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Repro II - PATH (Tobin) > Lecture 8: Fallopian Tubes and Ovaries > Flashcards

Lecture 8: Fallopian Tubes and Ovaries Flashcards

1
Q

Most common etiologies underlying suppurative salpingitis?

A
  • N. gonorrhea = 60% of cases
  • C. trachomatis = remainder
  • More than one organism can be involved; any pyogenic organism
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2
Q

Tuberculosis salpingitis is an important cause of what in endemic countries; what are the main histo features of this disorder?

A
  • Infertility
  • Caseating granulomas + multinucleated giant cells + epitheliod macrophages
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3
Q

What are the most common primary lesions of the fallopian tubes (excluding endometriosis)?

A
  • Paratubal Cysts = small translucent cysts filled w/ clear, serous fluid
  • Hydatids of Morgagni = larger cysts found near the fimbriated end of the tube or in the broad ligaments; remnants of müllerian duct.
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4
Q

Which uncommon benign tumor may arise in the fallopian tube?

A

Adenomatoid tumor (mesotheliomas)

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5
Q

Which rare tumor of the fallopian tube may present as dominant tubal mass on pelvic examination or due to abnormal discharge, bleeding, and occasionally abnormal cells on Pap smear?

A

Primary Adenocarcinoma

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6
Q

In terms of the fallopian tubes what are the most common disorders you must consider?

A
  • Ectopic pregnancy
  • Endometriosis
  • Inflammatory disorders –> Salpingitis
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7
Q

What stage do most primary adenocarcinomas of the fallopian tube present at; what is the prognosis of these tumors?

A
  • 50% of the tumors are stage I at diagnosis
  • But nearly 40% of pt’s are dead within 5-years
  • Higher stage tumors pursue an even more aggressive course
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8
Q

New data has suggested that a subset of serous ovarian cancers actually arise from where?

A

Epithelium of the fallopian tube

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9
Q

What is the most common cause of an ovarian mass in a reproductive age female?

A

Cystic follicle –> originating from unrutured graafian follicles

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10
Q

What are the growth characteristics of cystic follicles and how does size dictate their classification?

A
  • Usually multiple and discovered incidentally; BENIGN
  • If >2/2.5 cm then called follicle cyst –> may be palpable or cause pelvic pain
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11
Q

What are cystic follicles and the larger follicle cysts filled with; how do they appear morphologically?

A
  • Filled with a clear, serous fluid
  • Lined by gray, glistening membrane
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12
Q

How common are luteal cysts and what is their gross appearance that distinguishes them from cystic follicles?

A
  • Present in the normal ovaries of reproductive age females
  • Lined w/ rim of bright yellow tissue containing luteinized granulosa cells
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13
Q

Polycystic ovarian syndrome (PCOS) is a complex endocrine disorder characterized by what findings clinically?

A
  • Hyperandrogenism - hirsutism, acne, deep voice, male pattern baldness
  • Menstrual irregularities - amenorrhea
  • Chronic anovulation
  • ↓ fertility
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14
Q

Due to increase in free estrone levels, women with PCOS are at an increased risk for what?

A

Endometrial hyperplasia and cancer

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15
Q

What underlying metabolic disorders are common in women with PCOS?

A
  • Obesity due to altered adipose tissue metabolism
  • T2DM due to insulin resistance
  • Premature atherosclerosis
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16
Q

Majority of ovarian tumors are (benign/malignant) and how does age play a role in this?

A
  • 80% are benign, typically occur in younger women btw 20-45 y/o
  • Malignant tumors often older women btw ages of 45-65 y/o
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17
Q

What are the risk factors associated with malignant serous carcinomas of the ovary?

A
  • Nulliparity (low parity) = never given birth
  • Family hx
  • Heritable mutations: BRCA1 and BRCA2
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18
Q

The distinction between low-grade (well-differentiated) and high-grade (moderate to poor differentiated) serous ovarian carcinoma is based on what and correlates with?

