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Combined hormonal contraception ppt
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COMBINED ORAL CONTRACEPTIVES
Mechanism of action
The combined oral contraceptive (COC) pills currently available
in the UK are shown in Table 2. They combine an estrogen
(ethinylestradiol (EE) in all cases but one) with one of seven
progestogens.
Aside from secondary contraceptive effects on the cervical mucus
and to impede implantation, COCs primarily prevent ovulation.
This makes the method highly effective in ‘perfect’ use (Table 1),
but it removes the normal menstrual cyle and replaces it with a
cycle that is user-produced and based only on the end-organ, i.e.
the endometrium. So the withdrawal bleeding has minimal medical
significance, can be deliberately postponed or made infrequent
(e.g. tricycling, discussed below), and if it fails to occur, once
pregnancy is excluded, poses no problem. The pill-free time is the
contraception-deficient time, which has great relevance to advice
for the maintenance of COC efficacy (see below).
Benefits versus risks
Capable of providing virtually 100% protection from unwanted
pregnancy and taken at a time unconnected with sexual activity, the COC provides enormous reassurance by the associated
regular, short, light and usually painless withdrawal bleeding at
the end of the 21-day pack. Inevitably, most of this section will
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Combined hormonal contraception
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Pill type Preparation Estrogen Progestogen
(µg) (µg)
Table 2 Formulations of currently marketed combined oral contraceptives (COCs)a
a
Other names in use worldwide are on the website www.ippf.org.uk. b
Converted to norethisterone as the active metabolite.
c
Equivalent daily doses for comparison with monophasic brands.
d
Marketed primarily as acne therapy (see text), and not intended to be used
as a routine pill.
Monophasic
Ethinylestradiol/ Loestrin 20 20 1000 Norethisterone
norethisterone type acetateb
Loestrin 30 30 1500 Norethisterone
acetateb
Brevinor 35 500 Norethisterone
Ovysmen 35 500 Norethisterone
Norimin 35 1000 Norethisterone
Ethinylestradiol/ Microgynon 30 30 150
levonorgestrel (also ED)
Ovranette 30 150
Ethinylestradiol/ Mercilon 20 150
desogestrel Marvelon 30 150
Ethinylestradiol/ Femodette 20 75
gestodene
Ethinylestradiol/ Femodene (also ED) 30 75
gestodene Minulet 30 75
Ethinylestradiol/ Cilest 35 250
norgestimate
Ethinylestradiol Yasmin 30 3000
drospirenone
Mestranol/ Norinyl-1 50 1000
norethisterone
Bi/triphasic
Ethinylestradiol/ BiNovum 35 500 833c (7 tabs)
norethisterone 35 1000 (14 tabs)
Synphase 35 500 (7 tabs)
35 1000 714 (9 tabs)
35 500 (5 tabs)
TriNovum 35 500 (7 tabs)
35 750 750 (7 tabs)
35 1000 (7 tabs)
Ethinylestradiol/ Logynon (also ED) 30 50 (6 tabs)
levonorgestrel 40 32c 75 92 (5 tabs)
30 125 (10 tabs)
Trinordiol 30 50 (6 tabs)
40 32 75 92 (5 tabs)
30 125 (10 tabs)
Ethinylestradiol/ Tri-Minulet 30 50 (6 tabs)
gestodene 40 32 70 79 (5 tabs)
30 100 (10 tabs)
Triadene 30 50 (6 tabs)
40 32 70 79 (5 tabs)
30 100 (10 tabs)
Ethinylestradiol/ Dianetted 35 2000
cyproterone acetate
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be on possible risks and hazards associated with taking the Pill,
but the positive aspects should not be forgotten; they are listed
in the second box below. Although some of these findings await
full confirmation, the good news is rarely mentioned while the
suspected risks are widely publicized and often over-dramatized.
Space does not allow full discussion of all the work that has
been published in the 45 years during which the Pill has been
available in this country. Practitioners should form their own
opinion of the risks and benefits by their own reading, but the
following may help to summarize present medical opinion upon
which contemporary prescription of the Pill is based.
