Ovarian tumours

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Ovarian tumours

  1. 1. •www.doctor.sd
  2. 2. •www.doctor.sd Swellings of all kinds that involve the ovary.
  3. 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. •www.doctor.sd
  4. 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 •www.doctor.sd
  5. 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. •www.doctor.sd
  6. 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%. •www.doctor.sd
  7. 7. CLASSIFICATION  WHO (Serov et al 1973) – morphological, based on the relation of cell types of tmrs to tissues normally present in the ovary. •www.doctor.sd follicle surface epitheliumsurface epithelium Stroma (mesenchyme)
  8. 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 •www.doctor.sd
  9. 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 •www.doctor.sd
  10. 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. •www.doctor.sd
  11. 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. •www.doctor.sd
  12. 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. •www.doctor.sd

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