Chapter 50: Anexal Masses - Ovarian and Adnexal Disease Flashcards

1
Q

Define the adnexal space

A
  • Adnexal space: Area between the uterine cornu and lateral pelvic wall. Contains the ovaries, fallopian tubes, and upper broad ligament and mesosalpinx and remnants of the mullerian duct. Most commonly affected are ovaries and fallopian tubes
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2
Q

At what ages are the ovaries palpable?

A
  • Premenarchal ovaries should not be palpable
  • Reproductive group – ovaries palpable about half the time
  • Postmenopausal - Less responsive to gonadotropin, leading to surface follicular activity diminishment = non palpable within 3 years of normal menopause
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3
Q

Malignant potential of palpable ovaries in post menopausal women

A

o Take palpable ovaries in a postmenopausal woman seriously

o 1/4 will be malignant in this group, whereas only 10% in reproductive age women will be palpable

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4
Q

Etiology and presentation of a follicular cyst

A

When ovarian follicle fails to rupture, causing build up of hormone and enlargement. Only significant if it is large enough to cause pain or if it persists beyond one menstrual cycle. We are not sure why but the granulosa cells lining the cyst persist through the time when ovulation should have occurred and continue to enlarge in the second half of the cycle. Due to the thick layer, they sometimes won’t rupture. Can lead to amenorrhea and strange cycles due to the amount of estradiol, causing overstimulation of the endometrium

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5
Q

Imaging for follicular cyst?

A

o Imaging: US often warranted in reproductive age women with a cyst larger than 5cm.

We worry with the following findings: Thick septations, soft tissue elements, evidence of internal or external excrescences, and papillations

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6
Q

How long do follicular cysts last?

A

o Resolution: Most go away in 6 weeks. If not, consider something else.
 If contraceptive given, it won’t shrink what you got, but can prevent further development

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7
Q

Rupture of follicular cyst

A

o Rupture: Causes pelvic pain and transient symptoms due to spillage of fluid into the cavity with hormones in it. Intervention not indicated since symptoms are transient

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8
Q

What are corpus luteul cysts?

A

o The other common type of functional ovarian cyst. Basically just the corpus luteum that has grown beyond 3cm. Related to the post-ovulatory (progesterone dominant) phase of the menstrual cycle

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9
Q

There are two variations of the corpus luteum cysts. One that is enlarged beyond the normal 14 days of having a corpus luteum and one that is larger during the later portion of the luteal phase.

Discuss the first variant, the one that just lasts a long time

A

Enlarged corpus luteum that continues to produce progesterone beyond the 14 days.
• Delayed menstruation from a few days to a few weeks, although usually just 2 weeks of the missed period. Dull achy persistent ipsilateral pelvic pain also present. Enlarged adnexa on Pelvic Exam.
• This triad is also seen in ectopic so keep on the differential

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10
Q

There are two variations of the corpus luteum cysts. One that is enlarged beyond the normal 14 days of having a corpus luteum and one that is larger during the later portion of the luteal phase.

Discuss the second variant, the one that we see late in the luteal phase

A
  • Spontaneous hemorrhage with rupture in the luteal phase. Pt typically is not using oral contraceptives, has normal periods, with a sudden sharp pain late in the luteal phase.
  • Surgery indicated with hemiperitoneum or hypovolemia. Otherwise, expectant management with pain control.
  • At risk: Anticoagulation and clotting disorders
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11
Q

The last of the three functional ovarian cysts, theca lutein, presents how?

A

o Least common of the three. Associated with pregnancy. Usually bilateral, most commonly due to multiple gestations, trophoblastic disease, and ovulation that has been induced by clomiphine and hCG.
o Tend to regress spontaneously, but can get large and multicystic

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12
Q

Benign ovarian neoplasms are not in themselves malignant. How often do they become cancerous and when do we detect them?

A

Most cysts are functional, but about 25% can be benign masses with no functional component.

90% are benign in reproductive age group, with 25% malignant when including the post menopausal group

Due to no functional component usually, we only detect on physical exam or when they are large enough to cause a mass effect

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13
Q

Three types of benign ovarian neoplasms

A

o Three types: Epithelial cell, germ cell, and stromal cell

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14
Q

Let’s start with the epithelial based benign ovarian neoplasm. It also has three subtypes, which are:

A

Most common = Serous cystadenoma

2nd most common = Mucinous cystadenoma

Endometrioid (stupid really, essentially just uterine stuff)

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15
Q

How often are serous cystadenomas malignant potentially? How do we treat?