The data presented here have been derived mainly from the
prospective Royal College of General Practitioners (RCGP),
Oxford/FPA and US Nurses Studies, supplemented by numerous case–control studies and a few randomised controlled trials
conducted by the WHO and other bodies.
Contraceptive benefits of COCs
• Effectiveness
• Convenience, not intercourse related
• Reversibility
Non-contraceptive benefits of COCs
These at times may provide the principal indication for use
of the method (e.g. in the treatment of dysmenorrhoea in a
not-yet sexually active teenager)
• Reduction of most menstrual cycle disorders: less heavy
bleeding, therefore less anaemia, and less dysmenorrhoea;
regular bleeding, the timing of which can be controlled (no Pilltaker need have ‘periods’ at weekends; upon request, she may
tricycle and so bleed only a few times a year); fewer symptoms
of premenstrual tension overall; no ovulation pain
• Reduced risk of cancers of ovary and endometrium (see text),
and very possibly also colorectal cancer
• Fewer functional ovarian cysts, because abnormal ovulation is
prevented
• Fewer extrauterine pregnancies, because normal ovulation is
inhibited
• Reduction in pelvic inflammatory disease (PID)
• Reduction in benign breast disease
• Fewer symptomatic fibroids
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• Probable reduction in thyroid disease, whether over- or under-active
• Probable reduction in risk of rheumatoid arthritis
• Fewer sebaceous disorders, especially acne (with estrogendominant COCs such as Marvelon™ and Yasmin™)
• Possible reduced risk of endometriosis (a potential benefit
probably not as well realised as it would be if the Pill were
taken in a bleed-free regimen)
• Continuous use beneficial in long-term suppression of endometriosis
• Possibly fewer duodenal ulcers (not well established)
• Reduction in Trichomonas vaginalis infections
• Possible lower incidence of toxic shock syndrome
• No toxicity in overdose
• Some obvious beneficial social effects, to balance suggested
negatives
Even as we turn to unwanted effects, it is reassuring that,
according to the RCGP report in 1999, COCs have their main
(small) effect on every known associated cause of mortality
during current use and for some (variable) time thereafter. The
excess thrombotic risk has probably vanished by 4 weeks, and
by 10 years after use ceases, mortality in past-users is indistinguishable from that in never-users.
Tumour risk and COCs
No medication continues to receive so much scrutiny and investigation as the Pill. For some time, fears have been expressed about
its possible connection with breast, cervical and liver cancers.
Breast cancer
The incidence of this disease is high, and therefore it must
inevitably be expected to develop in women whether they take
COCs or not. Since the recognized risk factors include early
menarche and late age of first birth, use by young women was
rightly bound to receive scientific scrutiny. The literature to date
is copious, complex, confusing and contradictory!
The 1996 publication by the Collaborative Group on Hormonal
Factors in Breast Cancer reanalysed original data relating to
over 53 000 women with breast cancer and over 100 000
controls from 54 studies in 25 countries. This is 90% of the world
epidemiological data. The reanalysis showed disappearance of
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the risk in ex-users, but recency of use of the COC was shown
to be the most important factor: with the odds ratio unaffected
by age of initiation or discontinuation, use before or after first
full-term pregnancy, or duration of use. The main findings are
summarized in Table 3 and below. A 2002 study of 4575 breast
cancer patients and matched cancer-free controls in the USA
was congruent with this and particularly reassuring in that there
was nothing to suggest the so-called ‘time-bomb’: despite 75%
exposure to the COC in the population, there was no persistence of risk in long-time ex-users when they reached ages with
much higher incidence of this cancer, as shown in Figure 2.
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User status Increased risk
Table 3
The increased risk of developing breast cancer while taking the pill and in the 10 years
after stoppinga
Current user 24%
1–4 years after stopping 16%
5–9 years after stopping 7%
10 plus years an ex-user No significant excess
Cases
per 100
women
7
6
5
4
3
2
1
0
15 20 25 30 35 40 45 50 55 60 65 70
Age (years)
Figure 2
Background risk: cumulative number of breast cancers per 100 women, by age.
(Reproduced from statement by Faculty of Family Planning, June 1996.)
a
Collaborative Group on Hormonal Factors in Breast Cancer. Lancet 1996; 347: 1713–27.
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