AMENORRHEA

Miteku Andualem
[BSC, MSC]
 Principles of Menstrual Function

• Menses
Physiologic uterine bleeding due to interplay of hormones vi
a hypothalmo-pituitary-ovarian axis.
• For menses to occur,
Actively coordinated axis
Responsive endometrium
Patent out-flow tract
 CNS-Hypothalamus-Pituitary
Ovary-uterus Interaction

Dopamine Endorphines
(-) (-)

Hypothalamus
Gn-RH

_ Ant. pituitary –
FSH, LH
Estrogen Ovaries Progesterone

Uterus

Menses
 AMENORRHEA
Definition & Incidence
Amenorrhea literally means absence of menses
Physiological :- Before Puberty, Adolescence, Pregna
ncy, Lactation and Menopause. Accounts for 90-95
% of amenorrhea
Pathological :- Primary and Secondary Amenorrhe
a.
Primary Amenorrhea :-
Is defined as the absence of menses by age 13 years
in the absence of normal growth or secondary sexua
l development; or the absence of menses by age 15
years in the setting of normal growth and secondary
sexual development.
Secondary Amenorrhea :-
Defined as the absence of menses for more th
an 3 cycle intervals, or 6 consecutive months,
in a previously menstruating woman.
Its incidence varies, from 3% in the general po
pulation to 100% under conditions of extreme
physical or emotional stress.
 Etiologies of Amenorrhea

Compartm Site of defect Hormone level

ent

1 Out flow tract Eugonadotropic

obstruction hypogonadism

2 Ovary Hypergonadopropic
hypogonadism

3 Pituitary Hypogonadotropic
hypogonadism

4 Hypothalamus Hypogonadotropic
hypogonadism
 I. Out flow tract obstruction
Congenital causes

Müllerian anomalies
Transverse vaginal septum
Absent endometrium
Cervical agenesis
Imperforate hymen
Androgen insensitivity
True hermaphrodites
Acquired causes
Asher man's syndrome
Secondary to prior surgeries
Cesarean section
Myomectomy
Currettage, especially postpartum
Secondary to infections
Pelvic inflammatory disease
IUD–related
Tuberculosis
Schistosomiasis
Cervical stenosis
Cone biopsy
Loop electro excision procedure
 Out flow contd.
Imperforate hymen
Is one of the most common obstructive lesions of the
female genital tract

Imperforate hymen occurs 1 in 2,000 women

At birth, infants may have a bulging introitus due to m

ucocolpos from vaginal secretions stimulated by mate
rnal estradiol.

If the diagnosis is not made in the newborn period an

d the hymen remains imperforate, the mucus will be r
eabsorbed and the child usually remains asymptomati
c until menarche.
Adolescent girls present with cyclic abdominal
or pelvic pain & hematocolpos, which gives th
e hymenal membrane a bluish discoloration.

Marked distension of the vagina may also res

ult in back pain, pain with defection, or diffic
ulties with urination.

Retrograde menstruation may lead to develop

ment of endometriosis.
 Out flow contd.
Treatment 
Hymenectomy  or cruciate incision
 Repair of the hymen can be performed at any age;
however, the repair is facilitated if the tissues have
undergone estrogen stimulation.
Therefore, surgery is ideal in the newborn,
postpubertal, or premenarchal periods
Give certificate to the child
Out flow contd.
 Out flow contd.
Transverse vaginal septum
Results when there is failure of fusion and/or canaliz
ation of the urogenital sinus and müllerian ducts.
Occurs in approximately 1 in 30,000 to 1 in 80,000 w
omen.
These septa may be located at various levels in the v
agina;
Approximately 46 % are found in the upper vagina,
35 to 40 % in the middle portion, and 15 to 20 % in th
e lower vagina.
 The septa are generally less than 1 centimeter in
thickness and may have a small central or eccentr
ic perforation.
The external genitalia appear normal, but interna
lly the vagina is shortened (a blind pouch).
Children may present with mucocolpos, whereas
adolescents can develop hematocolpos or pyohe
matocolpos due to an ascending infection throug
h the small perforation.
 Out flow contd.
Treatment —  Excision and complete removal of the septum.
 Out flow contd.
Absent endometrium
This abnormality is rare
Physical findings are normal.
Absence of the endometrium is suspected in patients With:
1. Primary amenorrhea and
2. Normal secondary sexual characteristics
3. Hormone levels are normal and
4. No withdrawal bleeding after combined estrogen & progesterone r
eplacement.
 Out flow contd.
Asherman's syndrome
It is diagnosed by performing hysterosalpingography, saline infusion ultraso
nography, or hysteroscopy.
There is complete obliteration or multiple filling defects caused by synechiae
.
If tuberculosis or schistosomiasis is suspected, do endometrial cultures.
Treatment
Adhesions released using hysteroscopic resection with scissors or electroca
utery.
A pediatric Foley catheter is placed in the uterine cavity for 7 to 10 days pos
toperatively
Systemic administration of broad–spectrum antibiotic therapy
2–month course of high– dose estrogen therapy with monthly progesterone
withdrawal is used to prevent reformation of adhesions.
80% of patients treated achieve pregnancy , complications including miscar
riage, preterm labor, placenta previa, & placenta accreta occur.
Cervical stenosis can be treated by cervical dilation.
 Ovarian Failure
Primary dysfunction at the level of the ovary.
Termed premature menopause or premature ovarian failure
(POF).
POF is preferable, as it better describes the pathophysiology
of this condition.
Due to lack of negative feedback, the gonadotropins, LH and F
SH, have increased levels (hypergonadotropic).
Premature ovarian failure is defined as loss of oocytes and the
surrounding support cells prior to age 40 years.
The diagnosis is determined by two serum FSH levels greater t
han 40 Miu /mL that are obtained at least 1 month apart.
Incidence 1 in 1,000 women less than 30 years, and 1 in 100
women less than 40 years.
In most cases, the etiology of POF is not determined.
 Ovarian Failure contd.
1. Chromosomal Disorders 3. Acquired Abnormalities
Abnormal Karyotype Iatrogenic causes
Turner Syndrome Radiation
Normal Karyotype
Chemotherapy
"pure" gonadal dysgenesis
Oophorectomy
2. Specific Genetic Defects
Congenital Lipoid Adrenal Hyperplasia
Infections(mumps oophoritis)
Aromatase Deficiency Autoimmune disorders
Mutations in the LH & FSH recept Cigarette smoking
ors (impair follicular health)
Vanishing testes syndrome   Polycystic ovarian syndrome
Feminizing tumor of the ovary
Masculinizing tumor of the ovary
Idiopathic
 Pituitary Failure
Acquired Abnormalities Inherited Abnormalities
Pitutary adenomas Mutations in GnRH recepto
Sheehan syndrome r
Inflammation Mutations in LH /FSH subunits
Metastatic lesions
surgical removal or
Radiation treatment of pitui
tary adenomas.
 Pituitary contd.

Acquired Pituitary Dysfunction

Most pituitary dysfunction is acquired after mena
rche, and therefore, women present with normal
pubertal development followed by secondary am
enorrhea.
Nevertheless, in rare cases, these disorders may
develop prior to puberty, resulting in delayed pu
bertal development and primary amenorrhea
Pituitary adenomas are the most common cause
of acquired pituitary dysfunction.
 Pituitary contd.
Pitutary adenomas
Cause amenorrhea in two ways
1. Prolactin secretion
Elevated prolactin levels are associated with a reflex increase in cen
tral dopamine production, which alters GnRH neuronal function.
2. Mass effect
This mass may compress neighboring gonadotropes or may damage
the pituitary stalk, disrupting dopamine inhibition of prolactin secre
tion.
As many as one tenth of amenorrheic women have increased levels
of serum prolactin (the "galactorrhea-amenorrhea syndrome").
 Pituitary contd.
Sheehan syndrome refers to panhypopituitarism that d
evelops after massive postpartum hemorrhage complica
ted by hypotension.
Loss of gonadotrope activity results in anovulation and
subsequent amenorrhea.
Damage to the other pituitary cell types may present as
failure to lactate, loss of sexual and axillary hair, hypoth
yroidism, and adrenal insufficiency.
The pituitary cell types are differentially sensitive to da
mage.
Prolactin secretion deficiency is the most common, foll
owed by loss of gonadotropin and growth hormone rele
ase, loss of ACTH, and least commonly, by decreases in t
hyroid-stimulating hormone (TSH) secretion
 Hyperprolactinemia & Hypothyroidism fig.

Decreased thyroid hormones

-Ve

Increased TRH Increased Increased

+ prolactin dopamine

Change in pulsatile
Increased TSH GnRH secretion

Change in LH&FSH

Anovulation &
Amenorrhea
 Hypothalamic failure
Inherited Abnormalities Acquired abnormalities
Eating disorders
Idiopathic hypogonadotropic hyp
ogonadism Extreme exercise
Stress
Chronic disease
Anatomic Destruction
Radiation
 Hypothalamic failure contd.

Acquired Hypothalamic Dysfunction

Functional Disorders or Hypothalamic Amenorrhe
a
Most frequently, gonadotropin deficiency leading
to chronic anovulation is believed to arise from fu
nctional disorders of the hypothalamus or higher
brain centers.
Also called hypothalamic amenorrhea, this diagn
osis encompasses three main categories: eating d
isorders, extreme exercise, chronic disease and s
tress.
Each woman appears to have her own hypoth
alamic "set-point" or sensitivity to environme
ntal factors.

For example, individual women can tolerate si

gnificantly different amounts of stress without
developing amenorrhea.
 Hypothalamic failure contd.

