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FEMALE PATHOLOGY

CONTRACEPTION
PREGNANT WOMAN
PREMENSTRUAL SYNDROME( PMS)
MENOPAUSE ( M)
Contraception
The discovery of estrogen and progesterone and their potential
contraceptive effects stimulated research on the regulation of
fertility in women.
The effectiveness and safety of OC agents in controlling ovulation
and fertility are a result of these efforts.
Consequently, most research and application of fertility control
techniques continue to be directed toward the control of female
fertility, and there is no readily reversible and effective
pharmacologic contraceptitve for men.
The practice of C.is as old as human existence.
Today, the voluntary control of fertility is of paramount importance
to modern society. From a global perspective, countries currently
face the crisis of rapid population growth that has begun to
threaten human survival.
At the present rate, the
population of the world
will double in 40 years in
several of the more
socioeconomically
disadvantaged countries,
populations will double
in less than 20 years
CONTRACEPTION
HORMONAL CONTRACEPTION
NONHORMONAL CONTRACEPTION

A pacient s choice of C. method involves factors


such as efficacy, safely, non contraceptive benefits
and personal consideration.
HORMONAL CONTRACEPTION

COMBINATION ORAL CONTRACEPTIVES


PROGESTIN ONLY ORAL CONTRACEPTIVES
INJECTABLE CONTRACEPTIVE
TRANSDERMAL PACHES
SUBDERMAL IMPLANTS
CONTRACEPTIVE VAGINAL RING
INTRAUTERINE DEVICES ( IUD)
EMERGENCY POSTCOITAL CONTRACEPTION
FUTURE METHODS OF CONTRACEPTION
ORAL CONTRACEPTIVES
The development of hormonal forms of contraception
represents one of the greatest advances of modern
gynecology.
The concept of pregnancy prevention from administration of
hormones originated with the realization that ovulation was
inhibited by the presence of the corpus luteum.
A number of investigators showed that extracts of ovaries
and later progesterone or estrogen , inhibited ovarian
function.
Progestins were shown to inhibit ovulation; the addition of
estrogen was found both to regulate menstrual bleeding and
increase contraceptive effectiveness.
declined significantly in
the past 40 years.
The estrogenic
component of CO
consisted of either
ethinyl estradiol or
mestranol. Today ee is
used in all preparations
containing 35 mcg or
less.
Another major development is the reduction
in the dosage of ee to 20 mcg.
The major impetus for this change is to
improve the safety and reduce adverse
effects. ( weight gain, breast tenderness,
and nausea).
Monophasic CO have a constant dose of both
estrogen and progestin in each of the active
pills.
Phasic combinations can alter either or both
hormonal components.
The progestin
component
CONSISTS OF synthetic progestagenes
norethindrone,
levonorgestrel
norgestrel ( D, L- norgestrel or D- levonorgestrel ) ,
desogestrel,
norgestimat,
drospirenone.
Aditional progestagens ( gestodene, lynestrenol, and cyproterone
acetate) are used in CO marketed in western Europe.
The most recent addition to the progestin group is the addition of
DROSPIRENONE found in YASMINE birth control pills.
Mechanism of action
-inhibition of ovulation by suppression of follicle
stimulating hormone ( FSH) and luteinizing hormone
( LH).
-Alteration of cervical mucus to inhibit sperm transport
-Interference with ovum transport
-Inhibition of implantation by suppression of normal
endometrial development.
Either estrogen or progesterone alone is capable of
inhibiting both FSH and LH. The combination of the 2
steroids creates synergistic effect that greatly increases
their antigonadotropic and ovulation inhibitory effects.
NONCONTRACEPTIVE HEALTH
BENEFITS OF HORMONAL
CONTRACEPTION
Reduction or protection against diseases below:
Ovarian cancer- protective against hereditary ovarian cancer
Endometrial cancer
Benign breast disease- effect consistent across all age groups
PID - pelvic inflammatory disease
Ectopic pregnancy
Iron deficiency anemia
Bone mineral density
Colorectal cancer
Uterine leiomyomas
Functional ovarian cysts
Rheumatoid arthritis
Other Benefits
Regulation of Menstrual Dysfunction
CO can reduce and sometimes eliminate
Mittelschmerz and PID.
Can reduce functional cysts and ectopic
pregnancies by the cessation of ovulation.
Endometriosis
Women can manipulate the cycle to avoid menses
during certain events, such as vacations or
weekends by extending the number intake days of
hormonally active pills.
Androgen Excess and benign breast disease
POTENTIAL RISKS OF ORAL
CONTRACEPTIVES
Pregnancy
Hormonal contraceptives are among the most effective
methods for preventing pregnancy. While the theoretical
risk of pregnancy is lowest with combined CO, longacting
injections and contraceptive implants achieve higher
efficacy in actual use because compliance is ensured.
Stroke
Women with a history of hypertension and smoking are
at higher risk.
Myocardial Infarction
it is still prudent to continue to avoid using estrogen-
containing pills in women over 35 who smoke.
POTENTIAL RISKS OF ORAL
CONTRACEPTIVES
Venous Thromboembolism ( VTE)
In women who have a history of thromboembolism , CO
are contraindicated. If a patient has a family history of
VTE or stroke, it may be helpful to screen for factor V
Leiden and other thrombophilias, and if a defect is
noted, nonhormonal methods of contraception should be
used.
Neoplasms
The results of several studies have suggested an increase
in the development of cervical cancer in users of
CO( including dysplasia and cancer), about 70 percent
higher compared with intrauterine device (IUD) users
A strong association exists between CO use and the
development of benign hepatic adenomas.
Gallbladder Disease
Changes in clinical
laboratory values
Increased: insulin level, platelet count,
prothrombine time, coagulation factors, cholesterol
total, triglycerides, gamma GT, alkaline
phosphatase, bilirubine, thyroid binding globulin,
triiodthyronine

