lect 14 female contraception Flashcards

1
Q

to create contraceptives we manipulate which system for the release of what

A

endocrine system for the release of sperm or oocyte

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2
Q

major components of the endocrine system pertaining to contraception

A

GnRH (hypothalamus)–> LH, FSH (gonadotropic cell in anterior pituitary)–> testis, ovaries (gametogenesis, gonadal hormone production)

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3
Q

effect of LH and FSH on ovary

A

release of estrogen and progesterone, increase steroidogenesis, stimulate maturation of ovarian follicle

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4
Q

estrogen and progesteron stimulate what

A

folliculogenesis and secondary sex characteristics

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5
Q

negative feedback loop of HPO axis

A

negative feedback on hypothalamus and pituitary to reduce GnRH and LH and FSH

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6
Q

what does pulsatile mean for GnRH, LH, FSH

A

shape of the chemical message matters. rhythmic, intermittent propagation

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7
Q

FSH regulates what

A

follicle growth and maturation in the ovaries

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8
Q

primary follicles develop into what

A

oocytes

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9
Q

what happens to mature follicles

A

they get ovulated and become the corpus luteum

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10
Q

cells that surround to development of oocytes, make steroid hormones from interaction

A

granulosa and theca cells

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11
Q

theca cells make what

A

testosterone

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12
Q

granulosa cells make what

A

make estradiol from testosterone via aromatase

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13
Q

testosterone to estradiol process

A

cholesterol side chain cleavage to progesterone. progesterone becomes testosterone. aromatase makes estradiol from testosterone

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14
Q

what induces the production of estradiol in granulosa cells

A

FSH

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15
Q

what hormone acts on theca cells and what does it do

A

LH and it increases steroid synthesis and synthesis of FSH receptor to magnify FSH response

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16
Q

role of progesterone in steroidogenesis

A

cross roads. can be made into glucocorticoids in adrenal glands and also act in testes and ovaries to make testosterone and estrogen

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17
Q

estrogen and progesterone act with what receptors

A

nuclear hormone receptors in the same way that glucocort. do

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18
Q

two isoforms of estrogen receptors

A

alpha and beta

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19
Q

true or false? there are more selective estrogen receptor ligands and modulators that act differentially with ERalpha or ERbeta

A

true

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20
Q

estrogen also acts on receptors where for implantation of fertilized oocyte

A

acts in endometrium so that cells there can proliferate and become more receptive to implantation

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21
Q

possible binding for both estrogen and progesterone to cell membrane receptors may cause what

A

nongenomic changes

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22
Q

oocyte is released where

A

into fallopian tube

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23
Q

how many ovulated oocyte per menstrual cycle

A

one

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24
Q

goal of contraception

A

prevent release or fertilization by sperm of ocyte

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25
Q

contraceptive drugs can also be used for…

A

for ovulation induction

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26
Q

hormone replacement therapy use

A

decrease in estrogens and progesterones leading to menopause

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27
Q

chemical analogs of progesterone and estrogen can also be used for…

A

cancer chemotherapy

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28
Q

most effective contraceptives

A

implants, IUD, sterilization

29
Q

higher risks of pregnancy are with what contrceptives

A

male and female condoms, withdrawal

30
Q

what peak triggers follicle rupture and ovulation

A

LH peak

31
Q

estrogen peaks where

A

during follicle rupture

32
Q

progesterone peaks when

A

after ovulation, mature corpus luteum

33
Q

ovulation happens when during cycle

A

mid cycle

34
Q

what degenerates and produces steroids when woman not pregnant

A

corpus luteum

35
Q

if woman becomes pregnant what happens to uterine endometrium

A

hormones prepare the endometrium lining. increases after ovulation. to create a favorable environment for fertilized zygote to implant

36
Q

what creates menstruation

A

degeneration of endometrium lining

37
Q

positive feedback of HPO axis

A

increase in estradiol above a certain threshold stimulates GnRH and LH release which stimulates oocyte release

38
Q

negative feedback of HPO axis

A

constant release of estradiol and progesterone prevents LH and FSH release

39
Q

measuring temperature and detecting ovulation with thermometer method

A

fertility awareness based method

40
Q

in fertile woman temperature increase because of what

A

progesterone release after ovulation

41
Q

oral contraceptives contain what

A

analogs of estrogen and progesterone

42
Q

why use analogs in contraceptive pills

A

because they have longer half lives

43
Q

contraceptive pills use to be monophasic meaning?

