ulipristal Acetate?

A

MOA - similar to levonorgestrel, but longer duration of efficacy

Use - contraception, may interfere with established pregnancy

ENDO 2 (6 decks)

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