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Ovarian cancer

SNOMED: 762997004885 wordsUpdated 03/03/2026
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Exam Tips

  • In UK exams, persistent/frequent bloating, early satiety, pelvic pain, or urinary urgency (especially in women >50) should trigger CA125 then pelvic ultrasound in primary care.
  • A new IBS-type presentation after age 50 is a red flag; IBS rarely first presents at this age.
  • CA125 is helpful but non-specific: list benign causes (endometriosis, PID, pregnancy, heart failure) and malignant non-ovarian causes.
  • State the dominant spread pattern as transcoelomic peritoneal seeding (explains ascites/omental disease); see figure of peritoneal dissemination pathways in standard gynae-oncology atlases.
  • Management marks are gained by mentioning specialist MDT care, cytoreductive surgery goal (no macroscopic residual disease), platinum-based chemotherapy, and biomarker-led PARP maintenance.

Definition

Ovarian cancer is a malignant neoplasm arising from ovarian or related Mullerian epithelium, with most primary cases being epithelial and high-grade serous subtype predominating. Many so-called ovarian high-grade serous cancers are now understood to begin in the distal fallopian tube (fimbrial epithelium) and then involve the ovary/peritoneum, with spread commonly occurring throughout the peritoneal cavity before distant metastasis.

Pathophysiology

Most UK cases are epithelial cancers, especially high-grade serous carcinoma, often linked to TP53 mutation and homologous recombination deficiency (for example BRCA1/BRCA2 pathway dysfunction). Malignant cells exfoliate into peritoneal fluid and seed peritoneal surfaces (transcoelomic spread), classically involving omentum, bowel serosa, and diaphragm, which explains ascites, bloating, early satiety, and bowel obstruction in advanced disease. Lymphatic spread to pelvic/para-aortic nodes and haematogenous spread to liver/lung can occur. Non-epithelial tumours (germ cell, sex-cord stromal) are less common but important in younger patients.

Risk Factors

  • Increasing age (incidence rises with age; peak in later life)
  • BRCA1/BRCA2 pathogenic variants and hereditary cancer syndromes (including Lynch-associated families)
  • First-degree family history of ovarian or breast cancer
  • Nulliparity, early menarche, late menopause (greater lifetime ovulatory cycles)
  • Endometriosis (notably linked with endometrioid and clear-cell histotypes)
  • Hormone replacement therapy (small increased risk with both oestrogen-only and combined regimens)
  • Personal history of breast, bowel, or ovarian cancer
  • Obesity, tobacco smoking, and possible asbestos exposure
  • Diabetes (especially insulin-treated)

Clinical Features

Symptoms

  • Persistent abdominal distension/bloating (often >12 times per month)
  • Early satiety and reduced appetite
  • Pelvic or abdominal pain
  • Urinary urgency and frequency
  • Unexplained weight loss, fatigue, or malaise
  • Change in bowel habit (including new IBS-type symptoms in women >50 years)
  • Dyspepsia, nausea, or symptoms of bowel obstruction in advanced disease
  • Breathlessness from pleural effusion
  • Abnormal or postmenopausal bleeding can coexist

Signs

  • Abdominal or adnexal/pelvic mass
  • Ascites with abdominal fullness/shifting dullness
  • Pleural effusion signs (reduced breath sounds, stony dullness)
  • Cachexia or unintentional weight loss
  • Features of bowel obstruction in late-stage disease

Investigations

Serum CA125:Often elevated in epithelial ovarian cancer; normal result does not exclude disease, and raised levels are non-specific (for example endometriosis, PID, pregnancy, heart failure, other cancers).
Transvaginal/transabdominal pelvic ultrasound:Complex adnexal mass, multilocularity, solid components, papillary projections, bilateral lesions, ascites, or peritoneal nodularity suggest malignancy.
CT chest/abdomen/pelvis (staging):Defines disease extent: omental caking, peritoneal deposits, nodal disease, liver/lung/pleural involvement; guides operability and MDT planning.
Histology from surgical specimen or image-guided biopsy:Confirms diagnosis and subtype (serous, mucinous, endometrioid, clear cell, etc.) and enables molecular profiling.
Genetic testing (germline +/- somatic BRCA and homologous recombination deficiency assessment):Identifies hereditary risk and predicts suitability for PARP inhibitor maintenance.
Baseline pre-treatment bloods (FBC, U&E, LFTs, clotting profile):Assesses fitness for surgery/chemotherapy and detects complications such as anaemia, renal or hepatic dysfunction.

