Diseases of the female genital tract

DISEASES OF THE FEMALE
GENITAL TRACT

 Introduction of FGT
 Clinical manifestations of FGT pathology
 Pathology of Vulva
 Pathology of Vagina
 Pathology of Cervix
 Pathology of Myometrium
 Pathology of Endometrium
 Pathology of Fallopian tube
 Pathology of Ovary
 Pathology Gestational and placental disorders
Objectives

Female Reproductive System
-The female reproductive system consists of
-The ovaries
-Secondary sex organs - which are involved in
coitus, fertilization & development, birth & nursing
of the baby.
-

 Vulva
 Vagina
 Cervix
 Uterus
 Uterine tubes [ fallopian tubes]
 Ovaries ( The gonads )
Major Organs of FGT

-Diseases of the vulva
-Diseases of the vagina
-Diseases of the cervix
-Diseases of the Body of Uterus And Endometrium
-Diseases of the Fallopian tubes
-Diseases of the Ovaries
-Gestational and Placental disorders
DISEASES OF F.G.T. INCLUDE:

Pathological basis of signs & symptoms in the FGT
Sign or symptom Pathological basis
-Vaginal discharge Inflammation
-Vaginal bleeding
In pregnancy Hemorrhage from placenta
(placenta
(praevia, placental bed
(miscarriage) or decidua
(ectopic pregnancy)
Post-coital Hemorrhage from cervical
lesion (carcinoma, erosion)
Post-menopausal Hemorrhage from uterine
lesion (polyp, carcinoma)

-Abnormal menstruation Psychological disturbance
(timing or volume of loss) Hormonal dysfunction
Defect in local haemostasis
Uterine lesions (Fibroid,polyp, IUD)
-Pain Pathologic distension/rupture
(tubal ectopic pregnancy),Muscular
spasm (uterine),Ischemia or
infarction (ovarian torsion),
menstrual pain due to
adenomyosis, functional etc
-Abdominal distension Ascites (Ovarian tumors involving
peritoneum), uterine enlargement
(pregnancy), ovarian cyst.

ABNORMAL UTERINE BLEEDING:
The most common gynecologic problem in women during active
reproductive life
- Polymenorrhea: cycles shorter than 3 weeks
- Oligomenorrhea: cycles longer than 6-7 weeks
- Metrorrhagia: intermenstrual bleeding (MC organic )
- Hypermenorrhea: excessive flow (MC organic )
- Menorrhea: prolonged duration of flow
- Menorrhagia: increase amount & duration of flow
- Menometrorrhagia: prolonged flow with irregular
intermittent spotting ( organic)

Causes of abnormal uterine bleeding according to age group
Age group Causes
Pre-puberty Precocious puberty ( hypothalamic, pituitary, or ovarian
origin)
Adolescence Anovulatory cycles , coagulation disorders
Reproductive
age
- Complications of pregnancy ( abortion, ectopic pregnancy,
trophoblastic diseases)
- Organic lesions ( leiomyomas, adenomyosis, polyps,
endometrial hyperplasia , carcinomas)
- Anovulatory cycles
-Ovarian dysfunctional bleeding (i.e. inadequate luteal phase)
Perimenopausal -Anovulatory cycles
- Irregular shedding
Postmenopausal -Organic lesions ( carcinoma, hyperplasia, polyps)
- Endometrial atrophy

DYSFUNCTIONAL UTERINE BLEEDING (FUNCTIONAL
ENDOMETRIAL DISORDERS):
Definition: It is abnormal bleeding in absence of organic uterine lesions.
MCC is anovulatory cycles (hyperestrogenic states). It is due to:
- Endocrine disorders - : pituitary, adrenal, and thyroid diseases.
- Ovarian disorders - : polycystic ovaries, hormone secreting tumors.
- Metabolic causes - : obesity, malnutrition,..
- Unexplained causes - : (?? Cryptogenic).
Morphology:
- Premenstrual endometrial biopsy shows a persistent proliferation
pattern with variable degree of hyperplasia, cystic glandular change
- Sporadic endometrial breakdown & bleeding ( estrogen effect
unopposed by progesterone).

 Inflammatory lesions of the Vulva:
 All skin disorders can be seen
 Herpes virus infection:
STD, HSV type 2, Painful ulceration in the skin.
Intraepithelial blisters & viral inclusion &
eosinophilic swelling of epithelial cells
 Syphilis:
 Primary syphilis - : Chancre - indurated lesion with
central ulceration & LN – heals even without Tt.
 Secondary syphilis: Condyloma latum (inflammed
hyperplasia of epithelium with underlying chronic
inflammation rich in plasma cells & end arteritis
obliterans), Silver stain demonstrates the
spirochetes.

Granuloma inguinale (Donovanosis):
STD affecting the genitalia, inguinal & perianal region ,
gram negative bacilli (Calymmatobacterium donovani) -
Chronic valvular papule/nodule/ ulceration, tropical
areas, can spread to other parts of FGT, ulcer
margins show epithelial hyperplasia & Ulcer bed filled
with neutrophil abscesses. Sliver stain demonstrates
bacilli within macrophages (Donovan bodies)

Lymphogranuloma venereum:
STD, Chlamydia trachomatis, tropical areas, vesicles
that rupture and form punched out painless ulcer,
secondary infection, abundant granulation tissue,
fibrosis, fistula, lymphatic obstruction (chronic form
of the disease), necrotizing granuloma may occur

Candidiasis :
Chronic irritation & inflammation, white thick
discharge, DM, may be associated with vaginitis
Diagnosis: ME of skin scrapping or culture,
nonspecific histological picture, fungi can be
demonstrated within the keratin layer or
superficial epithelium by sliver stain
Bartholin’sAbscessCyst:
inflammatory occlusion of the main duct of
Bartholin’s vulvo-vaginal gland, most common
cause is gonorrhea
Vulvodynia (vestibular adenitis) : inflammation of
the minor vestibular glands (unkown cause)
causing very painful ulceration. Treatment is often
surgical.

Infection involving the lower and the
upper genital tract
(Pelvic inflammatory disease =PID)
Definition: an ascending infection that
begins in the vulva & spreads upward
to involve the entire genital tract.

Causes:
1- Sexually transmitted disease (STD):
gonococcal (MC) or chlamydial infection:
acute suppurative inflammation confined
to mucosa and submucosa (spread via
mucosa).
2- Postabortal or postpartal; caused by
staphylococci, streptococci, E. coli &
clostridium perfringens. Spread is through
uterine wall leading to affection of serosa
and peritoneum.

 Morphology: acute suppurative inflammation
of the Bartholin’s glands, periuretheral glands,
endocervical glands & fallopian tubes.
 Pathological lesions & complications: Acute
salpingitis, salpingo-oophoritis, tubo-ovarian
abscess, pyosalpinyx (distention of the
fallopian tube with pus). It may cause
peritonitis, septicemia, fibrous adhesion
(intestinal obstruction), tubal occlusion &
infertility or ectopic pregnancy.