Eating Disorders
Anorexia nervosa and bulimia, result in amenorr
hea.
Anorexia nervosa patient have abnormal body i
mage, intense fear of weight gain, often engage
d in compulsive exercise, mean age onset 13-14
yrs (range 10-21 yrs)
Low estradiol  risk of osteoporosis
Weight loss is generally less severe in bulimic wo
men, who eat in binges then purge to maintain w
eight.
Hypothalamic dysfunction is severe in anorexi
a and affect other hypothalamic-pituitary axes
in addition to the reproductive axis.
Amenorrhea in anorexia nervosa can precede,
follow, or appear coincidentally with weight l
oss.
Even with return to normal weight, not all wo
men with anorexia will regain normal menstr
ual function.
 Hypothalamic failure contd.

Exercise-Induced Ame
norrhea
Seen in women whose
exercise regimen is as
sociated with significa
nt loss of fat, such as
ballet, gymnastics, an
d long-distance runnin
g.
 Patient Approach

• History
– Age, parity
– Previous menstrual history
– Mode of onset-Sudden, Gradual
– Family history
– Past medical history or recent illnesses
– Weight fluctuation
– History of any stressful events
– History of drug intake
– Radiation exposure
– History of uterine curettage or uterine surgeries
– History of PPH or shock or infection
– Acne, hirsute
– Inappropriate galactorrhea
– Headache or visual disturbances
– Symptoms of estrogen deficiency
 Approach Contd.

• Physical examination
V/S
Weight, Height , BMI
Assess thyroid gland
breast
Presence of normal reproductive tract
Presence of secondary sexual characteristics
Axillary and pubic hair growth
Neurological examinations and determination of visual field
 Amenorrhea

Pelvic examination Absent uterus Sexual hair

Normal
Yes No
Negative HCG +Ve
Müllerian Agenesis
ANC

Prolactin TSH FSH

Increased Increased See next slide

Dopamine Vs
Thyroid
surgery
replacement
 FSH

Decreased Increased Normal

Stress, exercise & eating Gonadal failure

disorders Testosterone 17-OH-P
DHEAS
Karyotype
Increased Increased
Yes Increased
No
MRI Adrenal
POF Vs Gonadal Ultrasound CAH
treat tumors
MRI dysgenesis for ovarian
tumor
Abnormal
Normal

Tumor
 Approach Contd.

Clinical state Serum FSH Serum LH

Normal 5-20 IU/L 5-20 IU/L

Hypogonadotropic <5 <5
Hypergonadotrophic >20 >40
INFERTILITY

Miteku Andualem
[BSC, MSC]
 Infertility
 Infertility: is inability to conceive after 1 year of u
nprotected intercourse of reasonable frequency.

 Most couples are more correctly considered to be

subfertile, rather than infertile, as they will ultima
tely conceive if given enough time.

 Sterility: incapable of becoming pregnant or of in

ducing pregnancy
 INFERTILITY
Two types of infertility
 Primary infertility: no prior pregnancies
 Secondary infertility: infertility following at least one
prior conception.

Fecundity
 Is the probability that a single menstural cycle will re
sult in a live birth
 INFERTILITY
Fecund ability
 Is the ability to conceive in a single cycle , the monthl
y probability of conceiving is 20 to 25 %.

 In people attempting conception, approximately 50

% of women will be pregnant at 3 months, 75 % will
be pregnant at 6 months, and > 85 % will be pregnan
t by 1 year.
 ETIOLOGY OF INFERTILITY
 Successful pregnancy requires a complex sequence of eve
nts including:
Patent out flow tract
Ovulation
Sperm of adequate number & quality
Ovum pick-up by a fallopian tube
Fertilization
Transport of a fertilized ovum into the uterus
Receptive endometrial cavity.
 Infertility can be seen as male & female infertility
 ETIOLOGY
Female infertility
Ovulatory Dysfunction
Male factors
Tubal /Peritoneal Factor
Pre-testicular
Uterine Factor
Testicular
Cervical Factors
Vaginal Factors Post-testicular
Chronic systemic diseas Idiopathic
es
Social personal habit(illi
cit drugs)
Unexplained
 ETIOLOGY

Etiology of Infertility

Ovulatory dysfunction 27%

Male factor 25%

Tubal/uterine factors 22%

Unexplained infertility 17%

Other 9%
 Ovulatory Dysfunction

 Ovulation may be perturbed by abnormalities within

the hypothalamus, anterior pituitary, or ovaries.
 Hypothalamic disorders may be due to lifestyle, for e
xample, excessive exercise, eating disorders, or stres
s.
 Thyroid disease and hyperprolactinemia may also co
ntribute to menstrual disturbances
 Ovulatory contd.
 Different methods can be used to determine if and when ovulation
has occurred.
 Directly or indirectly, all are based on one or another of the hormon
al events that characterize the normal ovulatory menstrual cycle .
 Each of the available tests is useful and no one test is necessarily b
est.
 Some are very simple, noninvasive, and inexpensive, and others ar
e more complicated, invasive, and costly.
 A few can predict when ovulation is likely with varying accuracy.
 However, no test, regardless how sophisticated, can prove that ovul
ation has actually occurred; the only positive proof of ovulation is
pregnancy.
 The most appropriate test to use varies with the information requir
ed.
 Ovulatory contd.
Methods used to document ovulation include:
1. Indirect
Menstrual pattern
Basal body temperature
Ovulation predictor kits
Endometrial biopsy
Serum progesterone
Sonography
2. Direct: laparoscopic visualization of recent corpus luteum or detec
tion of ovum from aspirated peritoneal fluid
3. Conclusive: pregnancy
 Ovulatory contd.
Basal Body Temperature:
This test requires that a woman's morning oral temperature be grap
hically charted.
BBT is measured each morning, on awakening and before arising
Oral temperatures are usually 97.0° to 98.0°F during the follicular ph
ase.
A postovulatory rise in progesterone (thermogenic) levels increases
basal temperature by approximately 0.4° to 0.8°F.
This biphasic temperature pattern is strongly predictive of ovulation.
Nevertheless, although this test has the advantage of being inexpen
sive, it is insensitive in many women.
Furthermore, for a couple wishing to conceive, the temperature inc
rease follows ovulation, and therefore the window of maximal fertil
ity has been missed.
Ovulatory contd.
 Ovulatory contd.
Ovulation predictor kits
These kits, measure the concentration of urinary luteiniz
ing hormone (LH) by colorimetric assay.
Ovulation predictor kits turn positive when the urinary L
H concentration exceeds a threshold level normally seen
only during the LH surge
Begin testing 2 to 3 days prior to the predicted LH surge,
and testing should be continued daily.
In most instances, ovulation will occur the day following t
he urinary LH peak.
If equivocal results are obtained, the test can be repeate
d in 12 hours
 Ovulatory contd.
Serum Progesterone:
Ovulation can also be tested by measuring midluteal phase serum p
rogesterone levels.
In a classic 28-day cycle, serum is obtained on cycle day number 21
following the first day of menstrual bleeding, or 7 days following o
vulation.
Levels during the follicular phase are generally <2 ng/mL
Values above 4 to 6 ng/mL are highly correlated with ovulation and
subsequent progesterone production by the corpus luteum.
Progesterone is secreted as pulses, and therefore a single measure
ment is not indicative of overall production during the luteal phase.
Many clinicians choose to empirically treat any patient with a prog
esterone level below this value with natural progesterone.
 Ovulatory contd.
Endometrial Biopsy:
Inadequate progesterone levels are believed to result in lut
eal phase defect (LPD).
These investigators defined LPD as a lag in the histologic ap
pearance of the endometrium of greater than 2 days relati
ve to the actual day of the cycle.
This discrepancy in dating is termed an out-of-phase biopsy
.
Unfortunately, the utility of this test is severely hampered b
y high intra-observer and inter-observer variability.
The estimated frequency of LPD in the infertile population
has ranged widely, but is generally agreed to be between 5
and 10 percent.
 Ovulatory contd.
Sonography:
Serial ovarian sonography can demonstrate t
he development of a mature antral follicle and
its subsequent collapse during ovulation.
This approach is rather time consuming and o
vulation can be missed.
 Ovulatory contd.
Treatment of ovulatory dysfunction is ovulation induction

