PATH 16 OVARY

• a) CYSTIC AND INFLAMMATORY LESIONS
• - are relatively common:  
• • Cysts are common, ID'd on ultrasound.
• • Polycystic Ovarian Syndrome is a clinic-pathological syndrome of obesity, androgenism, insulin resistance, anovulation, infertility.
• • Inflammatory:  Lesions are uncommon, secondary to abdomino-pelvic sepsis, PID, autoimmune.

• b) ENDOMETRIOSUS
• - common condition (10-15% of women) char'd by growth of tissue resembling endometrium beyond or outside the uterus.
• - Often involves pelvic peritoneum, ovaries, rectosigmoid colon, and rarely distant sites (eg. lung).
• - Pathology: multifactorial involving retrograde menstruation (flow of menstrual blood into the fallopian tubes), immune and genetic factors.
• Morphology: ovarian lesions are often cystic and haemorrhagic (‘chocolate cysts’)
• Clinical: present with pain (may be cyclical), effects of adhesions and infertility.
• Managed by hormonal treatment or surgery (severe cases). - Increased risk of neoplasia (1-2%).

(70%) derived from mesothelium covering ovaries which is constantly scarred during ovulation.

Further divided into three categories each with various histological subtypes.

Overall, serous subtype tumours are the most common, others include mucinous, endometrioid etc.

Benign Tumours (serous/cyst adenomas) are characterised by a single layer of columnar epithelium that lines the cyst or cysts. Can have accompanying stromal component.

• Borderline Tumours (borderline serous tumours) mainly include serous or mucinous types.
• Epithelial proliferation and atypia but no destructive tissue invasion.
• Generally excellent prognosis.

Serous types: 30-40% have extraovarian ‘implants’, late recurrence/progression may occur

Malignant Tumours (serous/cyst adenocarcinoma) most ovarian malignancies are of epithelial type, hence ‘malignant surface tumours’ is used synonymously with ‘ovarian cancer’.

Ovarian carcinomas usu high grade, poor prog at later stages (most are detected late).

• Pathology: the progression is debated, and precursor lesions generally aren’t identified or accessible for sampling. There is a proposed ‘dual model’ describing the pathogenesis of ovarian cancer; types 1 and 2, each associated with different mutations.
• Type 1:  mainly low grade carcinomas arising in precursor lesions (endometriosis, benign or borderline tumours).
•  Type 2: high grade carcinomas probably arising from ovarian surface epithelium or fallopian tubes.

Cause: not known, but risk factors include multiple ovulation, environmental and hereditary factors. Hereditary ovarian cancer (10-15% cases) mainly associated with BRCA 1 (usually high Serous Cystadenocarcinoma)

Clinical: patients present as they would w most ovarian tumours, except in later stages when metastases occur.

Spread: mainly intraabdominal, paraaortic nodes, distant (liver, lung etc).

• Dx:
• clinical,
• radiology (ultrasound, CT),
• serology (serum CA125)
• or surgical.

Prog: depends mostly on stage, also grade, subtype, and response to therapy.

Screening: not yet established but could involve clinical examination, serum CA125 and ultrasound.

• Stage 1: confined to ovaries.
• Stage 2: spread to pelvis.
• Stage 3: spread to extrapelvic peritoneum, lymph nodes or bowel wall.
• Stage 4: distant metastases.

NB: most are detected in advanced stages.

• (20%)
• Often occur in kids/young adults, usu benign with mixed
• differentiation.

Mature Cystic Teratoma are most common, benign dermoid cysts (recognisable dermis).

• Malignant tumours are rare, with various types
• Often radio/chemosensitive with good prognosis.
• Tumour markers (AFP, HCG).

 (5-10%)  relatively uncommon stromal tumours that are mostly benign.

Thecoma-fibroma consist of solid grey fibrous cells to yellow (lipid laden) thecal cells.

• Granulosa-thecal cell tumours consist of granulosa and thecal cells with cystic spaces.
• - 3-5% of ovarian malignancies, usually post menopausal. Often with oestrogenic release (can lead to endometrial/breast cancer).
• - Late metastases common.

• Sertoli-Leydig cell tumours (androblastomas) result in androgen production and virilism.
• - Many are low grade (granulosa and sertoli tumours) and may present with effects of hormone secretion.

Clinical presentation of all ovarian tumours is similar despite their morphological diversity

Usually asymptmtic until large enough to cause local pressure problems.

-Exception: functioning neoplasms with hormonal effects (eg. granulosa-thecal tumour).

• Patients can present with:
• palpable abdominal/pelvic mass,
• abdominal swelling (tumour, ascites),
• GIT symptoms (diarrhoea, constipation),
• vascular obstruction (DVT, oedema)
• or distant metastases.

NB: although germ cell/stromal cell tumours make up around 30% of tumours, they are only responsible for <10% of malignant tumours as most are benign.

(5%)

Can be difficult to distinguish from a primary ovarian carcinoma histologically.

Primary sites include colorectal, appendix, stomach, pancreas, endometrium, breast etc.

Krukenberg Tumour a secondary ovarian malignancy with primary site from the GIT (gastric origin most common).

Metastatic carcinoma, usually bilateral with mucin producing signet ring cells. Prominent reactive stromal proliferation.

"Fail-lopianed the TEST"

• Tumours of Fallopian tube
• Ectopic Preg
• Salpingitis
• Tumours of Peritoneum

Usu due to ascending infxn of the genital tract.

Can be acute or chronic with variable microbiology.

Inflammatory infiltrate and fibrosis can lead to serosal adhesions distorting the fallopian tubes → adhesions can cause hydrosalpinx, due to obstruction → infertility.

• Very common (1/80)
• Fallopian tubes being the most common site.  

• Signs/symptoms:
• pain,
• post vaginal bleed,
• positive pregnancy test.

Increased risk with tubule abnormality (salpingitis, endometriosis)

• Dx- ultrasound.
• May be surgical emergency due to acute bleeding into peritoneal cavity.

• Uncommon, malignancies rarer
• Incidence depends on definition.

Some ovarian and peritoneal carcinomas may arise in the fallopian tube (and perhaps previous ovarian primaries are instead secondary to fallopian carcinoma).

• Increased risk with BRCA 1 patients.
• Usu serous carcinomas, may spread even when in-situ

Most are metastatic (GI, biliary, cervical, uterus etc) 

Primary malignancies include mesotheliomas and carcinomas.

Most primary carcinomas are high grade serous carcinomas (similar appearance, behaviour and treatment similar to ovarian serous carcinoma).

Diagnosis of exclusion, increased risk in BRCA 1 mutation