Block 2 Lecture 2 -- Contraception Flashcards
1
Q
Theoretical vs. actual efficacy of OCs.
A
99 vs 92
2
Q
Describe monophasic OC dosing
A
fixed E + P for 21 days, then 7 placebo
3
Q
Describe extended cycle OC dosing.
A
84 active + 7 placebo
4
Q
What brands are extended-cycle?
A
seasonale, yaz
5
Q
When are biphasics, triphasics, multiphasics used?
A
for breakthrough bleeding
- varied E + P dosing
- no evidence of bleeding improvement though
6
Q
What is Lybrel?
A
OC that eliminates hormonal cycle
– 365 active pills
7
Q
What is the dosing in Lybrel?
A
20 ug + 90 ug levonorgestrel
8
Q
What are the progestins with less androgenic activity?
A
1) desogestrel
2) norgestimate
3) drosperinone
9
Q
What is the advantage to drosperinone?
A
anti-aldosterone (MR antagonist) for less bloating, weight gain
10
Q
What is the disadvantage to drosperinone?
A
higher risk of VTE vs. levonorgestrel
11
Q
What is the difference in 3rd/4th gen OCs?
A
new progestins are less androgenic
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
13
Q
When are lo-dose OCs preferred?
A
adolescents, underweight (110 lb), older than 35, perimenopausal
14
Q
What is defined as very low dose OC?
A
20-25 ug EE
15
Q
What is defined as low-dose OC?
A
less than 35 ug EE (or less than 0.5 mg norethindrone or equivalent)
16
Q
What is defined as normal dose OC?
A
35-50 ug
17
Q
What dose should not be exceeded in any patient for OC?
A
50 ug (VTE)
18
Q
When is normal (35-50ug) dosing preferred?
A
160+ lb
19
Q
What is first choice in OC selection?
A
low-dose (since all OCs are equally effective)
20
Q
When are monophasics preferred?
A
if easy-management is a must
– can just skip placebo to lengthen cycle
21
Q
When are bi- and tri-phasics preferred?
A
when lessening spotting and progestin ADRs is a concern
22
Q
When are extended formulation OCs preferred?
A
when dysmenorrhea or menstrual issues are present
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
24
Q
What are the APIs in the transdermal patch (ortho evra)?
A
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