Drugs used for ovulation induction

Clomiphene citrate
FSH
hcG
GnRH analogs
 Tubal/Peritoneal Factor
Damage or obstruction of fallopian tube
Previous PID
Previous tubal surgery
Ectopic pregnancy
Benign polyps
Tubal endometriosis
Mucus debris
Tubal damage of unknown cause-sub clinical infection
Peritubal/periovarian adhesions
PID
Pelvic Surgery
Endometriosis
 Tubal/ peritoneal contd.
Symptoms such as chronic pelvic pain or dysmenorrhea may s
uggest the presence of tubal obstruction or pelvic adhesions o
r both.
Adhesions can prevent normal tubal movement, ovum pick-up
, and transport of the fertilized egg into the uterus.
Tubal infertility has been estimated to follow in 12 percent, 23
percent, and 54 percent of women following one, two, or thre
e cases of PID, respectively
Testing for tubal patency can be performed by Rubin test hys
terosalpingography (HSG), Falloposcopy , Salpingoscopy or b
y chromotubation during laparoscopy.
 Tubal/ peritoneal contd
1. HSG (hysterosalpingography):
Done on day 6-10 of cycle
Advantage: site & side of blockade determin
ation, detection of uterine malformation and
as treatment
Contraindicated in presence of pelvic infecti
on & undiagnosed adnexal mass
Could be oil based or water based
Tubal abnormalities on HSG
 Tubal/ peritoneal Contd.
2. Laparoscopy & chrome pertubation
Indications:
Abnormal HSG
Failure to conceive after 6 months with normal HS
G
Unexplained infertility
Age above 35 years
Better done in secretary phase
Drawbacks: more invasive and couldn’t detect uterine
cavity problems & tubal lumen
 Tubal/ peritoneal Contd.
Treatment of tubal and peritoneal factors is tuboplasty
Tuboplasty:
1. Adhesiolysis
2. Fimbrioplasty
3. Salpingostomy
4. Tubal anastmosis
5. Tubo-cornual anastmosis
Poor prognosis following tuboplasty is associated with
o Dense adhesions
o Loss of fimbriae
o Bilateral hydrosalpinx>3cm
o Length after construction<4cm
 Uterine Factor
Uterine causes of infertility include
Congenital malformation –didelphys
, unicornute, septate
Luteal phase defect
Endometritis –Tuberculosis
Endometrial polyps
Leiomyoma – large, solitary, submu
cous, distorting cavity
Asherman’s syndrome
 Uterine Factor contd.
There are five major approaches for evaluating pel
vic anatomy:
1. Hysterosalpingography
2. Transvaginal sonography with or without saline instill
ation
3. Hysteroscopy
4. Laparoscopy, and
5. MRI
 Cervical Factors
The cervical glands secrete mucus that is normally thic
k and impervious to sperm and ascending infections.
High estrogen levels at midcycle change the characteri
stics of this mucus, and it becomes thin and stretchy.
Estrogen-primed cervical mucus filters out nonsperm c
omponents of semen and forms channels that help dir
ect sperm into the uterus.
Midcycle mucus also creates a reservoir for sperm, allo
wing ongoing release during the next 24 to 72 hours an
d extending the potential time for fertilization.
 Cervical Factors contd.
Abnormalities in mucus production are secondary to
Cryosurgery, cervical conization, or a loop electrosur
gical excision procedure (LEEP) for an abnormal pap s
mear
Cervical infection (Chlamydia trachomatis, Neisseria
gonorrhoeae & Ureaplasma urealyticum)
Abnormalities of cervical factor can be assessed by p
ostcoital test
 Cervical Factors contd.
Postcoital Test: (Sims- Huhner test)
The couple are requested to have intercourse on the day of o
vulation.
Obtain the cervical mucus within few hours from cervical os wi
th forceps or by aspiration.
In the presence of high estrogen levels, mucus is copious, stret
chy, and relatively clear. Mucus should be able to be stretched
to >5 cm. These qualities are summarized by the term spinnba
rkeit.
Normal finding are:
1. Mucus is copious, stretchy
2. At least five motile sperm per high-power field,
3. There should be a minimal number inflammatory cells.
4. When dried, the mucus should form a ferning pattern
 Cervical Factors contd.
The most common reason for an abnormal test is improp
er timing.
There is limited consensus on the definition of a normal
test, and the predictive value for conception is poor.
Many infertility specialists recommend literally bypassing
the cervix with intrauterine insemination in any woman
with a history of cervical surgery, especially if she has not
ed a decrease in midcycle mucus production.
 Unexplained
No obvious cause for infertility following all st
andard investigations i.e. semen analysis, ovul
ation detection, tubal &peritoneal factors, end
ocrinopathy & post-coital test
With expectant management, 60 % conceive i
n three years
 Male factor
The hypothalamic-pituitary-testicular axis
 Spermatogenesis
Testes have two functions:
1. The generation of mature germ cells (sperm) and the
2. Production of testosterone
The testes have two distinct components, the seminiferous tubul
es (the site of spermatogenesis) and the Leydig cells (the source
of testosterone).
The seminiferous tubules are composed of germ cells, called sper
matogonia, and Sertoli cells.
The seminiferous tubules contain developing sperm and support
cells called Sertoli cells or sustentacular cells.
Leydig cells also called interstitial cells, which are responsible for
steroid hormone production. In simplistic terms, Leydig cells are s
imilar to the thecal cells of the ovary.
 Spermatogenesis contd.
After migration of the germ cells to the genital ridge
during embryogenesis, there are approximately 300,
000 spermatogonia in each gonad.
Each undergoes a series of mitotic divisions and, by p
uberty, there are about 600 million in each testis.
Continued proliferation during adult life supports the
production of 100- 200 million sperm each day and
more than 1 trillion during a normal reproductive life
span.
The spermatogenic process is directed by genes locat
ed on the Y chromosome & takes 70 days to comple
te.
Another 12- 21 days are required to transport sperm
from the testis through the epididymis to the ejacula
tory duct.
 Etiology of Male Infertility
Etiology of infertility Site of dysfunction Prevalence %

Pre-testicular Hypothalamic / pituitary 1 -2

Testicular Testis 30 - 40

Post-testicular defects Ducts of sperm transport 10 - 20

Idiopathic ----- 40 -50

Etiology of Male Infertility contd.
1. Pre-testicular causes
Are hypothalamic & pituitary disease
A. Congenital disorders 
B. Acquired diseases
1. Tumors
2. Infiltrative diseases
3. Chronic disease
4. Hyperprolactinemia
5. Drugs 
 Etiology of Male Infertility contd.
2. Testicular Causes
Congenital disorders
Cryptorchidism
Varicoceles

Acquired disorders
Infection
Drugs 
Radiation
Environmental factors
Smoking
Systemic disorders  

Y chromosome defects
Etiology of Male Infertility contd.
3. Post-testicular causes
Congenital or acquired disease in the ductal
system of a male
Absence, dysfunction, or obstruction of the
epididymis
Bilateral obstruction, ligation, or altered
peristalsis of the vas deferens
Etiology of Male Infertility contd.
4. Idiopathic male infertility 
 Despite careful assessment of all possible causal
mechanisms, a cause of abnormal sperm number
, morphology or function cannot be identified in a
substantial proportion of infertile men.
There are also men who have repeatedly normal
semen analyses but cannot impregnate an appar
ently normal female partner.
 Diagnostic work up of male infertility
1. Standard semen analysis
Cornerstone of the assessment of the male infertility
The standard semen analysis consists of the following:
1. Measurement of semen volume and pH
2. Microscopy for debris and agglutination
3. Assessment of sperm concentration, motility, and morphology
4. Sperm leukocyte count
5. Search for immature germ cells.
The semen sample should be collected after two to seven days o
f sexual abstinence, preferably at the doctor's office by masturba
tion.
If this is not possible, then the samples can be collected with co
ndoms without chemical additives and delivered to the laborator
y within an hour of collection.
Because of the marked inherent variability of semen analyses, at
least two samples should be collected one to two weeks apart.
Diagnostic work up of male infertility contd.

Normal semen analysis findings

Volume >1.5 mL

Count >20 million/mL

Motility >50%

Morphology >30%

WBCs <1 million/mL

PH 7.2-7.8
Terminologies in seminal fluid analysis

Aspermia: failure of formation or emission of

semen
Oligospermia: < 20 million/ml
Polyzoospermia:>350 million/ml
Azoospermia: no spermatozoa
Asthenozoospermia: abnormal motility
Teratozoospermia: abnormal morphology
Necrozoospermia: dead or motionless
Diagnostic work up of male infertility contd.

Semen volume 
The mean semen volume in the WHO study was 3.7 mL; the l
ower reference limit was 1.5 mL .
A low or absent ejaculate volume suggests the possibility of:
Failed emission
Incomplete collection
A short abstinence interval
Congenital bilateral absence of the vas deferens
Ejaculatory duct obstruction
Hypogonadism, or
Retrograde ejaculation.
 Diagnostic work up of male infertility contd.
2. Endocrine Evaluation
Endocrine disorders involving the hypothalamic-pituitary-te
sticular axis are well recognized but uncommon causes of
male infertility and are extremely uncommon in men havin
g normal semen parameters.
Indications for endocrine evaluation in infertile men include
An abnormal semen analysis (sperm count <10 million/ml),
Sexual dysfunction (decreased libido, impotence), and
Endocrinopathy
A basic endocrine evaluation of the infertile male are FSH a
nd total testosterone and will detect the vast majority of cli
nically significant endocrinopathies.
 Evaluation of infertility
Objectives:
Discover etiologic factor
Rectify the abnormality to improve fertility
Reassure the couples
When to investigate:
After one year
After 6 months in women older than 35 years
& after 40 years in men
 Evaluation of infertile couple
History
Childhood illnesses
Exposure to toxins, heat, radiation, metals
Infection, trauma, torsion, DES exposure
Precocious or delayed puberty
Galactorrhea
Change in the pattern of hair distribution
Drug exposure
Medical illnesses
Surgical illnesses & their treatment
 Evaluation of infertile couple
Physical Examination
– Features of hypogonadism secondary sexual characteristics
eunchoidal skeletal proportions, hair distribution.
– Testes evaluation: size, weight, volume
– Epididymis: irregularity
– Visual field loss
– Spermatic cord :vas deferens, varicose
– Prostate: size, tenderness
– Penile abnormalities
– Breast, liver, thyroid, neurological evaluation
 Treatment of the Infertile couple

I. Lifestyle Therapies
II. Correction of an Identified Cause
III. Assisted Reproductive Technologies
 Treatment contd.
I. Lifestyle Therapies
Weight Optimization
Stop Smoking
Exercise
Stress Management
 Treatment contd.