Management

Lifestyle Modifications

  • Urgent referral via suspected cancer pathway and management through a specialist gynaecological oncology MDT
  • Smoking cessation, weight optimisation, nutritional support, and physical activity within tolerance
  • Early symptom control and palliative care input where disease is advanced
  • Genetic counselling for patients and at-risk relatives when hereditary disease is suspected

Pharmacological Treatment

Platinum-taxane chemotherapy (first-line systemic therapy)

  • Carboplatin (dose by Calvert formula, commonly AUC 5-6 IV every 3 weeks)
  • Paclitaxel 175 mg/m2 IV every 3 weeks

Standard first-line regimen in many epithelial cases, neoadjuvant or adjuvant depending on resectability. Monitor FBC, renal function, and neuropathy; major risks include myelosuppression, hypersensitivity, and peripheral neuropathy.

Anti-angiogenic therapy

  • Bevacizumab 15 mg/kg IV every 3 weeks (with chemotherapy and/or maintenance in selected advanced disease)

Avoid or use extreme caution with uncontrolled hypertension, recent major bleeding, poor wound healing, GI perforation risk, or significant proteinuria; monitor BP and urine protein.

PARP inhibitor maintenance (biomarker-directed)

  • Olaparib 300 mg orally twice daily
  • Niraparib 300 mg orally once daily (or 200 mg once daily if lower body weight/platelets per protocol)

Used after response to platinum in appropriate BRCA/HRD contexts. Safety: monitor FBC regularly (anaemia, thrombocytopenia, neutropenia), blood pressure (niraparib), renal/hepatic function, and rare MDS/AML risk; adjust for interactions and organ impairment.

Supportive medicines during treatment

  • Ondansetron 8 mg orally twice daily for chemotherapy-induced nausea/vomiting prophylaxis
  • Dexamethasone 8 mg orally/IV pre-chemotherapy and short course after chemotherapy as antiemetic adjunct
  • Low molecular weight heparin prophylaxis (for example dalteparin 5000 units SC once daily in high VTE-risk inpatients, if no contraindication)

Tailor antiemetic and thromboprophylaxis plans to regimen and patient risk. Check contraindications: active bleeding, severe thrombocytopenia, uncontrolled infection, or steroid-related complications.

Surgical / Interventional

  • Primary cytoreductive (debulking) surgery aiming for no macroscopic residual disease
  • Typical procedures include total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy, peritoneal biopsies/washings, and nodal assessment as indicated
  • Interval debulking surgery after neoadjuvant chemotherapy when primary complete resection is not initially feasible
  • Fertility-sparing surgery may be considered in selected early-stage unilateral non-epithelial or low-risk epithelial cases after specialist counselling

Complications

  • Malignant ascites and recurrent pleural effusions
  • Bowel obstruction from peritoneal carcinomatosis
  • Cancer cachexia and malnutrition
  • Venous thromboembolism (high baseline and treatment-related risk)
  • Progressive metastatic disease to liver, lymph nodes, and lung
  • Treatment complications: neutropenic sepsis, neuropathy, renal toxicity, hypertension/proteinuria, and therapy-related marrow disorders (rare)

Prognosis

Outcome is strongly stage-dependent at diagnosis. Early-stage disease has markedly better survival than advanced-stage disease; UK data show very high 1-year and 5-year survival in stage I compared with major decline by stage IV. Many patients still present at stage III/IV, but survival has improved over recent decades with better surgery, systemic therapy, and maintenance strategies.

Sources & References

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