TUMORS OF THE VULVA
 Benign tumors
 Condyloma Accuminatum:
 Papillary Hidradenoma
 Vulvar Intraepithelial Neoplasia (VIN=
Vulvar Dysplasia)
 Malignant tumors
 Verrucous Carcinoma
 Invasive vulvar Squamous cell carcinoma
 Extramammary Paget’s Disease

Condyloma Accuminatum: multiple, benign, wart-like
verrucous STD, caused by HPV types 6&11. (vulva, perineum,
vagina, rarely cervix). It is squamous cell papilloma with
marked acanthosis,hyperkeratosis & parakeratosis, some
showing cells with cytoplasmic clearing and nuclear atypia (i.e.
koilocytic atypia = koilocytosis indicating viral infection).

Papillary Hidradenoma: benign, well
circumscribed nodule of modified apocrine
sweat gland. It is composed of tubular
structures lined by both epithelial(columner) &
myoepithelial cells.

 Vulvar Intraepithelial Neoplasia (VIN=
Vulvar Dysplasia):
- A premalignant intramucosal squamous neoplasm
that frequently precedes invasive carcinoma occurs
4th – 5th decades.
- Mucosal lesions with cellular anaplasia and marked
nuclear atypia, caused by HPV type 16. Synonyms:
VIN III= carcinoma in situ (CIS)= Bowen’s disease.
Tends to progress to invasive carcinoma ( in old &
immunosuppressed patients).
-

Differentiate (simplex) VINs
 Usually HPV-negative, associated with Lichen
sclerosus or Lichen simplex chronicus.
 These precancers usually arise after
menopause and leading to well differentiated
keratinized squamous cell carcinoma in the 6th
– 8th decade.

N.B.
HPV
- E6 protein of HPV type 16 & 18 can bind to P53 gene
leading to P53 inactivation
- E7 protein of HPV 16 & 18 binds to Rb gene products
Leading to promotion of neoplastic growth through:
1- Deregulation of cell cycle
2- Production of genomic instability
3- Increase telomerase expression
-Types 6 & 11 of HPV with no or low risk of malignancy
do not form a complex with P53 & typically give rise to
benign condylomas

Verrucous Carcinoma: A rare locally aggressive
neoplasm. Usually does not metastasize.
,
Invasive vulvar Squamous cell carcinoma:
may arise de novo or on top of VIN. Spreads to inguinal
LNs & is of poor prognosis. The prognosis depends on size,
depth of invasion, and lymph nodes status

1- Vaginitis
2- Tumors of vagina
DISEASES OF VAGINA

1-Vaginitis & vulvovaginitis
Since both vulva and vagina are anatomically close to each
other, often inflammation of one affects the other.
Common infections –
 Bacterial - streptococci,staphalococci, E.coli,
H. vaginalis
 Protozoal - Trichomonas vaginalis
 Viral - Herpes simplex
 Fungal – Candida albicans
The most common causes of vaginitis are Candida
albicans ( monaliasis) and Trichomonas
( Trichomonaliasis )

TUMORS OF THE VAGINA
 Benign tumors
 uncommon
 Squamous cell carcinoma
 Clear cell adenocarcinoma
 Embryonal rhabdomyosarcoma

Carcinoma: primary carcinoma of the vagina is rare, but 1-
2% women with cervical squamous cell carcinoma develop a
concomitant squamous cell carcinoma in the vagina. Age: 60-70
yrs. Morphology; plaque-like, fungating /ulcerative lesion that
infiltrates cervix, urethera, bladder or rectum.
Clear cell adenocarcinoma: is rare (MC in young women, whose
mothers had received Diethylstilbestrol (DES) during pregnacy for
treatment of threatened abortion). The tumor cells are vacuolated and
contained glycogen.

 Embryonal
rhabdomyosarcoma:
 uncommon, a highly
malignant tumor of
infants and children;
 polypoid bulky mass
(Botryoid= grape-like)
protruding from vagina.
That is why also known
as Sarcoma Botroides

Embryonal Rhabdomyosarcoma- vagina

Histopathology
 It is composed of rounded malignant (embryonal)
rhabdomyoblasts, some tumor cells have a “tennis-
racket” shape with striated cytoplastmic extension.
Tumor cells are +ve for desmin & myosin
immunostain. These cells are characterstically lying
underneath the vaginal epithelium, called CAMBIUM
LAYER
 The central core of polypoid masses composed of
loose and myxoid stroma with many inflammatory
cella

DISEASES OF THE CERVIX
 Inflammation of Cervix: Cervicitis
 Cervical Tumors

 Inflammation of Cervix: Cervicitis
- May be acute or chronic; specific or non-specific
- Non-specific: Strept., Staph., enterococci, E. coli
- Specific (STD): gonococci, Chlamydia, Mycoplasma,
Trichomonas, Candida….
- Acute cervicitis: - rare (postpartal and nonspecific)
- Neutrophilic infiltration beneath the lining mucosa

Chronic cervicitis:
- More common Bacterial growth & alteration in pH
- May be specific, non-specific or of unknown cause -- -----
- Common cause of leukorrhoea
Predisposing factors – sexual intercourse, trauma of child
birth, instrumentation and excess or deficiency of
estrogen.

Morphology:
 Gross- eversion of ectocervix with hyperemea, edema and
granular surface.Nabothian(retention cysts) may be
grossly visible as pearly grey vesicles.
 Histopathology - squamous metaplasia, chronic
inflammatory cells, columnar cell proliferation (micro-
glandular change), reactive epithelial atypia (mistaken for
CIN), and Nabothian cysts (due to occlusion of cervical
gland ducts ) & squamous metaplasia

Normal epithelium of cervix & Chr. Cervicitis

Cervical Tumors
 Benign tumors
 Endocervical polyp
 Cervical intraepithelial neoplasia (CIN)
 Malignant tumors
 Invasive cervical carcinoma
 Adeno-squamous & Endocervical type
Adenocarcinama

Cervical Tumors
•Endocervical polyp: benign tumors composed of C.T. stroma
showing dilated endocervical glands and lined by endocervical
epithelium
•Squamous intraepithelial lesions (SIL)
CERVICAL INTRAEPITHELIAL NEOPLASIA(CIN)
-It is caused by a sexually transmitted disease; 2nd – 3rd decades ,
caused by cancer-related (high risk) HPV type
16,18,31,33,35,39,51,52,53,56,58,59.
- It usually precedes invasive squamous cell carcinoma (4th – 5th
decades)

- Risk factors: early age of first intercourse,
multiple sex partners & high-risk male sex
partners; that suggests a sexually
transmitted oncogenic agent from male to
female at an early age. HPV acts as a
promotor, and herpes virus type II ,
tobacco, constitution , environment &
others may be cofactors.