II. Correction of an Identified Cause

Ovulation Induction for ovulatory dysfunction
Surgical correction of tubal ,peritoneal & uterine defects
Surgical and medical treatment of male ifertility.
 Treatment contd.
III. Assisted Reproductive Technologies
Is clinical and laboratory techniques used to achieve preg
nancy in infertile couples for whom direct corrections of
underlying causes are not feasible.
These techniques include, but are not limited to,
In vitro fertilization (IVF)
Intracytoplasmic sperm injection (ICSI)
Egg donation
Gestational carrier surrogacy
Gamete intrafallopian transfer (GIFT)
Zygote intrafallopian transfer (ZIFT)
THANK YOU
 Endometriosis
 Is the presence of actively growing and functioning
endometrial tissue out side the uterus
 Adenomyosis: is considered as endometrosis found
in the myometrium.
 The most common site of implantation are pelvic vi
scera and the peritoneum
 In case of endometrosis, the endometrial tissues ar
e responsive for oestrogen hormone where ever th
e site is.
 Incidence- Predominantly found in reproductive ag
e group(7%)
Etiology – theories proposed for the occurrence of en
dometriosis.
1.Ectopic translocation of endometrial:
 it is based on the assumption that endometriosis is
caused by the seeding or implantation of endometri
al cell by trance tubal regurgitation during menstru
ation
 Retrograde menstruation occurs in 70-90% of wom
en, but all person will not develop the case
2. Coelomic metaplasia:
 transformation of coelomic epithelium in to e
ndometrial tissue has been proposed as a me
chanism for the origin of endometriosis.
3. Induction theory:
 is proposed that endogenous( undefined) bio
chemical factor can induce undifferentiated p
eritoneal cells to develop in to endometrial ti
ssue.
• Genetic factor- risk of it is 7 times greater if th
eir is family hx
1. pain- Clinical features
 Dysmenorrhoea before and throughout menses
 Chronic pelvic pain
 Dyspareunia
2. Sub fertility
When endometriosis is moderate or sever involvin
g the ovaries and causing adhesion then block tub
o - ovarian motility and ovum pick up
 Clinical finding
• Infertility
• Dysparunia classical triads
• Dysmenorrheal
• Chronic pelvic pain
• Bloody urine or stool in pre menstrual interval
• Elevation cancer antigen( CA-125)
 Physical examination
 Tender nodule in posterior vaginal fornix
 Pain upon uterine motion
 Fixed and retroverted uterus secondary to cul-de-sac adhesio
n
 Tender abdominal mass secondary endodermoma
 Final diagnosis is confirmed by laparoscopy
P/E
 In many women with endometriosis no abnormality
is detected during PE
 Inspection of the genitalia especially episiotomy site
scar
 Pain full swelling of the recto vaginal septum
 Uterosacral or cul-de-sac nodularity
 In sever case fixed, retroverted uterus, and reduced
mobility of fallopian tubes and ovaries
 Implantation site
 Cervix(50%)
 Uterine cul de sac
 Posterior broad ligament
 Utero-sacral ligament
 Ux, fallopian tube, sigmoid colon, appendix…
 pathology
 Small implant-red, petechial lesion on peritoneal sac
 Large- cystic, dark brown
 Surrounding peritoneal surface become thickened and scarre
d(POWDER BURN)
 On ovary, cyst become enlarged in size and called chocolate c
yst
Powder burn Flame like lesion
 Risk factors
 Deficient cellular immunity
 Genetic infuluence;First degree female relative
 Cervical stenosis
 Transverse vaginal septum
 Prolonged menstrual flow
 Short menstrual flow
 treatment
Depend on
 pts future fertility desire
 Severity of the disease(stage of the disease)
 Patients age
 Expectant management
Mild discomfort
 minimal or mild endometriosis
Management includes;
Analgesic therapy by NSAID
 patient with mild premenstrual pain
 No abnormalities on pelvic examination
 No desire for immediate fertility
 Hormonal therapy
 Is to interrupt the cycle

A. OCP
 good with minimal or mild symptoms.
 are prescribed either cyclically or continuously
for 6–12 months.
 B. progestin
 cause decidualization in the endometriotic tissue.
 Oral medroxy progesterone acetate = 10- 30mg daily dose.
 Depot medroxy progesterone acetate 150 mg IM can also be
given as a single injection every 3 months.
 C. Danazole
 Danazol has progestin like effects.
mechanism of action
 On hypothalamus-inhibit gonadotropin release, F
SH, LH inhibited
 inhibits steroidogenic enzymes in the ovary.
• hypoestrogenic environment is created.
• has androgenic effects
prevents the growth of endometriotic tissue.
dose is 400 to 800 mg/d in divided doses for 6 months.
 D. GnRH agonist
 suppression of gonadotropin secretion
 inhibit stereodogenesis
 Pain relieved within 2-3 months of initiation
 Can be given; as leuprolide acetate 3.75 mg/month(IM)
 Nafarelin 400-800mg daily(intra nasally)
 GnRH agonist
Rx limited to 6 months because of S/E such as
 loss of bone mineral density.
 vasomotor symptoms,
 vaginal dryness, and mood changes.
Surgical management-conservative
Indication for conservative surgery
 infertility
 severe disease
 adhesions
Laparatomy / laparoscopy is done
 excise or destroy all endometriotic tissue,
 remove all adhesions, and restore pelvic anatomy
to the best possible condition.
 Definitive surgery
 Hystrectomy,salphingo-oopherectomy
 Indicated for patient who
• Do not desire future childbearing and
• has severe disease or symptoms,
 This entails total abdominal hysterectomy, bilateral salpingo-
oophorectomy, and excision of remaining adhesions or impla
nts.
 ENDOMETRIAL HYPERPLASIA

 It is a spectrum of morphologic and biologic al

teration of endometrial glands and stroma

 It is associated with un opposed estrogen

(absence of progesterone influence) stimulation
of the endometrium.
 ENDOMETRIAL HYPERPLASIA

 Its usually clinical symptom is AUB, chance of chang

ed in to endometrial ca.
Caused by:
 Estrogen producing tumor
 Hormonal therapy
 The malignant potential of this hyperplasia is depen
d on: age, underlying ovarian disease, obesity and e
xogenous hormone exposure
 TREATMENT
 Progestin therapy
Option:
A.cyclic progestin therapy( MPA 10- 20mg /day
for 14 days per month)
B.continuous progestin therapy( megestrol acet
ate 20-40mg/ day for 2-3 months)
 Ovulation induction
 Uterine myoma/ leiomyoma/ fibroids are the
most common benign uterine tumor.
 It is estimated to be present in at least 20 % of
all women of reproductive age
 50% of all women older than 35yrs of age
 It is asymptomatic in many women and may b
e discovered incidentally during routine physic
al examination.

114
 It occurs as single, but often multiple
Classification /Location –anatomic
 Subserosa - subperitoneal leiomyomata may lie ju
st at the serosal surface of the uterus
 Intramural/ interstitial, leiomyomas lie within the
uterine wall
 Submucousal leiomyomas lie just beneath the en
dometrium
 May located out side the uterus(cx, broad ligamen
t)

115
 Etiology and origin
 Myoma arises from single smooth muscle cells
 The cause of uterine myoma is unknown, but sai
d to be oestrogen dependent tumour
Evidence
 Rarely found before puberty, stop growing after
menopause and actual regretion of size may occ
ur
 New myoma rarely occur after menopause
 There is rapid growth of myoma during pregna
ncy
116
 Etiologic...
 Associated with other conditions of hyper oest
roginisim including anovulation and endometr
ial hyperplasia.
 Older nulliparas women have high risk of deve
loping myoma

117
 Pathology
 Myomas are nodular tumour that vary in size a
nd number
 It may be microscopic or huge
 May cause symmetric uterine enlargement or i
t may distort the uterine contour significantly
 Consistency- may be hard and stony( as when c
alcified), soft as with cystic degeneration), firm
or rubber which is usually description of myom
a

118
 Are usually separated from the myometrium b
y pseudo capsule of connective tissue

119
 Degenerative Change

Reported in two third of specimen

 Hayaline Degeneration- most common change, almo
st all mayoma have this change except the smaller on
e.
 Caused by overgrowth of the fibrous element which
deal to hayalinization of the fibrous tissue and event
ually calcify as its blood supply diminished
 Cystic Degeneration-follow liquification of the hayali
ne degeneration.

120
Mucoid Change- when arterial input is impaired, areas
of hayalinization may convert to mucoid type, it may
further leads to cystic degeneration.
Necrosis- when the blood supply is impaired the tissue
may be necrotized.
 seen in pedenculated subserous, when twist occur o
r sometimes necrosis occurs in the centre of large t
umour simply as a result of poor circulation.
 necrtotic mayomas are dark and hemorrhagic in the
interior and eventually the tissue may break complet
ely.
121
Red or corneous degeneration:
 is seen occasionally, especially in association
with pregnancy as a result of poor circulation f
or the rapidly growing tumor.

122
 Clinical features
 Asymptomatic- most myoma do not produce symto
m
 Abnormal uterine bleeding- 1/3 of pts presents with
AUB
- menorrahagia
- metrorrhagia
- combination
 Mechanism of abnormal bleeding is not well establis
hed, but several theories have been postulated.
123
1. Ulceration over a sub mucus tumour
2. Increased endometrial surface area
3. Interference of mayoma with normal uterine
contractility
4. Compression on venous plexus of the adjace
nt myometrium and endometrium.

124
 Pain
 Pressure symptoms
 Urinary frequency & urgency, urinary retentio
n, hydronephrosis, constipation
 Pain- abdominal and pelvic pain, heaviness, d
yspareunia, dysmenorrhoea
 Acute pain due to torsion, red degeneration, i
nfarction, secondary dysmenorrhea, crampy p
ain with delivered myoma

125
• Reproductive disorder
Increased incidence of abortion and preterm labour d
ue to:
 Disturbance of uterine blood flow
 Alteration of endometrial blood flow
 uterine irritability
 Rapid growth of myoma during pregnancy
 Uterus may not accommodate the growing fetus
 Interference with the implantation and placental gr
owth by poorly developed endometrium.