Decreased: glucose tolerance, antithrombina III,


erythrocyte count, magnesium, zinc,
immunoglobuline A,G,M
CONTRAINDICATIONS
Cerebrovascular disease or coronary artery
disease.
History of deep vein thrombosis.
Pulmonary embolism
Untreated hypertension and age older than 35
years and also cigarette smoking.
Active liver disease and pregnancy suspected
Diabetes with vascular complications
Estrogen dependent neoplasia and breast
cancer
Undiagnosed abnormal vaginal bleeding
INJECTABLE CONTRACEPTIVE
STEROIDS
DMPA:-Depo- Provera
-is a progestin only
-administration site is in gluteus or deltoid
-dosage: 150mg every 12-13 weeks
-the fertility return 7-15 months after discontinuation
MPA/ E2 C - medroxyprogesterone acetate estradiol cypionate
-Is a combined progestin- estrogen
-Administration is : gluteus, deltoid or anterior thigh
-Dossage: 25 mg medroxyprogesterone acetate/ 5 mg estradiol
cypionate every 28-33 days
-The fertility return 35-84 days after discontinuation
SUBDERMAL IMPLANTS

Levonorgestrel IMPLANTS NORPLANT etonogestrel


Progestin containing 6 silicon rods that have multiple modes
of action that include inhibition of ovulation, changes in
cervical mucus, and a thinning of the endometrial lining.
These methods are highly effective , and fertility improves
rapidly on removal. Implants have minimal metabolic effect.
The principal problem with implants includes the need for
surgical insertion and removal and potential problems with
removal of the implant, requiring hospitalization and removal
under anesthesia.
TRANSDERMAL PACHES
ORTHO EVRA
The transdermal contraception patch contains once-
a- week dosing of 150 microg. norelgestromin and
20 microg. ee. each day, and it is applied for 3 weeks
followed by a 1-week rest , when the patient
experiences withdrawal bleeding.
The mechanism of action of the hormonal patch is
similar to that of CO pills , primarily by preventing
ovulation.
The advantage of the patch is that it may increase
compliance in women who have a problem taking a
daily oral pill and decreased nausea and vomiting
due to avoidance of the first pass effect.
CONTRACEPTIVE VAGINAL
RING
The most recent contraceptive device available consists
of a vaginal ring that contains the progestin etonogestrel
and ee.
The ring is a combined hormonal contraceptive method
that the women inserts in the vagina herself.
The ring is inserted for a-3 week period, after wich it is
removed , followed by 1- week hormone free period in
which withdrawal bleeding is anticipated.
Once it is inserted , the ring releases continuous doses of
hormones into blood , and the mechanism of action are
similar to those of the contraceptive patch.
Cycle control appears to be similar to that of the patch
and CO pills. The efficacy and other aspects of safety are
similar to that of CO pills , and the contraindications are
also the same.
HORMONE - CONTAINING
INTRAUTERINE DEVICE ( IUD)
Once in place, the IUD provides contraception for up to 5 years.
Progestasert contains38 mg progesterone and barium sulfat for greater
visibility on x-ray films. This IUD must be replaced yearly.
Mirena has a reservoir that contains levonorgestrel. This releases 20
microgr of levonorgestrel per day into the uterine cavity for as long as
5 years.
T Cooper T 380 mm is covering with cooper and it must be replaced for
10 years.
Its mechanism of action includes cervical mucous tickening, reduced
sperm motility, endometrial suppression, and a week foreign- body
reaction in the uterine cavity and, in a small percentage of patients, the
inhibition of ovulation.
Its safety has been well established and is similar to that of the copper
IUD.
Although infections are rare with IUD if used in monogamous couples
EMERGENCY POSTCOITAL
CONTRACEPTION
The most experience available is with the use of combined
contraceptive pills , also known as the morning after pill.
To be effective, the first dose of medication must be
administered within 72 hours of unprotected intercourse and
a second dose within 12 hours of the first.
Other options include a product known as plan B that
contains 75 mg levonorgestrel given in two doses within 72
hours of exposure.
Side effects of emergency oral contraceptive pills are upper
gastrointestinal symptoms , including nausea and vomiting,
breast tenderness, fatigue, headache, abdominal pain, and
dizzines. Ectopic pregnancy is possible if treatment fails.
NONHORMONAL
CONTRACEPTION
Abstinence or natural familly planning
Lactational amenorrhea
Coitus interruptus
Rhythm method
Condoms
Diaphragms
Cervical caps
Female condom
Intrauterine device
Spermicides
Surgery permanent method (vasectomy in men, and interupting the
fallopian tubes , hysterectomy, possibly endometrial ablation, and
hysteroscopic tubal occlusion in women)
ABNORMAL UTERINE
BLEEDING
A normal cycle has an average length of 28
days , but can range from 21 to 35 days. The
average duration is 4 days, with a range of 1-8
days. Blood loss is usually about 35 ml and is
considered abnormal when it is greater than
80ml.