A

each tablet contained a fixed amount of estrogen and progestin

44
Q

contraceptive pills are now multiphasic meaning?

A

concentration vary during the cycle to try to mimic natural hormones

45
Q

how is release of oocyte prevented and LH surge prevented and FSH

A

constant low amounts of estrogen given to prevent cycling. constant negative feedback

46
Q

contraceptive effect on fsh

A

no fsh stimulation of follicle maturation in ovary

47
Q

contraceptive effect of sperm

A

less able to swim to oocyte by changing composition of the protein the sperm has to swim. decreased fertilization

48
Q

perfect use failure rate of contraceptive vs typical failure rate

A

0.3% vs 9%

49
Q

failure of pill contraceptive is related to what

A

poor compliance like forgetting pill

50
Q

metabolism of analogs

A

metabolized in the liver and gets conjugated to be released in GI tract.
Deconjugated by bacteria so that it can be reabsorbed in liver and released on circulation

51
Q

problems with taking some antibiotics with contraception

A

antibiotic alters enterohepatic circulation such that they kill bacteria that would help remove congugated compound in drug and allow it to get reabsorbed. But antibiotics makes no reabsorption and drug excreted so no recycling of estrogen and progesterone, lower levels and cause normal cycle to come back

52
Q

advantages of oral contraceptive (6)

A
  1. periods more regular
  2. can be used by women over 40
  3. may decrease menstrual cramps, acne
  4. does not interfere with sexual intercourse
  5. reduces risk of ovarian cancer
  6. increases bone density
53
Q

disadvantages of oral contraceptives (3)

A
  1. increase risk of blood clots
  2. my by related to slight increase in breast cancer
  3. cant be used by smokers over the age of 35
54
Q

risk of oral contraceptives relating to others

A

very low risk compared to others

55
Q

contraceptive patch Evra mechanism

A

steroids penetrate the skin and into circulation so they cana be delivered to the hypothalamus and other tissues

56
Q

pearl index of patch

A

0.88 so better than pill. half the rate of pregnancy in women after 6 cycles of taking the pill

57
Q

compounds in patch

A

150 microg NGMN and 20 microg EE

58
Q

contraceptive implants effectiveness

A

99%

59
Q

IUD mechanism and types

A

inserted in uterus. Copper T delivers copper and progstin iud delivers progesterone

60
Q

common analog of progesterone

A

levonorgestrol

61
Q

emergency contraceptive and mechanism

A

plan b: levonorgesterol.

temporary block of ovulation

62
Q

when should we take plan b

A

within 72 hours of unprotected sex

63
Q

effectiveness of plan b

A

75-97% depending on time after intercourse

64
Q

selective progesterone receptor modulator and is a partial antagonist and agonist

A

ulipristal acetate

65
Q

ulipristal acetate efficacy and days

A

similar to that of progestin. effective for up to 5 days after intercourse

66
Q

what drugs interact with contraceptive by inducing p450s and how

A

barbiturates, phenytoin (anti-epileptics), rifampicin. Contraceptives get metabolized by p450s that have been induced by these drugs

67
Q

why should the pill not be taken for smokers over 35

A

increased mortality in smokers who take the pill after the age of 35 even more at 45 compared to smokers who are younger

68
Q

patch compliance vs pill compliance

A

more compliance in patch and is not affected by age

more compliance in pill for older people, less compliance in younger people

69
Q

implants contraceptives most contain what

A

progesterone analog levonorgestrel