Transcript CHAPTER 10 Family Planning ’S GYNECOLOGY NOVAK OBGY R1 Lee Eun Suk

NOVAK’S GYNECOLOGY
CHAPTER 10 Family Planning
OBGY R1 Lee Eun Suk
Family Planning

The rapid growth of the human population in this century
threatens the survival of all

At this present rate, the population of the world will double
in 47 years

That of many of the poorer countries of the world will double
in about 20 years
Family Planning

For the individual and for the planet, reproductive health
requires careful use of effective means


Prevent both pregnancy and sexually transmitted diseases
The contraceptive choices made by American couples in 1995

For couples older than 35 years of age


Sterilization is the number one choice
For younger couples


Oral contraceptives (OCs) are the most used methods
The condom ranks second
T10.1
Family Planning

Abortion is an obvious indicator of unplanned pregnanacy

Abortion ratios by age group indicate that the use of abortion


Greatest for the youngest women
Least for women in their late 20s and early 30s
Family Planning

Young people are much more likely to experience
contraceptive failure


Their fertility - greater than of older women
More likely to have intercourse without contraception
Efficacy of Contraception

Factors affecting whether pregnancy will occur






fecundity of both partners
timing of intercourse in relation to the time of ovulation
method of contraception used
intrinsic effectiveness of the contraceptive method
correct use the method
A pregnancy rate per year can be calculated using the Pearl
formula


The
The
The
The
The
Dividing the number of pregnancies by the total number of months
contributed by all couples, then multiplying the quotient by 1,200
Rates of pregnancy with different methods are best calculated
by reporting two different rates derived from multiple studies
T10.2
Safety

Some contraceptive methods have associated health risks
; Areas of concern are listed in Table 10.3

Most methods provide noncontraceptive health benefits in
addition to contraception

Oral contraceptives reduce the risk for ovarian and endometrial
cancer and ectopic pregnancy

Barrier methods and spermicides provide some protection against
STDs, cervical cancer, and tubal infertility
T10.3
Cost

Intrauterine devices (IUDs) & subdermal implants



Expensive initial investment
Prolonged protection for a low annual cost
Sterilization & the long-acting methods

The least expensive over the long term
T10.4
Nonhormonal Methods

Coitus Interruptus

Lactation Amenorrhea

Periodic Abstinence or Natural Family Planning

Condoms

Vaginal Spermicides

Vaginal Barriers

Intrauterine Devices
Coitus Interruptus

Withdrawal of the penis from the vagina before ejaculation

Advantages




Immediate availability
No cost
Reduced the risk for STDs
Failure rate ( reported by The Oxford Study )


6.7 per 100 woman-years
The penis must be completely withdrawn both from the vagina
and from the external genitalia
Lactation Amenorrhea


Ovulation is suppressed during lactation
The suckling of the infant





prolctin levels↑
gonadotropin-releasing hormone (GnRH)↓
luteinizing hormone (LH)↓
follicular maturation↓
Another method of contraception should be used from 6 months
after birth, or when menstruation resumes



→
→
→
→
Progestin only OCs, implants, injectable contraception
Barrier methods, spermicides, IUDs
The risk for the breast cancer↓
Periodic Abstinence or Natural Family Planning

Couples attempt to avoid intercourse during the fertile period
around the time of ovulation

A variety of methods

The calendar method


The mucus method (Billings or ovulation method)


The least effective
To predict the fertile period by feeling the cervical mucus
The symptothermal method


The first day of abstinence is predicted either from the calendar,
by subtracting 21 from the length of the shortest menstrual cycle
in the preceding 6 months
The end of the fertile period – by use of basal body temperature
Periodic Abstinence or Natural Family Planning

Efficacy



3.1% probability of pregnancy in 1 year for the small proportion of
couples who used the method perfectly
86.4% for the rest
Vaginal infection increase vaginal discharge


↑ Complicating the use of the method
Accurate advance prediction of the time of ovulation

↑ Facilitate both the use & efficacy
Periodic Abstinence or Natural Family Planning

Risks

Conceptions resulting from intercourse remote from the time of
ovulation


↑ Spontaneous abortion
than contraceptions from midcycle intercourse
→ Malformations are not more common
Condoms

Latex rubber condoms

1840s due to vulcanization

Hold the seminal fluid → preventing its position in the vagina

Prelubricated with the spermicide
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
↑ More effective
The risks for condom breakage

About 3%
Condoms

Sexually Transmitted Diseases

Latex condoms and other barrier methods





↓ the risk for STDs
↓ Gonorrhea, ureaplasma, and PID and its sequelae (tubal infertility)
Chlamydia trachomatis , herpes virus type 2,HIV, and hepatitis B
→ did not penetrate
Some protection from cervical neoplasia
Latex allergy could lead to life-threatening anaphylaxis