Bleeding at irregular time intervals , or bleeding


that is excessive but at the time of expected
menses.
ABNORMAL UTERINE
BLEEDING
The causes of abnormal uterine bleeding:
Pregnancy related (Misscariage, Ectopic pregnancy, Gestational
trophoblastic disease)
Infection (Cervicitis, Endometritis)
Neoplasm (Cervical dysplasia/ carcinoma, Endometrial
hyperplasia/ polyps/ carcinoma, Submucous leiomyomas,
Estrogen producing ovarian tumors
Systemic (Thyroid disease, Liver disease, Coagulation disorders,
Sepsis )
Iatrogenic (Oral contraceptives, Progestin only contraceptives,
Intrauterine devices
Hormone replacement therapy, Steroids )
PELVIC INFLAMMATORY
DISEASE ( PID)
The term PID describes a spectrum of infection and inflammation involving , in
varying degrees depending on the severity of the disease , the upper genital tract
( endometrium, tubes, and ovaries)as well as the surrounding peritoneum.
PID comprises , for the most part , sequelae of cervical infection with sexually
transmitted organisms, chiefly Neisseria gonorrhoeae and Chlamydia
trachomatis.
Cervical infection with these organisms breaks down cervical barriers to
ascending infection, allowing endogenous superinfection of the upper genital tract
by aerobic as well as anaerobic organisms normally inhabiting the lower genital
tract. In addition , though less commonly the cause , instrumentation of the cervix
and uterus during surgical procedures can cause auto-inoculation of the
endometrium with endogenous bacteria and lead to PID.
Criteria for the diagnosis of PID
Minimum criteria
sexually active or history of recent instrumentation of cervix or uterus
lower abdominal pain
adnexal tenderness
cervical motion tenderness
Additional criteria that support the diagnosis of PID:
oral temperature > 38,3 gr.C
abnormal cervical or vaginal discharge
elevated C-reactive protein and/or erythrocyte sedimentation rate
elevation of WBC count
laboratory documentation of positive cervical testing for GC or Chlamydia
ultrasound with documentation of hydrosalpinx/ pyosalpinx and/ or tubo-ovarian complex
laparoscopic documentation of tubal inflammation and/ or pyosalpinx
AMENORRHEA (A)
Primary A:
No period by age 14 in the absence of growth and
secondary developmental characteristics ( breasts and
pubic hair), or
No period by age 16 regardless of the extent of
secondary development
The incidence of primary A is < 1%
Secondary A:
The absence of menses for longer than 6 months, or
The absence of menses for a total of three previous cycle
intervals
The incidence of secondary A is approximately 0,7%
DISMENORRHEA (D)
Is pelvic pain associated with menstrual periods. The pain is
usually described as cramping in nature. Pain can also be felt
outside of the pelvis; women can experience backache,
headache, and extremity pain.
It can also be accompanied by many other systemic symptoms ,
including lightheadedness, insomnia, and gastrointestinal
symptoms such as nausea, vomiting, and diarrhea.
Primary, or intrinsic dismenorrhea is not associated with
identifiable pathology
Secondary dismenorrhea can be caused by a number of
gynecologic conditions ( uterine myomas,adenomyosis,
endometriosis, and pelvic infection)
It is less common and less severe in women who have given
birth.
DISMENORRHEA (D)
Both primary and secondary D can be managed medically, at least
initially.
The two mainstays of medical treatment are NSAID, COX-2 inhibitors,
and CO . NSAID decrease prostaglandin production, which helps
improve symptoms.
CO cause atrophy of the endometrium , the principal site of
prostaglandin production. They also can reduce the amount and
duration of bleeding , which can improve a woman experience.
The COX-2 inhibitors ( rofecoxib and others) are a new class of oral
analgesics originally developed to treat arthritis. They have been
shown effective in the management of D. Short- term therapy with
oral narcotics ( codeine, oxycodone) can be used for the few days of
severe , debilitating symptoms. Side effects, particularly the sedation,
make this therapy unattractive to many healthy women.
PREMENSTRUAL
SYNDROME( PMS)
A constellation of symptoms that occurs in a cycling pattern,
always in the same phase of the menstrual cycle , interfering
with work or lifestyle and followed by a period entirely free of
symptoms.

