This document discusses ovarian masses and cancer of the ovary. It covers the classification, symptoms, diagnosis and management of ovarian tumors. Ovarian masses can be cystic or solid, benign or malignant. The majority are epithelial in origin. Risk factors include early menarche, late menopause, years of ovulation and low parity. Diagnosis involves medical history, physical exam, tumor markers and imaging tests. Treatment consists of surgery along with chemotherapy and/or radiation depending on staging. The prognosis is poor since many cases are diagnosed at late stages.

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Swellings of all kinds that involve the ovary.

3. The adnexal mass could be:
 I] Functional cysts
 II]Inflammatory masses
 III]Endometriosis
 IV]Ectopic pregnancies
 V]Neoplastic
Differential diagnosis from:
I)Pedunculated uterine fibroids,2)Colonic
masses,3)Peritoneal or UT lesions.
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4. Ovarian masses are:
 Cystic, solid or partially cystic/solid
 Benign or malignant
 Unilocular or multilocular
 Having thick or thin septa
 Freely , strictly mobile or fixed
 Unilateral or bilateral.
 Functional or organic
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5. Aetiology & Epidemiology
 Aetiology is unknown
 Ca ovary is commoner in developed world
 Most ovarian tumours are epithelial in origin
 Incidence: rare at <35 yrs. Peak at 50-70 yrs
 Only 3% of ovarian Ca are seen at < 35 yrs.The vast
majority are non-epithelial [germ cell tmrs].
 Contributory factors ; 1) Early menarche
2) Late menopause
3) Years of ovulation
 Now, reproductive factors – like parity and the use of oral
contraceptives are considered most influential.
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6. Aetiology (continued);
1. Parity: Smoothly decreasing risk of Ca ovary with
increasing parity.
2. Oral contraceptives: protective role is evident even
for ten yrs after stopping them.
3. Years of ovulation: Fathalla’s hypothesis- active
ovulation time increases the risk.
4. Other environmental factors: Alcohol and tobacco,
coffee – have weak evidence.
5. Genetic factors: play an important role. First –
degree relative, having the disease under the age
of 50, the risk will increase by 6 – 10 fold. If > 2
relatives are affected the life-time risk rises to
40%.
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7. CLASSIFICATION
 WHO (Serov et al 1973) – morphological,
based on the relation of cell types of tmrs to
tissues normally present in the ovary.
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follicle
surface epitheliumsurface epithelium
Stroma
(mesenchyme)

8.  Classification(continued);
1]Epithelial: 85%
Serous 40% Epithelial tmrs;
Mucinous 10% Serous-- resemble endosalpinx
Endometiroid 20% Mucinous-- cervical
Clear cell(mesonephroid) 5% Endometrioid-- endometrium
Brenner Clear cell-- mesonephros
Mixed
Undifferentiated Ca
Unclassified
2]Sex cord gonadal{stromal}: 6%
Granulosa-theca cell
Sertoli-Leydig cell
Gynandroblastoma
3]Germ cell: 2%
Dysgerminoma
Yolk sac
Teratomas(immature & mature)
4]Others: 1%
lymphoma
5]Secondary( metastatic ) 6%
Breast, gastrointestinal, endometrial
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9. PATHOLOGY
 Epithelial:[1] Serous;*majority= cystic/solid
*bilaterality= 50-90%.Mrscly-papillary pattern
psammoma bodies(calcospherules) exist.
Mucinous;*multilocular,*largest (d-r = 25cm)
Endometrioid;*most-cystic,*often-unilocular,
*associated end.Ca in 15%.Clear cell;*thick-
Walled,*unilocular,*containing turbid brown
Fluid,*solid projections,*bilateral in 15%.
 Borderline tmrs: 10% -- nuclear atypia, mitotic
Activity, multilayering cells.No stromal invation
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10. MANAGEMENT
1. History; [a] 2/3 present too late, [b] poor prognosis, [c] 5-yr survival is ~
25%.
2. Metastasis; [a] direct-- to pelvic peritoneum + pelvic organs,to diaphragm
& omentum, to surfaces of bowel + liver.[b] lymphatic- via ovarian vessels
to renal & para-aortic region,via broad ligament to pelvic nodes, to neck
and groin. [c] blood – to liver and lung .
3. Clinical staging; is redefined by FIGO in 1889, by adding 3 substages to
stage III etc.
Stage I: Growth limited to ovaries ( Ia, Ib, Ic)
Stage II: Growth involving one or both ovaries (IIa,b,c)
+ pelvic extension.
Stage III: Growth involving one or both ovaries (IIIa,b,c)
+ extension outside the pelvis.
Stage IV: Growth involving one or both ovaries
+ distant metastasis.
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11. DIAGNOSIS
 Symptoms:1] Abd.pain & discomfort
2] Distension or feeling a lump
3] indigestion,urinary symptoms
4] weight loss and AUB.
 Examination: Feeling a pelviabdominal mass
Lymph-node enlargement
Ascites
 Investigations:1} Hb,grouping,urea & electrolytes liver function tests. 2}
Chest X-ray & barium enema. 3} IVU
 Imaging techniques: USS,CAT and MRI.
 Cytology:From pleural effusion or ascites. FNA from lymph nodes .
 Tumour markers: None of them is accurate;
1) CA 125 – rises in endometriosis,rapidly falls after chemotherapy.
2) CEA [carcinoembryonic antigen rises in mucinous cystadenoCa.
3) OCCA & OCA – tumour-associated a. :rises in both serous & mucinous.
 Screening: routine USS, colour Doppler, Serum CA 125, Family history.
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12. TREATMENT
 Surgery: the mainstay of both diagnosis and treatment.Vertical incision is
required. A sample of ascitic f. is taken.Exploration of omentum, bowels and
other organs. The therapeutic objective is to remove the tumour completely.
Cytoreduction to<1.5c may have the same prognosis.TAH+BSO+ Omentectomy
is advisable.
 Radiotherapy: is indicated in st.(I+II).In st.(III) – irradiation to the whole abdomen
& pelvis is needed.In st. (IV) radiotherapy is ineffective.
 Chemotherapy: plays major role ;
a) Stage Ia -------------- surgery alone.
b) Stage Ib–IIIa ------ Chemotherapy+ Radiotherapy.
c) > minimal residuum-------- Chemotherapy.
Single + combination therapy can be used: Alkylating agents --- ( Melphan,
Cyclophosphamide). Antimetabolites (5-fluorouracil, Methotrexate). Antibiotics
(Adriamycin).
 Other treatments: 1) Hormonal – Tamoxifen + LHRH agonists and others have
been used with little success. 2) Immunotherapy – has no proven benefit.
Combination of BCG (Bacille Calmette-Guerin) + alpha-interferon +
chemotherapy showed some encouraging results.
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