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PHS 933 > Block 2 Lecture 2 -- Contraception > Flashcards

Block 2 Lecture 2 -- Contraception Flashcards

1
Q

Theoretical vs. actual efficacy of OCs.

A

99 vs 92

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2
Q

Describe monophasic OC dosing

A

fixed E + P for 21 days, then 7 placebo

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3
Q

Describe extended cycle OC dosing.

A

84 active + 7 placebo

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4
Q

What brands are extended-cycle?

A

seasonale, yaz

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5
Q

When are biphasics, triphasics, multiphasics used?

A

for breakthrough bleeding

    • varied E + P dosing
    • no evidence of bleeding improvement though
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6
Q

What is Lybrel?

A

OC that eliminates hormonal cycle

– 365 active pills

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7
Q

What is the dosing in Lybrel?

A

20 ug + 90 ug levonorgestrel

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8
Q

What are the progestins with less androgenic activity?

A

1) desogestrel
2) norgestimate
3) drosperinone

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9
Q

What is the advantage to drosperinone?

A

anti-aldosterone (MR antagonist) for less bloating, weight gain

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10
Q

What is the disadvantage to drosperinone?

A

higher risk of VTE vs. levonorgestrel

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11
Q

What is the difference in 3rd/4th gen OCs?

A

new progestins are less androgenic

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12
Q

Describe efficacy of progestin-only birth controls.

A

less effective; associated with regular bleeding

    • 40% still ovulate (ectopic risk)
    • must be taken at same time q day
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13
Q

When are lo-dose OCs preferred?

A

adolescents, underweight (110 lb), older than 35, perimenopausal

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14
Q

What is defined as very low dose OC?

A

20-25 ug EE

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15
Q

What is defined as low-dose OC?

A

less than 35 ug EE (or less than 0.5 mg norethindrone or equivalent)

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16
Q

What is defined as normal dose OC?

A

35-50 ug

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17
Q

What dose should not be exceeded in any patient for OC?

A

50 ug (VTE)

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18
Q

When is normal (35-50ug) dosing preferred?

A

160+ lb

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19
Q

What is first choice in OC selection?

A

low-dose (since all OCs are equally effective)

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20
Q

When are monophasics preferred?

A

if easy-management is a must

– can just skip placebo to lengthen cycle

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21
Q

When are bi- and tri-phasics preferred?

A

when lessening spotting and progestin ADRs is a concern

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22
Q

When are extended formulation OCs preferred?

A

when dysmenorrhea or menstrual issues are present

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23
Q

When are progestin-only OCs preferred?

A

if any of the following:

1) migraines w/ aura
2) thromboembolic disease
3) cerebrovascular disease
4) SLE
5) 35+ yo and smoker, obesity, OR HTN

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24
Q

What are the APIs in the transdermal patch (ortho evra)?

A

EE + norelgestromin, a norgestimate metabolite

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25
Q

When should a transdermal patch be avoided?

A

1) if 198+ lbs.

2) if thromboembolic risk is a concern

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26
Q

What effect do CHCs have on dyslipidemia?

A

none

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27
Q

theoretical vs actual efficacy of Ocs

A

99 vs 92

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28
Q

Describe monophasic OC dosing

A

fixed E+P for 21 days, then 7 placebo

How well did you know this?
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29
Q

Describe extended-cycle OC dosing

A

84 active + 7 placebo

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30
Q

What brands are extended cycle?

A

seasonale, yaz

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31
Q

When are biphasics, triphasics, multiphasics used?

A

for breakthrough bleeding. varied E+P dosing; no evidence of bleeding improvement though

How well did you know this?
1
Not at all
2
3
4
5
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32
Q

What is Lybrel?

A

OC that eliminates hormonal cycle (365 active pills)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the dosing of lybrel?

A

20 ug EE + 90 ug levonorgestrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the progestins with less androgenic activity?

A

1) desogestrel; 2) norgestimate; 3) drosperinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the advantage to drosperinone?

A

anti-aldosterone (MR antagonist) for less bloating, weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the disadvantage to drosperinone?