A

Degree of nuclear atypia; correlates with patient survival

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19
Q

Ovarian and endometrial serous tumors have what characteristic morphologic finding?

A

Psammoma bodies (concentric calcifications)

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20
Q

Which precursor lesion associated with sporadic high-grade serous ovarian cancer has been described as originating in the fallopian tube?

A

Serous tubal intraepithelial carcinoma (STIC)

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21
Q

Which cystic lesions of the ovary may be the origin of a vast majority of serous ovarian carcinomas?

A

Cortical inclusion cysts

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22
Q

How do the genetic mutations observed in low- vs. high-grade serous ovarian carcinomas differ?

A
  • Low-grade = mutations in KRAS, BRAF, or ERBB2;* withwild-type*TP53
  • High-grade = high frequency of TP53 mutations and lack mutations in either KRAS or BRAF.
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23
Q

What are the morphological features of benign serous ovarian tumors both grossly and microscopically?

A
  • Smooth glistening cyst wall w/ NO epithelial thickening or have small papillary projections
  • Abundant cilia are found in benign tumors
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24
Q

What gross morphological features of serous ovarian carcinomas are features of malignany?

A
  • Larger areas of solid or papillary tumor mass
  • Tumor irregularity
  • Fixation or nodularity of the capsule
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25
Q

What epithelial proliferation pattern is thought to be the precursor to low-grade serous carcinomas?

A

Growth in a delicate, papillary pattern known as “micropapillary carcinoma”

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26
Q

Serous tubal intraepithelial carcinomas consist of cells morphologically identical to high-grade serous ovarian carcinomas, but are distinguished how?

A

LACK of invasion

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27
Q

Both low- and high-grade serous ovarian tumors have a propensity to spread where; assoc. w/ what common presenting sign?

A
  • Spread to peritoneal surfaces and omentum
  • Commonly assoc. w/ presence of ascites
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28
Q

What is the 5-year survival rate for borderline and malignant serous ovarian carcinomas confined to the ovaries; what is prognosis for same tumor involving the peritoneum?

A
  • Confined to ovary = 100% (borderline) and 70% (malignant)
  • Peritoneum = 90% (borderline) and 25% (malignant)
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29
Q

What is the prognosis of serous ovarian carcinomas dependent on?

A

Pathologic classification of the tumor and growth pattern on the peritoneum

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30
Q

Which genetic mutation is a consistent alteration observed in all type of mucinous tumors of the ovary?

A

KRAS proto-oncogene

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31
Q

What are some of the major difference between mucinous and serous ovarian tumors in terms of growth patterns?

A
  • Mucinous RARELY involve the surface of the ovary (unlike serous)
  • Mucinous are RARELY bilateral
  • Mucinous produce larger cystic masses
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32
Q

How do mucinous tumors of the ovary appear grossly and what are they filled with?

A

Multiloculated tumors w/ sticky, gelatinous fluid rich in glycoproteins

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33
Q

What type of differentiation is observed with benign mucinous ovarian tumors?

A
  • Gastric or intestinal differentiation = common
  • Endocervical type = uncommon
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34
Q

How are mucinous borderline tumors distinguished from benign mucinous (cystadenomas) based on morphology?

A
  • Epithelial stratification + tufting; and/or papillary intraglandular growth
  • Often appear similar to tubular adenomas or villous adenomas of the intestine
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35
Q

What type of growth pattern is characteristic of malignant mucinous carcinomas?

A

Confluent glandular growth = “expansile” invasion

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36
Q

What is the 10-year survival for stage I (noninvasive) mucinous carcinoma vs. invasive mucinous carcinoma?

A
  • Stage I = 95%
  • Invasive = 90%
  • Spread beyond ovary is usually fatal
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37
Q

Since mucinous ovarian carcinomas are uncommon, what must they be distinguished from especially with bilateral presentation?

A

Metastatic mucinous adenocarcinomas

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38
Q

What does pseudomyxoma peritonei refer to and what is it related to?

