Block 2 Lecture 2 -- Contraception Flashcards Preview

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Flashcards in Block 2 Lecture 2 -- Contraception Deck (105):
1

Theoretical vs. actual efficacy of OCs.

99 vs 92

2

Describe monophasic OC dosing

fixed E + P for 21 days, then 7 placebo

3

Describe extended cycle OC dosing.

84 active + 7 placebo

4

What brands are extended-cycle?

seasonale, yaz

5

When are biphasics, triphasics, multiphasics used?

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

6

What is Lybrel?

OC that eliminates hormonal cycle
-- 365 active pills

7

What is the dosing in Lybrel?

20 ug + 90 ug levonorgestrel

8

What are the progestins with less androgenic activity?

1) desogestrel
2) norgestimate
3) drosperinone

9

What is the advantage to drosperinone?

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

10

What is the disadvantage to drosperinone?

higher risk of VTE vs. levonorgestrel

11

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

new progestins are less androgenic

12

Describe efficacy of progestin-only birth controls.

less effective; associated with regular bleeding
-- 40% still ovulate (ectopic risk)
-- must be taken at same time q day

13

When are lo-dose OCs preferred?

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

14

What is defined as very low dose OC?

20-25 ug EE

15

What is defined as low-dose OC?

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

16

What is defined as normal dose OC?

35-50 ug

17

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

50 ug (VTE)

18

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

160+ lb

19

What is first choice in OC selection?

low-dose (since all OCs are equally effective)

20

When are monophasics preferred?

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

21

When are bi- and tri-phasics preferred?

when lessening spotting and progestin ADRs is a concern

22

When are extended formulation OCs preferred?

when dysmenorrhea or menstrual issues are present

23

When are progestin-only OCs preferred?

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

24

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

EE + norelgestromin, a norgestimate metabolite

25

When should a transdermal patch be avoided?

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

26

What effect do CHCs have on dyslipidemia?

none

27

theoretical vs actual efficacy of Ocs

99 vs 92

28

Describe monophasic OC dosing

fixed E+P for 21 days, then 7 placebo

29

Describe extended-cycle OC dosing

84 active + 7 placebo

30

What brands are extended cycle?

seasonale, yaz

31

When are biphasics, triphasics, multiphasics used?

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

32

What is Lybrel?

OC that eliminates hormonal cycle (365 active pills)

33

What is the dosing of lybrel?

20 ug EE + 90 ug levonorgestrel

34

What are the progestins with less androgenic activity?

1) desogestrel; 2) norgestimate; 3) drosperinone

35

What is the advantage to drosperinone?

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

36

What is the disadvantage to drosperinone?

higher risk of VTE vs. levonorgestrel

37

What is the FDA-required warning on drosperinone?

higher risk of VTE vs. levonorgestrel

38

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

new progestins are less androgenic

39

Describe efficacy of progestin-only birth controls

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

40

When are low-dose OC's preferred?

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

41

What is defined as very low dose OC?

20-25 ug EE

42

What is defined as low-dose OC?

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

43

What is defined as normal dose OC?

35-50 ug

44

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

50 ug (VTE risk)

45

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

160+ lbs

46

What is first choice in OC selection?

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

47

When are monophasics preferred?

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

48

When are bi- and tri-phasics preferred?

when lessening spotting and progestin ADRs is a concern

49

When are extended-formulation OC's preferred?

when dysmenorrhea or menstrual issues are present

50

When are progestin-only OC's preferred?

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

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

EE + norgestimate (active metabolite = norelgestromin)

52

When should a transdermal patch be avoided?

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

53

Why does the transdermal patch carry a higher thromboembolic risk?

estradiol 60% higher due to first-pass avoidance

54

Describe application of ortho evra.

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

55

What are the APIs in nuvaring?

EE + etonorgestrel

56

What are the advantages to nuvaring?

as effective as COC's but lower systemic estrogen dose

57

Describe administration of nuvaring?

insert x 3 weeks then remove

58

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

97% (better)

59

What is the MoA of DMPA?

suppress estradiol production to inhibit ovulation for 3 months

60

What are ADRs of DMPA?

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

Describe dosing of DMPA.

150 mg DMPA IM or SQ

62

What are the warnings for DMPA?

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

63

What is the API in the implant (implanon)?

etonorgestrel

64

What is the dosing of the implant?

3 yr implant in skin of upper arm

65

What is the effectiveness of the implant?

suppresses ovulation in 97%

66

What are the ADRs of the implant?

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

67

What is the most widely used form of contraception?

IUD

68

What is the actual effectiveness of IUDs?

99% (paragard has slightly higher failure rate)

69

What is the MoA of IUDs?

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

70

What are the active ingredients in IUDs?

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

71

How long is paragard active?

10 years

72

How long is mirena active?

5 years

73

What is the dosing in mirena?

10 ug/day

74

What is an ADR of paragard?

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

75

What is an ADR of mirena?

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

76

When should progestin-only emergency contraception be used?

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

77

What is the MoA of progestin-only EC?

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

78

What is the dosing of progestin-only EC?

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

79

What are ADRs of progestin-only EC?

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

80

How is progestin-only available?

to all-age patients without rx

81

What is the Yuzpe regimen?

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

82

When was the Yuzpe regimen approved?

1997

83

Describe the effectiveness of the Yuzpe regimen.

74%

84

What is a disadvantage to Yuzpe regimen?

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

85

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

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

86

How does a copper IUD work for EC?

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

87

What are the options for EC?

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

88

What are the anti-progestins?

ulipristal (Ella) and mifepristone (off-label)

89

What is the MoA of anti-progestins in EC?

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

90

Describe timeframe of anti-progestin use.

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

91

Describe ADRs of anti-progestins in EC.

minimal - ab pain, menstrual irregularity

92

Describe metabolism of anti-progestins.

3A4 (do not use in severe liver disease)

93

What are the sxs of estrogen excess?

nausea, breast tenderness, HA, fluid retention

94

what are the sxs of estrogen deficiency?

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

95

What are the sxs of progestin excess?

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

96

What are the sxs of progestin deficiency?

dysmenorrhea, late-cycle breakthrough bleeding/spotting

97

Solution to excess estrogen:

decrease E dose, use progestin-only, use IUD

98

Solution to estrogen deficiency:

increase E dose

99

Solution to progestin excess:

decrease P dose or use less-androgenic progestin

100

Solution to progestin deficiency:

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

101

How do CHCs differ?

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

102

Function of progestins in CHCs

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

103

Function of estrogens in CHCs:

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

104

How does mestranol compare to EE?

50% less potent but converted to EE in liver

105

What are the non-contraceptive benefits of CHCs?

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