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Combined hormonal contraception ppt
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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 activ￾ity, 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 numer￾ous 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 Pill￾taker 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 estrogen￾dominant 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 indistin￾guishable from that in never-users.

Tumour risk and COCs

No medication continues to receive so much scrutiny and investi￾gation 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 persis￾tence 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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