A
  • Extensive mucinous ascites + cystic epithelial implants on peritoneal surface + adhesions + frequently involves ovaries
  • Almost all cases due to extraovarian source (usually APPENDICEAL)***
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39
Q

What are the 3 classifications of endometrioid ovarian tumors?

A
  • Benign = endometrioid adenofibromas
  • Borderline
  • Malignant
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40
Q

How are endometrioid ovarian tumors distinguished from serous and mucinous tumors?

A

Presence of tubular glands resembling benign or malignant endometrium

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41
Q

Endometrioid ovarian tumors commonly arise in what settings?

A
  • In association w/ endometriosis and borderline tumors
  • 10-30% are accompanied by carcinoma of the endometrium
42
Q

How does the age of pt with endometrioid ovarian tumor in setting of ovarian endometriosis differ?

A

Occur earlier, on average pt’s 10 years younger than normal

43
Q

Is ovarian endometrioid carcinoma in the setting of carcinoma of the endometrium due to metastasis?

A
  • No, relatively good prognosis suggests the 2 arise independently
  • Synchronous primaries
44
Q

Which mutations are commonly associated with endometrioid ovarian carcinomas?

A
  • Alterations that ↑ PI3K/AKT signaling = PTEN, PIK3CA, ARID1A, and KRAS
  • -* Mutations in DNA mismatch repair and CTNNB1
  • TP53 mutations common in poorly differentiated tumors
45
Q

How common are bilateral endometrioid ovarian carcinoma and what does bilaterality imply?

A
  • 40% are bilateral
  • Usually implies extension of neoplasm beyond genital tract
46
Q

What is 5-year survival for pt’s with stage I endometrioid ovarian carcinoma?

A

75%

47
Q

What are the 3 B’s for remembering Brenner tumors?

A
  • Resemble bladder epithelium (transitional cell tumor)
  • “Coffee bean” nuclei on H&E stain
  • Usually benign
48
Q

What is the gross morphology, growth pattern and characteristics of Brenner tumors of the ovary?

A
  • May be solid or cystic, and 90% are unilateral
  • Can be small or massive
  • Fibrous stroma resembling normal ovary w/ sharply demarcated nests of epithelium resembling that or urinary tract often w/ mucinous glands in center
49
Q

What stage do the majority of ovarian carcinoma present in and what are the signs and sx’s?

A
  • Majority present w/ high stage disease; primary reason for relatively poor prognosis of these tumors
  • Weakness, weight loss —-> cachexia
  • Peritoneal disease –> massive ascites (positive cytology part of staging)
50
Q

Common sites of metastasis for ovarian carcinomas?

A
  • Regional LN’s
  • Lungs
  • Liver
  • GI
  • Opposite ovary (50% of cases)
51
Q

Which serum marker is used in patients w/ known ovarian carcinoma to monitor disease recurrence and progression?

A

CA-125 and HE4 (new)

52
Q

What are the 3 categories of teratomas?

A
  1. Mature (benign)
  2. Immature (malignant)
  3. Monodermal or highly specialized
53
Q

What are the majority of benign teratomas are cystic referred to as?

A

Dermoid cysts, due to almost always being lined by skin-like structures

54
Q

Mature benign (aka cystic teratomas) are most often seen in whom?

A

Young women during active reproductive years

55
Q

Occasionally benign teratomas are associated with what paraneoplastic syndrome?

A

Inflammatory limbic encephalitis

56
Q

What is the characteristic gross and microscopic morphology of mature (benign) teratomas?

A
  • Unilocular cysts containing hair + sebaceous material
  • Teeth and calcification frequently found within wall
  • May contain cartilage, bone, thyroid and neural tissue
57
Q

About 1% of dermoid cysts (benign teratomas) undergo malignant transformation, most often to what?

A

Squamous cell carcinoma

58
Q

What is the karyotype of almost all benign ovarian teratomas?

A

46, XX

59
Q

What are struma ovarii composed of and are the bilateral or unilateral teratomas?

