Oral contraceptives, menopause and HRT Flashcards

1
Q

oestradiol as a hormone/drug

A
  • well absorbed

- low bioavailability (due to first pass metabolism)

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2
Q

what are the 3 forms of oestrogen contraceptive?

A

1) oestrogen sulphate (conjugated oestrogen)
2) estriol
3) ethinyl oestradiol (ethinyl group protects the molecule from first pass metabolism)

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3
Q

what are the consequences of a lack of oestrogen?

A

increased chance of osteoporosis and fracture

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4
Q

what other problems does oestrogen contribute to?

A
breast growth --> cancer
CVS problems (when there is low oestrogen)
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5
Q

how is progesterone as a hormone/drug?

A
  • poorly absorbed
  • rapidly metabolised in the liver
  • given IM
  • oral therapy e.g. norethisterone
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6
Q

what does Combined Oral Contraceptive consist of?

A

oestrogen (ethinyl oestradiol)

progestogen (levonorgestrel or norethisterone)

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7
Q

what is the effect of using the COC?

A

suppresses ovulation

  • feedback of E and P on hypothalamus and pituitary
  • P thicken cervical mucus
  • E upregulates P receptors
  • E counteracts androgenic effect of synthetic P
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8
Q

what is the treatment plan of COC?

A

taken for 21 days, then stop for 7 days, then start again

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9
Q

what are the unwanted effects of oestrogens?

A
  • nausea
  • headache
  • increased weight (water retention and fat deposition)
  • CVS problems
  • breast cancer
  • endometrial proliferation
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10
Q

when is progesterone-only contraceptive given?

A

when using oestrogen in contraindicated e.g in smoker, CVS problems, history of thrombosis

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11
Q

examples of emergency contraception (post-coital pill)

A
  • levonorgestrel: E+P or P only
    within 72 hours
  • copper IUD: affects sperm viability and function
  • ulipristal: delays ovulation unto 5 days with anti-progestin activity
    within 120 hours
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12
Q

what is menopause?

A

permanent cessation of menstruation

leads to loss of ovarian follicular activity

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13
Q

what is the average age of menopause?

A

51 (45-55)

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14
Q

what is the climacteric?

A

period of transition from predictable ovarian function through the postmenopausal years

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15
Q

what is premature ovarian insufficiency?

A

menopause before the age of 40

1% in women

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16
Q

what are the causes of POI?

A

autoimmune
secondary to surgery
chemo or radiation

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17
Q

what are the hormone levels in menopause?

A

high GnRH
high FSH and LH
low follicle

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18
Q

what are the menopause symptoms?

A
  • hot flushes
  • sleep disturbance
  • depression
  • decreased libido
  • urogenital atrophy
  • joint pain
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19
Q

what are the complications of menopause?

A

-osteoporosis:
loss of bone matrix
risk of fracture
loss of bone mass

  • CVS
    women are protected from CVS disease before menopause but have the same risk as men by age 70
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20
Q

what is the treatment of menopause?

A

HRT- combined to prevent endometrial hyperplasia , reduce risk of cancer

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21
Q

how is HRT administered?

A

oral, transdermal, transvaginal

  • oral oestradiol
  • oral conjugated equine oestrogen

cyclical (E given everyday, P every 12-14 days)
continuous

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22
Q

what are the risks of HRT?

A
  • breast cancer
  • VTE
  • stroke
  • gallstones

however very low absolute risk for postmenopausal women <50
older women have a much more increased risk

23
Q

what is the treatment of menopause?: drugs

A

tibolone (synthetic prohormone)
raloxifene (SERM, agonist)
tamoxifen (SERM, antagonist)

24
Q

what is tibolone? what are the associated risks?

A

oestrogenic, progestognenic and weak androgenic actions

increased risk of stroke
possible increase in risk of breast cancer

25
Q

HRT, when is oestrogen-only treatment used?

A
  • for women with hysterectomies i.e. have no endometrium

- post-menopausal (don’t want further kids)

26
Q

what is raloxifene?

A

selective oestrogen receptor modulator
tissue selective:
- oestrogenic in bone
- anti-oestrogenic in breast and uterus

used to treat and prevent postmenopausal osteoporosis

27
Q

which risks are prevented and which are increased by raloxifene?

A

risk of vertebral fractures and breast cancer reduced

risk of fatal stroke, VTE increased

does not affect vasomotor symptoms

28
Q

what is tamoxifen?

A

SERM, anti-cancer drug
- anti-oestrogenic in breast
- BUT oestrogenic in uterus
used to treat oestrogen-dependent breast tumours and metastatic breast cancers

29
Q

what are the phases of the ovarian cycle?

A

follicular
ovulatory
luteal

30
Q

what are the phases of the endometrial cycle?

A

menstruation
proliferative
secretory

31
Q

what are the main stages of follicle growth?

A

primordial follicle
Graffian follicle
corpus luteum

many follicles present
some mature
only one ovulates

32
Q

what is the pre-antral follicle?

A

ovum surround by cells

33
Q

what is the early antral follicle?

A

ovum with granulosa and thecal cells
antral filled space

becomes the late antral

34
Q

what will the dominant follicle release and what effect does this have before ovulation?

A

secretes oestrogen

this lowers LH (before LH surge) and causes the other follicles to undergo atresia

35
Q

at what stage of the endometrial cycle does the dominant follicle release oestrogen?

A

proliferative phase

36
Q

where is aromatase found in the ovary? what is the function?

A

in granulosa cells (oestrogen producer)

convert androgens created by thecal cells into oestrogen

37
Q

what is the role of cervical crypts?

A

produce mucus to create a less hostile environment for sperm

38
Q

what effect does high oestrogen have on basal temperature?

A

decreases

progesterones do the opposite

39
Q

what stimulates follicle maturation?

A

FSH

40
Q

what are the target sites for oestrogen?

A
  • bone
  • muscle
  • endometrial growth
  • glands and breast
41
Q

what is the corpus luteum?

A

a hormone-secreting structure formed after the ovum has been expelled, it is degraded after a few days if no pregnancy

42
Q

what is menopause?

A

permanent cessation of mensturation

loss of ovarian follicular activity

43
Q

simply, what are the complications of menopause?

A

CVD and osteoporosis

44
Q

why is HRT used in menopause?

A

to control the vasomotor symptoms e.g. hot flushes

nb SERMs have no effect on these symptoms

45
Q

what is combined in HRT to prevent endometrial hyperplasia?

A

oestrogen and progesterone

46
Q

when is oestrogen given alone in HRT?

A

only in hysterectomy (no endometrium for unnecessary proliferation)

47
Q

how is HRT administered (frequencies)?

A

cyclical

oestrogen every day
progesterone evert 12-14 days

48
Q

what is a benefit of tibolone?

A

reduced fracture risk

49
Q

what are the risks with using raloxifene?

A

increases risk of DVT/

fatal stroke

50
Q

what are these drugs oestrogenic in?

  • raloxifene
  • tamoxifen
A
  • raloxifene: in bone (not breast or uterus)

- tamoxifen: in endometrium/uterus and bone

51
Q

where is raloxifene anti-oestrogenic?

A

breast and uterus

52
Q

what sort of cancers should tamoxifen be used for given its oestrogenic effects in the uterus?

A

for oestrogen- DEPENDENT breast tumours/
metastatic breast cancers

it is anti-oestrogenic in the breast by antagonism

53
Q

what effect does the combined contraceptive have on ovulation?

A

suppresses ovulation by negative feedback on hypo-pit

54
Q

what effect does progesterone have when used in contraceptive?

A

thickens cervical mucus to make a hostile environment for the sperm