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PHAR 300 > Contraception > Flashcards

Contraception Flashcards

1
Q

what are the modern methods of contraception?

A
  • female and male
    sterilization
  • oral hormonal pills
  • the intra-uterine device (IUD)
  • male and female condoms
  • injectables
  • the implant (including Norplant)
  • vaginal barrier methods
  • emergency contraception.
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2
Q

what are traditional or natural methods of contraception?

A
  • rhythm (periodic abstinence)
  • withdrawal
  • lactational amenorrhoea
    method (LAM)
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3
Q

What are the different family planning (contraception) methods? what is their effectiveness and reversibility?

A
  • male condom (18% - reversible)
  • female condom (21% - reversible)
  • withdrawal (22% - reversible)
  • fertility awareness-based method (24% - reversible)
  • sponge (12-24% - reversible)
  • spermicide (28%- reversible)
  • injectable (6% - reversible)
  • pill (9% - reversible)
  • patch (9% - reversible)
  • ring (9% - reversible)
  • diaphragm (12% - reversible)
  • implant (0.05% - reversible)
  • IUD (0.12% - reversible)
  • female/male sterilization (0.15% (male) and 0.5% (women) - irreversible)
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4
Q

what are the main components of the endocrine system regarding male and female reproduction?

A
  • GnRH produced and released by hypothalamus
  • goes to anterior pituitary where it releases LH and FSH
  • goes to testes or ovary where hormones are produced
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5
Q

what is a hormone?

A

a chemical messenger that circulates in the body and has an effect on distant cells

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6
Q

explain the hypothalamic-pituitary-ovarian axis with their feedback loops.

A
  • hypothalamus releases GnRH and stimulates pituitary
  • releases LH and FSH, which stimulates ovary
  • stimulates maturation of ovarian follicles and production estrogen and progesterone
  • estrogen has negative feedback on hypothalamus
  • progesterone has negative feedback on pituitary
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7
Q

is GnRH, LH, and FSH released in a constant way?

A

no they are released in a pulsatile way

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8
Q

on which cells does LH act on and what does it do? (In women)

A
  • acts on theca cells
  • increases steroid synthesis
  • increases amount of FSH receptors
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9
Q

on which cells does FSH act on and what does it do? (In women)

A
  • acts on granulosa cells
  • regulates follicle growth and maturation
  • increases activity of cholesterol side chain cleavage (by CYP11A1 – to make progesterone)
  • increases activity of aromatase (to make estradiol)
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10
Q

What is the action of progesterone?

A

two response types:
- slow genomic process where receptor goes to nucleus and activates genes
- fast nongenomic process where receptor activates secondary messengers

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11
Q

what are the two types of estrogen receptors and what do they do?

A
  • ER-alpha: leads to nuclear response
  • ER-beta: leads to nongenomic response
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12
Q

what are the uses of estrogens and progestins as drugs?

A
  • contraception
  • ovulation control
  • hormone replacement therapy
  • cancer chemotherapy
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13
Q

what is the positive feedback regulation seen when looking at the menstrual cycle?

A
  • estradiol concentration increases above a threshold (right before ovulation –after menses)
  • this triggers GnRH
  • this causes the LH surge
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14
Q

what is the effect of the LH surge in ovulation regulation?

A

it stimulates follicle rupture and ovulation

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15
Q

what is the negative feedback regulation seen when looking at the menstrual cycle?

A
  • after ovulation there are high levels of estradiol, which causes negative feedback so decreases levels of FSH and LH
  • corpus luteum releases high levels of progesterone, so there is an increase in luteal phase, which causes even further inhibition of FSH
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16
Q

how does fertility-awareness based contraceptive methods work?

A

basal body temperature is lower during follicular phase and higher during luteal phase due to progesterone levels

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17
Q

what are the different types of oral contraceptive pills?

A

combination pills: contain both estrogen and progestin analogues
- monophasic: 1 month cycle (all pills are the same)
- multi-phasic: active pills contain different amounts
- extended cycle: typically 12 weeks of active pills

progestin-only pills

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18
Q

How do oral contraceptives pills work?

A
  • prevent the ovary from releasing an egg
  • thicken the cervical mucus to make it difficult for sperm to reach the egg
  • thin the lining of uterus to make implantation of a fertilized egg more difficult
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19
Q

what is perfect use failure rate of contraceptive pills vs typical use rate? why is this seen?

A
  • perfect: 0.3%
  • typical: 9%
  • due to poor compliance
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20
Q

What are different drug-drug interaction mechanisms which may affect oral contraceptives?

A
  • induction of P450s: would metabolize hormone faster
  • entero-hepatic circulation change: affects absorption and distribution
  • binding to plasma proteins
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21
Q

what are advantages of oral contraceptive pills?

A
  • periods more regular
  • can be used for women over age 40
  • may decrease menstrual cramps, bleeding, anemia
  • may be associated with decreased risk of ovarian and endometrial cancer, and colorectal cancer
  • may decrease breast tenderness and acne
  • does not interfere with sexual intercourse
  • may increase bone density
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22
Q

what are disadvantages/contradictions of oral contraceptive pills?

A
  • increased risk of venous thromboembolism
  • slight increase in breast cancer
  • increased risk for smokers (more risk change with increased age)
23
Q

how do contraceptive patches work?

A
  • slowly release hormones (estradiol and progestin derivatives)
  • must reapply new patch weekly (in reversible)
24
Q

How does the efficacy and compliance of the patch compare to the pill?

