68 by 6pVau3



       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
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
       The   fecundity of both partners
       The   timing of intercourse in relation to the time of ovulation
       The   method of contraception used
       The   intrinsic effectiveness of the contraceptive method
       The   correct use the method

   A pregnancy rate per year can be calculated using the Pearl
       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
   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
   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
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 least effective
        The mucus method (Billings or ovulation method)
             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

            ↑ Spontaneous abortion
             than contraceptions from midcycle intercourse

            → Malformations are not more common
   Latex rubber condoms
       1840s due to vulcanization

   Hold the seminal fluid → preventing its position in the vagina

   Prelubricated with the spermicide
       ↑ More effective

   The risks for condom breakage
       About 3%
   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
   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
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
   ↑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
       A first-year pregnancy rate of 11.3 per 100 women
            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
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
   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
   The ParaGard and the Mirena IUDs

       Protect against ectopic pregnancy

       Progesterone or levonorgestrel → Menstrual bleeding & clamping↓
   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
   Pelvic Inflammatory Disease

       When PID is suspected in IUP-wearing woman

            → The IUD should be immediately removed

            → High-dose antibiotic therapy should be started
   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
   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

       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
        The cervix is exposed with a speculum
        The uterine cavity should be measured with a uterine sound
        A paracervical block
             →10mL of 1% lidocaine mixed with atropine (0.5mg)
        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
             → 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
            To prevent later septic abortion, premature rupture of the memb-
             ranes & premature birth
       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
            → 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
       Replaced at the end of 1 year
   Copper T380A
       Approved for 10 years
   Levonorgestrel T
       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
       Female sex steroids , Synthetic estrogen
        Synthetic progesterone (progestin) , Progestin only

   Combination OCs
       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
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

       In the United States, OCs contain either of two estrogens
            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)
            40%   of cycles : ovulatory
            25%   : inadequate luteal function
            18%   : follicular maturation without ovulation
            18%   : complete suppression of follicle

       At moderate blood levels of progestin
            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
       Pregnancy rates as low as two to three per 1,000 women per year,
        when used consistently

   Progestin-only OCs
       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 estrogen-
    containing 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 )
            → Modest increased risk for venous thrombosis than older progestins

       Lewis and colleagues
            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
            Major causes of death blamed on OC use in the past

       Principal determinants of risk
            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
       Dose-related effect on blood pressure
       Older high-dose pills → 5% higher than 140/90mmHg
       Estrogen → renin substrate↑ → BP ↑

   Glucose Metabolism
       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

       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
             Less advanced than those in women who had never used OCs

        Greater risk in women who started OC use before 20 years of age
             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

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