30. Ovarian and Fallopian tube Tumors Flashcards

1
Q

Second most common cancer of the female genital tract… responsible for over 50% of deaths from cancer of the female genital tract

A

Ovarian cancer

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2
Q

Pathogenesis

A

Tumors of the ovaries are associated with one of the three distinct components of the ovary:

  • surface epithelium
  • ovarian germ cells OR
  • ovarian stroma
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3
Q

Over 65% of all ovarian tumors and 90% of all ovarian cancers​ are what kind of tumors?

Krukenberg tumors?

A

Epithelial tumors on the ovary capsule

About 5-10% of ovarian cancer is metastatic from other primary tumors in the body… usually the GI tract, known as Krukenberg tumors, or the breast and endometrium

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4
Q

Pathogenesis:

How does ovarian cancer spread? (4)

A

Primarily by direct exfoliation of malignant cells from the ovaries

As a result, the sites of mets often follow the broad circulatory path of the peritoneal fluid

Lymphatic spread can also occur, most commonly to the retroperitoneal pelvic and para-aortic lymph nodes.

Hematogenous spread = responsible for more rare and distant mets to lung and brain

In advanced disease, intraperitoneal tumor spread leads to accumulation of ascites in the abdomen and encasement of the bowel with tumor. This results in intermittent bowel obstruction known as carcinomatous ileus. In many cases, this progression results in malnutrition, slow starvation, cachexia, and death.

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5
Q

Pathogenesis:

Cause of ovarian cancer?

A

Unclear but believed to result from malignant transformation of ovarian tissue after prolonged periods of chronic uninterrupted ovulation

Ovulation disrupts the epithelium of the ovary and activates the cellular repair mechanism. When ovulation occurs for long periods w/o interruption, this mech is believed to provide the opportunity for somatic gene deletions and mutations during the cellular repair process.

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6
Q

Pathogenesis:

Familial component?

A
  • 10-15% of women with ovarian cancer have familial cancer syndrome
  • Pts with mutations in BRCA1 gene have 85% chance of developing breast cancer and 30-50% chance of developing ovarian cancer
  • Smaller proportion of patients with BRCA2 gene mutations (25%) also have inc. risk of ovarian cancer
  • Pts with Lynch II syndrome (HNPCC) have high rate of familial breast, ovarian, colon, and endometrial cancer
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7
Q

Classification of various ovarian neoplasms (benign, borderline, malignant)

A
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8
Q

Risk Factors and Protective Factors for Ovarian Cancer

A
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9
Q

Symptoms of Ovarian Cancer

A
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10
Q

Evaluation of Pelvic and Abdominal Masses found on physical exam

U/S findings in patients with a pelvic mass

A
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11
Q

Epithelial Tumors

Pathogenesis

A

Derived from malignant transformation of the epithelium cells of the surface of the ovary

These cells come from the primitive mesoderm and are capable of undergoing metaplasia.

Six primary types = serous, mucinous, endometrial, clear cell, Brenner, and undifferentiated.

The neoplasms in this group range in malignant portential from benign to borderline (tumors of low malignant potential) to malignant. Serous cystadenocarcinomas = most malignant epithelial cell tumors

Malignant epithelial tumors extend from the capsule of the ovary to seed the peritoneal cavity. In more than 75% of patients, tumors have spread beyond the ovary at the time of dx; thus the prognosis is v poor.

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12
Q

When ovarian cancer metastasizes to umbilicus, it is known as…

A

Mary Joseph nodule

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13
Q

Most common type of epithelial ovarian tumor?

A

Serous tumors (serous cystadenocarcinomas) = large, cystic, and bilateral 65% of time

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14
Q

Staging of Ovarian Carcinoma

A
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15
Q

CA-125

A

Serum tumor marker is elevated in 80% of epithelial cell cancers

B/c CA-125 levels correlated with the progression and regression of these tumors, it has been useful in tracking the effect of treatment and recurrence of epithelial ovarian carcinoma

Its value as a screening tool for detection of ovarian cancer has not yet been established

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16
Q

Tx?

A

SURGERY including TAH-BSO, ementectomy, cytoreduction or “debulking”, and bilateral pelvic and para-aortic lymph node sampling

Goal of debulking = leave behind no visible tumors or tumor nodules no greater than 1 cm

After surgery, epithelial ovarian cancer is treated with combo chemotherapy, most commonly IV carboplatin and paclitaxel (Taxol) or docetaxel (Taxotere)

17
Q

Germ Cell Tumors

Classification

A
18
Q

Many germ cell tumors produce serum tumor markers that can be useful in the dx of a pelvic mass and in assessing a patient’s response to therapy.