A

higher risk of VTE vs. levonorgestrel

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37
Q

What is the FDA-required warning on drosperinone?

A

higher risk of VTE vs. levonorgestrel

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38
Q

What is the difference in 3rd/4th-gen Ocs?

A

new progestins are less androgenic

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39
Q

Describe efficacy of progestin-only birth controls

A

less effective; associated with regular bleeding. 40% still ovulation (ectopic risk). Must be taken at same time q day

How well did you know this?
1
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40
Q

When are low-dose OC’s preferred?

A

1) adolescents; 2) underweight (110 lb); 3) older than 35; 4) perimenopausal

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41
Q

What is defined as very low dose OC?

A

20-25 ug EE

How well did you know this?
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42
Q

What is defined as low-dose OC?

A

less than 35 ug EE (or less than 0.5 mg norethindrone or equivalent)

How well did you know this?
1
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2
3
4
5
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43
Q

What is defined as normal dose OC?

A

35-50 ug

44
Q

What dose should not be exceeded in any patient for OC?

A

50 ug (VTE risk)

45
Q

When is normal (35-50 ug) dosing preferred?

A

160+ lbs

46
Q

What is first choice in OC selection?

A

low-dose (since all OC’s are equally effective)

47
Q

When are monophasics preferred?

A

if easy-management is a must. Can just skip placebo to lengthen cycle

48
Q

When are bi- and tri-phasics preferred?

A

when lessening spotting and progestin ADRs is a concern

49
Q

When are extended-formulation OC’s preferred?

A

when dysmenorrhea or menstrual issues are present

50
Q

When are progestin-only OC’s preferred?

A

if any of the following: 1) migraines w/ aura; 2) thromboembolic dz; 3) cerebrovascular disease; 4) SLE; 5) 35+ yo and smoker, obesity, or HTN

51
Q

What are the APIs in the transdermal patch (ortho evra)?

A

EE + norgestimate (active metabolite = norelgestromin)

52
Q

When should a transdermal patch be avoided?

A

1) if 198+ lbs; 2) if thromboembolic risk is a concern

53
Q

Why does the transdermal patch carry a higher thromboembolic risk?

A

estradiol 60% higher due to first-pass avoidance

54
Q

Describe application of ortho evra.

A

1-2x/week to ab/hip/butt for 3 weeks

55
Q

What are the APIs in nuvaring?

A

EE + etonorgestrel

56
Q

What are the advantages to nuvaring?

A

as effective as COC’s but lower systemic estrogen dose

57
Q

Describe administration of nuvaring?

A

insert x 3 weeks then remove

58
Q

What is the actual effectiveness of depo provera (DMPA)?

A

97% (better)

59
Q

What is the MoA of DMPA?

A

suppress estradiol production to inhibit ovulation for 3 months

60
Q

What are ADRs of DMPA?

A

1) 10-18 month delay to fertility upon cessation; 2) decreased BMD; 3) menstrual irregularities with spotting/heavy bleeding (30% in first year, 10% after, may get amenorrhea)

61
Q

Describe dosing of DMPA.

A

150 mg DMPA IM or SQ

62
Q

What are the warnings for DMPA?

A

don’t use longer than 2 yrs (BMD) and monitor bone density

63
Q

What is the API in the implant (implanon)?

A

etonorgestrel

64
Q

What is the dosing of the implant?

A

3 yr implant in skin of upper arm

65
Q

What is the effectiveness of the implant?

A

suppresses ovulation in 97%

66
Q

What are the ADRs of the implant?

A

irregular menstrual bleeding/spotting; BMD effect and fertility delay probable

67
Q

What is the most widely used form of contraception?

A

IUD

68
Q

What is the actual effectiveness of IUDs?

A

99% (paragard has slightly higher failure rate)

69
Q

What is the MoA of IUDs?

A

1) reduce sperm motility by thickening mucous; 2) interfere with implantation; Paragard also reduces sperm viability

70
Q

What are the active ingredients in IUDs?

A

mirena/skyla/liletta = levonorgestrel; paragard = cu ions

71
Q

How long is paragard active?

A

10 years

72
Q

How long is mirena active?

