Contraception (COCs) Flashcards
What are some COCs? (general) Name some pro’s/cons
Oral that contain both progestogen and oestrogen
- pros = regular, light, minimal pain period, control over period, improved acne/period disorders
- cons = drug interactions, daily tablet, spotting, nausea, mood/weight change, BP inc, headache, inc stroke MI risk in smokers >35
Noova ring = COC hormonal vag ring
What are some progesterone only contraceptive methods?
Drosperidone tab = when COC C/I
Levonorgestrel or norethisterone tabs = when COC C/I
Medroxyprogesterone IM depot = 12 wkly injec
Etonogestrel implant = every 3 yrs, long term
Levonorgestrel IUD = long term (5 yrs)
What are some non-hormonal contraceptives?
Barriers = condoms (male/female), diaphragm
Copper IUD = unaffected by drugs, long term 5-10yrs
How do COCs prevent pregnancy? (general)
Inhibit ovulation
Reduce receptivity of endometrium to implantation
Thicken cervical mucous to form barrier to sperm
What are some indications for COCs?
Contraception
Acne
Menstrual disorders (e.g. dysfunctional uterine bleeding)
Endometriosis
PMS
Outline some COC Precautions
Migraine (can worsen), diabetes (effects glucose metabolism maybe)
BMI >30kg/m2 (inc VTE risk)
Cardiovascular health
Smokers (inc VTE risk, <35 support smoking cessation)
Surgery = inc thromboembolism risk, stop COC 4 wks before surgery, restart >2 wks post-mobilisation
Preg (estrogen can dec milk supply, use progest-only if must)
Post-partum = delay use until 21 days pp, or 42 day if high VTE risk
Outline some COC C/I
C/I patients w/ hormone sensitive breast cancer
Migraines w/ aura and/or >35 yrs
CV risk factors –> affects BP, inc stroke/MI
Hx VTE
Smokers >35yrs
end organ damage
How long do ADRs last for COCs?
Tolerance to ADR develop in first 3 months
Reduced risk of ovarian cysts, PID, dec ovarian/endometrial cancers
List some common ADRs for COCs
Mood changes (watch mental health)
N/V, headache
breast enlargement/tenderness
change in libido, inc BP, fluid retention
Chloasma (melasma, esp preg women)
acne, thrush
List some infrequent ADRs for COCs
Contact lense intolerance (+dry eyes)
Rash, hirsutism
Alopecia, altered lipid profiles
Hyperinsulinaemia (esp w/ levonorgestrel-containg COCs)
Insulin resistance
List some rare ADRs for COCs
VTE
Allergies, hypertension, stroke
Photosensitivity, jaundice, pancreatitis, liver cancer
Cervical cancer (inc w/ duration, declines to that of never users)
Breast cancer (small inc w/some, decline to never exposed after 10 yrs)
What influences the risk of VTE with COC use?
Dose of estrogen
type of progestogen
presence of other risk factors
Risk of VTE is higher in the 1st year of COC use, peak in 3 months
Which drugs types interact with COCs?
Drugs which increase CYP3A4 (progest, estro are metabolised by it)
Taking COC w/in 4 weeks of CYP3A4 inducers –> contraceptive failure
Which drug classes interact with COCs? (give e.g.)
Anti-epileptics = Carbamazepine, oxcarbazepine, phenytoin, phenobarbital, topiramate, primidone
Antibiotics = Rifampicin, Rifabutin, griseofulvin
Discuss the interaction between anti-infectives with COCs
No evidence that other anti-infectives alter COCs
What should be done if enzyme-inducing drugs are taken with COCs?
Use monophasic COC w/ levonorgestrel and ethinylestradiol AND inc COC dose to 50mcg ethinylestradiol
Two ways:
- 2 tablets of COC containing 30mcg or
- 1 tablet of 20 mcg and 1 tablet of 30mcg COC
Use additional contraceptive methods, reduce hormone free periods
Microgynon 50 ED is unsuitable as progestrogen dose is insufficient for contraceptive efficacy in this situation
What is a monophasic COC regimen?
Each tablet contains same dose of oestrogen and progesterone
classified further by low, standard, high estrogen doses
What is Multiphasic COC regimen?
