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Bloc I - Reproduction > Sept6 M1,2-Contraception > Flashcards

Sept6 M1,2-Contraception Flashcards

1
Q

pearl index def

A

pregnancy rate after 1 year of exposure per 100 women years, using this method only

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2
Q

best methods of contraception

A
  • sterilization (surgical)
  • injection
  • implants
  • IUD
  • OCP
  • vaginal ring
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3
Q

common point between non surgical contraception methods with lowest pearl index

A

contain chemicals

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4
Q

why OCP has 98-99% efficacy

A

some individuals metabolize the steroids in the pill faster, shorter half life and may still get pregnant
very low nbr of people but till possible

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5
Q

OCP component and mech

A

E + P

  • estrogens blocks hypoth and pit level release of LH and FSH (no LH surge + no FSH so follicle can’t become secondary antral) so block ovulation
  • progestin affects ovary and prevents folliculogenesis, alters secretions of endometrial lining to make it thicker and harder for sperm to fertilize the egg
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6
Q

follicles seen and not seen when using OCP

A
  • primordial present
  • primary present
  • antral ABSENT (bc still have LH, FSH, P and E but no LH surge). have less steroids in circulation
  • no Graafian follicles
  • REPRESSED FOLLICULOGENESIS*
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7
Q

endothelial lining in woman using OCP

A
  • thinner bc no stim by steroids. lower steroids level than normal. + diminished blood loss (halved)
  • endo not receptive for implantation
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8
Q

SEs of OCP

A

Are beneficial SEs

  • repression of folliculogenesis bc of steroids (indep of FSH, LH)
  • P makes repro tract more visquous, more protein secretions, thicker and harder for egg to move + prevents sperm from getting there
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9
Q

sx reduced with the OCP

A
  • PMS
  • menstrual cramps
  • acne
  • bleeding
  • anemia
  • ovarian cysts
  • breast tenderness
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10
Q

why OCP helps reduce sx of menstrual cycle

A

bc no big surge in steroids

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11
Q

OCP reduces risk of what diseases

A
  • ovarian, endometrial, GI and uterine cancer
  • ovarian cysts
  • PID
  • iron deficiency anemia
  • ectopic pregnancy
  • fibrocystic breast disease
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12
Q

OCP SEs

A
  • nausea
  • breast tenderness
  • mid cycle bleeding
  • weight gain
  • go away in 1-6 mo*
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13
Q

why imp to monitor OCP pt in first 3 months

A

risk of

  • migraine headaches
  • liver disease
  • high BP
  • gallbladder disease
  • blood clots
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14
Q

does OCP cause breast cancer

A

no. if it does, risk increase is very low

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15
Q

absolute contraindications to OCP

A
  • hx of breast ca
  • hx of blood clots (if high dose OCP)
  • liver, kidney dz
  • unexplained uterine bleeding
  • pregnancy
  • smokers over 35
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16
Q

OCP is given how

A
  • 3 weeks of E and P

- 1 week of nothing

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17
Q

emergency contraception works how

A
  • smaller endometrium, not receptive for implantation, if fertilization has occured
  • decrease in progestin after the effect of pill goes away causes the withdrawal bleed
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18
Q

how to use emergency contraception

A

within 72 hours of unprotected sex, use one or two doses to induce withdrawal bleed

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19
Q

effectiveness of emergency contraception

A

75-97%

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20
Q

ulipristal acetate is what

A
  • drug used in morning after pill*
  • selective progesterone R modulator.
  • antag or agonist
  • both work bc even if agonist, when effect goes away, P stops and get the menses
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21
Q

contraceptive patch haract

A
  • no first pass effect
  • replaced weekly
  • steroids are lipophilic so easy abso
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22
Q

patch efficacy and compliance

A
  • efficacy = or less than OCP (bc not weight adjusted)

- compliance >than OCP

23
Q

options other than monthly bleed OCP

A
  • continuous OCP with no monthly bleeds
  • three-month cycle OCP
  • one a year bleed OCP
  • does no harm, no increase in cancer or complications*
24
Q

E and P of OCP effect on HPO axis

A
  • E blocks LH from rising + affects endo lining
  • P blocks effect of E on cells
  • they bind steroid binding proteins*
25
Q

meds that reduce the half life of OCP (P and E)

A

drugs that induce the p450s in the liver and are metabolized by it. make the steroids metab faster

  • rifampin (for TB)
  • any drug blocking entero-hepatic circulation like Abx (kill bugs that prolong steroid half life)
26
Q

goal of the morning pill

A

cause a menses

27
Q

what happens when stop OCP

A

body readapts immediately. phase where follicle grows rapidly (secondary antral) can occur. menses immediately when stop