A

5 years

73
Q

What is the dosing in mirena?

A

10 ug/day

74
Q

What is an ADR of paragard?

A

PID, may increase blood flow by 35% leading to dysmenorrhea

75
Q

What is an ADR of mirena?

A

PID, overall reduced menstrual blood flow, but may increase spotting in first year

76
Q

When should progestin-only emergency contraception be used?

A

within 72h (89% effective); but may be effective up to 5 days

77
Q

What is the MoA of progestin-only EC?

A

prevent ovulation and reduce sperm motility; effective in early stages of LH surge still (no effect on implantation or post-implantation)

78
Q

What is the dosing of progestin-only EC?

A

1.5 mg levonorgestrel in 2 doses; or 1 dose in OneStep

79
Q

What are ADRs of progestin-only EC?

A

nausea, withdrawal bleeding in 7 days, 2-3 day delay in menstruation

80
Q

How is progestin-only available?

A

to all-age patients without rx

81
Q

What is the Yuzpe regimen?

A

within 72h: 2 doses of 100 ug EE + 0.5 mg levonorgestrel 12h apart

82
Q

When was the Yuzpe regimen approved?

A

1997

83
Q

Describe the effectiveness of the Yuzpe regimen.

A

74%

84
Q

What is a disadvantage to Yuzpe regimen?

A

worse ADRs vs. progestin only; also only 74% effective

85
Q

When can a copper IUD be used for EC? What is the effectiveness?

A

up to 5 days post-sex (99% effective)

86
Q

How does a copper IUD work for EC?

A

may also prevent implantation in addition to motility and viability of sperm

87
Q

What are the options for EC?

A

1) progestin-only; 2) yuzpe; 3) anti-progestins; 4) copper IUD

88
Q

What are the anti-progestins?

A

ulipristal (Ella) and mifepristone (off-label)

89
Q

What is the MoA of anti-progestins in EC?

A

block ovulation; impair endometrial proliferation; embrotoxic (but probably not abortifacient at 30 mg dose w/o prostaglandin)

90
Q

Describe timeframe of anti-progestin use.

A

60% effective if within 5 days; effective up to day of LH surge

91
Q

Describe ADRs of anti-progestins in EC.

A

minimal - ab pain, menstrual irregularity

92
Q

Describe metabolism of anti-progestins.

A

3A4 (do not use in severe liver disease)

93
Q

What are the sxs of estrogen excess?

A

nausea, breast tenderness, HA, fluid retention

94
Q

what are the sxs of estrogen deficiency?

A

breakthrough bleeding, amenorrhea, vasomotor sxs, anxiety, decreased libido

95
Q

What are the sxs of progestin excess?

A

appetite, weight gain, bloating, acne, oily skin, hirsuitism, depression, fatigue, irritability

96
Q

What are the sxs of progestin deficiency?

A

dysmenorrhea, late-cycle breakthrough bleeding/spotting

97
Q

Solution to excess estrogen:

A

decrease E dose, use progestin-only, use IUD

98
Q

Solution to estrogen deficiency:

A

increase E dose

99
Q

Solution to progestin excess:

A

decrease P dose or use less-androgenic progestin

100
Q

Solution to progestin deficiency:

A

increase P dose, use extendend-cycle/continuous regimen, progestin-only, or IUD

101
Q

How do CHCs differ?

A

1) estrogenic effects (metabolism); 2) androgenic effects (direct and indirect -SHBG)

102
Q

Function of progestins in CHCs

A

most of effect: 1) block LH surge; 2) inhibit ovulation; 3) thicken mucous; 4) induce endometrial atrophy

103
Q

Function of estrogens in CHCs:

A

1) suppress LH, 2) prevent LH surge, 3) stabilize endometrium

104
Q

How does mestranol compare to EE?

A

50% less potent but converted to EE in liver

105
Q

What are the non-contraceptive benefits of CHCs?

A

these effects persist after discontinuation.. 1) reduce dysmenorrhea and acne; 2) reduce risk of ovarian/endometrial cancer, 3) reduce risk of ovarian cysts, PID

PHS 933 (14 decks)

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