What symptoms are associated with PMS?


Symptoms may be both: physical and emotional. Physical
symptoms include weight gain, breast swelling and tenderness,
skin changes such as acne, hot flashes, diarrhea or
constipation, headache, craving of sweets, and pelvic pain.
Emotional symptoms include irritability, insomnia, depression,
confusion or forgetfulness, anxiety, fatigue, and a feeling of
being out of control.
PREMENSTRUAL
SYNDROME( PMS)

Healthy diet that is low in fat, salt, and sugar but more
moderate in proteins and complex carbohydrates ( whole
grains, vegetables, and fruit) is most beneficial to the patient
with PMS.
Prostaglandin PGE1 may be low in some women with PMS,
particularly those women whose symptoms are associated with
alterations in carbohydrate metabolism.
Prostaglandins also contribute to dysmenorrheal; thus an
inhibitor such as a nonsteroidal anti- inflammatory drug can be
beneficial.
MENOPAUSE (M)
M is permanent cessation of menstruation resulting from the loss of
ovarian follicular activity. Natural M is defined as 12 months of
amenorrhea without another pathologic cause. The average age at which
this occurs is 51,4 years. M before age 40 is called premature ovarian
failure.
Perimenopause is the period immediately prior to M and the first year
after M. The average age that perimenopause starts is the 47,5 years
and it lasts on average 4 years.
The climacteric is the phase during the aging of women marking the
transition from the reproductive to the non- reproductive state. This time
period includes events such as decreased fertility that precedes
perimenopause and extend beyond M.
MENOPAUSE (M)
M is due to a gradual depletion of functioning ovarian follicles.
Declining inhibin levels from the granulose cells lead to increased
FSH production from the pituitary that accelerates the follicular
phase of the menstrual cycle.
High basal estradiol levels during menses can be seen, often in
association with follicular cysts.
As the granulosa cells gradually lose their ability to produce
estradiol, FSH levels rise ( as do LH levels, to a lesser extent).
After M, androgen levels decline by 50%, but the greater decline
of estradiol favors a higher androgen- to- estrogen ratio, leading to
signs of hirsutism and alopecia in some women.
Estrogen production after M is principally estrone produced by
aromatazation of androstendione in adipose tissues.
MENOPAUSE (M)

the irregularity of the menstrual cycles


hot flash (a sudden sensation of warmth, often accompanied
by a flushed sensation of the upper body and face, typically
lasting 1-5 minutes)
Sleep and mood disturbances
dyspareunia
vulvar pruritus
incontinence
Hormone therapy ( HT) in
HT with estrogen ( andM
a progestin if a uterus is
still present) has been given in M to replace
ovarian hormones. Studies have shown a 70-
80% improvement in vasomotor symptoms and
urogenital atrophy , 25 -50% decrease risk of
vertebral and hip fractures.
Other studies have suggested a 20% decrease in
risk of colorectal cancer, possible decreased risk
of Alzheimers disease, a 25% reduction in risk
of tooth loss, and a possible decreased risk of
age-related macular degeneration when HT is
utilized post- menopausally.
While observational studies have pointed to a
cardioprotective benefit of HT
Hormone therapy ( HT) in
M
HT is contraindicated in
pregnancy,
in patients with active thromboembolic disease,
chronic liver impairment,
undiagnosed genital bleeding,
or estrogen dependent neoplasms.

Estrogen therapy has been associated with an


increased risk of cholelithiasis and deep venous
thrombosis.

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