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Ovarian tumor

Ovarian tumor is one of the most common


tumors of the female generative system. Little
progress has been made in identifying
precursory or in situ stages of these lesions.
The 5-year survival rate for all stages is still
35-38%little better than 35 years ago.

Table 1 Histology of ovarian tumors (WHO, 1972)

1. Epithelial ovarian tumors
(1) Serous
(2) Mucinous
(3) Endometrioid
(4) Clear cell
(5) Brenner
(6) Mixed epithelial
(7) Undifferentiated
2. Gonadal sex cord stromal tumor
(1) Granulosa stromal cell tumor
Granulosa cell tumor
Thecoma-fibroma tumor
(a) Theca cell tumor (b) Fibroma
(2) Sertoli leydig cell tumor
(androblastoma)
(3) Gynandroblastoma
3. Lipid (lipoid) cell tumor
4. Ovarian germ cell tumors
(1) Dysgerminoma
(2) Endodermal sinus tumor (yolk-sac
tumor)



(3) Embryonal carcinoma
(4) Polyembryoma
(5) Choriocarcinoma
(6) Teratoma
Immature
Mature
(a) Solid (b) Cystic
Monodermal and highly
specialized:
(a) Struma ovarii (b)
Carcinoid (c) Others
(7) Mixed germ cell tumors
5. Gonadoblastoma
6. Non-ovarian specific soft tissue
tumor (sarcoma, fibrosarcoma,
lymphosarcoma)
7. Unclassified tumor
8. Metastatic tumor
9. Tumor like condition Follicle
cysts, lutein cysts, and so on



Epethelial tumors account for more than
50~70% of all primary ovarian neoplasia and
more than 85%-90% of ovarian malignant
tumors.
Ovarian germ cell tumors account for 20%-
40% of ovarian tumors. They include
dysgerminoma, embryonal carcinoma,
teratoma, endodermal sinus tumour,
choriocarcinoma , and so on.

Sex cord stromal tumors account for about
5% of all ovarian tumors. These tumors are
potentially functional, that is, producing
hormones, so we call them ovarian functional
tumors.
Metastatic tumors account for 5%-10% of
ovarian tumors. The primary sites are
commonly gastrointestinal tract, breast,
genital organs.
High risk factors
1. The factors of heredity and family
2. Environmental factors
3. Endocrine factors
Pathophysiology
1. Epithelial tumors
Epithelial ovarian tumors present at an
average age of 30-60 years.
Cellular proliferation, atypia, and the presence
of stromal invasion are the histologic criteria
used to classify malignant potential.

SEROUS CYSTADENOMA
BENIGN TUMORs
comprises approximately 25% of benign
ovarian neoplasms.
divided 2 categories, simple and papillary.
Psammoma bodies (small irregular
calcifications) are characteristic of serous
tumors.

BORDERLINE SEROUS CYSTADENOMA
papillary formation
good differentiation
lack of stromal invasion
SEROUS CYSTADENOCARCINOMA
external papillary excrescences covered
by stratified epithelium (usually over 4-5
layers)
nuclear atypia
occasional mitotic figures and stromal
invision
MUCINOUS CYSTADENOMA
BENIGN TUMORs
Account for approximately 20% of benign ovarian
neoplasms
Generally unilateral, rounded or ovoid, smooth,
grayish-white
Cut section reveals the multilocular cysts strikingly
filled with a viscous and tremellose mucin.
The rate of malignant alteration is 5%-10%.

BORDERLINE MUCINOUS CYSTADENOMA
The tumor generally is rather large.
Microscopically, cellular stratification occurs.
No stromal invasion
Cellular atypia may be mild to moderate and
a moderate number of mitoses may be present.

MYXOMA PERITONEI
the progressive accumulation of mucin witnin the
abdomen
arise from either a mucinous ovarian tumor or
from a mucocele of the appendix
account for approximately 2%-5% of mucinous
cystadenomas
tumor cells secrete mucin
rare cellular atypier and mitotic activity

MUCINOUS CYSTADENOCARCINOMAS
account for 10% of ovarian malignant
neoplasms.
Cut section reveals the multilocular cysts
filled with a turbid or bloody mucin.
Microscopically, glands are crowded and
stroma are rather few. Stromal invasion and
cellular atypia may occur strikingly.
In contrast to serous cystadenocarcinoma, this
tumor has a more favorable prognosis.
OVARIAN ENDOMETRIOID TUMOR
The malignant kinds of these neoplasms are
endometrioid carcinomas, account for 10%-24% of
primary ovarian malignant neoplasms.
The histologic type are adenocarcinoma or
adenoacanthoma, as in uterine carcinomas.
Endometrial cancer found in the uterus and ovary
commonly represents multifocal and not metastatic
disease.
OVARIAN GERM CELL TUMOR
They are found in the gonad or at any site
from which the germ cell arises or to which it
migrates.
This tumor occurs principally in young
females60%-90% in prepuberal and only
4% in postmenopausal women.
Germ cell tumors may contain germ cells as
the predominant component.