126
 Red degeneration due to pregnancy
 Dystocia during labour
 PPH – uterus failed to contract, entrapment of placenta by su
b mucus myoma.
Infertility- account for < 3% of the case due to:
 unovulatory cycles
 Interference with sperm transport
 Tubal blockage
 Interference with prostaglandin induced uterine contraction
which is important for the sperm transport.
 Endometrial ulceration, continuous bleeding.

127
 Physical Signs

Abdominal mass
 Irregular, nodular, firm, mobile
 Asymmetrical /symmetrical uterine enlargem
ent
 Pedunculated, sub mucous myoma (delivere
d myoma) .

128
 Treatment
A. Observation and follow-up
 For asymptomatic myomas, in the absence of
pain, AUB or pressure symptoms especially fo
r premenopausal women
 Follow-up - every 6 month, detect and treat
anaemia, u/s
- Hysteroscopy
- laparoscopy

129
B. Medical management
 Used for perimenopausal women
 Menorrahagia
 As an adjuvant to surgical treatment
GnRH analogues
 Causes a temporarily increase in the level of Gonadotro
pine and steroid followed by chronic suppression or gona
dotropin and gonadal steroids within 1 to 3 weeks and p
ersists as long as treatment lasts but promptly.
 It is called “medical oophrectomy” or “medical menopa
use”

130
 Patients may manifest with symptoms of men
opause, hence the Rx not recommended for m
ore than 6 months.
Effect of the drug on myoma
 reduce vascularity and individual cell size, i.e.,
its size is reduced by 40 to 50% after 3 to 6 mo
nths of Rx.

131
C. Surgery
Indications:
 AUB with severe anaemia
 Pain, size > 12 to 14 wks , rapid growth, pressure sym
ptoms, complications on reproductive process (aborti
on and preterm labour)
Surgical procedure depends on:
 age, nature of symptom and size of myoma, desire for
future fertility, site of the mass

132
 Types of surgery
 Myomectomy
 complication- intra or post op bleeding, recur
rence (30% in 10 yrs)
 Hysterectomy (TAH)
 Vaginal myomectomy
 Hysteroscopy resection for sub mucus myoma
 Laparoscopy myomectomy

133
Premalignant & Malignant
Disease of Cervix
Squamocolumnar junction
Cervical Intraepithelial neoplasia (CIN)
CIN means disordered growth and development of the epithelial linin
g of the cervix.
CIN is used to describe histologic findings of cervical biopsy.
Nearly all cervical neoplasia, both squamous and columnar, develops
within the transformation zone, usually adjacent to the new SCJ.
Theoretically, cervical cells undergoing metaplasia are particularly vul
nerable to the oncogenic effects of HPV and co-carcinogens.
Metaplasia is most active during adolescence and pregnancy.
This may explain why early age of sexual activity and first pregnancy a
re known risk factors for cervical cancer
 CIN Contd.

Lower genital tract squamous intraepithelial neoplasia is mul

ticentric.
It affects multiple anatomic sites which embryologically are d
erived from the same anogenital epithelium:
1. Cervical intraepithelial neoplasia (CIN)
2. Vaginal intraepithelial neoplasia (VAIN)
3. Vulvar intraepithelial neoplasia (VIN)
4. Perianal intraepithelial neoplasia (PAIN)
 CIN Contd.
CIN has three degrees of severity:
CIN 1:Mild atypical cellular changes in the lower third of the e
pithelium (formerly called mild dysplasia).
CIN 2: Moderate atypical cellular changes confined to the bas
al two-thirds of the epithelium (formerly called moderate dys
plasia)
CIN 3: Severe atypical cellular changes encompassing greater
than two-thirds of the epithelial thickness, and includes full-th
ickness lesions (formerly called severe dysplasia or carcinoma
in situ).
 CIN Contd.

Natural History of Cervical Intraepithelial Neoplasia Lesions

CIN grade Regression (%) Persistence (%) Progression to Progression to
CIS (%) Invasion (%)
CIN 1 57 32 11 1
CIN 2 43 35 22 5
CIN 3 32 <56 – >12
 CIN Contd.
10% of women with CIN have concomitant preinvasive neopla
sia of the vulva, vagina, or anus.
Conversely, 40–60% of patients with VIN or VAIN have synchr
onous or metachronous CIN.
Historically, dysplasia was the terms used to describe prema
lignant squamous cervical cellular changes. This nomenclature
is currently replaced by the term CIN.
CIN is most commonly detected in women in their 20s
Prevalence figures for CIN vary according to the socioeconomi
c characteristics and geographic area
The epidemiologic risk factors for CIN are similar to those for
cervical cancer
Risk Factors for Cervical Neoplasia
Demographic risk factors
Ethnicity (Latin American countries, U.S. minorities)
Low socioeconomic status
Age
Behavioral risk factors
Infrequent or absent cancer screening Pap tests
Early coitarche
Multiple sexual partners
Male partner who has had multiple sexual partners
Tobacco smoking
Dietary deficiencies(vitamins such as A, C, E, beta carotene, and folic acid)
Medical risk factors
Cervical high-risk human papillomavirus infection
Parity
Immunosuppression
 Human papiloma virus
Human papillomavirus is a nonenveloped DNA virus with a protein c
apsid.
It infects epithelial cells exclusively and approximately 30 to 40 HPV
types have an affinity for infecting the lower anogenital tract.
Viral Life Cycle
The circular, double-stranded HPV genome consists of nine identifie
d open reading frames.
The "early" (E) genes govern functions early in the viral life cycle su
ch as DNA maintenance, replication, and transcription.
The "late" (L) genes encode capsid proteins needed late in the viral l
ife cycle to complete assembly into new, infectious viral particles.
Completion of the viral life cycle takes place only within an intact sq
uamous epithelium.
HPV is a nonlytic virus, and therefore infectiousness depends upon d
esquamation of infected cells
 HPV contd.
Viral Types
More than 100 HPV types have now been identified.
Clinically, HPV types are classified as high-risk (HR) or low-risk (LR) based u
pon their cervical cancer oncogenicity.
Low-risk HPV types 6 and 11 cause nearly all genital warts and a minority
of subclinical HPV infections. Low-risk HPV infections are rarely, if ever, o
ncogenic.
In contrast, the HR HPV types include 16, 18, 31, 33, 35, 45, and 58 and ac
count for approximately 95% of cervical cancer cases worldwide.
Other HR HPV types less often associated with neoplasia include 39, 51, 5
2, 56, 59, 68, 73, and 82.
The most common HR HPV types (16, 18, 45, and 31) found in cervical can
cer are also the most prevalent in the general population.
HPV 16 is the dominant cancer-related HPV, accounting for 40 to 70 perc
ent of invasive squamous cell cervical cancers worldwide.
 HPV Contd.
Transmission
Sexally transmitted
Vertical infection (Conjunctival, laryngeal, vulvar, or perianal warts pr
esent at birth or develop within 1 to 3 years)
Outcome of HPV Infection
HPV infection can be transient or persistent
HPV infection may be latent or expressed.
Expression is either productive, with formation of new virus, or neopl
astic, causing preinvasive disease or malignancy.
 HPV Contd.
Latent Infection :
Latent infection refers to that in which cells are infected, but HPV re
mains quiescent.
Expressed Productive Infection
Productive infections have little or no malignant potential because
eventual host cell death is required to complete the viral life cycle.
The intact, circular HPV genome remains unintegrated into the infe
cted cell's chromosomes and its oncogenes are expressed at only ve
ry low levels .
In both the female and male genital tracts, productive HPV infectio
ns produce either visible genital warts, called condylomata acumin
ata, or much more commonly, subclinical infections known as low-
grade squamous intraepithelial lesions (LSILs).
 HPV Contd.
Expressed Neoplastic Infection
In cancerous lesions, the circular HPV genome integrates line
arly at random locations into a host chromosome and unrestr
ained transcription of the E6 and E7.
Their products, the E6 and E7 oncoproteins, interfere with th
e function and accelerate degradation of p53 and pRB, key ho
st tumor suppressor proteins.
This leaves the infected cell vulnerable to malignant transfor
mation by loss of cell cycle control, cellular proliferation, and
accumulation of DNA mutations .
 HPV Contd.
Cofactors that lead HPV infection to persist
• HPV-related cofactors:
Viral type;
Simultaneous infection with several oncogenic types;
High virus load
• Host-related cofactors
Immune status
Parity
• Exogenous :
Smoking,
OCP
 Risk factors
Strong association
- sexual risk factors
- Low socio economic status
- Multiparty
- Cigarette smoking
- Immunosuppression
- In utero DES exposure
Weak risk association/controversial
OCP, Nutrition
 HPV Contd.
Diagnosis of Infection
Clinical lesions and results of cytology, histology, and colposcopy, al
l of which are subjective and often inaccurate.
Definitive diagnosis is made by direct detection of HPV DNA. Using
In situ hybridization,
Polymerase chain reaction (PCR)
Hybrid capture (HC) technique
Treatment
The only indications to treat HPV infection are the presence of neop
lasia or symptomatic warts.
 HPV Contd.
Prevention
Behavioral Interventions
Condoms use
Prophylactic Vaccines
Recombinant quadrivalent vaccine against types 6, 11, 16,
and 18 (Gardasil)
Indicated for women aged 9 to 26 years
Administered in three intramuscular doses over 6 months
.
Testing for HPV is not recommended prior to vaccination
It elicits humoral antibodies that neutralize HPV before it
can infect host cells
Prevent establishment of persistent infection and therefo
re, the development of cervical neoplasia.
 Cervical cancer screening
Aims to detect disease before symptoms occur.
Basis for cervical cancer screening are:
long preinvasive state (10-15yrs) of the disease
Existence of effective treatment for pre cancerous lesions
Screening can be organized or opportunistic
Organized screening
Is designed to reach the highest possible number of women a
t greatest risk of cervical cancer with existing resources.
Opportunistic screening
Is screening done on women who are visiting health services
for other reasons
 Screening Contd.
Methods of cervical cancer screening include:
1. Cervical Cytology
Conventional PAP collection
Liquid-based PAP collection
2.HPV DNA testing
3.Combined test
4.Visual method
 1. Cervical Cytology
Conventional pap smear
Introduced in 1941 by Papanicolaou
Standard screening test for lower genital tract neoplasm
Historical success in developed countries in reduction of cervi
cal cancer.
The Pap test's specificity is 98 % with sensitivity of 51
In conventional pap sample is taken,
Sample is then quickly spread as evenly as possible over one
half to two thirds of a glass slide.
Then, after fixation immediately by spray or immersion of slid
e with 95% alcohol
 Cervical Cytology Contd.
Liquid-Based Testing
Sampling and cell transfer to a liquid medium should be perfo
rmed according to manufacturer specifications.
LBC is more sensitive and accurate for the detection of both s
quamous lesions and adenocarcinomas of the cervix
 Cervical Cytology Contd.
Timing of sample
Avoid menstruation period
Abstain for 24 to 48 hours from
Vaginal intercourse,
Douching, and use of
Vaginal tampons and
Medicinal or contraceptive cream preparations
Location of sample
Sample transformation zone
Sampling Tools are
Spatula, broom, and endocervical brush
 American cancer society cervical cancer screening guide line
Initiation of screening 3 years after onset of vaginal intercourse; no later than age 21

