Ovarian Cancer Flashcards

1
Q

Incidence of ovarian cancer

A

The second most common gynaecological malignancy (sixth most common cancer in women- lifetime risk of 1.4%.) Ovarian cancer is more common in White women than Asian or Black women.

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2
Q

Types of ovarian cnacer

A

Epithelial carcinomas account for around 90% of primary ovarian cancers
* Most arise from the ovarian surface epithelium and the distal fallopian tube. Primary ovarian-type tumours may also develop within the peritoneum
* Classification divides ovarian tumours into: serous, mucinous, endometrioid, clear cell, transitional cell and squamous.
* Tumours can benign, malignant and intermediate.

Non-epithelial cancers account for the remaining 10% of ovarian cancers
* These include germ cell tumours, sex cord and stromal tumours, neuroendocrine tumours, SCC arising within a teratoma etc.

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3
Q

Where do secondary ovarian tumours generally arise from, where might they spread to

A
  • Secondary tumours generally arise from: endometrium, breast, GI tract, cervix
  • Ovarian cancer may spread to: liver, intraperitoneal structure, para-aortic lymph nodes, the lungs
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4
Q

Risk factors for ovarian cancer

A
  • Increasing age (incidence increases with age and peaks in the 8th decade)
  • Genetic factors (FHx- 2.7-3.5x increased risk, BRCA1 and BRCA2 (TSG) gene mutations)- BRCA1 more commonly than BRCA2
  • Lynch syndrome- hereditary non-polyposis colorectal cancer
  • Nulliparity, early menarche and late menopause (increased ovulatory cycles)
  • IVF
  • Use of HRT (both oestrogen-only and combined HRT)
  • PMH of cancer, endometriosis, PCOS
  • Lifestyle factors including tobacco smoking, being overweight and oesity, occupational exposure to asbestos
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5
Q

What are some protective factors against ovarian cancer

A

(conditions that decrease the number of ovulatory cycles)- An increasing number of pregnancies, breastfeeding, use of COCP, early menopause tubal ligation, prophylactic oophorectomy

  • When you ovulate, the epithelial lining of the ovary is damaged and hence cell division occurs to repair this damage (risk of dysplasia)
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6
Q

Classifications of epithelial ovarian tumours

A

Borderline- Malignant histological features are present but not invasive
* May become malignant so surgery is advised
* In younger women- close observation may be offered following removal of the cyst or unaffected ovary to preserve fertility
* Recurrence can occur up to 20 years later

Serous cystadenoma- adenocarcinoma, most common malignant ovarian neoplasm accounting for 50% of malignancies. Have ‘fluid filled cyst’- typically a single cyst. Benign serous tumours are called serous cystadenomas, whereas malignant ones are called serous cystadenocarcinomas.
* Classed as high grade or low grade
* Often contain psammoma bodies

Mucinous cystadenoma- adenocarcinoma accounting for around 3% of ovarian malignancies- can become very large and abdominal cavity fills with gelatinous mucin secretions (‘pseudomyxoma peritonei’)

Endometrioid carcinoma- 10% of ovarian cancer which are similar histologically to endometrial cancer- ectopic, has a poor prognosis.
* Often have cysts that are filled with dark blood

Transitional- also called Brenner tumours. Made up of transitional cells which are usually found in the lining of the bladder.
* Histology shows ‘coffee bean nuclei’

Clear cell carcinoma- malignant variant that accounts for 10% of ovarian malignancies

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7
Q

What are germ cell tumous. How can they be classified

A

Undifferentiated primordial germ cells of gonad and present in young, premenopausal women.