A
  • Composed of mature thyroid tissue, may be functional, causing hyperthyroidisim
  • ALWAYS unilateral
60
Q

How do immature malignant teratomas differ from benign teratomas based on their components; who is most often affected?

A
  • Component tissues resemble embryonal and immature fetal tissue; most often primitive neuroepithelium
  • Prepubertal adolescents and young women, mean age = 18 y/o
61
Q

What is the ovarian counterpart of testicular seminoma?

A

Dysgerminoma

62
Q

Which tumor accounts for 50% of malignant ovarian germ cell tumors?

A

Dysgerminoma

63
Q

Dysgerminomas are most commonly seen in what age group?

A

10-30 y/o; may also be seen in children

64
Q

Which proteins expressed by dysgerminomas are useful diagnostic markers and which may serve as therapeutic target?

A
  • OCT-3, OCT-4, and NANOG = maintain pluripotency
  • KIT may serve as therapeutic target
65
Q

Dysgerminomas that produce ↑ levels of hCG correlates with the presence of what cell type?

A

Syncytiotrophoblastic GIANT cells

66
Q

What are the characteristic morphological features of dysgerminomas and are they typically bilateral or unilateral?

A
  • Majority are UNILATERAL; may be small or fill entire abdomen
  • Large vesicular cells w/ clear cytoplasm + well-defined borders + central nuclei growing in sheets or cords
67
Q

What is the prognosis of dysgerminomas?

A
  • ALL are malignant, but only 1/3 are aggressive
  • Unilateral tumor that has not broken capsule or spread outside ovary has excellent prognosis
  • Overall survival >80%
68
Q

Treatment options for dysgerminoma?

A
  • Salpingo-oophorectomy for low-grade
  • These neoplasms ARE responsive to chemotherapy
69
Q

What is the 2nd most common malignant germ-cell tumor of the ovary?

A

Yolk Sac Tumor (aka endodermal sinus tumor)

70
Q

What is the characteristic histologic feature of yolk sac tumors (aka endodermal sinus tumor)?

A

Glomerulus-like structure composed of central blood vessel enveloped by tumor cells within a space also lined by tumor cells (Schiller-Duval body)

71
Q

What tumor marker is elaborated by yolk sac tumors?

A

α-fetoprotein (AFP)

72
Q

Who are yolk-sac tumors most commonly seen in and what is the most common presentation?

A
  • Child or young woman presenting w/ abdominal pain + rapidly growing pelvic mass
  • Typically involving single ovary
73
Q

What is the prognosis of yolk sac tumors?

A

80% survival w/ combination chemotherapy

74
Q

What do choriocarcinomas of the ovary elaborate which may be useful for diagnosis and detecting recurrences?

A

↑↑↑ chorionic gonadotropins (hCG)

75
Q

How do choriocarcinomas of the ovary differ from those found in the placenta?

A
  • Generally unresponsive to chemotherapy
  • More aggressive and often fatal due to hematogenous metastases at time of dx
76
Q

Granulosa cell tumors of the ovary are divided into adult and juvenile forms, which is more common and peak age range?

A
  • Adult tumors account for 95% of all granulosa cell tumors
  • Majority (2/3’s) occur in postmenopausal women
77
Q

What small, distinctive, glandlike structures filled with acidophilic material are sometimes seen in granulosa cell tumors and make the diagnosis straight forward?

A

Call-Exner bodies

78
Q

For what 2 reasons are granulosa cells tumors of clinical importance?

A
  1. May elaborate large amounts of estrogen
  2. May behave like low-grade malignancies
79
Q

How would a juvenile granulosa cell tumor commonly present in a child and what age?

A
  • Early breast development
  • Early menarche
  • Pubic or underarm hair

*ALL before the age of 8

80
Q

How would an adult present with a granulosa cell tumor?

A
  • Proliferative breast disease
  • Endometrial hyperplasia
  • Endometrial carcinoma
  • Dysfunctional uterine bleeding
81
Q

Elevated tissue and serum levels of what product of granulosa cells can be useful for identifying granulosa and other sex cord-stromal tumors + monitoring treatment?