Screening intervals for women at Age <30: annual if conventional smear; every 2 years if LBC
average risk test
Age >30: every 2 to 3 years after 3 consecutive negative tests
Screening intervals for women at higher HIV + or other immunocompromised state: 2 tests during first
risk year after immune disease diagnosis, then annually

Discontinuation of screening Age 70: consider if 3 documented negative (and no abnormal)

Screening after hysterectomy
tests in prior 10 years
Continue if screening history uncertain, history of cervical
cancer, DES, recent HPV +, HIV + status, other
immunocompromised state
Not indicated if removal confirmed for benign indication
Subtotal hysterectomy: continue screening per guidelines
Continue screening if history of DES or cervical cancer

WHO recommendation: once, 35-40 yrs

 Cervical Cytology Contd.
Reporting of PAP smear results for both Conventional & liquid based is by
the Bethesda System
In 1988, standardization of cervical cytology reporting took place with the
development of the Bethesda System nomenclature.
Subsequently it was revised 2001.
The 2001 Bethesda System: Epithelial Cell Abnormalities
Squamous cell
Atypical squamous cells (ASC) of undetermined significance (ASC-US) cannot
exclude HSIL (ASC-H)
Low-grade squamous intraepithelial lesion (LSIL)
High-grade squamous intraepithelial lesion (HSIL)
Squamous cell carcinoma
Glandular cell
Atypical glandular cells (AGC)
Endocervical, endometrial, or not otherwise specified
Atypical glandular cells, favor neoplastic
Endocervical or not otherwise specified
Endocervical adenocarcinoma in situ (AIS)
Adenocarcinoma
 Cervical Cytology Contd.
Limitations of cytology
Moderate to low sensitivity
High rate of false-negative test results ( may be due to
poor sample collection , poor reading or poor interpretation of findings)
Women must be screened frequently
Requires complex infrastructure
Results are not immediately available
Requires multiple visits
Less accurate among postmenopausal women
Cervical Cytology: Initial Management of Epithelial Cell Abnormalities
Epithelial Cell Abnormality
ASC-US
LSIL
ASC-H, HSIL, squamous cell
carcinoma
AGC, AIS, adenocarcinoma
General Recommendation Special Circumstances
Repeat cytology at 6 and 12 Refer to colposcopy for
months recurrent abnormal cytology,
Reflex HPV DNA testing or initial positive HPV DNA test;
Colposcopy adolescents managed with
repeat annual cytology
Colposcopy for non-adolescent Adolescents managed with
women repeat annual cytology; HPV
DNA test at 12 months or
repeat cytology at 6 and 12
months are also acceptable for
postmenopausal women
Colposcopy
Colposcopy, endocervical Endometrial sampling indicated
curettage; HPV DNA testing for if age >35 years, abnormal
AGC bleeding, chronic anovulation,
or atypical endometrial cells
specified
 Colposcopy

Colposcopy is an outpatient procedure that is simple, q

uick, and well-tolerated.
It allows examination of the lower genital tract and an
us with a microscope.
Indicated for patients with abnormal Pap test results a
nd visible epithelial abnormalities
Clinical objectives
Provide a magnified view of the lower genital tract
Identify SCJ cervix
Detect lesions suspicious for neoplasia
Direct biopsy of lesions
 Colposcopy Contd.
Abnormal findings of colposcopy indicative of
dysplasia and carcinoma in situ (CIS) are those of:
Leukoplakia or hyperkeratosis
Acetowhite epithelium
Mosaicism or punctation vessels
Atypical vessels with bizarre capillaries with corkscrew, comm
a-shaped, or spaghetti-like configurations
Abnormal colposcopic finding are indication for
colposcopic directed biopsy.
Findings of biopsy may indicate CIN.
 Management of CIN
Management of low grade lesions (CIN I)
CIN 1 can be observed indefinitely, especially in adolescents, or
Treated if it persists for at least 2 years
Management of High Grade lesions
CIN 2 adolescents same as CIN I
CIN 2 in adult women and
CIN 3 are treated by excision or ablation
Before using ablative treatment modalities, there must be no indica
tion of invasive cancer or glandular lesion by cytologic or histologic
colposcopic or evaluation.
 Management of CIN Contd.
Ablative therapies are :
1. Cryosurgery
Delivers refrigerant gas, usually nitrous oxide, through flexible tubing to a metal
probe.
Which freezes tissue on contact by crystallizing intracellular water.
2. Carbon Dioxide Laser
Treatment with amplification by stimulated emission of
radiation, or laser,
Is delivered using colposcopic guidance with a
micromanipulator.
This modality vaporizes tissue to a depth of 5 to 7 mm
Management of CIN Contd.
Excisional Treatment Modalities
• Lesions suspicious for invasive cancer and AIS of the cervix must un
dergo a diagnostic excisional procedure
1. Loop Electrosurgical Excision Procedure (LEEP)
uses a thin wire on an insulated handle through which an elec
trical current is passed.
This creates an instrument that simultaneously cuts and coag
ulates tissue under direct colposcopic visualization
2. Cold-Knife Conization
This surgical procedure removes the entire cervical transform
ation zone including the cervical lesion by scalpel
Management of CIN Contd.
Place of hysterectomy
If fertility is not needed
If surgical margins are positive for abnormal cell
Recurrent high-grade cervical disease
 2. HPV DNA testing

Rational for using HPV testing in cervical screening

The strong causal associates of HPV& cervical ca &its precur
sors.
The high HPV –attributable fraction (90-99% of cervical ca).
The long time interval (15yrs)b/n infection and HSIL.
The minimal invasive nature of sampling procedure.
The availability of one standardized ,FDA approved test.
The high sensitivity of the available tests (for HSIL).
 HPV DNA testing Contd.

Indication
For triaging women with ASC-US
Alternative 1st degree screening for cervical ca( HSIL)
Testing method: PCR
Sensitivity=50-95% (85%)
Specificity=50-95% (84%)
 3. Combination Screening

Combination screening is Cytology + HPV testing in wo

men > 35yrs
Alternative 1st degree screening approach
FDA approved, 2003
Interval of screening=3yrs
 4. Visual Method
Screening of cervical cancer using visual methods are
a) Visual inspection with acetic acid (VIA)
b) Visual inspection with Lugol’s iodine(VILI)
Visual Inspection with Acetic Acid

Viewing the cervix with the naked eye to identify color change
s on the cervix.
Acetic acid is a mucolytic agent.
It reversibly clumps nuclear chromatin causing lesions to ass
ume various shades of white depending on the resultant degr
ee of abnormal chromatin density.
Applying 3- to 5-percent acetic acid to mucosal epithelium res
ults in the acetowhite change characteristic of neoplastic lesi
ons as well as some non-neoplastic conditions
VIA Contd.
VIA Contd.
 Visual inspection with Lugol’s iodine (VILI)

Lugol iodine solution stains mature squamous epithelial cells maho

gany in estrogenized women due to high cellular glycogen content.
Due to attenuated cellular differentiation, dysplastic cells have low
er glycogen content and fail to fully stain, appearing various shades
of yellow. This is called Schiller Test
Lugol solution should not be used in patients allergic to iodine, radi
ographic contrast, or shellfish.
Lugol solution is particularly useful when abnormal tissue cannot be
found using acetic acid alone, and to better define the limits of the
transformation zone.
VILI has Sensitivity =87.2 Specificity =84.7%
(VILI) Contd.
 Strengths of Visual Method

Simple, easy-to-learn
Minimal infrastructure requirement
Low start-up and sustaining costs.
Many types of health care providers can perform the
procedure.
Test results are available immediately.
Requires only one visit.
May be possible to integrate VIA screening into prim
ary health care services.
 Limitations of Visual method

Moderate specificity
No conclusive evidence regarding the health or cost i
mplications of over-treatment.
There is a need for developing standard training met
hods and quality assurance measures.
Likely to be less accurate among post-menopausal w
omen
Rater dependent.
 Management of abnormal VIA /VILI

What to do if the VIA (VILI) test is positive?