28
Q

intrauterine devices rules

A

bigger and more nasty looking = works better

*larger surface area = lower pregnancy rate but higher bleeding rate

29
Q

2 types of IUD

A
  • with copper

- with progestin (Mirena for ex)

30
Q

charact of copper IUDs and IUDs in general

A
  • fertility returns as soon as removed
  • copper = only working on ability of endo to receive blastocyst
  • copper = cause 2x normal menstrual blood flow
31
Q

contraindications to IUDs

A
  • severe pain with periods (dysmenorrhea)
  • copper allergy
  • gono or chlam infection
  • endometriosis or other current abnormal vaginal bleeding (bc copper IUD witll cause more blood less and pain in endometriosis)
  • etc
32
Q

progesterone IUD mech of action

A
  • continuously stims endo to make proteins
  • suppresses endometrial prolif (stim by estrogen Rs)
  • blocks lymphocyte recruitments (which would help implantation)
33
Q

progesterone vs copper IUD

A

less bleeding with P IUD

34
Q

medicated vaginal ring is what

A

same principle as progesterone IUD but as a vaginal ring

35
Q

contraceptive implant def

A
  • injection of 6 tubes of silicone silastic polymer that are permeable to steroids (one used is progesterone)
  • progesterone is released over 5 years
36
Q

main problem with contraceptive implant

A

possible irregular bleeding or spotting (but no cycles per se).
-bleeding is also a problem of copper IUDs

37
Q

contraindications to contraceptive implant (sustained progestin)

A
  • liver disease
  • breast cancer
  • unexplained uterine bleeding (same contraindication as copper IUD)
  • blood clots
38
Q

immunocontraception for females is what

A

immunize a woman to the zona pellucida proteins (Zip-1), to GNRH LH or FSH, to sperm proteins and to bHCG

39
Q

how vaccine against ZP would work

A

an antibody binds the ZP. this prevents the sperm from entering it

40
Q

how vaccine against beta unit of HCG would work

A
  • this unit is what makes it diff from FSH and LH (bc HCG, FSH and LH have the same alpha unit
  • vaccine blocks HCG ability to rescue CL of pregnancy
41
Q

immunocontraception success rates%

A
  • to ZP = 75%
  • to bHCG = 90-95% (reversible effect)
  • to sperm proteins = 75%
42
Q

hormonal male contraception groups what

A

injections, implants or creams of

  • testo alone
  • testo + P + E
  • novel androgens
43
Q

how male contraception works

A

want to keep the serum testo normal to block LH and FSH

44
Q

what happens to serum testo if give testo only as male contraceptive

A
  • low dose = not changing, normal
  • interm dose = not changing, normal
  • high dose = testo goes up
45
Q

what happens to spermatogenesis if give testo only as male contraceptive

A
  • low dose = working
  • interm dose = not working (very low testo)
  • high dose = working again
46
Q

in testo only male contraception, why spermatogensis blocked at interm dose and works at high dose

A
  • interm dose = testo suppresses LH secretion (axis) so Leydig cells prod of testo drops so less intragonadal testo
  • high dose = even though Leydig cells suppressed, we’re giving enough testo exogenously to maintain spermatogenesis
47
Q

effect of the testo + estrogen male contraception

A
  • serum LH goes down
  • serum testo increases transiently and back noral
  • intragonadal testo goes down
48
Q

charact of testo + estrogen male contraception

A

complete spermatogenesis is achieved if wait lng enough. + will take long to reverse the action

49
Q

alternatives to testo in T and T+E male contraception

A

can use analogs that are more potent like MENT (10x more potent)

50
Q

dimenthandrolone undecanoate is what

A

new male contraceptive that is both an androgen and progestin R agonist

51
Q

non hormonal male contraception is what

A
  • chemo (causes azoospermia)
  • WIN18446 (inhibits enzyme in testis making retinoic acid into retinol (vitA). vitA is essential for spermatogenesis
  • Gossypo (antispermatogenic effect via mt K+ channel suppression) bad SEs
  • JQ1 (block hyperacetylation of histones necessary for sperm nucleus condensation)
  • inhibitors of EDD maturation process
  • other targets like proteins for fertilization, maturation in EDD, etc.
52
Q

male contraception acting on inhibition of fertilizing ability of sperm and on EDD maturation

A
  • EDD 5a reductase inhibitors (less testo in EDD = less sperm motility + binds egg less)
  • nifedipine (CCB), blocks enzyme action for fertilization
  • mifepristone (progesterone R on sperm necessary for sperm to enter egg)
  • EPPIN (block EDD protease eppin, necessary for maturation)
53
Q

immunocontraception in males

A
  • nonexistent

- no research on it atm

Bloc I - Reproduction (57 decks)

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