A

 70% are benign. 10% have intraepithelial cellular characteristics which suggest they are of low malignant potential. 20% are frankly malignant.
 High rate of becoming malignant = treat by surgical resection. In younger patient, consider preserving ovary.
 Increased risk of malignancy in contralateral ovary, so in older patients, take both ovaries and potentially the uterus as well

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16
Q

Presentation and treatment for the second most common benign ovarian tumor, mucinous cystadenoma. How often are they malignant?

A

 Malignancy rate of 15%
 Become large, potentially filling entire pelvic cavity
 US: Multilocular septations
 Surgery to treat

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17
Q

What is a Brenner Cell Tumor? Malignant potential?

A

 Uncommon benign epithelial tumor
 Solid ovarian tumor 2/2 large amount of stroma and fibrotic tissue surrounding the epithelial cells
 More common in older women. Sometimes occur in the setting of mucinous tumors of the ovary.
 Small, rarely malignant

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18
Q

The second subset of benign ovarian tumors, germ cell, are known for having what inside of them?

A

o Contain hair and bones and stuff
o Tissue from all 3 embryonic tissue layers. Most common ectodermal origin, primarily squamos cell tissue such as skin appendages (sweat sebaceous glands, hair follicles, sebum (dermoid stuff, hence the name). Others includeCNS, teeth, cartilage, intestines, etc.

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19
Q

Imaging of germ cel ltumors

A

o Imaging: CT shows high density fat, making it bouyant and often leading to ovarian torsion (15%)

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20
Q

Who gets these germ cell tumors and what is the most common type?

A

o Most common = Benign cystic teratoma AKA dermoid cyst AKA dermoid
o 80% during reproductive years, median age of 30 years

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21
Q

Treatment for germ cell tumors?

A

o Tx: Surgery, even though malignancy potential is

22
Q

The last of the three benign ovarian neoplasms, the stromal cells, come from what?

A

o Sex cord, solid tumors

o Female cell type = Granulosa theca cell, male tissue = sertoli leydig cell. Equal prevalence.

23
Q

Functional vs non functional stromal cell benign masses

A

“Functional” = make hormones
 Theca makes estrogen, causing feminization
 SL make androgenic components leading to hirsuitism and virilization

“Non functional”
 Ovarian fibroma - Result of collagen production by spindle cells. 4% of ovarian tumors, most common in middle age. Linked with ascites.

24
Q

Meigs syndrome?

A

• Benign ovarian fibroma coupled with ascites and right pleural effusion = Meigs syndrome

25
Q

Top 5 most common cancer related killers of women

A

lung, breast, colorectal, pancreatic

5th = ovarian

26
Q

Out of all gyn cancers, how bad is ovarian?

A

o Highest rate of mortality of all gynecological cancers 2/2 difficulty in detection.
 60% of the 25,000 found per year will die in 5 years.
 65-70% diagnosed in an advanced state when the 5 year survival rate is 20-30%

27
Q

Impact of genetics on ovarian cancers

A

 Genetics: 8-13% BRCA1 or 2. 5% risk with a first degree relative with ovarian carcinoma. 20-30% if you have two first degree relatives.

28
Q

Lynch syndrome impact on ovarian cancer

A

 Cancer: 13 fold increase seen in women with HNPCC (hereditary nonpolyposis colorectal cancer AKA Lynch syndrome)

29
Q

What is the most protective thing against ovarian cancer

A

 Protective: Long term suppression of ovulation (5 years) = 50% reduction lifetime risk

30
Q

What hormones are linked to ovarian cancers

A

 Hormones: NO evidence to support postmenopausal hormone therapy linked to this cancer.

31
Q

Sxs of ovarian cancer and what age we see them

A

 Sxs: Abdominal bloating or distension, abdominal or pelvic pain, decreased energy or lethargy, early satiety, urinary urgency.

Ages: 50-60s

32
Q

Risk factors of ovarian cancer besides age, genetics.

A

Nulliparity, infertility, endometriosis

33
Q

Why is ovarian cancer so lethal? The ovaries are so small…

A

 Spread primarily via direct extension within the peritoneal cavity as a result of direct cell sloughing from the ovarian surface. Can spread via blood and lymph, but they don’t really need to. We can see extensive disease even with a small precursor lesion on the ovary.

34
Q

How helpful is CA-125?

A
  • Elevated CA-125: pregnancy, PID, endometriomas, uterine leiomyomata, adenomyosis, even menstruation, cirrhosis, pleural effusion, peritoneal effusion.
  • Really only use it in post-menopausal women to indicate whether a mass may be benign or malignant
  • 50 % of early stage and 20-25% of late stage cancers associated with normal levels.
35
Q

Types of carcinomas and what they come from

A

 Serous cystedenomas –> SC’s with proliferating activity with nuclear abnormalities but no infiltrative growth (low potential malignancy) –> Serous cystadenocarcinoma

 Mucinous cystadenomas –> MC’s with proliferating activity with nuclear abnormalities but no infiltrative growth (low potential malignancy) –> Mucinous cystadenocarcinoma

 Endometrioid benign cyst –> EBC’s with proliferating activity with nuclear abnormalities but no infiltrative growth (low potential malignancy) –> Edometrioid carcinoma (essentially a uterine cancer, almost all are malignant)

 Adenocarcinoma

36
Q

How often are the ovarian cancers of the epithelial type? (mucinous/serous)

Why?