Morphology:
 CIN I = dysplasia in the
deeper 1/3rd of the
epithelium & preserved
maturation in the upper
2/3rd.
CIN II = dysplasia in the
deeper 2/3rd & less
maturation.
CIN III = dysplasia in all
layers & no maturation i.e
carcinoma in situ (CIS)

Bethesda system : a new classification for CIN (National
Cancer Institute) for reporting cervical & vaginal cytology.
Besthesda
system
HPV
type
Morphology CIN Dysplasia
-Low grade SIL
(L-SIL) –
-High grade
SIL (H-SIL)
6,11
16,18
Koilocytic atypia, flat
condyloma
Progressive cellular
atypia , loss of
maturation
CIN I
CIN
II &
CIN
III
Mild
Moderate,
severe,
carcinoma in
situ
N.B.:
The oncoproteins (E6 &E7) of high-risk HPVs deregulate the cell cycle, produce
genomic instability, and increase telomerase expression. All these molecular events
promote neoplastic cell growth.
The low risk HPVs (HPV 6,11) do not possess these properties and typically give
rise to benign condyloma.
L-SIL –Low grade – Sq. Intraepithelial Lesion

INVASIVE CERVICAL CARCINOMA:
-Up to 70% of CIN III (CIS) progress to invasive carcinoma.
-Gross: fungating, ulcerative or infiltrative lesions
-Histology: most cases are squamous cell carcinoma of varying
degree of differentiation (65% = large cell non-keratinizing, 25%
large cell keratinizing, 10% small cell poorly differentiated sq.c.c.)
-Other non-squamous carcinomas (adenocarcinoma,
adenosquamous, neuroendocrine=small cell undifferentiated) are
less common and strongly associated with HPV type 18.

 Clinical staging:
- Stage 0: CIS Stage I: confined to the cervix
- Stage II: extending beyond the cervix but not into
- the pelvic wall; into vagina but not to
- lower 1/3 of vagina
- Stage III: reaching the pelvic wall or lower 1/3 of
- vagina
- Stage IV: spreading out side the pelvis
 Prognosis: depends on stage ( 100% cure for stage 0 &
10% of stage IV).

DISEASES OF THE ENDOMETRIUM
 ENDOMETRITIS:
 ADENOMYOSIS & ENDOMETRIOSIS:
 ENDOMETRIAL HYPERPLASIA
 TUMORS OF THE ENDOMETRIUM

ENDOMETRITIS:
 Acute endometritis:
Histological : Neutrophilic infiltration of the endometrium,
caused by Staph., Strept., …; following abortion, delivery or
instrumentation.
 Chronic endometritis:
Clinically : Abnormal endometrial bleeding
Histological : Mononuclear (plasma cell & macrophages
infiltration of the endometrium.
Etiology : in chronic PID, tuberculous, in user of IUDs,
actinomycosis and due to retained gestational tissue.

ADENOMYOSIS & ENDOMETRIOSIS:
Adenomyosis : Defined as presence of nests of benign
endometrial glands & stroma within the myometrium, deep in
the wall of the uterus. It leads to uterine enlargement &
irregular thickening of the uterine wall.
-Possible cause – metaplasia or oestrogenic stimulation due to
endocrine dysfunction of ovary
-Clinically- menorrhagia, colicky dismenorrheoa and
menstrual pain in the sacral or sacrococcycygeal regions.
- Criteria for diagnosis – The minimum distance between the
endometrial islands within the myometrium and the basal
endometrium should be one low power microscopic field (2-3
mm ).

Endometriosis:
- Presence of nests of endometrial glands & or stroma
outside the uterus in ovaries, fallopian tubes, pelvic
peritoneum, uterine ligaments, and rarely in vulva,
vagina, laparotomy scar, umbilicus, and appendix.
- Ectopic endometrium may undergo cyclic menstrual
changes and periodic bleeding.
- Clinically: dysmenorrhea, dyspareunia , pelvic pain &
infertility.
- Diagnosis depends on the presence of 2 out of 3
following features :
1- Endometrial glands ,
2-Stroma, and
3- RBCs or hemosiderin pigment.

Theories of endometriosis:
- Tubal spread
- Lymphatic spread
- Hematogenous spread

ENDOMETRIAL INTRAEPITHELIAL NEOPLASIA = EIN
( ENDOMETRIAL HYPERPLASIA )
Definition: It is abnormal proliferation of
endometrial glands.
The most common cause of dysfunctional uterine
bleeding (DUB) & is associated with
hyperestrogenemia.

Types:
1- Simple hyperplasia= cystic hyperplasia, mild hyperplasia:
Cystic dilated glands, non-neoplastic, due to
anovulatory cycles.
2- Complex hyperplasia= adenomatous hyperplasia:
Overcrowded, closely opposed glands. Some of these are
neoplastic (contain PTEN (Phosphatase and tensin
homolog ) mutations & considered as EIN). PTEN- tumor
suppressor gene
3-Atypical hyperplasia = complex / adenomatous hyperplasia
with atypia:
Overcrowded glands with cytological atypia. Most cases of
this category are neoplastic (EIN) and many contain
PTEN mutations

N.B.: Endometrial hyperplasia:
- It is an important cause of
abnormal uterine bleeding.
- A subset (EIN) is considered a
risk factor for endometrial
carcinoma.
-The risk of carcinoma increases
as function of the degree of
atypia.
- Both endometrial hyperplasia
and adenocarcinoma are
associated with
hyperestrogenism, microsatellite
instability, and mutation of
PTEN gene.

Simple (cystic)glandular hyperplasia
Complex (adenomtous) hyperplasia without
atypia
Complex (adenomatous) hyerplasia with
atypia

TUMORS OF THE ENDOMETRIUM
 Benign tumors
 Endometrial polyp
 Malignant tumors
 Endometrial carcinoma
 Papillary serous adenocarcinoma
 ENDOMETRIAL STROMAL SRCOMA
(MALIGNANT MIXED
MESODERMAL=MULLERIAN TUMOR)

TUMORS OF THE ENDOMETRIUM
Endometrial polyp:
- Sessile tumors composed of endometrial glands and stroma.
- May be associated with hyperestrogenism or Tamoxifen therapy.
- Usually benign, but may show foci of hyperplasia or cancer.

Endometrial carcinoma:
- 7% of all invasive carcinomas in women
- Most common invasive cancer of the female genital
tract.
Epidemiologic & pathophysiologic types:
1- Endometrial adenocarcinoma: Common,55-65 yrs.
Old.
- Risk factors: Obesity, nulliparity, early menarche &
late menopause, granulosa cell tumor of the ovary,
breast cancer, diabetes,
hypertension,infertility&unopposed estrogen..
-

 Gross: Fungating polypoid or infiltrating mass
(diffuse involving the entire endometrial surface).
- Histopathology: Adenocarcinoma usually well
differentiated with often associated with metaplastic
changes ( squamous, secretory or mucinous
differentiation). Other histological forms:
adenosquamous or clear cell adenocarcinoma.
- Containing mutations in PTEN gene, microsatellite
instability, often pre-exciting EIN.

