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Hannah's Reproductive > Oral Contraceptives > Flashcards

Oral Contraceptives Flashcards

1
Q

From what tissues is oestradiol released?

A

Ovary
Placenta
Small amount from testes and adrenal cortex

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2
Q

From what tissues is progesterone released?

A

Ovary
Placenta
Small amount from testes and adrenal cortex

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3
Q

From what tissues is testosterone released?

A

Testes

Small amount from ovaries and adrenal cortex

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4
Q

What is the problem with using natural oestrogens as part of an oral contraceptive?

A

Broken down quickly by hepatic first pass metabolism

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5
Q

Why can’t natural progesterone be used as part of the oral contraceptives?

A

Not orally effective/available

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6
Q

What is the feedback effect of oestrogen on the HPG axis?

A

Effectively inhibits FSH release

May inhibit or stimulate LH release depending on concentration

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7
Q

What is the feedback effect of progesterone on the HPG axis?

A

Inhibits GnRH release
Does not have much of an effect on FSH release
High doses will inhibit LH

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8
Q

Give an example of a synthetic oestrogen

A

Ethinyloestradiol (most commonly used)

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9
Q

Give an example of a 1st generation synthetic progestogen

A

Levonorgestrel (commonly used in OCs as well as HRT and the morning after pill)

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10
Q

What are the disadvantages of the 1st generation progestogens?

A

Androgenic (can cause hirsutism)

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11
Q

What are the disadvantages of the 2nd generation progestogens?

A

Expensive

Increased incidence of thromboembolic events

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12
Q

What conditions are 3rd generation progestogens (cyproterone, drospirenone) used to treat?

A

Dysmenorrhea/menorrhagia (prevents IDA)

PCOS

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13
Q

What is the disadvantage of cyproterone?

A

Highest risk of thromboembolic events

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14
Q

What is drospirenone?

A

A 3rd generation progestogen/analog of spironolactone that acts as an antiandrogenic diuretic

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15
Q

What are the 2 main effects of drospirenone?

A

Antimineralocorticoid

Antiandrogenic

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16
Q

What drugs are used to treat PCOS?

A

OCs with 3rd gen progestogens
Spironolactone
Metformin

17
Q

What are some of the possible serious complications of untreated PCOS?

A

Insulin resistance
CVD
Endometrial cancer

18
Q

What are the 3 different forms of OCs available, in order from most to least effective?

A

Combined preparations
Sequential preparations
Progestogen-only oral preparations (mini-pill)

19
Q

What is the difference between combined and sequential preparations of OCs?

A

Combined: mixture of oestrogen and progestogen in a fixed ratio of doses
Sequential: ratio of doses varies to correspond approximately to changes in endogenous oestrogen and progestogen

20
Q

Why can the mini-pill be used by lactating women?

A

Progestogen at this dose does not inhibit PLN release, where the addition of oestrogen would

21
Q

What kind of progestogens are generally included in the mini-pill?

A

Usually 1st gen

22
Q

What is the problem with low dose oestrogen OCs?

A

May get breakthrough bleeding (but less other adverse effects)

23
Q

For which OCs is it essential to take the pill at the same time every day?

A

Sequential preparations

Progestogen-only oral preparations

24
Q

List 15 possible adverse effects of COCs

A 
Hypertension
VTE
Cancer (some evidence for breast, cervical and uterine)
Nausea/vomiting
Dizziness
Flushing
Breast discomfort
Headache (especially in women who get headaches normally before onset of menses)
Weight gain
Decreased libido
Chloasma
Acne
Depression
Irritability
Fatigue
25
Q

Is the risk of developing or exacerbating existing hypertension with COC use reversible or irreversible?

A

Reversible

26
Q

What is the risk of VTE with COC use dependent on?

A

Dose of oestrogen (main factor; higher dose confers higher risk)
Type of progestogen
Presence of other risk factors

27
Q

When is risk of VTE highest with COC use?

A

In the 1st year of use

28
Q

What is the risk of VTE with use of COCs containing cyproterone?

A

60/100,000 patient-years (risk in pregnancy is 60/100,000 pregnancies)

29
Q

Describe the increase in risk of cervical cancer with COC use and how this can be managed

A

Risk is slight but increases with duration of COC use

Women should be regularly screened for cervical cancer

30
Q

Describe the influence of COCs on uterine cancer risk

A

The increased incidence of uterine cancer caused by OCs is diminished when progestogen is given concurrently to women with an intact uterus (overall effect is protective)

31
Q

What is the proposed mechanism of weight gain with OC use?

A

Due to water retention (oestrogen can act similarly to aldosterone) and possibly anabolic effects

32
Q

List 6 benefits of COC use

A

Decreased risk of endometrial cancer
Decreased incidence of ovarian cancer and ovarian cyst formation
Decreased risk of colorectal cancer
Protective effect on benign breast tumours
Decreased risk of bone fractures
Decreased dysmenorrhoea and menorrhagia (and therefore protection against IDA)

33
Q

What is the mechanism of action of the vaginal ring? What is its advantage over OCs?

A

Vaginal ring with ethinyloestradiol and etonogestrel is inserted into the vagina, left for 3 weeks and removed for 1 week; the process is repeated
Effective with lower doses of hormones as it bypasses the portal circulation

34
Q

List 3 non-oral forms of progestogen-only contraceptives, their method of administration and the duration of effectiveness

A

Medroxyprogesterone: IM, every 12 weeks
Etonorgestrel: subdermal implant, up to 3 years
Levonorgestrel: IUDs, up to 5 years

35
Q

What is emergency contraception? How does it work? How effective is it and over what timespan?

A

1 tablet of 1500ug of levonorgestrel (10x that of OCP dose)
May inhibit LH to prevent ovulation, changes the uterine tubing and lining to prevent implantation
~85% effective within 72 hours of unprotected intercourse

36
Q

What other form of emergency contraception besides the morning-after pill is available? How effective is this?

A

Copper IUD

99% effective but must be inserted by a doctor (morning-after pill can be obtained without prescription)

37
Q

What is the role of progestogens as contraceptive agents?

A

May inhibit LH release to prevent ovulation if high enough dose is delivered
Continuous exogenous progestogen administration makes the endometrium unfavourable for implantation and the vaginal/cervical mucus more inhospitable
May also interfere with coordinated contractions of the cervix, uterus and uterine tubes which ordinarily aid fertilisation and implantation

Hannah's Reproductive (5 decks)

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