Nonlatex condoms of polyurethane and Tactylon are now available
Condoms

Female Condoms

Vaginal pouches made of polyurethane are available

Efficacy trials


The pregnancy rate : only 2.6%
No signs of trauma, and the bacterial flora is not changed
Vaginal spermicides

Nonionic surface-active detergents that immobilize sperm

Aerosol foams provided rapid dispersal throughout the vagina


the best protection
Nonoxynol-9


↓ the risk for bacterial vaginosis and other STDs, including HIV
Toxic to the lactobacilli that normally colonize the vagina


vaginal colonization with bacterium Escherichia coli
Concerns about possible teratogenicity

No greater risk for miscarriage, birth defects, or low birth weight
Vaginal Barriers

Vaginal diaphragm, cervix cap, vault cap, vimule (Fig. 10.4)

They are safe

The noncontraceptive benefit

Protection from STDs, tubal infertility & cervical neoplasia
F10.4
Vaginal Barriers

Diaphragm

Circular spring covered with fine latex rubber (Fig 10.5)

Coil-spring & flat –spring → flat oval compressed for insertion

Proper fitting & proper use are key to its effect

Spermicide is always prescribed for use
Fig 10.5
Risks


↑The risks for bladder infection

Relative risk : 1.42, 2.83, and 5.68 for use 1, 3, or 5days in a week

→ Smaller-sized, wide-seal diaphragm or cervical cap
An study comparing cases of toxic shock with controls

No increased risk from diaphragm use
Cervical caps

Much smaller than the diaphragm
Does not contain a spring in the rim
Covers only the cervix with spermicide

Efficacy

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A first-year pregnancy rate of 11.3 per 100 women
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Near perfect use → a first-year pregnancy rate of 6.1 per 100
The cap worn for more than 72 hours → pregnancy rate ↑
The failure rates with “perfect use” → higher than the diaphragm

Parous women more failures than nulliparous women
Fitting Cervical caps

The cervical size is estimated and palpation

The cap is inserted by compressing it between finger and thumb
and placing it through the introitus, dome outward

Before use, the cap is one-third filled with spermicidal jelly or
cream
Cervical caps - Risks

Negative cervical cytology progressed to dysplasia in 4%


Other studies - not found this effect
In contrast, Koch - to be protected from dysplasia

Not associated with cystitis

Toxic shock – not reported
Intrauterine Devices

Very important worldwide but play a minor role in contraception
for the U.S.

High-dose copper IUD : TCU380, or ParaGard


Safe, long-term contraception with effectiveness equivalent to
tubal sterilization
The third copper IUDs

T380A (ParaGard) : the progesterone-releasing T (Progestasert)




Bands of copper on the cross arms of the T
Copper wire around the stem
Total surface area of 380 mm of copper
Levonorgestrel-releasing T (Mirena)
Mechanism of Action

Formation of “biologic foam” within the uterine cavity


Contains strands of fibrin, phagocytic cell & proteolytic enzymes
Copper IUDs


→ Release a small amount of the metal
→ Producing an even greater inflammatory response



Stimulate the formation of prostaglandin
Smooth muscle contraction & inflammation
→ The altered intrauterine environment


↓ Sperm passage
↓ fertilization
Mechanism of Action

The natural progesterone in the Progestasert


→ endometrial atrophy
The levonorgestrel in the Mirena


Much more potent than natural progesterone
Blood levels of the hormone



Half of the levonorgestrel subdermal implant (Norplant)
→ Block ovulation
The IUD is not an abortifacient

Contraceptive effectiveness

→ not depend on interference with implantation
Effectiveness

The copper T380A and the levonorgestrel T

Remarkably low pregnancy rates


Less than 0.2 per 100 woman-years
Total pregnancies over a 7-year period


The levonorgestrel T : 1.1 per 100 woman
The copper T380A : 1.4 per 100 woman
Benefits

The ParaGard and the Mirena IUDs

Protect against ectopic pregnancy

Progesterone or levonorgestrel → Menstrual bleeding & clamping↓
Risks

Infection

The relative risk for PID




Progestasert : 2.2
Copper 7 : 1.9
Saf-T-Coil : 1.3
Lippes Loop : 1.2

↑Risk was detectable within 4 months of insertion
The rate of diagnosis of PID →1.6 cases per 1,000 women per year

Exposure to sexually transmitted pathogens



More important determinant of PID than the wearing of an IUD
PID with actinomycosis → only in women wearing an IUD
Risks