2) Papillary serous adenocarcinoma: -
Associated with older age , - Often arising in endometrial
polyps or endometrial surface epithelium, and - Associated
with multiple P53 mutations.
-Spread: invades the myometrium, and spread by
lymphatics & blood (MC to the lung). Serous tumors can
spread quickly, even when non-invasive

- Prognosis: depends on extend of spread (stage).
Excellent prognosis when the carcinoma is
confined to corpus uteri itself. However papillary
serous tumor spreads quickly even when non-
invasive.
Biologically: more aggressive neoplasms are
poorly differentiated carcinomas including clear
cell & papillary serous carcinoma.
Clinically Abnormal uterine bleeding

ENDOMETRIAL STROMAL SRCOMA ( MALIGNANT MIXED
MESODERMAL = MULLERIAN TUMOR ): TUMORS WITH
STROMAL DIFFERENTIATION
-Rare tumors. Highly malignant. Derived from primitive stromal
cells (mullerian mesoderm origin). Consists of glandular
(carcinomatous) & stromal (sarcomatous) elements. The stromal
elements may show muscle, cartilage or osteoid differentiation.
--Gross: bulky polypoid tumor protruding into endometrial cavity
and vagina.

- Other variants of endometrial stromal
tumors:
 1)Benign stromal nodules: discrete nodules of
stromal neoplasm within the myometrium.
 2)Endometrial stromal sarcoma (Endolymphatic
stromal myosis): well & poorly differentiated
stromal neoplasm, may penetrate into lymphatic
channels.
 3)High-grade sarcoma not otherwise specified:
high grade unclassified tumor capable of
widespread metastases. Occurs in postmenopausal
females; presents with uterine bleeding. Overall 5-
years survival is 25%.

 Benign tumors
 Leiomyoma
 Leiomyosarcoma
TUMORS OF THE MYOMETRIUM

Leiomyoma:
-Benign smooth muscle tumor, MC overall tumor of females
in the active reproductive age, related to increased estrogen
stimulation, and associated with a number of specific
cytogenetic abnormalities.
- Sharply circumscribed, round
gray-white firm nodules, located -
1-within the myometrium (intramural),
2-beneath the serosa (subserous)
3-beneath the endometrium (submucous).

 It may undergo cystic degeneration and
calcification.
- May be asymptomatic or associated with
abnormal uterine bleeding, pain, urinary
disorders.
- Malignant transformation is exceptionally rare
(?almost none).

LEIOMYOSARCOMA -:
- Uncommon, most arise de novo and not from leiomyomas.
- Bulky, fleshy, infiltrative mass in the uterine wall
-Disseminate in the peritoneal cavity & widely by blood
stream.
- Overall 5-years survival is 40%

Histologically distinguished
from leiomyomas by:
1- More than 10 mitotic
figures/ 10 H.P.F. ( with or
without cellular atypia), or
2- Between 5-10 mitotic
figures with cellular atypia.
N.B.: Smooth muscle tumor of
uncertain malignant
potential: A subset of
smooth muscle tumors
displays some but not all of
the features of malignancy

 1-INFLAMMATORY - SALPINGITIS:
 2- TUMORS OF FALLOPIAN TUBE-
DISEASES OF THE FALLOPIAN TUBES

1-INFLAMMATORY - SALPINGITIS:
Suppurative salpingitis:
-Infection by pyogenic organisms: streptococci,
staphylococci, & gonococci (PID)
-May cause tubo-ovarian abscesses, pyosalpinx, peritonitis
& “violin string” adhesion that may cause intestinal
obstruction.
Tuberculous salpingitis:
-Hematogenous dissimination from other foci . May be
associated with T.B. of endometrium & peritoneum.
Histologically: caseating granulomas with giant cells.
-May cause infertility, or ectopic pregnancy

 Benign tumors
 Uncommon
 Adenocarcinoma
TUMORS OF FALLOPIAN TUBE

- Rare. Most common is adenocarcinoma (like
serous adenocarcinoma of the ovary).
- Recently, adenocarcinoma of the fallopian tubes
has been associated with BRCAI & BRCA 2
mutations?.
- Many arise in the fimbriated portion of the
tube.
2- TUMORS OF FALLOPIAN TUBE-

 Anatomy
 Manifestations of ovarian diseases
 Inflammatory - Oophritis
 Non-Neoplastic Ovarian Cysts
 Ovarian Tumors
 Classification of ovarian tumors
 Pathology of individual tumors
OVARY

Embryological development
Precursor Ovarian component Other female genital tract
structures
1.Coelomic epithelium
2. Ectopic endometrial
epithelium—Mullerian
Epithelium
Surface epithelium 1.Fallopian tubes( ciliated
columnar serous cells)
2.Endometrial lining(non
ciliated columnar cells)
3. Endocervical glands
(mucinous non ciliated)
1.Yolk Sac Germ cells(toti potent)
1. Sex cords Stroma of the ovary Endocrine apparatus of post
natal ovary.

Importance of embryological
development
1.Primary Ovarian tumours are classified on the
basis of their site of origin.
2.Still some tumours do not fall in any of the
categories and are put into Malignant (Not
Otherwise Specified)
3.A third category of neoplasms of the ovary are
Metastatic tumours from non ovarian primaries.

Manifestations of ovarian diseases:
- Pelvic pain
- Menstrual irregularities ( abnormal pattern of ovarian
hormone secretion).
- Infertility; failure of ovulation (Stein-Leventhal).
- Ovarian mass : either non-neoplastic (cysts) or neoplastic
(cystic or solid).
OVARIAN DISEASES

 INFLAMMATORY - OOPHORITIS:
- Inflammation of the ovaries is always secondary to
salpingitis or peritonitis.
- If chronic & bilateral leading to extensive fibrosis &
infertility.

NON-NEOPLASTIC OVARIAN CYSTS
1- Follicular and Luteal cysts: Common, 1-8
cm in diameter. They are lined by follicular
(granulosa) cells or luteinized cells.
Asymptomatic, but may rupture, causing
peritoneal reaction & pain.
2 - Chocolate cysts: Blood-filled cysts, due to
endometriosis of the ovaries.

NON-NEOPLASTIC OVARIAN CYSTS
3 – Polycystic Ovarian Cystic Disease ( Stein -
Leventhal syndrome (PCOD) -:
It is important cause of infertility. There is excessive
production of androgens, increase conversion of androgens to
estrogen, insulin resistance, and inappropriate gonadotrophin
production by the pituitary.
Morphology: Ovaries are large, white, many subcortical
follicular cysts(0.5-1 cm.) in diameter, and covered by
thickened fibrosed outer tunica. No corpora lutea (= no
ovulation).
Manifestations: Young females with Oligomenorrhea,
infertility, obesity & hirsuitism.

OVARIAN TUMORS
- Common forms of neoplasia in women.
- 80-90% of ovarian tumors are benign.
- Most ovarian tumors occur between 20-45 years.
- Ovarian cancer is second MC malignancy of the female genital
tract (after endometrial cancer).
- Most ovarian tumors are derived from surface epithelium, and
“CA-125” is the tumor marker for surface epithelial tumors of the
ovary.
- Malignant ovarian tumors present at a late stage, thus are
associated with high mortality rate.
- Known risk factors are nulliparity, family history, and specific
inherited mutations (BRCAI & BRCAII) genes.

