Oral Contraceptives Flashcards
Synthetic progestogens are used in OCP because
progesterone (naturally occurring) are not orally active
Synthetic oestrogens are used in OCP becuase
oestradiol (natural oestrogen) is absorbed but rapidly broken down; synthetics enter the enterohepatic circulation and tf last longer
What is the mechanism of OCPs?
negative feedback on anterior pituitary and hypothalamus to inhibit release of FSH and LH thereby stopping ovulation
In the menstrual cycle, oestrogen is responsible for
proliferative phase and proliferation of the endometrium
Oestradiol (natural estrogen) will always inhibit
FSH
Oestradiol will sometimes inhibit
LH depending on concentration; surge in oestrogen causes LH surge and rupture of the follicle for ovulation
Progesterone only comes from
the corpus luteum following ovulation
Prolific cervical secretion of mucous occurs
When oestrogen peaks just prior or at ovulation
Progesterone drives which phase of the menstrual cycle?
Secretory/luteal
Progesterone in the secretory phase is dependent upon
oestrogen previously priming the endometrium
What happens to the endometrium during the secretory/luteal phase?
synthesizes proteins necessary for implantation, increases blood supply to increase nutrients
If fertilization occurs, the corpus luteum serves to
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)
Testosterone is released from
testes and small amounts from ovaries and adrenal cortex
Progesterone is released from
the ovary, placenta, adrenal cortex, and testes as an intermediary to testosterone
Oestrogens are released from
ovary and placenta, small amounts from adrenal cortex and testes
Ethinyloesrtradiol is a
synthetic estrogen
Levonorgestrel is a
synthetic progestogen
Cyproterone is a
synthetic progestogen
Drospirenone is a
synthetic progestogen
Combined preps of OCP contain
mixture of oestrogen and progesterone in a fixed ratio of doses
Sequential OCP preps contain
ratio of O and P doses corresponding approximately to endogenous changes of these hormones
Progestogen-only oral prep OCP (mini pill) contains
Only progestogen, for when oestrogen is contraindicated eg during lactation - these are the LEAST effective OCPs
The most frequently used synthetic oestrogen in OCP is
ethinyloestradiol
Levonorgestrel is used in
in older OCPs along with norethisterone; tx of menstrual irregularities, HRT, and the morning after pill
What was the downside to older progestrogens levonorgestrel and norethisterone?
many side effects: androgenic (hirsutism)
Newer progestrogens include
cyproterone and drospirenone
Which OCPs can be used to tx symptoms of PCOS?
newer OCPs with fewer androgenic SEs eg cyptoretone and drospirenone which have anti-androgenic effects
How do OCPs help in tx of PCOS?
overcome the symptoms of hyperandrogenism: acne, hursutism, weight gain; combat insulin resistance, CVD risk factors, and endometrial cancer risk
Drugs used in the management of PCOS include
OCP (cyproterone and drospirenone), sprionolactone (aldosterone receptor antagonist), metformin
Cyproterone is said to have the highest risk of
venous thromboembolic disorder and clotting - removed from market in france (Diane)
Cyproterone is a derivative of
progesterone
Drospirenone is a derivative of
spironalactone
Activity of drospirenone includes
progestogenic, anti-mineralocorticoid (mild diuretic), anti-androgenic
Drospirenone is marketed as
Yasmin, Yaz
Which progestogens are most commonly used in the mini-pill?
Levonorgestrel, norethisterone (older progestogens)
Why is oestrogen-containing OCP contraindicated in breastfeeding women?
Oestrogen will negatively feed back on the anterior pituitary to prevent prolactin release and hence stop lactation
The mechanism of the oestrogen component of OCPs is to
inhibit FSH (sometimes LH depending on the dose)
The mechanism of the progesetogenic component of the OCP is to
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
T/F women on the mini-pill do not ovulate
False; if they are having regular periods they are likely ovulating because progestogen is not high enough to inhibit LH
How do progestrogens act as OCPs if they do not fully inhibit LH?
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
What are the adverse effects of COCs?
Hypertension (reverisble); increased risk of venous thromboembolism; increased risk of cancer (breast, cervical, and uterine)
Which OCPs are least likely to give rise to increased risk of VTE?
earlier OCPs with oestrogen and the older progestogens (levonorgestrel and norethisterone)
Which component of the OCP is attributed to for the increased risk of VTE?
Oestrogen - increasing dose increases risk; type of progestogen (older = safer)Why
Why is it recommended that women on OCP (and HRT) have regular cervical cancer screening?
increased risk of cervical cancer; increases with duration of use but declines to normal after 10 years cessation of OCP
Increased risk of uterine cancer while taking OCP is abolished if
oestrogen is prescribed with a progestogen (and the woman has an intact uterus)
What are the benefits of COCs?
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)
The morning after pill contains
1500ug of levonorgestrel
MAP must be taken within
72 hrs
Effectiveness of MAP is
~85%