Pelvic Inflammatory Disease

When PID is suspected in IUP-wearing woman

→ The IUD should be immediately removed

→ High-dose antibiotic therapy should be started
Risks

Ectopic Pregnancy

In 5% of IUD wearers

d/t the fallopian tubes are less well protected against pregnancy
than uterus

Copper T380A or levonorgestrel T

Compared with women using no contraception
→ 80% to 90% reduction in the risk for ectopic pregnancy

Greater reduction than that seen for users of barrier methods
Risks

Fertility

↑Twofold in the risk for infertility associated with tubal factors

The Oxford Study : giving birth just as promptly after IUD removal

Exposure to sexually transmitted pathogens

→ Confers risk for infertility
IUD – Clinical Management

Contraindications to IUD use
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Pregnancy
A history of PID
Undiagnosed genital bleeding
Uterine anomalies
Large fibroid tumors
Chronic immune suppression
Copper allergy and Wilson’s disease
Clinical Management

Insertion

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The cervix is exposed with a speculum
The uterine cavity should be measured with a uterine sound
A paracervical block


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Use of a tenaculum for insertion is mandatory to prevent perforation
With the ParaGard and the Progestasert, the outer sheath of the
inserter is withdrawn a short distance to release the arms of the T


→10mL of 1% lidocaine mixed with atropine (0.5mg)
→ gently pushed inward again to elevate the now-opened T
against the fundus
With the Mirena IUD, insertion is somewhat different


The inserter tube loaded with the IUD is introduced into the uterus
Until the preset sliding flange on the inserter is 1.5 to 2cm from the
external os of the cervix
Clinical Management

Intrauterine Devices in Pregnancy

IUD should be removed as soon as possible


Options for management (if the IUD is present)




Therapeutic abortion
Ultrasound-guided intrauterine removal of the IUD
Continuation of the pregnancy with the device left in place
If the IUD is not in a fundal


To prevent later septic abortion, premature rupture of the membranes & premature birth
→ Ultrasound-guided intrauterine removal of the IUD
If the IUD is in a fundal

→ Continuation of the pregnancy with the device left in place
IUD – Duration of Use

Progestasert
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
Copper T380A


Approved for 10 years
Levonorgestrel T


Replaced at the end of 1 year
Approved for 5 years
Actinomyces-like particles should be found


Removal of the IUD
Treatment with oral penicillin
IUD – Choice of Devices

Copper T380A & levonorgestrel T




Protection for many years
Low pregnancy rates
↓Risk for ectopic pregnancy
Progestasert





Must be replaced annually
Risk for infection with each insertion
Increasing cost
↑Risk for ectopic pregnancy
↓ The amount of menstrual bleeding & dysmenorrhea
Hormonal Contraception
Hormonal Contraception


Combination OCs



Female sex steroids , Synthetic estrogen
Synthetic progesterone (progestin) , Progestin only
The most widely used hormonal contraception
Administered for 21days beginning on the Sunday after a menstrual
period → discontinued for 7 days to allow for withdrawal bleeding
Progestin-only formulations

Take every day without interruption
Hormonal Contraception




Injectable progestins
Estrogen-progestin combinations
Subdermal implants releasing progestin
Experimental vaginal ring


Release either estrogen-progestin or progestin alone
Silastic ring



Worn in the vagina release steroid hormones
Absorbed at a constant rate
Containing levonorgestrel or combinations of levonorgestrel and
estrogen
Hormonal Contraception - Steroid Hormone Action

Progestins


Progestins are synthetis compounds that mimic the effect of
natural progesterone but differ from it structurally
Three classes



Estranes ┓ 19-nor progestin & used in oral contraceptives in US
Gonanes ┛
Pregnane (or 17-acetoxy compounds)
 Similar to progesterone → bound by the progesterone receptor
 Medroxyprogesterone acetate (Provera) : major injectable progestin

Some directly bound to the receptor( levonorgestrel, norethindrone)


Require bioactivation ( i.e. desogestrel )
Three newer progestins

Norgestimate , desogestrel, and gestodene → little androgenic effect
Hormonal Contraception - Steroid Hormone Action

Estrogens
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In the United States, OCs contain either of two estrogens
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
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Mestranol or ethinyl estradiol
Mestranol requires bioactivation releasing the active agent EE
OCs with 35µg of EE provide the same blood levels of hormone as
do OCs containing 50 µg of mestranol
Antifertility Effects

Combination Oral Contraception

Suppress basal follicle-stimulating hormone (FSH) and LH

↓ Ability of the pituitary gland to synthesize gonadotropines




→
→
→
→
Ovarian follicles do not mature
Little estradiol is produced
There is no midcycle LH surge
Ovulation does not occur
Antifertility Effects