Tumour types-- a basic classification
Site of origin Types Frequency Age group
Surface epithelial
tumours
1.Serous
2.Mucinous
3.Endometroid
4.Clear cell
5.Brenner
60%-70% 20 years and greater
Germ cell 1.Teratoma
2.Dysgerminoma
3.Endodermal Sinus(Yolk Sac
Tumour)
4.Choriocarcinoma
15%-20% 0 to 25 years and
greater
Sex cord stromal
tumours
1.Granulosa Theca cell tumours
2.Sertoli-Leydig cell tumours
3.Gynandroblastoma
5%-10% All ages
Miscellaneous 1.Lipid cell tumour
2.Gonadoblastoma
Variable variable
Metastasis Krukenberg tumours 5% variable

CLASSIFICATION OF OVARIAN TUMORS
(A) PRIMARY OVARIAN TUMORS:
(B) METASTATIC NON-OVARIAN CANCER (Krukenberg’s tumor)
A: PRIMARY OVARIAN TUMORS:
I. Surface mullerian epithelial tumors: (Benign, Borderline, and
Malignant)
II. GERM CELL TUMORS:
III. SEX CORD-STROMAL TUMORS:

 I. SURFACE MULLERIAN EPITHELIAL
TUMORS: (Benign, Borderline, and Malignant)
 1-Serous tumors: composed of ciliated columnar
(tubal type) epithelium
 2- Mucinous tumors: composed of mucus-secreting
(cervical canal type) epithelium
 3- Endometrioid tumors: composed of glandular
(endometrium-like) epithelium.
 4- Brenner’s tumors: composed of transitional
(urothelium-like) epithelium
 5- Clear cell tumors.

II. GERM CELL TUMORS:
1- Teratoma
2- Dysgerminoma (seminoma ovarii)
3- Yolk sac tumor= Endodermal sinus tumor
4- Embryonal carcinoma (MC mixed with other
types)
5- Choriocarcinoma (MC mixed with other types)

III. SEX CORD-STROMAL TUMORS:
 1- Granulosa-Theca cell tumor: secrete
estrogen
 2- Sertoli-Leydig cell tumor: secrete androgens
 3- Fibroma: associated with Meig’s syndrome
 4- Sex cord stromal tumor with annual tubules
 5- Gynandroblastoma
 6- Steroid (Lipid)cell tumors

SEROUS TUMORS
-The MC cystic neoplasms of the ovary.
- Cysts are lined by tall columnar, ciliated epithelial cells (fallopian tube
type) & filled with serous fluid. Types:
1-Benign Serous Tumors (Cystadenomas):
(60%), smooth lining & no papillary or solid areas. 20% are
bilateral.
2- Borderline Serous Tumors (low malignant potential):
(15%), epithelial atypia, solid areas, but no stromal invasion. 30% are
bilateral.
3- Malignant Serous Tumors (Cystadenocarcinomas):
(25%); multilayered epithelium, solid areas & papillary structures
invasing the stroma. 65% are bilateral. The prognosis depends on
stage, and the presence of peritoneal implants means poor prognosis.

Diagrammatic representation of
aggressiveness

Borderline serous cystadenoma-
ovary

MUCINOUS TUMORS
Large cystic masses, huge size, and multiloculated. Cysts filled with sticky
gelatinous fluid. They either lined by tall columnar mucus-secreting
epithelium (intestinal-type mucinous cystomas) or show papillary
architectures and focal cilia (mullerian mucinous tumors), which may be
associated with endometriosis. Types:
1- Benign Mucinous Tumors (cystadenomas):
80%; large cysts with smooth lining & no atypia. 5% are bilateral.
2- Borderline Mucinous Tumors (of low malignant potential):
10-15%; cellular atypia, but no stromal invasion.
3- Malignant Mucinous Tumors (Cystadenocarcinomas):
5-10%; atypia, solid sheets & stromal invasion.
20% bilateral.
Seeding in the peritoneum with malignant deposits causes
pseudomyxoma peritonei.
Usually mucinous cystadenocarcinomas are of intestinal type.

Borderline mucinous cystadenoma-
ovary

SEROUS TUMOUR
 Serous papillary cystic tumor
of borderline malignancy.
There is extensive, orderly
invagination of the neoplastic
glands, most with intraluminal
papillae, into the stromal
component of the neoplasm.
The stroma is unaltered in
appearance.
MUCINOUS TUMOUR
 Mucinous cystic tumor of
borderline malignancy,
endocervical type. Many cells
have abundant eosinophilic
cytoplasm.

SEROUS
TUMOURS
 Cystadenocarcinomas–
complex growth pattern, frank
effacement of stroma, usual
features of malignancy and
extremes of atypia. Concentric
calcifications (Psammoma
Bodies) may be seen.
MUCINOUS
TUMOURS
 Cystadenocarcinomas– more
complex and solid growth
pattern with atypia and
stratification, loss of glandular
architecture and necrosis.

ENDOMETROID TUMOURS
• 20% of all ovarian tumours.
• Majority are carcinomas, if benign forms are
present they are cyst adenofibromas.
• Distinguished from serous and mucinous
tumours by presence of tubular glands bearing
close resemblance to benign or malignant
endometrial glands.
• 30% associated with carcinoma endometrium
and 15% with endometriosis whereas 40%
involve both ovaries.

ENDOMETRIOD CARCINOMA
 Gross: presence of both solid
and cystic areas
 Microscopic: Tubular
glands resemble those of
typical endometrial
adenocarcinoma.

CLEAR CELL TUMOUR
These are uncommon and aggressive tumours.
Grossly can present in solid and or cystic pattern (figure
solid tumour with cysts and necrosis)
Microscopically: large epithelial cells with abundant clear
cytoplasm.

BRENNER TUMOUR
 Uncommon adenofibromas
 Epithelial components– nests of transitional cells
resembling urinary bladder.
 Most are benign,variable size(1cm to 30 cm).
 Gross—solid or cystic
 Microscopic – fibrous stroma resembling normal
ovarian stroma seperated by sharply demarcated
nests of urinary tract, with mucinous glands.

BRENNER TUMOUR
 Gross:A sharply
demarcated, yellow-white
fibromatous tumor
occupies a portion of the
sectioned surface of the
ovary.
Microscopically:Nests of
transitional cells, some
containing cysts, lie in a
fibromatous stroma.

GERM CELL TUMORS
- 15-20% of all ovarian tumors. It arises from
totipotent germ cells capable of differentiation into
the three germ layers.
- Mostly benign cystic teratomas while Other
tumours are found principally in children
and young adults.
- Homologous to germ cell tumours in male testis.

TERATOMAS
Mature
Benign
teratomas
Immature
Malignant
Monodermal
or highly
specialized

1-TERATOMAS
1-Mature (Benign) Teratoma: MC germ cell tumors of the ovary, cystic
(dermoid cysts), lined by skin & hairs, and filled with sebaceous
secretion. There may be mature cartilage, bone (teeth) & other
structures. 10-15% are bilateral. < 1% undergo malignant
transformation (MC sq.c.c.).
2-Immature (Malignant) Teratoma: Rare , solid, bulky, with areas of
hemorrhage and necrosis. It contains embryonic elements of he three
germ layers. Age: adolescent & young women. Grading is based on the
amount of immature neuroepithelium. It causes wide spread
extraovarian metatases depending on the degree of the immaturity of
the including tissues.
3- Monodermal (Specialized )Teratomas: differentiate along the line of single
tissue. Examples:- Strauma ovarii is MC (mature thyroid tissue) –
Carcinoid tumor.