Refer for confirmatory diagnosis or adjunctive test.
Offer to treat immediately.
Cryotherapy
 Cervical cancer
Cervical cancer is the most common gynecologic cancer in wo
men
Worldwide, cervical cancer is common, and ranks second amo
ng all malignancies for women
Compared with other gynecologic malignancies, cervical cance
r develops in a younger population of women
Most early cancers are asymptomatic
Advancing cervical cancer present with bleeding, watery disch
arge, and signs associated with venous, lymphatic, neural, or u
reteral compression
The median age at diagnosis ranges from 40 to 59 years
 Cervical cancer Contd.
Risks factors
Cervical cancer is a unique in that it is a confirmed seq
uela of a STI
Risk factors of cervical cancer are similar with risk fact
ors for CIN
Tumorigenesis of cervical Ca
Squamous cell carcinoma of the cervix typically arises at the s
quamocolumnar junction from a pre-existing dysplastic lesion,
which in most cases follows infection with HPV
Following tumorigenesis, the pattern of local growth is exoph
ytic if a cancer arises from the ectocervix, or may be endophy
tic if it arises from the endocervical canal
 Cervical cancer Contd.
Diagnosis
Symptoms
Vaginal bleeding that follows coitus or douching
Watery, blood-tinged vaginal discharge
Phsical Examination
Exophytic or endophytic growth
Polypoid mass, papillary tissue, or barrel-shaped cerv
ix
Cervical ulceration or granular mass
Testing Used during Cervical Cancer Staging
Testing To Identify:
Laboratory
CBC Anemia prior to surgery, chemotherapy, or
radiotherapy
Urinalysis Hematuria
Liver function Liver metastasis
Creatinine and BUN levels Hydronephrosis
Chest radiograph Lung metastasis
Intravenous pyelogram (IVP) Hydronephrosis
CT scan (abdomen and pelvis) Lymph node metastasis, metastasis to other
distant organs, and hydronephrosis
MR imaging Local extracervical invasion + those for CT
scan
Procedural
Cystoscopy Tumor invasion into the bladder
Proctoscopy Tumor invasion into the rectum
Examination under anesthesia Extent of pelvic tumor spread
Clinical Stages of Cervical Cancer (FIGO, Revised 1994)

Stage Characteristics

0 Carcinoma in situ, cervical intraepithelial lesion (CIN) 3

I Carcinoma is strictly confined to cervix (extension to corpus should be

disregarded)

IA Invasion is limited to measured stromal invasion with a maximum depth of

5 mm and no wider than 7mm

IA1 Measured invasion of stroma no greater than 3 mm in depth and no wider

than 7 mm

IA2 Measured invasion of stroma greater than 3 mm and no greater than 5 mm

in depth and no wider than 7mm

IB Clinical lesions confined to the cervix or preclinical lesions greater than IA

IB1 Clinical lesions no greater than 4 cm in size

IB2 Clinical lesions greater than 4 cm in size

II Carcinoma extends beyond cervix but has not extended to pelvic wall; it
involves vagina, but not as far as the lower third

IIA No obvious parametrial involvement

IIB Obvious parametrial involvement
III Carcinoma has extended to the pelvic wall; on rectal examination there is no
cancer-free space between tumor and pelvic wall; tumor involves lower third
of vagina; all cases with hydronephrosis or nonfunctioning kidney should be
included, unless they are known to be due to another cause

IIIA No extension to pelvic wall, but involvement of lower third of vagina

IIIB Extension to pelvic wall, or hydronephrosis or nonfunctioning kidney due to
tumor

IV Carcinoma has extended beyond true pelvis or has clinically involved mucosa
of bladder or rectum

IVA Spread of growth to adjacent pelvic organs

 Cervical cancer Contd.
Treatment of cervical cancer
Early stage disease( stage I to IIA) surgery
Late stage disease ( stage IIB and beyond )radiation
 Differential diagnosis
• Cervical tuberculosis
• Fibroid polyp
• Syphilitic ulcer
Thank you
Endometrial cancer
 Uterine cancer is the most common malignant neoplas
Introduction
m of the female genital tract and the fourth most com
mon cancer in women.
 About 6,000 women in the United States die of this dis
ease each year.
 It is more frequent in affluent and white, especially ob
ese, postmenopausal women of low parity. Hypertensi
on and diabetes
 Types of endometrial ca
1. Estrogen- dependant :
 Most common type
 Tumors begins hperplastic endometrium
 occurs in younger perimennopausal women with of exposure to u
nopposed estrogen
2. Estrogen -independent :
 not associated to endometrial hyperplasia
 May arise in in aback ground of atrophic endometerium
 Characteristic that increases exposure to unopposed estrogen increases th
Risk factors
e risk for endometrial cancer.
 Conversely, decreasing exposure to estrogen limits the risk.
 Unopposed estrogen therapy, obesity, anovulatory cycles and estrogen-sec
reting neoplasm , all increase the amount of unopposed estrogen and ther
eby increase the risk for endometrial cancer.
 Smoking seems to decrease estrogen exposure, thereby decreasing the can
cer risk, and oral contraceptive use increases progestin levels, thus providi
ng protection.
 Unopposed estrogen treatment of menopause is associated with an eightf
old increased incidence of endometrial cancer.
 The addition of progestin decreases this risk dramatically.
oRisk Factors for Endometrial
Unopposed estrogen exposure
Cancer
o Median age at diagnosis: 59 years

o Menstrual cycle irregularities, specifically menorr

hagia and menometrorrhagia Postmenopausal ble
eding Chronic anovulation
 Risk Factors for Endometrial Cancer
 Nulliparity
 Early menarche (before 12 years of age)
 Late menopause (after 52 years of age)
 Infertility
 HRT
 Ovarian dysfunction
 Obesity
 Diabetes mellitus
 Arterial hypertension with or without atherosclerotic heart disease
 History of breast or colon cancer
 Clinical evaluation
History
o Abnormal uterine bleeding-90%

o Pelvic pressure-due to uterine enlargement

o Hematometra

o <5% asymptomatic

.
 Clinical evaluation
 Physical examination
 It should be performed, with particular attention to su
praclavicular , inguinal lymph nodes breast and liver.
 Bimanual rectovaginal examination to evaluate the siz
e and mobility of the uterus is important.
 The size and consistency of the cervix; the adnexal stru
ctures and parametrium; and the entire vagina, vulva,
and rectum are important
 Clinical evaluation
Endometrial sampling
 Endometrial aspiration biopsy-MVA accurate dia
gnosis
 D&C
 Hysteroscopy
 PAP smear
 Histological types
1. Endometrid adenocarcinoma-most commn typ
e(80%)

2. Muccinious carcinoma-5%

3. Papillarry serious carcinoma-3-4%

4. Clear cell carcinoma-5%,tend to occur in older

women and it is aggressive type

5. Squamous carcinoma-rare type

 Clinical staging
Stage I Disease - confined to uterus

Stage II Disease - extends to cervix

Stage III Disease - extends to pelvis

Stage IV - Distant metastasis

 Treatment
Treatment and prognosis depends on

1.Stage of the disease

2.Histological type

3.Depth of myometrium invasion

4.age
 Treatment
1. Surgery-TAH+BSO is a primary operative proce
dure for endometrial cancer

N.B. any suspected lesion should be biopsed

2. Radiotherapy

primary surgery followed by radiation therapy is

the most widely accepted treatment for late sta
ge of endometrial cancer
PELVIC ORGANS PROLAPSE

202
 Uterine prolapse(UVP)
Definition: is a protrusion/descent of uterus and cervix
to or out of the vaginal canal
Factors associated
 Damage to pelvis diaphragm by :prolonged labor ,ea
rly first stage pushing , inappropriate instrumental de
livery ,3rd stage mismanagement, frequent child birth
 Aging –estrogen deficiency
 Congenital weakness of pelvic floor supports

203

---
Increased intra abdominal pressure by-chronic cough
,constipation, ascites ,obesity
 Race-white are more affected
Differential diagnosis
 Cyctocele , rectocele
 Delivered myoma
 Vaginal wall cyst
 Chronic uterine inversion
 Polyps(cervical and endometrial)
 Vaginal vault prolapsed

204
 Clinical grading of UVP
0 degree: no prolapsed
1st degree: cervix descend in to vagina but not as
far the interoitus
2nd degree: descends as far as the interoitus
3rd degree: body of uterus out side the interoitus

205
 Patient evaluation with UVP
Hx
 Feeling of pressure in the pelvis
 Protrusion through the vagina
 Backache
 Heaviness and dragging sensation
 Ulceration
 Coital difficulty
 Urinary problems
 Constipation
 Cough

206
 Age ,parity
PE
 Cough –chest examination
 Abdominal mass
 Pelvic exam –degree of UVP ,ulcer
INV
 CBC, urine culture ,IVP,RFT

207
 MX -UVP
Non –surgical
 Estrogen supplement
 Treat precipitate factors(cough ,ascites--- )
 Pelvic floor exercise
 Pessaries
Surgical
 Vaginal hysterectomy
 Manchester operation
 Lefort`s operation
 Ventro suspention
208
 Cystocele
 Down ward displacement of the bladder which appears as bulge in
the anterior vaginal wall
 Anterior vaginal prolapsed describes an anterior vaginal wall defec
t where the bladder is associated with the prolapsed
Rx
 kegles exercise in mild cases
 Estrogen supplementation for post term woman
 Vaginal pessaries
 Surgery –anterior vaginal colporrhaphy