Progestin-only Preparations

Progestin-only “minipill”→ 0.3mg of norethindrone per day (Micronor)





of cycles : ovulatory
: inadequate luteal function
: follicular maturation without ovulation
: complete suppression of follicle
At moderate blood levels of progestin




40%
25%
18%
18%
Normal basal levels of FSH and LH
Some follicle maturation → estradiol trigger LH releasing
However, no answering LH surging & no ovulation
At higher blood levels of progestin

FSH↓ & Follicular activity↓ → Estradiol producton↓ & no LH surge
Antifertility Effects

Hormonal Implants

Release levonorgestrel (Norplant)
In the first year of use, ovulation occurs in about 20% of cycles
The proportion of ovulatory cycles increases with time

Mechanism



Low-dose progestins include effects on the cervical mucus ,
endometrium & tubal motility → sperm migration↓

Nuclear estrogen receptor levels↓& progesterone receptor ↓
→ Activity of the enzyme 17-hydroxysteroid dehydrogenase ↑
that metabolizes natural estradiol 17β

Antiprogesterone mefipristone (RU486)
→ Given before ovulation it can be delayed for several days
Oral contraceptives

Combination OCs


Progestin-only OCs



Pregnancy rates as low as two to three per 1,000 women per year,
when used consistently
Less effective
Three to four per 1,000 women per year
Injectable progestins & implants


Much less subject to user error
Comparable to pregnancy rates after tubal sterilization
Oral contraceptives - Metabolic Effects and safety

Venous Thrombosis

Older studies linked OC use to venous thrombosis & embolism,
cerebral vascular accidents, and heart attack

More recent studies found a much lower risk

Other obvious predisposing causes of thrombosis
→ Contraindications to OC use






Previous thrombosis
Preexisting vascular disease
Coronary artery disease
Leukemia
Cancer
Serious trauma
Oral contraceptives - Metabolic Effects and safety

Venous Thrombosis

Estrogens affect procoagulant & anti-coagulant systems


Fibrinolysis (anticoagulant) is increased as much as coagulant
Balance at increased levels of production & destruction of fibrinogen

The lower estrogen dose reduces the risk for a thromboembolic
event when compared with higher-dose

Smokers taking low-dose OCs

↑ Activation of the coagulation system than nonsmoker
Oral contraceptives - Metabolic Effects and safety

The absolute risk for thrombosis in OC users taking pills
containing 30 to 35㎍ EE is 3 per 10,000 per year


Compared with 1 per 10,000 reproductive-aged women
not using OCs & 6 per 10,000 in pregnancy
Thrombosis risk is apparent by 4 months after starting estrogencontaining OCs

Not increase further with continued use

Risk is highest during the first year of use
Oral contraceptives - Metabolic Effects and safety

Thrombophilia

Hemostatic variables in women given lower-dose OCs who had
previous thrombosis with OCs and compared with no thrombosis
( Bloemenkamp and colleagues)
 ↑Factor VII,VIII, and protein C
 ↓Antithrombin III, activated protein C sensitivity ratio, and protein S
 Women who had previous thrombosis with OCs → pronounced changes

Factor V Leiden



Genetic variation : 3% to 5% of the white population
Mutation in the factor V protein, inhibiting cleavage of the protein by
activated protein C
Risk for thromboembolic episode : 27.2 per 10,000 woman-years
Oral contraceptives - Metabolic Effects and safety

Thrombophilia

OCs containing newer agents ( i.e., prodestins, desogestrel,or gestodene )


Lewis and colleagues




→ Modest increased risk for venous thrombosis than older progestins
Attrition of susceptibles & adverse selection
Venous thrombosis attributable to OCs during the initial months of use↑
Compared new users to women already taking OCs for some time
without incident → risk ↑
A large European study of thrombosis with different OCs

Apparent risk for thrombosis was lowest with the first low-does pills
introduced & highest with those recently introduced
Oral contraceptives - Metabolic Effects and safety

Ischemic Heart Disease

Ischemis heart and stroke


Principal determinants of risk


Major causes of death blamed on OC use in the past
Advancing age & cigarette smoking
With the higher-does OCs used in the 1980s


Smoking had a profound effect on risk
Smoking 25 or more cigarettes per day had a 30-fold increased risk
for myocardial infarction if they used OCs , compared with nonsmokers
not using OCs
Oral contraceptives - Metabolic Effects and safety