MATURE CYSTIC
GROSS: unilocular cysts with
hair and cheesy material. Thin
walled gray white wrinkled
epidermis.hair, tooth and
calcification are found within
walls.
TERATOMA
MICROSCOPIC: cyst wall stratified
squamous epithelium and
underlying sebaceous,sweat glands
and other adnexa.other structures
like thyroid tissue,cartilage bone
may be seen.

2- Dysgerminoma
The ovarian counterpart of testicular seminoma.
GROSS- Yellowish white to gray pink solid, fleshy
tumors, of children & young adults
-10% are bilateral.
Microscopic picture: sheets of large cells
separated by fibrous stroma infiltrated by small
lymphocytes
- Non-functional, but may be mixed with other
germ cell elements that produce hCG
- Malignant, but radiosensitive & chemosensitive,
with relative good prognosis if treated early.

DYSGERMINOMA
 GROSS: Small nodules to
very large size.Cut surface:
yellow white to gray pink
appearance and are soft
and fleshy.
 Microscopic:large vesicular
cells, clear cytoplasm and well
defined boundaries and
centrally placed regular
nuclei.cells in sheets or cords
seperated by scant fibrous
stroma, which has mature
lymphocytes.

3- Endodermal Sinus Tumor ( Yolk Sac Tumor =
Infantile embryonal carcinoma)
-It arises from mutlipotent embryonal carcinoma cells
differentiating towards yolk sac structures.
- Affects children & adolescents; grows rapidly & spreads widely,
but is radio- & chemosensitive.
- Histologically: it shows cystic spaces into which papillary
structures with central blood vessels , the cyst spaces and
papillary structures are lined by immature epithelium
giving glomeruloid or “Schiller-Duval” bodies; There are
intracellular and extracellular hyaline droplet
(characteristic feature). Tumor cells are positive for Alpha-
fetoprotein (tumor marker).

Endodermal Sinus Tumour(Yolk Sac Tumour)
Schiller Duval Bodies

 - It is due to teratogenous development of germ cells.
- Most cases exist in combination with other germ cell
tumors.
- Resembles gestational choriocarcinoma, highly
malignant, spreads widely & elaborates hCG (tumor
marker).
- Microscopic picture: malignat syncitiotrophoblasts
& cytotrophoblasts in a hemorrhagic stroma.
N.B. Gonadal choriocarcinomas are more resistant to
chemotherapy than Gestational choriocarcinomas.
4- Choriocarcinoma

1- GRANULOSA - THECA CELL TUMOR
- 5% of all ovarian tumors, of peri & post-menopausal
women.
- Usually unilateral, solid white yellow, consisting of theca
cells & granulosa cells, arranged in “Call-Exner”
rosettes.
- Elaborated large amount of estrogen & may cause
precocious sexual development in children, endometrial
hyperplasia, cystic changes of the breast or endometrial
carcinoma (estrogen effects).
- Pure granulosa cell tumors are potentially malignant, clinical
malignancy occurs in 5-25% of cases, but they are slowly growing &
10-years survival is above 85%.
- Pure Theca cell Tumors - THECOMA

GRANULOSA CELL TUMOUR
 Gross: small partly solid,
partly cystic and mostly
unilateral.The neoplasm
composed of yellow-
white tissue with
hemorrhage, some of
which is intracystic

 Microscopically:
granulosa cell arranged in
various patterns like
micro,macro follicular,
trabecular,bands and
sheets.CALL-EXNER
BODIES characterstic
rosette like structures
having central rounded
pink mass surrounded by
granulosa

THECOMA
 Pure thecoma are almost always benign.
 Occur in post menopausal women.
 Oestrogen dominant tumours– endometrial
disorders , carcinoma and cystic disease of
breast.
 If androgen secreting – virilizing effects.

THECOMA
 Gross: a solid firm mass
upto 10 cm in
diameter.Section shows.
solid, lobulated, yellow
tissue.
 Microscopically : spindle
shaped theca cells along
with variable amount of
hyalinized collagen,
cytoplasm of these cells is
vacuolated and lipid laden.

2- SERTLOI-LEYDIG CELL TUMORS ( Androblastoma=
Arrhenoblastoma= Hilus Cell Tumors = Gonadoblastomas)
.Androgen producing neoplasm (rarely produce estrogen)
-Recapitulate the testicular counterpart & produce
masculinization or defemenization (Androgen)
effeect.
-Usually unilateral & benign.
-Gross: cut surface is solid and colour gray to golden
brown.
-Microscopic picture: Tubules lined with Sertoli cells
and Leydig cells interspersed in the stroma.
3- GYNANDROBLASTOMA: Extremely rare
- It consists of a mixture of granulosa/theca & sertoli/
leydig cells.
- It may be benign or malignant.

Sertoli Leydig Cell Tumor-Ovary

4) FIBROMA
 Common ovarian tumours. Usually bilateral
 Harmonally inactive
 Meig’s syndrome: fibroma with pleural
effusion and benign ascites.
 Gross large firm fibrous usually bi-lateral mass.
 Microscopic composed of spindle shaped well
differentiated fibroblasts and collagen.
 Fibrothecoma: combination of fibroma and
thecoma.

METASTATIC TUMOR
- Very common,
- The primary tumors is from abdominal and breast
tumors.
A bilateral metastatic ovarian carcinoma, composed of
mucin-producing signet ring cells, metastasizing from
GIT, mostly from the stomach, it may produce
pseudomyxoma peritonei like well differentiated
appendicial tumors.
Krukenberg tumor

HISTOPATHOLOGY OF
KRUKENBERG TM.

OVARIAN CYSTS
Neoplastic cysts Non-neoplastic cysts
-Cystadenoma
-- Benign cystic teratoma
(Dermoid cyst).
-Cystadenocarcinomas
- Follicular & Luteal cysts
- Polycystic ovarian disease
(PCOD).
- Chocolate (Endometriotic)
cyst.

GESTATIONAL & PLACENTAL
DISORDERS

ECTOPIC PREGNANCY : Disorders of early
pregnancy
Definition: implantation of the embryo in any
site other than uterus; Most common- the
fallopian tube (> 90%), rarely in ovary or
abdominal cavity.
Associated with PID & endometriosis; but
50% occur with no known cause.

 May end in:
 1- Spontaneous regression with resorption of the products
of conception
 2- Intratubal hemorhage (hematosalpinx)
 3- Tubal abortion or rupture & extrusion into abdominal
cavity →
 intraperitoneal hemorrhage and shock i.e. acute
abdomen
 (medical emergency).
- Diagnosis:
 High hCG, sonography & endometrial biopsy showing
decidual reaction but no chorionic villi.

Disorders of late pregnancy
1- Placental inflammation or infection:
A) Disorder of ascending infection
(Chorioamnionitis):
- infection of the fetal membrane
- Usually ascending from the vagina, in case of
premature rupture of the membranes.
- Most common cause is group B streptococci.
- Acute suppurative inflammation of the chorion &
amnion, and acute vasculitis of the umbilical
cord (funisitis).
B) Hematogenous (transplacental ) infection:
- It is derived from maternal septicemia (Listeria,
streptococcus & TORCH = Toxoplasma, Rubella,
Syphilis, Cytomegalovirus, Herpes) → villous
inflammation (villitis) and acute intervillositis.