A

Inhibin

82
Q

Almost all adult granulosa cell tumors have mutations of what gene?

A

FOXL2

83
Q

What is the prognosis, chance of malignancy and recurrence like for granulosa cell tumors?

A
  • All are potentially malignant; but histology does NOT predict behavior
  • Malignant tumors = generally indolent course and local recurrences may be amendable to surgery
  • Recurrences may appear 10-20 years after removal
  • 10-year survival = 85%
84
Q

How is the course of granulosa tumors composed predominantly of theca cells different?

A

Almost never malignant

85
Q

What’s an ovarian fibroma, thecoma, and fibrothecoma?

A
  • Fibroma = composed of fibroblasts
  • Thecoma = composed of plump spindle cells w/ lipid droplet
  • Fibrothecoma = mixture of the cells
86
Q

How does the hormonal activity of thecomas and fibromas differ?

A
  • Pure thecomas = RARE; but if predominant cell type of fibrothecoma may be hormonally active
  • Fibromas as a rule are hormonally inactive
87
Q

Fibromas of the ovary are typically (bilateral or unilateral) and how do they appear grossly?

A
  • 90% are unilateral
  • Usually solid, spherical or slightly lobulated, encapsulated, hard, gray-white masses covered by glistening, intact ovarian serosa
88
Q

Most ovarian fibromas come to attention how?

A
  • Pelvic mass, sometimes w/ pain
  • Large tumors (>6 cm) assoc. w/ ascites and uncommonly hydrothorax, usually only on right side = Meigs Syndrome
  • Also assoc. w/ basal cell nevus syndrome
89
Q

What is the triad of Meigs Syndrome?

A
  • Ovarian tumor (majority are fibromas)
  • Ascites
  • Pleural effusion (hydrothorax) on the right
90
Q

Fibromas, thecomas, and fibrothecomas are benign or malignant?

A

Benign

91
Q

What is the peak incidence for Sertoli-Leydig cell tumors in women?

A

10-30 y/o; can occur at all ages

92
Q

Mutation of which gene is common to Sertoli-Leydig cell tumors?

A

DICER1, gene encoding endonucleases needed for micro-RNA processing

93
Q

Sertoli-Leydig cell tumors arise (unilaterally or bilaterally) and may appear like what other tumor?

A

Unilateral and may resemble granulosa cell tumors

94
Q

Sertoli-Leydig cell tumors are functional and commonly lead to what signs/sx’s in children and adults?

A
  • Block normal female sexual development in children
  • Defeminization –> atrophic breasts, amenorrhea, sterility, and loss of hair
  • May progress to striking virilization (hirsutism) assoc. w/ male pattern baldness, hypertophy of clitoris and voice changes
95
Q

Pure Leydig cell tumors are also known as what; what distinguishing cell type is seen?

A
  • Hilus cell tumor
  • UNILATERAL tumor w/ large lipid-laden Leydig cells w/ distinct borders and characteristic cytoplasmic structures called Reinke crystalloids
96
Q

What is the predominant hormone elaborated by Hilus cell tumors (pure Leydig cell tumors)?

A

Testosterone –> hirsutism, voice changes, and clitoralmegaly

97
Q

Which uncommon tumor is composed of germ cells and sex cord-stroma derivatives resembling immature Sertoli and granulosa cells?

A

Gonadoblastoma

98
Q

In 50% of Gonadoblastoma cases there is co-existence of what other tumor?

A

Dysgerminoma

99
Q

What is the prognosis of Gonadoblastomas?

A

Excellent if completely excised

100
Q

The most common metastatic tumors of the ovary are derived from tumors of which origin?

A

Müllerian origin = uterus, fallopian tubes, contralateral ovary, or pelvic peritoneum

101
Q

What is a Krukenberg tumor and what is it characterized by?

A
  • Bilateral tumor of the ovaries from a mestastic GI carcinoma (diffuse-type)
  • Composed of mucin-producing, signet-ring cancer cells

Repro II - PATH (Tobin) (7 decks)

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