A
  • high efficacy of patch: after 6 cycle, pregnancy possibility is half than pill users
  • patch may be less efficacious in women more than 90kg (198lbs)
  • much higher compliance for patch than pill (we see lower pill compliance with lower age but no change seen with patch)
25
Q

What do implants contain?

A

Progesterone analogu

26
Q

How do mean LH levels differ in women who use implants?

A

When there is normally an LH surge, there is a very slight increase but it is much lower

27
Q

What are two types of IUD? How long do each last?

A
  • hormonal: release progesterone analog (levonorgestrel) — lasts 3-5 years
  • copper: copper wrapped around the base — lasts 10 years
28
Q

What are the two types of morning after pills?

A
  • plan B: progesterone analog
  • Ella: selective progesterone receptor mediator
29
Q

How do morning after pills work?

A
  • temporarily block ovulation
  • prevent fertilization
30
Q

How is pregnancy medically terminated in the first 9 weeks?

A
  • mifepristone: progesterone receptor antagonist
  • misoprostal: prostaglandin analog which dilates the cervix and indices uterine contractions
31
Q

What is the path of sperm in the male reproductive system?

A

Testis to epididymis to vas deferens

32
Q

Where are leydig cells located? What do they produce?

A
  • are outside the seminiferous tubules
  • produce high local testosterone
33
Q

How much testosterone do adult male produce daily?

A

5-7 mg

34
Q

What does the inside of a seminiferous tubules contain? What cells?

A
  • the outer ring of the inside has Sertoli cells
  • then from outer to inner: primary spermatocyte, immature spermatid, mature spermatid
35
Q

How long is spermatogenesis?

A

64 days

36
Q

what are the feedback mechanisms operating in the male?

A
  • negative feedback on hypothalamus and pituitary from testosterone and estradiol from leydig cells
  • negative feedback on pituitary by sertoli cells
37
Q

where is the human androgen receptor gene located?

A

on the X-chromosome

38
Q

explain testosterone biosynthesis?

A
  • inside of leydig cells biomolecules come together (cholesterol)
  • makes pregnenolone
  • converted to progesterone by 3B-HSD
  • converted to androstenedione by CYPc17
  • converted to testosterone by 17B-HSD, which can also be metabolized into estradiol
39
Q

what molecules can interact with the androgen receptor? how is each molecule made/released?

A
  • testosterone: made and released from leydig cells
  • DHT: testosterone converted to DHT with 5a-reductase
40
Q

what do testosterone, DHT, and estradiol each affect (which parts of body and how)?

A
  • testosterone: muscle (increase strength), bone marrow (stem cells), bone (linear growth), brain (libido, aggression)
  • DHT: external genitalia, prostate, skin, hair
  • estradiol: bone, brain, breast
41
Q

is a vasectomy reversible?

A

a procedure does exists (vasovasostomy) but doesn’t always work

42
Q

what is the effect of increasing sustained doses of testosterone in rabbits for serum testosterone and spermatogenesis?

A
  • serum: constant for many doses until reach a threshold point where concentration drastically increases since that is point where exogenous testosterone is used
  • spermatogenesis: high when body still used endogenous hormone, but at some point it decreases until there is no spermatogenesis (before the threshold point seen in serum concentration), then increases again since body uses exogenous hormone
43
Q

how does suppression of spermatogenesis compare in rabbits, rats, and monkeys?

A
  • works fully in rabbit
  • doesn’t work in rats but does get to a pretty low point
  • not effective in monkeys
44
Q

what is the effect of exogenous testosterone implants?

A
  • it inhibits LH secretion, which causes decreased LH and FSH so there is low intratesticular testosterone
45
Q

what is the response of T-E implants in rats over time for: serum LH, T secretions, serum T, serum E2, spermatogenesis.

A

-serum LH: completely gone
- T secretions: decreases until a basically zero point after 9-16 days
- serum T: stays the same
- serum E2: increases at first then decreases to a stable point (higher than normal but not too high)
- spermatogenesis: completely gone after 57 days

46
Q

what is dimethandrolone undecanoate and why would it be a good option for male contraception?

A
  • androgen and progesterone receptor agonist
  • not aromatized (no estrogenic activity)
  • not a substrate for 5a-reductase
47
Q

why are drugs that cause azoospermia not a good option for contraception?

A
  • they block spermatogenesis by blocking meiosis so is cytotoxic
  • also would probably be an irreversible effect
48
Q

is targeting retinoic acid a good option for male contraception?

A
  • could maybe be but drugs that do do that have adverse effects when mixed with alcohol, so men would have to never drink when taking this
49
Q

is the inhibition of BRDT a good option for male contraception?

A
  • no since would inhibit other bromodomain proteins leading to toxicity
50
Q

what are possible way of inhibiting the fertilizing ability of sperm?

A
  • blockers of epididymal function: steroid 5a-reducatse inhibitors
  • nifedipine (Ca+ channel blocker): prevent enzyme action needed for fertilization
  • mifepristone: makes sperm temporarily immotile
  • EPPIN (small protein coating sperm): affects sperm motility
51
Q

what are the serum testosterone concentrations throughout male lifespan?

A
  • fetal: medium
  • drops when born
  • neonatal: back to medium
  • drops when get to pre-pubertal
  • increases in pubertal
  • adult: gets to a stable point
  • slowly decreases when gets older to a point similar to beginning
52
Q

what are symptoms associated with testosterone deficiency?

A
  • sexual dysfunction
  • adverse metabolic effects
  • decreased bone density
  • cognitive function change
53
Q

testosterone therapy is useful in ______

A

androgen deficiency

PHAR 300 (12 decks)

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