A

90% of all ovarian malignancies are of the epithelial cell type, derived from mesothelial cells, which directly overly the stroma. Every rupture of a follicle with ovulation causes metaplastic change, hence repeated ovulation being prognostic

37
Q

Where do we see serous tumors and what do we see on histology?

A

 Malignant epithelial serous tumors (serous cystadenocarcinoma) - 50% from benign precursors with 30% being bilateral.
 Multiloculated with external excrescences on an otherwise smooth capsular surface. Calcified laminated structures, psammoma bodies, are found in more than one half of serous carcinomas

38
Q

If we see a REAL BIG mass in there, we aren’t thinking serous ovarian cancer, we are thinking Mucinous. Talk about it

A

o Mucinous cystadenocarcinoma = 5%. Can be largest, measuring up to 20cm, not often bilateral.May be associated with widespread peritoneal extension with thick mucinous ascites, termed pseudomyxoma peritonei

39
Q

Breast/ovarian familial cancer syndrome and how often we see it linked to ovarian cancer

A

o Breast/ovarian familial cancer syndrome = BRCA1/2 = Cumulative life risk of 50-85% for breast cancer and 15-45% for ovarian cancer. 10x more likely to carry a gene if Ashkenazi Jew.

40
Q

Most common ovaran cancer in women younger than 20

A

Germ cell cancer

41
Q

When do we see the germ cell cancer Dysgerminoma?

A

o Dysgerminoma - Often seen in those with gonadal dysgenesis, usually unilateral, and arise from radiosensitive/chemosensitive gonadoblastomas.

42
Q

Treatment for ovarian cancer

A

 Tx with unilateral conservative resection with just that ovary and fallopian tube in young population with size

43
Q

Dysgerminoma survival rate

A

 5 year survival for only one ovary is 90-95%, very good prognosis

44
Q

What are immature teratomas and what do we do with em

A

o Immature teratomas - Malignant counterpart of benign cystic teratomas. Often found in women under 25, and while rare, are dangerous due to rapid growth, with early symptoms due to hemorrhage and necrosis. Due to this, 2/3 of the time it is found early. Remove affected ovary and treat with chemo, good turnout.

45
Q

Discuss the granulosa subtype of the gonadal stromal cancers

A

o Granulosa: Large amounts of estrogen, showing up as endomerial hyperplasia or endometrial carcinoma in older populations. 20-30% of recurrence so keep watching these folks after surgical management.

46
Q

Discuss how Sertoli-Leydig gonadal stromal cell tumors present

A

o Sertoli-Leydig (arrhenoblastoma) are rare testosterone-secreting counterparts to granulosa cell tumors. Suspect with adnexal mass, virilization, and hirsuitism

47
Q

What is a krukenburg tumor? What does it mean?

A
  • Krukenburg = Metastasis to the ovary from some other location like the GI tract or breast
    o Signet ring cell types. Often bilateral with widespread met disease
48
Q

How does a primary fallopian carcinoma present?

A

o Primary fallopian tube carcinoma is usually adenocarcinoma, and only represents less than 1% of gynecologic cancers. 2/3 are postmenopausal. Often large looking like a hydrosalpinx, unilateral.

Suspect with postmenopausal bleeding and vaginal discharge (hydrotubae profluens = serosanguinous discharge).

We see metastasis and ascites with this, just like with ovarian.

49
Q

Basic management of ovarian and fallopian tumors

A

o Begin with tumor debulking. he logic is that radiation and chemo are more effective when the mass is less than 1cm. Often seeds nearby organs, so debulking is usually extensive.

50
Q

Long ass procedure list for surgery in the case of ovarian and fallopian cancers

A

 Enter the abdomen, get peritoneal cytology.
 Gross ascites is aspirated and also sent for cytology.
 Wash the gut, send to cytology
 Inspect and palpate all surfaces
 Partial omentectomy to see if invasion is present
 Sample pelvic and periaortic lymph nodes
 If no gross disease, biopsy from anterior and posterior cul-de-sac, right and left pelvic walls, right and left pericolic gutters, and diaphragm
 After surgery, use chemotherapy (Taxol with carboplatin or cisplatin)
 If recurring, try something else like tamoxifen, 5-fluorouracil, doxorubicin, cyclophosphamide.
 Radiation therapy has limited role