What is one major difference between epithelial and germ cell tumors?

A

In contrast to epithelial tumors, most germ cell tumors grow rapidly, are limited to one ovary, and are at stage I at the time of dx.

The prognosis for germ cell tumors is therefore far better than that for epithelial tumors. In most cases, these tumors are considered curable.

19
Q

Most common ovarian malignancy in women less than 20 years of age

A

Germ cell tumors

20
Q

Clinical Manifestations:

Germ Cell Tumors

A

Unlike the slow-growing epithelial ovarian cancers, germ cell tumors grow rapidly and thus cause sx leading to earlier dx.

Most commonly, distension of the ovarian capsul from rapid growth, hemorrhage, and necrosis results in acute pelvic pain

pts may also complain of pressure sx on the bladder or rectum or pain from the rupture of the tumor

21
Q

Treatment: germ cell tumors

A

Benign such as mature teratomas –> ovarian cystectomy / oophorectomy

B/c most germ cell cancers are dx in the early stage and are rarely bilateral, surgery is typically unilateral salpingo-oophorectomy if fertility is desired

However, if childbearing is complete or if the cancer is bilateral, total abdominal hysterectomy and bilateral salpingo0oophorectomy (TAH/BSO) is required + surgical staging

22
Q

Treatment: germ cell tumors

chemotherapy indicated?

A

With the exception of stage Ia dysgerminomas and immature teratomas, all germ cell malignancies require multiagent chemotherapy after surgery

Bleomycin, etoposide, and cisplatin (BEP)

23
Q

Sex cord-stromal tumors

Pathogenesis

A

Originate from either the cells surrounding the oocyte (before the differentiation into male or female) or from the ovarian stroma

These tumors are low-grade malignancies, which can occur at any age. They are usually unilateral and rarely recur.

Granulosa-theca cells are low-grade malignancies and the most common (70%) type of tumor in this group. Sertoli-Leydig tumors are very rare.

Both granulosa-theca cell tumors and Sertoli-Leydig cell tumors = functional tumors b/c they are characterized by hormone production.

24
Q

Ovarian stroma can develop into an ovary or a testis. As a result, what do ovarian granulosa-theca cell tumors resemble and what do they produce?

What do you see microscopically?

A

Fetal ovaries… produce large amounts of estrogens

Microscopically, the granulosa cells have grooved “coffee-bean” nuclei, and the cells are arranged in small clusters around a central cavity (Call-Exner bodies)

25
Q

Sex Cord-Stromal Tumors:

Ovarian fibroma

Meigs syndrome

A

Derived from mature fibroblasts and, unlike the other sex cord-stromal tumors, is NOT a functioning tumor.

Occasionally, fibromas are associated with ascites. The triad of an ovarian tumor, ascites, and right hydrothorax = Meigs syndrome

26
Q

Sex Cord-Stromal Tumors:

Clinical Manifestations

A
  • Granulosa-theca cell tumors:
    • Often produce estradiol and inhibin A/B
    • Estrogen stimulation –> feminization, precocious puberty, menstrual irregularities, secondary amenorrhea, postmenopausal bleeding
    • Estrogen stimulation –> endometrial hyperplasia and/or endometrial cancer –> therefore, endometrial sampling is very important
  • Sertoli-Leydig cell tumors:
    • Produce androgens (testosterone, androstenedione) that can cause virilizing effects in 75% of patients, including breast atrophy, hirsutism, deepened voice, acne, clitoromegaly, and receding hairline
27
Q

Sex Cord-Stromal Tumors

Treatment

A

Low-grade lesions, unilateral, and do not often recur –> therefore, usual tx = unilateral salpingo-oophorectomy

28
Q

Cancer of the fallopian tubes

Pathogenesis

A

EXTREMELY RARE - comprising only 0.5% of all cancers of the female genital tract

Progression of these tumors is similar to that of ovarian cancers including wide peritoneal spread and ascites accumulation

Most are adenocarcinomas

29
Q

Fallopian tube cancer

Clinical manifestations: Latzko’s triad

Tx:

A

Typically asymptomatic and is usually diagnosed during pelvic surgery for other indications

Classic triad:

Profuse watery discharge, pelvic pain, and pelvic mass = Latzko’s triad

Although only seen in 15% of cases, considered pathognomonic for fallopian tube carcinoma

Tx: surgical staged… same as that of epithelial ovarian cancer (TAHBSO, omentectomy, cytoreduction, peritoneal cytologic studies, RPLN sampling) –> carboplatin + paclitaxel