Ischemic Heart Disease

Use of OCs is now much safer




Because most women are taking low-dose pills
Physicians prescribe selectively, excluding women with major
cardiovascular risk factors
Nearly all current users took OCs with less than 50 ㎍ of EE
Current users of low-dose OCs had no increased risk for myocardial
infarction (California study and a study from Washington State)


Adjustment for major risk factors and sociodemographic factors
 Age, illness, smoking, ethnicity, and body mass index
After adjustment → risk for myocardial infarction was not increased
Oral contraceptives - Metabolic Effects and safety

Ischemic Heart Disease

One study of so-called third-generation OCs

OCs containing the new progestins desogetrel or gestodene
→ myocardial infarction↓than OCs with similar estrogen dose

Myocardial infarction risk is strongly increased among smokers
→Smokers who used OCs containing the new progestins
→ less likely to have myocardial infarction than the older OCs
Oral contraceptives - Metabolic Effects and safety

Oral contraceptive and Stroke

OC use appeared to be linked to risk for both hemorrhagic &
thrombotic stroke (1970s)
New information shows no risk for women who are healthy

Petitti and colleages study




Hypertension, diabetes, obesity, current smoking, and black race
→ strongly associated with stroke risk
Neither current nor past OC use was associated with stroke
WHO study


European women using low-dose OC
→ no increased risk for either type of stroke, thrombotic or hemorrhagic
European women using high-dose OC → risk↑
Oral contraceptives - Metabolic Effects and safety

Oral contraceptive and Stroke

Smokers and women with hypertension and diabetes


Increased risk for cardiovascular disease whether or not use OCs
WHO study ( if they use low-dose OCs )



Smokers taking OCs → 7 times the risk for ischemic (thrombotic) stroke
Hypertension → 10-fold increased risk (if they took OCs)
The current U.S. practice of limiting OC use by women older than 35
years of age to nonsmokers without other vascular risk factor is prudent
Oral contraceptives - Metabolic Effects and safety

Blood Pressure




Glucose Metabolism



Dose-related effect on blood pressure
Older high-dose pills → 5% higher than 140/90mmHg
Estrogen → renin substrate↑ → BP ↑
Progestins exhibit insulin antagonism → insulin level ↑
The effect is related to androgenic potency of the progestin & dose
Lipid Metabolism



Androgens & estrogens → competing effects on hepatic lipase
Estrogens → LDL↓ & HDL↑ TG ↑
Androgens → LDL ↑ & HDL ↓
Oral contraceptives - Metabolic Effects and safety

Other Metabolic effects

Estrogen in OCs

Circulating-thyroid-bind globulin ↑

Total thyroxine (T4) ↑ & triiodothyronine (T3) resin uptake↓

The results of actual of TFT → normal by free T4 & radioiodine tests
Oral contraceptives and Neoplasia

Endometrial Cancer and Ovarian cancer


Combination OCs reduced the risk for subsequent
endometrial cancer and ovarian cancer

A recent study found that as little as 1 year of OC use was
protective & continued use reduced risk by 7% per year

Benefit persisted for 15 years after last use , with little
diminution
50% reduction in ovarian cancer risk was observed for women
who took OCs for 3 to 4 year

80% reduction was seen with 10 or more years use
Oral contraceptives and Neoplasia

Cervical cancer


A weak association between OC & squamous cancer of the cervix
Risk factors





Early sexual intercourse
Exposure to human papillomavirus
If a woman already has HPV, OC use does not further increase her
risk for cervical neoplasia
Among women who are HPV negative, OC use doubles the risk of
having such a lesion
Adenocarcinoma of the cervix


Rare but not easily detected → incidence↑
Doubling of risk with OCs use
Oral contraceptives and Neoplasia

Breast Cancer

Generally, no increase in overall risk is found from OC use

Some studies → the risk may increase in women OC use





Used OCs For many year
Nulligravid
Young at the time of diagnosis
Continue using OCs in their 40s
Progestin-only OCs → protective effect

OC users who developed breast cancer were more likely to be diagnosed
in early stages & less likely to have LN involvement
Oral contraceptives and Neoplasia

Breast Cancer (Collaborative Group’s study)

Diagnosed while women were taking OCs


Greater risk in women who started OC use before 20 years of age



Less advanced than those in women who had never used OCs
Breast cancer is rare before 20 years of age
No increase in actual numbers
A term pregnancy → short-term increase in breast cancer risk


Growth-enhancing effects of estrogen
The effects of OCs may promote growth of existing cancers
Oral contraceptives and Neoplasia

Liver Tumors

OCs implicated as a cause of benign adenomas of the liver

Newer low-dose product → less risk

No association between OC use & subsequent liver cancer