Teratoma (dermoid cyst)- common (15-20% of germ cell tumours) and benign
* Contains fully differentiated tissue of all cell lines (commonly hair and teeth)
* Commonly bilateral and asymptomatic (rupture is painful)
* Requires surgical removal
* The inner lining contains single or multiple white shiny masses projecting from the wall towards the centre of the cysts- ROKATANSKY PROTUBERENCE
* A malignant form, the solid teratoma, also occurs in this age group but is rare
* ‘Immature teratomas’ can develop from neuroectoderm cells (ectoderm layer) and may be malignant and metastasise quickly

Yolk sac tumour- highly malignant and present in young women/ children
* Made up of germ cells that differentiate into yolk sac tissue- secrete alpha-fetoprotein.
* Large solid tumours- can be very aggressive
* On histology contain ’Schiller-Duval’ bodies

Dysgerminoma- female equivalent of a seminoma- most common malignancy in younger women and sensitive to radiotherapy
* Made up of germ cells that turn into oocytes as normal but the start to grow uncontrollably (50% of germ cell tumours)- bilateral in 20%.
* Histologically have a central nuclei surrounded by clear cytoplasm

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8
Q

What are sex cord tumours, how are they categorised

A

Tumour which arises from the stroma of the gonads (cells which hold the ovaries together and produce female hormones). Mainly occurs in young pre-menopausal or post-menopausal women.

Granulosa cell tumour- rare, malignant but slow growing (generally occurs in post-menopausal women), secretes oestrogens and inhibin
* Stimulates the endometrium, leading to PMB, endometrial hyperplasia and precocious puberty
* Serum inhibin is used as a biomarker
* Histology will show ‘Call-Exner bodies’

Thecoma- benign, rare, secretes androgens and oestrogens

Fibroma- rare and benign.
* Made up of fibroblasts- looks like thin needle strands with elongated nuclei on histology
* Often seen in conjunction with Meig’s syndrome (ascites and right pleural effusion), cured by mass removal

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9
Q

Presentation of ovarian cancer

A
  • May have vague or absent symptoms (70% present in stages 3-4)
  • Should suspect ovarian cancer in any woman (particularly over the age of 50) if they have any of the following symptoms persistently or frequently (particularly more than 12 times per month)
    o Abdominal distension (bloating)
    o Feeling full (early satiety) and/or loss of appetite
    o Pelvic or abdominal pain
    o Increased urinary urgency and/or frequency
  • Should also be considered in any woman over 50 if she has symptoms suggestive of IBS
  • Other unexplained symptoms:
    o Weight loss
    o Malaise or fatigue
    o Change in bowel habit
    o Abnormal or postmenopausal bleeding, GI symptoms (dyspepsia, nausea, bowel obstruction), SOB
  • Ovarian adenocarcinomas spread directly within the pelvis and abdomen- transcoelomic spread. Can also be lymphatic and blood-borne spread
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10
Q

What are some causes of a raised serum CA125

A

Peritoneal trauma, disease or irrigation, endometriosis, PID, ovarian cyst torsion, rupture, haemorrhage, pregnancy

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11
Q

Differentials for ovarian cancer

A
  • Other cancers including cancer of the cervix, uterus, rectum and bladder
  • Other causes of abdominal distension and bloating- uterine fibroids, ascites, adenomyosis and altered bowel habit (IBD, constipation coeliac, IBS, infection)
  • Other causes of early satiety including gastric cancer
  • Urinary conditions causing frequency of urgency or frequency
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12
Q

Investigations for ovarian cancer

A
  • Abdominal and pelvic examination: If there is ascites, or a pelvic or abdominal mass (which is not caused by known uterine fibroids), refer the woman urgently to gynaecology (2-week-wait)
  • Serum CA125 (present in 80%of women with epithelial ovarian cancer): If serum CA125 concentration is raised (35 IU/mL or greater), arrange an urgent ultrasound scan of the abdomen and- If USS is suggestive of ovarian cancer refer to gynaecology on a 2-week-wait