2- Toxemia of pregnancy:
-Occurs in 6% of pregnancies, in the last trimester & most common in
primiparas.
1- Pre-eclaspia = hypertension , proteinuria & edema, headache & visual
disturbances
2- Eclampsia = severe pre-eclapsia + convulsions & coma.
Associated with widespread endothelial injury & DIC
(Desseminated Intravascular Coagulation) affecting kidneys, liver,
brain & other organs.
- Resembles GVH( Graft Versus Host Reaction , but etiopathogenesis is poorly
understood.
- Delivery is the only definitive treatment for pre-eclampsia and eclampsia.
Pathogenesis of Toxemia of pregnancy: Unclear;
- The primary cause may be immune or genetic factors → mechanical or
functional obstruction of the uterine spiral arterioles → placental ischemia →
endothelial injury & activation of disseminated intravascular coagulation, leading
to decrease in glomerular filtrate, CNS disturbances, abnormal liver functions,
and fibrin thrombi and ischemia in most organs.

THEORIES OT TOXEMIA OF PREGNANCY:
1- Inadequate placental implantation → decrease in
uteroplacental perfusion and placental ischemia →
increase production of vasoconstrictors (e.g.
thromboxane , angiotensin) & decrease of
vadodilators(e.g. prostaglandin I2, prostaglandin E2)
→ arteriolar vasocontriction & hypertension.
2- Recently ; Factors imbalance → premature
termination of placental vascular growth. There is
abnormal increase in an anti-angiogenic factor
(sflt-1) and reduction in pro-angiogenic factors
(Vascular endothelial-derived growth factor=
VEGF & placental growth factor =PLGF ).

GESTATIONAL TROPHOBLASTIC DISEASES
1- HYADATIDIFORM (VESICULAR) MOLE: defined by-
1- Enlarged edematous and hydropic change of chorionic villi
which become vesicular(Cystic swelling). Gross -Grape like
2-Variable trophoblastic proliferation.
Two types:
- Complete (diploid) &
- Partial/Incomplete (triploid).
- 10% develop into invasive mole, and 2.5% develop into
choriocarcinoma.
2- INVASIVE MOLE:
- Penetrates the uterine wall, produce hemorrhage but does
not metastasize. - Responds well to chemotherapy.

Feature Complete mole Partial mole
-Karyotype
- Fetal parts
- Villous edema
- Trophoblastic
proliferation
- Atypia
-Serum hCG
-hCG in tissue
- Behavior
-Diploid (46 xxor 46xy), two
sperms fertilize an empty egg. All
genetic material is paternal
-Rarely seen or absent
- All villi
- Diffuse & circumferential
-Often present
- Elevated
- ++++
- 2% choriocarcinoma
-Triploid (69 ). Two sperms fertilize an
egg with normal chromosomes
- Usually present with abnormalities
- Some villi
- Focal and slight
-Abscent
- less elevated
- +
- Rare choriocarcinoma

3- Choriocarcinoma:
- 50% follow hydatidiform mole & 25% follow normal
pregnancy, 20% follow abortion & 5% follow
ectopic pregnancy.
- Highly malignant & metastasize widely.
-Gross: Large, soft, yellowish white & fleshy with areas of
hemorrhage and necrosis.
-Histology: Abnormal proliferation of both cytotrophoblasts
& cyncytiotrophoblasts invading the endometrium,
blood vessels, lymphatics, no chorionc villi are seen.
- Spread:
To lung, bone marrow, liver & other organs.

Clinical features:
Vaginal bleeding & discharge in the course of
apparently normal prgnancy, after miscarriage, or
high hCG titers.
N.B.: All gestational trophoblastic
disorders are associated with high level of
hCG (tumor marker).

4- Placental site trophoblastic Tumor:
- A rare tumor composed of proliferating
intermediate trophoblasts (larger than
cytotrophoblasts but mononuclear than cyncytial).
- D.D. from choriocarcinoma by the absence of
cytotrophoblastic elements and low level of hCG
production.
- Mostly are locally invasive only, but malignant
variants are distinguished by:
- A high mitotic index,
- Extensive necrosis, and
- local spread.
- About 10% result in metastases and death.

Contraception
 Contraception is the prevention of conception by methods
other than abstinence , its used to limit the size of family
( birth control )
or
( Family planning)

Ideal Contraception
An ideal contraception should fulfill the following:
 Highly efficient
 Free from unwanted side effect
 Absolute safety
 Simplicity of use
 Reversible
 Well tolerated

FEMALE CONTRACEPTION
Barrier Methods
 Diaphragm
 Cervical cap
 Female condom
Hormonal Methods
 Oral contraceptive - Combined oestrogen/
progestogen
- Progestogen only
 Depot progestogens – Injections
- Subcutaneous silicone

Intra Uterine Devices
 Inert
 Copper bearing
 Progestogen releasing.
Natural Methods
 Rhythm
 Breast feeding (while baby is totally breast fed)
Spermicides
 Creams, Films, Foams, Jellies, Pessaries,

Surgical Methods
 Laparoscopic sterilisation - Rings
- Clips
- Bipolar diathermy
- Laser
 Tubal ligation
Immunological Methods
- These are still at an investigative stage.

MALE CONTRACEPTION
 Condom
 Vasectomy
 Male oral contraception with androgens
and with cotton seed oil
 Immunological contraception
Still at
investigative
stage.

SIDE-EFFECTS
Minor side-effects commonly occure during the 1st
3 cycles & may lead to unnecessary
discontinuation
1. Irregular bleeding (breakthrough bleeding/ spotting)
 10-30% in the 1st month of use
 improves with time over 3 cycles
 amenorrhea 2-3% of the cycles
2. Breast tenderness & nausea
 Improve with time
 Less with lower estrogen dosage

SIDE-EFFECTS
3-Wt gain
 Placebo controlled trials have failed to show any
association between wt gain & COCP
4-Mood changes
 Women report depression & mood changes
 Placebo controlled trials have failed to show any
significantly increased risk of mood changes
with COCP

RISKS OF OCP
1-Venous thromboembolism
 VTE 3-4 X higher in users than nonusers
 Absolute risk of VTE in COCP users –
1-1.5/10 000/year
 Risk of VTE is higher during the 1st year of use than
subsequent years
 Incidence of VTE in nonpregnant women is 0.3/
10000/year at 20-24 Y------0.6 at 40-44 Y
 Incidence of VTE in pregnancy is 13/ 10000 deliveries
 The risk is attributed to the estrogen component of the
pill & decline with lower dosage

RISKS OF OCP
3-Stroke
 Some studies showed 2X ↑↑ risk of stroke
 Smoking & HPT ↑↑ risk of stroke
4-Gallbladder disease
 COCP ↑↑ secretion of cholic acid in bile ↑↑ incidence of gallstone
formation
 No significant ↑↑ risk of gallstone formation in COCP users
5-Breast cancer
 Still controversial
 A large meta-analysis 1996  significant ↑ risk of breast
ca in women currently taking the COCP( Relative Risk
1.24 ) & in the 1st 10 Y after discontinuing it