TERATOMA
Teratoma is one of the most
fascinating of all neoplasms.
This tumor may contain tissues of
ectoderm, endoderm, and mesoderm.
MATURE TERATOMA
Mature teratoma is the most common tumor of
ovary.
This tumor often occurs in patients 20-40 years old.
Cut section reveals the unilocular cysts strikingly
filled with adipose and hair, sometimes with bone
and teeth.

Special varieties of teratoma may produce unusual
symptoms.
Malignant change in a primarily benign cystic
teratoma is uncommon.
Any tissues may occur malignant change to form
every kind of malignant tumors.
The epithelium of scolex easily occur malignant
change.
IMMATURE TERATOMA
The tumor commonly occurs during the early
reproductive years.
The degree of malignance is bases on the
proportion of immature tissues, the cellular
differentiation, and the neuroepithelium content.
Maturation at a secondary site has even occurred
in some instances.
DYSGERMINOMA
Occurs principally in young females.
Comprises approxmately 5% of all malignant
ovarian neoplasms.
Radiation therapy is very effective in this tumor.
The 5-year survival rate is 90%.

ENDODERMAL SINUS TUMOR
Occurs principally in young female.
The biologic marker is alpha-fetoprotein
(AFP).
The survival time has been prolonged by
combination chemotherapy and surgery.
OVARIAN GONADAL SEX CORD
STROMAL TUMOR
GRANULOSA STROMAL CELL TUMOR
GRANULOSA CELL TUMOR:
Found in all age groups and associated with
pseudoprecocious puberty.
Early breast development , menstrual disorder,
postmenopausal vaginal bleeding make up the
characteristic symptom.
Laboratory studies demonstrate an increase in the
numbers of mature epithelial cells in the vaginal
cytologic specimen, elevated urinary and serum
estrogen levels, and variant degrees of endometrial
proliferation.
The characteristic cell is the round or slightly
ovoid granulosa cell with its dark nucleus.
Mitoses are common, and the ovumlike Call-
Exner bodies are classic.

THECA CELL TUMOR
This tumor offen exists with granulosa cell tumor.
The classic cell is short spindle, with abundant
cytoplasm.
The endometrium offen becomes proliferative, and
postmenopausal vaginal bleeding may occur.
The prognosis is better than that of other ovarian
carcinomas.

FIBROMA
These tumors account for about 2%-5% of all
ovarian tumors.
These solid ovarian tumors may be associated with
Meigs syndrome.
SERTOLI LEYDIG CELL TUMORS
also be called androblastoma
often affect females beneath the ages of 40 years
usually be luteinized, simulating the classic pattern
of the testes and producing steroids
generally benign, may produce the masculinization
The 5-year survival rate is 70%-90%.

