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Reproduction > Oral Contraceptives > Flashcards

Oral Contraceptives Flashcards

1
Q

Synthetic progestogens are used in OCP because

A

progesterone (naturally occurring) are not orally active

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2
Q

Synthetic oestrogens are used in OCP becuase

A

oestradiol (natural oestrogen) is absorbed but rapidly broken down; synthetics enter the enterohepatic circulation and tf last longer

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3
Q

What is the mechanism of OCPs?

A

negative feedback on anterior pituitary and hypothalamus to inhibit release of FSH and LH thereby stopping ovulation

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4
Q

In the menstrual cycle, oestrogen is responsible for

A

proliferative phase and proliferation of the endometrium

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5
Q

Oestradiol (natural estrogen) will always inhibit

A

FSH

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6
Q

Oestradiol will sometimes inhibit

A

LH depending on concentration; surge in oestrogen causes LH surge and rupture of the follicle for ovulation

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7
Q

Progesterone only comes from

A

the corpus luteum following ovulation

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8
Q

Prolific cervical secretion of mucous occurs

A

When oestrogen peaks just prior or at ovulation

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9
Q

Progesterone drives which phase of the menstrual cycle?

A

Secretory/luteal

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10
Q

Progesterone in the secretory phase is dependent upon

A

oestrogen previously priming the endometrium

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11
Q

What happens to the endometrium during the secretory/luteal phase?

A

synthesizes proteins necessary for implantation, increases blood supply to increase nutrients

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12
Q

If fertilization occurs, the corpus luteum serves to

A

release progesterone and oestrogen to negatively feed back on the anterior pituitary and hypothalamus to prevent ovulation until the placenta takes over to support the pregnancy (10-12 weeks)

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13
Q

Testosterone is released from

A

testes and small amounts from ovaries and adrenal cortex

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14
Q

Progesterone is released from

A

the ovary, placenta, adrenal cortex, and testes as an intermediary to testosterone

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15
Q

Oestrogens are released from

A

ovary and placenta, small amounts from adrenal cortex and testes

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16
Q

Ethinyloesrtradiol is a

A

synthetic estrogen

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17
Q

Levonorgestrel is a

A

synthetic progestogen

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18
Q

Cyproterone is a

A

synthetic progestogen

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19
Q

Drospirenone is a

A

synthetic progestogen

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20
Q

Combined preps of OCP contain

A

mixture of oestrogen and progesterone in a fixed ratio of doses

21
Q

Sequential OCP preps contain

A

ratio of O and P doses corresponding approximately to endogenous changes of these hormones

22
Q

Progestogen-only oral prep OCP (mini pill) contains

A

Only progestogen, for when oestrogen is contraindicated eg during lactation - these are the LEAST effective OCPs

23
Q

The most frequently used synthetic oestrogen in OCP is

A

ethinyloestradiol

24
Q

Levonorgestrel is used in

A

in older OCPs along with norethisterone; tx of menstrual irregularities, HRT, and the morning after pill

25
Q

What was the downside to older progestrogens levonorgestrel and norethisterone?

A

many side effects: androgenic (hirsutism)

26
Q

Newer progestrogens include

A

cyproterone and drospirenone

27
Q

Which OCPs can be used to tx symptoms of PCOS?

A

newer OCPs with fewer androgenic SEs eg cyptoretone and drospirenone which have anti-androgenic effects

28
Q

How do OCPs help in tx of PCOS?

A

overcome the symptoms of hyperandrogenism: acne, hursutism, weight gain; combat insulin resistance, CVD risk factors, and endometrial cancer risk

29
Q

Drugs used in the management of PCOS include

A

OCP (cyproterone and drospirenone), sprionolactone (aldosterone receptor antagonist), metformin

30
Q

Cyproterone is said to have the highest risk of

A

venous thromboembolic disorder and clotting - removed from market in france (Diane)

31
Q

Cyproterone is a derivative of

A

progesterone

32
Q

Drospirenone is a derivative of

A

spironalactone

33
Q

Activity of drospirenone includes

A

progestogenic, anti-mineralocorticoid (mild diuretic), anti-androgenic

34
Q

Drospirenone is marketed as

A

Yasmin, Yaz

35
Q

Which progestogens are most commonly used in the mini-pill?

A

Levonorgestrel, norethisterone (older progestogens)

36
Q

Why is oestrogen-containing OCP contraindicated in breastfeeding women?

A

Oestrogen will negatively feed back on the anterior pituitary to prevent prolactin release and hence stop lactation

37
Q

The mechanism of the oestrogen component of OCPs is to

A

inhibit FSH (sometimes LH depending on the dose)

38
Q

The mechanism of the progesetogenic component of the OCP is to

A

negatively feed back on LH in some cycles (not much of an effect on FSH) - higher doses are needed to do it EVERY cycle but are associated with side effects

39
Q

T/F women on the mini-pill do not ovulate

A

False; if they are having regular periods they are likely ovulating because progestogen is not high enough to inhibit LH

40
Q

How do progestrogens act as OCPs if they do not fully inhibit LH?

A

continuous, exogenous progestogens make the endometrium unfavourable to implantantion and the cervical mucous inhospitable to sperm preventing fertilization; interference with contractions of uterus, cervix, and FTs that facilitate fertilization and implantation

41
Q

What are the adverse effects of COCs?

A

Hypertension (reverisble); increased risk of venous thromboembolism; increased risk of cancer (breast, cervical, and uterine)

42
Q

Which OCPs are least likely to give rise to increased risk of VTE?

A

earlier OCPs with oestrogen and the older progestogens (levonorgestrel and norethisterone)

43
Q

Which component of the OCP is attributed to for the increased risk of VTE?

A

Oestrogen - increasing dose increases risk; type of progestogen (older = safer)Why

44
Q

Why is it recommended that women on OCP (and HRT) have regular cervical cancer screening?

A

increased risk of cervical cancer; increases with duration of use but declines to normal after 10 years cessation of OCP

45
Q

Increased risk of uterine cancer while taking OCP is abolished if

A

oestrogen is prescribed with a progestogen (and the woman has an intact uterus)

46
Q

What are the benefits of COCs?

A

decreased risk of endometrial cancer; decreased incidence of ovarian cancer and ovarian cyst formation; reduction in risk of colorectal cancer (HRT too); protective effect on benign breast tumours; reduction in risk of bone fractures; reduction in dysmenorrhoea and menorrhagia (and tf protection against iron deficiency anaemia)

47
Q

The morning after pill contains

A

1500ug of levonorgestrel

48
Q

MAP must be taken within

A

72 hrs

49
Q

Effectiveness of MAP is

A

~85%

Reproduction (11 decks)

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