RISKS OF OCP
5-Breast cancer
 Cumulative breast ca risk up to age 35 is 2 / 1000
with COCP --------------------------------------- 3 / 1000
 It is not known whether this ↑ is due to the pills or due to delaying
the 1st full term birth
 More recent study > 9000 women  no significant ↑↑ in breast ca
risk
No ↑↑ risk with different dosage of estrogen, longer periods of use,
or with different progestin components
No ↑↑ risk in Pt with family Hx of breast ca
No ↑↑ risk in Pt who started using the pills at an earlier age
↑↑ risk in Pt who carry BRCA1, BRCA2 genes

RISKS OF OCP
6-Cervical cancer
 One study ↑↑ risk of Cx ca in long term COCP users
who are HPV positive
 A review of 28 studies of women with Cx ca ↑↑ risk of
Cx ca with ↑↑ duration of COCP use
 Probably due to ↑↑ risk of HPV (a major risk factor for cx
ca) that might be related to sexual behavior which differs
in users & non users of COCP
 Another study HPV + ve women follwed up for 10 years
showed no increased risk

IUCD MECHANISM OF
ACTION
 Prevention of fertilization the chief mechanism
 Inhibition of implantation
 Presence of foreign body & copper biochemical &
morphological changes in the endometrium adversely affect
sperm transport
 Copper ion have direct effect on sperm mobility  ↓↓ in its
ability to penetrate Cx mucous
 Levonorgestrel releasing devices  weak foreign body reaction
& endometrial decidualization & glandular atrophy estrogen &
progestrone receptors are ↓↓ Cx mucous becomes thick &
impermeable to sperms ovulation may be inhibited in some
women

INDICATIONS FOR IUCD
 In the absence of contraindications may be considered for any
woman seeking a reliable, reversible, coitally independent
method of contraception
 Women seeking long term birth control
 A method requiring less compliance
 Women with contraindications to estrogen
 Breast feeding women
 Copper IUCD used for postcoital contraception within 7 days
 LNG- IUCD ↓↓ menstrual flow & cramping suitable for
women with menorrhagia & dysmenorrhea

IUCD CONTRAINDICATIONS
Absolute contraindications
 Pregnancy
 Current, recurrent or recent (within 3 M) PID or sexually
transmitted disease
 Puerperal sepsis
 Immediate post septic abortion
 Severely distorted uterine cavity
 Unexplained vaginal bleeding
 Cx or endometrial ca
 Malignant trophoblastic disease
 Copper allergy Copper -IUCD
 Breast Ca  LNG -IUCD

IUCD CONTRAINDICATIONS
Relative contraindications
 Risk factor for sexually transmitted diseases or HIV
 Impaired response to infections:
-HIV +ve women
-Women on corticosteroid Rx
 48hrs- 4 wks postpartum
 Ovarian ca
 Benign gestational trophoblastic disease

IUCD NON-
CONTRACEPTIVE BENIFITS
 Nonmedicated IUCD or copper IUCD ↓ risk of
endometrial ca
 LNG-IUCD  ↓ menstrual blood loss 74-97% 
improved Hb
 LNG-IUCD users  ↓ hysterectomy for menorrhagia 64-
80%
 LNG-IUCD  ↓ dysmenorrhea
 ---------------  protects against enometrial hyperplasia in
women on tamoxifen
 --------------  beneficial effects in fibroid related
menorrhagia

IUCD SIDE EFFECTS
1-Bleeding
Copper / nonmedicated IUCD
 Irregular menstrual bleeding
 ↑↑ amount of menstrual bleeding 65% in copper IUCD users
 NSAID or tranexamic acid ↓↓menstrualblood loss
 The days of bleeding or spotting ↓↓ overtime 13 days inth 1st months
 6 days at 1 year
 Discontinuation due to bleeding 20%
LNG-IUCD
 ↓↓menstrualblood loss 74-97%
 Spotting 16 days at 1 M ↓↓ 4 days at 12 M
 Discontinuation due to bleeding 14%
 Amenorrhea 16-35% at 12 M

IUCD SIDE EFFECTS
2-Pain or dysmenorrhea
 6% discontinue use due to pain
 Pain may be physiological
 LNG-IUCD ↓↓ dysmenorrhea
3-Hormonal LNG-IUCD
 Depression
 Acne
 Headache
 Breast tenderness
 Low incidence ,maximal at 3 M then ↓↓
 No change in Wt

IUCD SIDE EFFECTS
4-Functional ovarian cysts/ LNG-IUCD
 30% of users
 Resolve spontaneously

IUCD RISKS
1-Uterine perforation
 A rare complication at insertion
 0.6-1.6/1000 insertion
Risk factors
 Postpartum insertion
 Inexperienced operator
 Immobile uterus
 Extremely ante or retro –verted uterus
2-Expulsion
 2-10% in the 1st year of use
 5 year expulsion  5.8-6.7
 Risk factors: postpartum insertion, nulliparity,previous
expulsion(30% chance)

IUCD RISKS
3-Infection
 Risk is ↑↑ only in the 1st few months after insertion
 Inverse relation between infection & time since insertion
 Risk of PID 3.8 in 1st month
Baseline risk at 4 M
4-Filure
 If a woman become pregnant with an IUCD  exclude
ectopic
 Abortion is ↑↑ in women pregnant with IUCD in place
Copper IUCD abortion 75% if left in situ
Live birth 89% if IUCD removed
 Preterm delivery ↑↑ in women pregnant with IUCD in
place

IUCD MYTHS &
MISCONCEPTION
 Nulliparous woman can not use IUCD
 IUCD ↑↑ risk of ectopic
Fact  IUCD work primerly by preventing fertilization
Ectopic in IUCD users : nonusers
0.02-0.25/100WY:0.12-0.5/100WY
 IUCD ↑↑ risk of infertility
Fact  Women who discontinue IUCD use concieve at the same
rate of women who never used IUCD
 IUCD ↑↑ risk of long term PID
Fact after the 1st M the risk of infection is not higher than non
users/ PID < 2/ 1000 year of use
 IUCD are not effective contraceptives
Fact LNG –IUCD as effective as tubal ligation

INITIATION
 Counselling
 Inserted any time during a menstrual cycle once pregnancy
excluded
 During menses  exclude pregnancy & mask insertion related
bleeding
 Infection & expulsion ↑ with insertion during menses
 It can be removed any day of the menstrual cycle
 Cost effectiveness of gonorrhea & chlamydia screening
is not clear
 If there is mucpurulent discharge Cx swabs must be
taken & insertion delayed
 Antibiotic prophylaxis is not indicated

FOLLOW UP
A follow up visit must be scheduled in 6 wks then yearly
Women must be instructed to come if;
 IUCD thread can not be felt
 She feels the lower end of the IUCD
 ? Pregnant
 Abdominal pain, fever or unusual discharge
 Pain or discomfort during intercourse
 Sudden change in menstrual period
 Wants to remove the device or concieve

Diseases of the female genital tract

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Diseases of the female genital tract