209
 Rectocele
 Posterior vaginal wall prolapsed describes a posterior
vaginal wall defect.
 The rectum develops traps stool and constipation res
ults
Rx
 In severe –surgery to repair the defect

210
 Clinical presentation
Symptoms of POP
 Sensation of vaginal fullness, pressure, "something fa
lling out," or "heaviness."
 Sensation of "sitting on a ball."
 Discomfort in the vaginal area.
 Presence of a soft, reducible mass bulging into the va
gina and distending through vaginal introitus.
 With straining or coughing, increased bulging and de
scent of the vaginal wall.
 Back pain and pelvic pain

211
 Urinary symptoms are also common.
– Feeling of incomplete emptying of the bladder
– Stress incontinence
– Urinary frequency
 Defecation difficulty in rectocele

PE –inspection and palpate with PV of prolapse

212
 ct
Tra
ar y
r i n n
r U t i o
w e n c
Lo s f u
Dy
 Introduction
 lower urinary tract symptoms account for
significant gynecologic visits
 disturbances in the bladder function produce a wide variety o
f urinary symptoms
 Urinary incontinency
Definition:
 it is involuntary loss of urine that is asocial or hygienic pr
oblem and that is objectively demonstrable
 it is symptom not diagnosis
 Why is Incontinence Important?
 Social stigmata - leads to restricted activities and depression
 Medical complications - skin breakdown, increased urinary tra
ct infections
 Hospitalization
 Epidemiology
It is allways be improved and can be cured
It affacts 26% of reproductive age group
30-50%of post menopausal women
 Urinary Incontinence is Often
Under-Diagnoses and Under-Treated
• Only 32% of primary care physicians routinely ask about incon
tinence
• 50-75% of patients never describe symptoms to physicians
• 80% of urinary incontinence can be cured or improved
 Anatomy of Micturition
• Detrusor muscle
• External and Internal sphincter
• Normal capacity 300-600cc
• First urge to void 150-300cc
• CNS control
• Hormonal effects - estrogen
 Peripheral Nerves in Micturition
• Parasympathetic (cholinergic) - Bladder contraction
• Sympathetic - Bladder Relaxation
• Sympathetic - Bladder Relaxation (β adrenergic)
• Sympathetic - Bladder neck and urethral contraction (α adren
ergic)
• Somatic (Pudendal nerve) - contraction pelvic floor musculatu
re
Peripheral Nerves in
Micturition
 Potentially Reversible Causes
D - Delirium
I - Infection
A - Atrophic vaginitis or urethritis
P - Pharmaceuticals
P - Psychological disorders
E - Endocrine disorders
R - Restricted mobility
S - Stool impaction
Medications That May Cause Incontin
ence
• Diuretics
• Anticholinergics - antihistamines, antipsychotics, antidepressa
nts
• Saditives/hypnotics
• Alcohol
• Narcotics
• α-adrenergic agonists/antagonists
• Calcium channel blockers
 Evaluation of Urinary Incontinence
• History
age,parity, type of delivery
frequency of leakage
,what provokes, what help to stop the leakage
what makes the lleakage worse
has been treated priviosly
DM
HTN
PTB
 History……….
Is she medicated like
 blockers
 Sedatives
• smoking and alcohol consumption
• 3 P’s
• Position of leakage (supine, sitting, standing)
• Protection (pads per day, wetness of pads)
• Problem (quality of life)
 Physical examination
Chest pathologies
Neurologic abnormalities
Pelvic examination done with full bladder
o Vaginal rugea-estrogen status
o stress test
o asses pelvic muscle tone
o Q tip test-using cotton applicator and ask the patient to cough
 Investigation
 U/A
 Urodynamic studies
 cystomethery
 Grading urinary incontinence
 Grade 0 - Continent
 Grade 1 - Loss of urine with sudden increases
in abdominal pressure, not in bed at
night
 Grade 2 - Incontinence worsens with lesser
degree of physical stress
 Grade 3 - Incontinence with walking, standing
erect from sitting position, or sitting
up in bed
 Grade 4 - Total incontinence occurs and urine
is lost without relation to physical
activity or position
 Differential diagnosis
1. Extra urethral incontinence
a) Congenital
ectopic urether
b) Acquired
fistula
 2.Trans urethral incontinency
A. Genuine incontinency
B. Deturesor over activity
C. Functional incontinnency
D. Over flow incontinency
Extra urethral causes of incontinency
Fistula
 Epidemology

• Accounts 0.5-3% of gynacological complications

 Risk factors
 Obstructed labor
 Infection (TB)
 Pelvic surgery
 Maignancy
 Radaition
 Pathophisiology
• Fistula commonly caused by obstructed labor
• In obstructed labor ,the head of the fetus compresses the trig
one or the bladder neck against the anterior arch of the pubic
symphysis. This may result in tissue ischemia, necrosis, and ev
entual fistula formation
 Types of obstetric fistula
These can be
• vesicovaginal
• Urethro viginal
• Vesico uterine
• rectovaginal
 Clinical feature
• Continios leakage of urine
• constitutional symptoms of fever, chills, malaise, flank pain, a
nd gastrointestinal symptoms .
• Constitutional symptoms may result from hydronephrosis sec
ondary to ureteral obstruction or urinary extravasation into th
e retroperitoneal space.
 Diagnosis
History
• Primigravidea
• Obstructed labor
• Continious leakage of urine
 Physical examination
• Ammonic smell
• flank or abdominal tenderness due to hydronephrosis
• Identify the site and number of fistula
 Investigation
• U/A
• HCT
• RFT
• Cystometery
• Intravenious pylography
• 3 tampons test
 Management
prevention
 FANC
 Good intraparthal care
 Catheterization for 10 days
 Surgical treatment
• Done after 3 month of diagnosis of fistula
• Supratrigonal fistulas (fistulas above the interureteric ridge) w
ere typically approached transabdominally.
• Infratrigonal fistulas (fistulas below the interureteric ridge) w
ere corrected transvaginally.
• The transvaginal approach is the safest and most comfortable
for the patient
 Post operative care
 Stool softeners for 21 days
 Keep the catheter for 14 days
 On discharge
- Advise to pass urine aduquately
- Avoid coitus for 2-3 days
- Avoid pregnancy for 3 years
- Subsequent delivery with elective C/S
 Trans uretheral causes of incontinency
Stress incontinence
Involuntary leakage on effort or exertion, or on sneezin
g or coughing
• the generated intra-abdominal pressure causes a coinci
dent rise in intravesical pressure
• Hypermotility of bladder neck and urethra; associated
with aging, hormonal changes, trauma of childbirth or
pelvic surgery (85% of cases)
• Intrinsic sphinctor problems; due to pelvic/incontinenc
e surgery, pelvic radiation, trauma, neurogenic causes
(15% of cases)
 Overflow Incontinence
• Over distention of bladder
• Bladder outlet obstruction; stricture, BPH, cystocele, fecal im
paction
• Non-contractile baldder (hypoactive detrusor or atonic bladde
r); diabetes, MS, spinal injury, medications
 Urge incontinence

1. Also called detrusor hyperactivity, detrusor instability, irrita

ble bladder, spastic bladder
2. Most common cause of UI >75 years of age
3. Abrupt desire to void cannot be suppressed
4. Usually idiopathic
5. Causes: infection, tumor, stones, atrophic vaginitis or urethr
itis, stroke, Parkinson’s Disease, dementia
 Functional Incontinence
• Does not involve lower urinary tract
• Result of psychological, cognitive or physical impairment
Physical Examination
• Mental status
• Mobility
• Fluid overload
• Abdominal exam
• Neurologic exam
• Pelvic
• Rectal
 Diagnostic Tests
• Stress test (diagnostic for stress incontinence; specificity >90%)
• Post-void residual
• Blood Tests (calcium, glucose, BUN, Cr)
• Urine Culture
• Simple (bedside) Cystometrics
 Interpretation of Post-Void Residual
PVR < 50cc - Adequate bladder emptying
PVR > 150cc - Avoid bladder relaxing drugs
PVR > 200cc - Refer to Urology
PVR > 400cc - Overflow UI likely
 Treatment Options
• Reduce amount and timing of fluid intake
• Avoid bladder stimulants (caffeine)
• Use diuretics judiciously (not before bed)
• Reduce physical barriers to toilet (use bedside commode)
 Treatment Options
• Bladder training
• Patient education
• Scheduled voiding
• Positive reinforcement
• Pelvic floor exercises (Kegel Exercise)
• Caregiver interventions
• Scheduled toileting
• Habit training
• Prompted voiding
 Pharmacological Interventions
• Urge Incontinence
• Oxybutynin (Ditropan)
• Propantheline (Pro-Banthine)
• Imipramine (Tofranil)
• Stress Incontinence
• Phenylpropanolamine (Ornad
e)
• Pseudo-Ephedrine (Sudafed)
• Estrogen (orally, transdermally
or transvaginally
 Surgical Interventions
• Urethral Hypermotility
• Needle neck suspension
• Intrinsic sphincter defici
ency
• Sling procedure
 Other Interventions
• Pessaries
• Periurethral bulking age
nts (periurethral injectio
n of collagen, fat or silic
one)
• Diapers or pads
• Chronic catheterization
• Periurethral or suprapubic
• Indwelling or intermittant
PISSIARIES
Indwelling Catheter
257