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Ovarian tumours

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  • 1.
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  • 2. Swellings of all kinds that involve the ovary.
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  • 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);
    • Parity : Smoothly decreasing risk of Ca ovary with increasing parity.
    • Oral contraceptives: protective role is evident even for ten yrs after stopping them.
    • Years of ovulation : Fathalla’s hypothesis- active ovulation time increases the risk.
    • Other environmental factors : Alcohol and tobacco, coffee – have weak evidence.
    • 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 epithelium surface 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
    • History; [a] 2/3 present too late, [b] poor prognosis, [c] 5-yr survival is ~ 25%.
    • 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 .
    • 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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