Establishing the diagnosis in secondary care:
* Ca125 + TVUSS
* Women under 40: measure AFP and hCG (both raised in germ cell tumours)- may also use LDH and CEA
* Calculate the Risk of malignancy index (RMI):
- U x M x Ca125 level
- U= USS score- 1 point for each of the following (1-1 feature, 2- 2 or more features) Multilocular cysts , solid areas, metastases, ascites bilateral esions
- M= Menopausal status (1-pre, 2-post)
- Should refer all women with an RMI >250 to a specialist MDT

CT Abdo-pelvis should be performed for initial assessment of extent of disease
MDT should be involved in complex cases

Other investigations include: imaging guided biopsy, exploratory laparoscopy/ laparotomy, ascitic tap for cytology

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13
Q

How can ovarian cancer be staged

A
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14
Q

How can ovarian cancer be prevented

A
  • Women who are positive for BRCA mutations are offered prophylactic bilateral salpingo-oophorectomy (BSO) when they have completed their families- reduces he risk of ovarian cancer by 90%
  • May also do a salpingectomy with delayed oophorectomy (offsets morbidity associated with early menopause)
  • Tubal ligations and hysterectomy can also reduce ovarian cancer risk
  • COCP reduces ovarian cancer risk by up to 50% in both BRCA mutation carriers and women at average risk of ovarian cancer
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15
Q

What is optimal surgical staging

A
  • Involves midline laparotomy to allow thorough assessment of the abdomen and pelvis
  • Total abdominal hysterectomy, bilateral salphingo-oophorectomy and infracolic omentectomy (if fertility needs to be preserved only the affected ovary may be removed- only possible in 1a)
  • Biopsies of any peritoneal deposits
  • Random biopsies of the pelvic and abdominal peritoneum
  • Retroperitoneal lymph node assessment- Should do systemic retroperitoneal lymphadenectomy where cancer is not confined to the ovaries
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16
Q

How is ovarian cancer managed

A
  • Optimal surgical staging is the mainstay of treatment at all stages of disease
  • DO NOT offer adjuvant chemotherapy to women how have had optimal surgical staging and have low-risk stage 1 disease
  • Offer women with high-risk stage 1 disease (1c and above) adjuvant chemotherapy consisting of 6 cycles of carboplatin

Stage 2-4: Debulking surgery to remove as much of tumour as possible + carboplatin or cisplatin alone or combination with paclitaxel (most effective)
* Platinum compounds cross-link DNA leading to cell-cycle arrest (doses calculated according to GFR)
* Paclitaxel prevents replication and cell division- given with sterouds to reduce SEs
* Most are given as an outpatient, 3 weeks apart for 6 cycles
* 2/3 of women whose tumours initially respond to first-line chemo will relapse within 2 years of completing tx
* Bevacizumab is a monoclonal antibody which may be used though not routinely prescribed (available for treatment of recurrent disease)
* In stage 4 palliative care is more likely

17
Q

How should ovarian cancer be followed up

A

CT scan and CA125 should be followed up after treatment

Poor prognostic indicators
* Advanced stage
* Poorly differentiated tumours
* Slow or poor response to chemotherapy
* Death due to bowel obstruction or perforation

18
Q

How can patients with ovarian cancerbe managed symptomatically

A

Pain
* Analgesic ladder
* Co-analgesics = antidepressants, steroids and cytotoxics
* Opioid analgesia can be patient-controlled and usually accompanied by anti-emetics
* Alternative therapies e.g. acupuncture also used

Nausea and vomiting
* 60% patients with advanced carcinoma
* Due to opiates, metabolic causes (uraemia), vagal stimulation or psychological factors
* Antiemetics include anticholinergics, antihistamines, dopamine antagonists of 5HT-3 antagonists

Heavy vaginal bleeding
* High dose progestogens
* Radiotherapy if not already used

Ascites – drained by repeated paracentesis

Mx of obstruction at home – 1/3 spontaneous resolution
* Metoclopramide used if partial obstruction
* Can use dexamethasone for tissue oedema
* Complete obstruction: cyclizine and ondansetron for N&V, with hyoscine for spasm