OVARIAN METASTATIC TUMORS
Krukenbergs tumor
PATTERNS OF SPREAD
At the time of diagnosis, over 70% of patients with
epithelial carcinomas have metastased outside the
pelvis.
The most common location of metastases
Peritoneum 85%
Omentum 70%
Contralateral ovary 70%
Liver 35%
Pleura 33%
Lung 25%
Uterus 20%
Vagina 15%
Bone 15%
STAGING
The extent of the disease determines the stage
and the appropriate form of management.
Growth limited to the ovaries
A Growth limited to one ovary; no ascites present containing malignant cells;
no tumor on the external surface; capsule intact
B Growth limited to both ovaries; no ascites present containing malignant
cells; no tumor on the external surface; capsule intact
C Tumor either stage A orB, but with tumor on the surface of one or
both ovaries; or with ruptured capsule; or with ascites containing malignant
cells or with positive peritoneal washings
Growth involving one or both ovaries, with pelvic extension
A Extention and/or metastases to the uterus and/or tubes
B Extention to other pelvic tissues
C Tumor either stage A or B, but with tumor on the surface of one or
both ovaries; or with capsule(s) ruptured; or with ascites present containing
malignant cells or with positive peritoneal washings
Tumor involving one or both ovaries, with peritoneal implants outside the
pelvic and/or positive retroperitoneal or inguinal nodes; superficial liver
metastasis equals stage . Tumor is limited to the true pelvis, but with
histologically proven malignant extention to small bowel or omentum
A Tumor grossly limited to the true pelvis, with negative nodes but with
histologcally confirmed microscopic seeding of abdominal peritoneal surfaces
B Tumor involving one or both ovaries, with histologically confirmed
inplants of abdominal peritoneal surfaces, none exceeding 2 cm in diameter;
nodes are negtive
C Abdominal inplants greater than 2 cm in diameter and/or positive
retroperitoneal or inguinal nodes
Growth invoving one or both ovaries with distant metastases. If pleural
effusion is present, there must be positive cytologic findings to allot a case to
stage ; parenchymal liver metastasis equals stage
Table 2. FIGO stages for primary carcinoma of the ovary (1985)
CLINICAL FIDINGS
1. BENIGN OVARIAN TUMORS
These tumors are generally asymptomatic and are
found on routine pelvic examination.
On physical examination the most common signs of
an ovarian tumor include an adnexal mass (or
masses), an abdominal mass.
If the tumors are large enough, they may produce
pelvic pain, urinary retention or frequency
micturition, rectal discomfort, and bowel
obstruction, no ascites.

2. MALIGNANT OVARIAN TUMORS
The evaluation includes a carful history and complete
physical examination in addition to a pelvic examination.
Most neoplastic ovarian tumors produce few symptoms.
On physical examination the most common signs include
an adnexal mass (or masses), an abdominal mass ascites,
or evidence of metastasis.
When interpreting an adnexal mass,it must be
remembered that any palpable ovarian mass in a
premenarcheal or postmenopausal woman is abnomal.
DIAGNOSIS
Although most ovarian tumors have not
special symptoms, they may be diagnosed
by patitnts age, careful histories and
complete physical examination in addition
to a pelvic examination.
1. CELLULAR ANALASIS
Ascites or peritoneal washing is of greatest value
when the process appears to be early or to be
unilateral.
If there is clear extension of malignancy to
peritoneal surfaces, if there is omental tumor
extension, or if the entire tumor cannot be
removed, the peritoneal washing are less value.
2. FINE-NEEDLE PARACENTESIS
Routine paracentesis to obtain samples for
cellular analysis is not recommended but may
be useful in the diagnosis of advanced or
inoperable diseases.
3. OTHER ACCESSORY EXAMINATIONS
Ultrasonography (endovaginal ultrasound) and
computed tomography are accurate techniques.
A laparotomy at least for histological purposes is
mandatory.
CA125 is the best known marker for ovarian cancer.
In young patients, serum human chorionic
gonadotrophin (-hCG) , -fetoprotein (AFP) titres
should be determined.
DIFFERENTIAL GIAGNOSIS
1. Benign ovarian tumors and malignant
ovarian tumors See table 3
Table 3. Benign ovarian tumors and malignant
ovarian tumors
Content Benign Malignant
History Long, growth
slowly
Short, growth rapidly
Sign Generally
unilateral, active,
cystic, smooth,
no ascites
Generally bilateral, fixed, solid
or semisolid, nodular or
lobulated, often with bloody
ascites containing malignant
cells
General physical
condition

Good Cachexia present
Ultrasound Opaque dark area
of fluid, with
interval band,
edge clearly
Opaque dark area of fluid with
light beam or sport, edge not
clearly
2. DIFFERENTIAL DIAGNOSIS OF
BENIGN OVARIAN TUMORS
(1) OVARIAN TUMOR LIKE CONDITION
Follicle cysts and lutein cysts are the most common.
Indeed, in a normally menstruating woman any
adnexal mass larger than 5cm should be
concidered suspect if it persists for more than 6
weeks.
(2) SALPINGO-OOPHORY CYSTS
These are inflammation cysts and often
produce infertility.
(3) LEIOMYOMA
Leiomyomas are generally multiple, linked with
uterine, often associated with a menstrual
abnormality.
On physical examination, the tumor moves when
corpus uteri and cervix move.
(4) UTERINE PREGNANCY
The careful menstrual history, the HCH
study, and untrasonography scane may be
useful to differentiate the two conditions.
(5) ASCITES