Progestogen, or estrogen and progestogen, content varies throughout pack
More complex, cyclic symptoms (fluid retention, PMS, etc)
No advantage over monophasic, difficult to change timing of w/drawal bleeds
What types of estrogen is used in COCs?
Ethinylestradiol = synthetic estradiol derivative, more potent than natural form
Mestranol = synthetic estradiol, metabolised by ethinylestradiol
Estradiol = natural oestrogen
No clinical benefit between either
Discuss the use of estradiol in COCs
Natural oestrogen
seen in Qlaira (estradiol valerate multiphasic), Zoely (17-b estradiol monophasic)
No change in libido, better tolerate in women with mood disorders
Discuss the use of estradiol in COCs
Natural oestrogen
seen in Qlaira (estradiol valerate multiphasic), Zoely (17-b estradiol monophasic)
No change in libido, better tolerate in women with mood disorders
Discuss the use of ethinylestradiol in COCs
Ethinylestradiol = synthetic estradiol derivative, more potent than natural form
- low dose --> 20mcg - standard dose --> 30-35mcg - high dose --> 50mcg
Discuss the use of Mestranol in COCs
Mestranol = synthetic estradiol, metabolised by ethinylestradiol
- standrad dose 50mcg mestranol (=35mcg ethinylestradiol)
What progesterone is used in COCs?
2nd Gen = levonorgestrel and norethisterone
3rd Gen = gestodene, desogestrel, cyproterone
4th Gen = drospirenon, dienogest, nomegestrol
Discuss the use of 2nd generation progesterones in COCs
Levonorgestrel and norethisterone
Reduced risk of VTE compared to other COCs
COCs with 2nd gen progestogens are PBS subsidised
Discuss the use of 3rd generation progestogens in COCs
Gestodene and desogestrel = less androgenic activity than levenorgestrel (2nd gen), greater VTE risk compared to 2nd gen
Cyproterone = progestogenic and andti-androgenic (treat androgenisation), highest VTE risk
NOT indicated in absence of androgenisation
Discuss the use of 4th generation progesterones in COCs
Drospirenone = anti-mineralocorticoid activity (mild diuretic, K+ retention), anti-androgenic
Dienogest = anti-androgenic activity, VTE risk, no clear benefit over others
nomegestrol = anti-androgenic activity, no data about VTE risk (inc in HRT/MHT)
What is the benefit of newer progestreogen components in COCs?
More beneficial on acne
Less hirsutism
Less weight gain
What are some counselling points about COCs?
Active pills must be take consecutively w/ <36 hrs between doses
Hormone free interval must not exceed 7 days
Commence after menses to exclude preg, contraception provided 7 days after starting pill
When is contraceptive efficacy affected with COCs?
2 or more active pills missed (>48 hrs between active pills)
Medications taken that interfere w/ COC effectiveness
Severe vom/diarrhoea persists >24 hrs
Outline the 7 day rule for COCs
7 conseq days of active pill = reliably prevent ovulation
7 active pills may be omitted w/out ovulation (e.g. pill free period)
Missing more than 7 consec active pills = risk ovulation
Risk of preg greatest if missed pill is at the start or end of active pill cycle
What is the advice given for missing a COC during the first week of active pills?
> 48 hrs since last active or first active >24hr late
Take EC if unprotected sex
Take most recent missed pill, discard any other ones –> continue pills as normal
use barrier protection for 7 days
What is the advice given for missing a COC during the second week of active pills?
Safest time to miss
If >48 hrs since last active pill –> take most recent missed pill (discard others) –> use barrier protection for 7 days
No EC req
What is the advice given for missing a COC during the third week of active pills?
> 48 hrs since active tablet –> take most recent active, discard other missed pills –> use barrier for 7 days
Skip hormonal free interval (discard inactive pills) –> straight on to new pack
What is an extended pill regimen for COC?
Shorten or eliminate HFI –> reduce menses from every month to every 3-4 months
Seen in: seasonique, Yaz, Zoely
What are the benefits of seasonique?
Extended pill regimen
Reduced breakthrough bleeding/improve cycle control, dec PMS, inc ovarian suppression
Period lasts 3 days during 7 monopills