The patient often has history of hepatic disease, or
cardiac disease.
When the patient lies down, the shape of her
abdomen likes as frog-belly.
Percussion note is tympany in the middle abdomen,
dullness in the lateral abdomen. The shifting
dullness is positive.
3. DIFFERENTIAL DIAGNOSIS OF
MALIGNANT OVARIAN TUMORS

(1) ENDOMETRIOSIS
The lesion generally produces progressive
dysmenorrhea, hypermenorrhea, premenstrual
irregular vaginal bleeding, and so on.
Ultrasound, laparoscopy are the promising
adjuvant examination.
Laparotomy should be performed if ovarian
neoplasms cannot be ruled out.
(2) PELVIC INFLAMMATION OF
CONNECTIV TISSUE
The patient may have history of abortion or
puerperal inflammation.
Use of antibiotic may remit symptoms, and make
the mass or masses small or disappear.
(3) TUBERCULOUS PERITONITIS
The lesions often occur in young or infertility
women, generally have history of lung tuberculosis,
often produce leanness, asthenia, low fever, night
sweat, anorexia, infrequent menstruation or
amenorrhea.
Ultimately the dignosis of this lesion depends on
surgical exploration.
(4) EXTRA-GENERATIVE TRACT
TUMORS
Ovarian malignant neoplasms must be
differentiated from retroperitoneal masses,
rectal cancer or sigmoid cancer.
Untrasound, barium enema, intravenous
pyelography may assist in establishing the
diagnosis.

(5) METASTATIC OVARIAN TUMORS
The metastatic ovarian neoplasms should be
suspect if the adnexal mass or masses were
bilateral, median large, kedney shape, active
and solid.
The patient has gastrointestinal symptoms,
history of gastrointestinal cncer, and breast
cancer.
COMPLICATION
Complications include pediculotorsion, capsule
ruptured, inflammation, and malignant
transformation. They may produce pelvic pain or
abdominal pain, fever, ascities, abdominal mass or
masses, and so on.
TREATMENT
1. BENIGN TUMORS
Operation should be performed while the
diagnosis is established.
The extent of surgery depends on the patients
age, the patients desire of childbearing, and
contralateral ovary.
Frozen section should be used at the time of
surgery.
2. MALIGNANT TUMORS
(1) SURGERY
Surgery is usually performed to establish the type,
histologic grading, and stage of the tumor.
In certain early or borderline cases, surgery may also be
curative, and in nearly all cases it is a major part of
therapy.
At the time of surgery, peritoneal fluid or peritoneal
washing should be aspirated for cytologic analysis.
A second-look operation is indicated when an
inoperable tumor responds so remarkably to adjunctive
therapy that surgery becomes feasible.

(2) CHEMOTHERAPY
Since the introduction of cisplatin-based combinations in
the 1980s, the outcome of treatment has improved
markedly.
Generally, a pulse therapy regimen ie, 5 days of
therapy per month for 6-8 courses, has been the most
commonly accepted program.
Some new drugs (hexamethylmelamine, cisplatin,
Carboplatin, adriamycin) are the promising
chemotherapeutic agents.
It must be appreciated that these agents are toxic, and
the combinations are more noxious than the single
agents.(Table 4)
Table 4. Toxicity of chemotherapeutic agents
System Drug
Hepatic toxicity Methotrexate (esprcially chronic low-dose)
Renal toxicity Methotrexate (esprcially high-dose), Cisplatin
Myelosuppressive toxicity Many agents
Peripheral neuropathy Vincristine, Hexamethylmelamine
Ototoxicity Cisplatin
Pulmonary toxicity Bleomycin, Methotrexate, Cyclophosphamide
Cardiac toxicity Doxorubicin (acute or cumulative)
(3) RADIOTHERAPY
Radiation therapy was the prime therapeutic
modality for many years, but inability to deliver
effective dosages to the upper abdomen without
damaging the liver or kidneys limited its usefulness.
Because of the availability of a multitude of
chemotherapeutic agents, chemotherapy has
recently replaced radiation.
PREGNOSIS
The grade of tumor differentiation and FIGO
substage are most likely the strongest factors
predicting for recurrence in early stage.
In the advanced stages, prior to treatment,
performance status, FIGO classification,
differentiation grade, size of the residual
tumor, presence or absence of ascites, and cell
type all influence the survival outcome.

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