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68 Cards in this Set
- Front
- Back
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Most common infections of the tube
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Paratubal cysts
Infection Ectopic pregnancy Other |
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Paratubal cysts - Walthard Nest cells
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Transitional cell appearance
May be cystic Probably of mesothelial origin |
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Serous cysts (hydatid cysts, mullerian cysts)
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Lined by tubal-type epithelium
May have thin layer of muscle in the wall |
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Wolffian (mesonephric) cysts
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Single layer of cuboidal epithelium
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Salpingitis
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Pelvic Inflammatory Disease (PID)
Inflammation begins in the tube, spreads to ovary, etc. Usually due to ascending infection Gonorrhea and chlamydia most common Polymicrobial (B.fragilis, peptostreptococci, peptococci) |
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How would you know there was active inflammation int eh salpinx
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Active inflammation
Infiltrate in mucosa and submucosa Reactive hyperplasia of mucosa |
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Follicular salpingitis
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Fusion of plicae and fimbriae leads to gland-like spaces seen after resolution of inflammation
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Result of granulomatous salpingitis
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Infertility and uncommon in the US
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Ectopic pregnancy
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Over 95% of ectopic pregnancies are tubal
Implantation in the tube is often due to underlying tubal abnormality A history of PID is seen in 35-45 % |
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Ectopic pregnancy : Outcome if untreated
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May expel conceptus through fimbriated end of tube (tubal abortion)
Spontaneous death and involution Continued growth will result in hemorrhage into tube (hematosalpinx) and rupture of tube around 8th week |
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Treatment of ectopic pregnancy
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Salpingectomy:
Fewest complications May not be an option for women with only one functioning tube Salpingostomy 20% will recur in that tube Single dose of methotrexate 10% fail and risk future rupture; must continue to surgery |
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When would you diagnose a tumor of the salpinx ?
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When you have excluded everything else
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Adenomatoid Tumor
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Arises on the serosal surface: well-circumscribed yellow-white nodule
Rarely bilateral Derived from mesothelium |
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3 factors to dx a tubal tumor
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Bulk of tumor is in there
The mucosa is involved and has a papillary growth pattern Transition from benign to malignant epithelium |
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FT Carcinoma
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Grossly
Distended tube filled with tumor Microscopically Identical to ovarian counterparts (usually serous) |
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Prognosis of a tubal carcinoma
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Approximately half are stage 1 (confined to tube) at diagnosis, but the 5 year survival is still only about 60%
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Follicular cyst : Non neoplastic ovary
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Distended (> 2.5 or 3 cm) developing or atretic follicles
Cyst wall= theca cells with or without granulosa cell layer Most will regress spontaneously within 2 months |
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Corpus luteum cysts
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Exceed 2.5 or 3 cm
Grossly Yellow, undulating adrenal-like appearance Often hemorrhagic center Lined by luteinized granulosa and theca cells Abundant pink cytoplasm (lipid) Also generally will resolve within 2 months |
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Endometriosis
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Gross:
Bilateral in 1/3 to ½ Ovary is the most common site Hemorrhagic, shaggy lining, “CHOCOLATE” fluid Microscopic: Endometrial glands and stroma |
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Can you make a clinical diagnosis of POS at the microscope ?
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No, you need the following
Increased LH:FSH ratio Chronic anovulation Obesity (40%) Hirsutism (50%) Virilism (rare) |
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Polycystic ovaries
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2-5 times normal size
Fibrotic, hypocellular superficial cortex At least eight cortical cysts 2-8 mm in size Cysts are atretic follicles lined by granulosa cells with an outer layer of luteinized theca interna Rare or no corpora lutea or corpora albicantia (no ovulation) |
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PCOD and the endometrium
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The lack of ovulation and subsequent progesterone production means the secretory phase never happens
Patients have abnormal bleeding May develop hyperplasia (unopposed estrogen effect), and about 1% of patient’s develop endometrial carcinoma Well-differentiated endometrioid tumors, with no or only minimal myometrial invasion |
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Ovarian Neoplasias
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80% are benign- Patients usually 20-45 yrs
Malignancies - women over 40 Sx - Symptoms Lower abdominal pain Abdominal enlargement Pressure on neighboring organs |
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Risk factors for ovarian carcinoma
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Nulliparity
Family History Heritable Mutations (BRCA) Risk of developing ovarian cancer by the age of 70 in patients with BRCA mutations is estimated at 20-60% |
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Surface Epithelial Tumors
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Most primary ovarian tumors (65-70%) are in this category
The large majority of malignant ovarian tumors are in this category (90%) Rare in children |
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Types of epithelial cell tumors
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Serous
Mucinous Endometrioid Clear Cell Transitional |
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Serous tumors
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Usually cystic
Filled with clear (serous) fluid Often are bilateral Comprise about 25% of all ovarian tumors |
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What characteristic of serous epithelium helps decide if it is benign ?
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The presence of ciliated cells
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Serous cystadenoma, adenofibroma, cystadenofirboma
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Serous Cystadenoma
Lining may be smooth (no papillae) May have broad, firm, bulbous papillae Serous Adenofibroma Cauliflower-like exophytic growth on surface Serous Cystadenofibroma Cystadenoma with component of fibrous growth |
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Serous Tumors of Low malignant potential
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Proliferative epithelium without invasion
Nuclear atypia Complex glandular formations Cribriform Slender branching fronds Tufting, budding Proliferation Mitotic activity Stratification WITHOUT STROMAL INVASION |
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Serous Carcinoma
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Solid areas of tumor, often with necrosis and hemorrhage
Not always cystic and does not always have obvious papillae Microscopic Not necessarily papillary Pronounced nuclear atypia Abundant mitotic figures Bridging and coalescence of papillae producing slit- like glandular spaces Destructive invasion |
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Prognosis for serous tumors
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Pretty good. 70-100%
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Mucinous tumors
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Less common than serous
Bilateral in 5-10% 80% are benign Can grow extremely large (over 25 kg!) Usually multicystic |
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Mucinous cystadenoma
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Remember the blown up picture and then punctured picture revealing cysts
Mucinous epithelium lines the cystic structures in a single cell layer of bland cells with no mitotic activity This is the intestinal type of epithelium, with goblet cells |
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Mucinous LMP
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Epithelium becomes pseudostratified; “piled up”, “tufted”
Mitoses are evident Mucin depletion (like GI tumors) The changes can be very focal, so must sample extensively These changes must be present in 10% of the tumor Mu |
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Mucinous Carcinoma
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Very uncommon (metastatic mucinous carcinoma is much more common)
Gross Lots of solid tumor growth Microscopic Atypia Abundant mitoses Complex architecture Bridges Cribriform Invasion of stroma |
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Prognosis
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Ten year survival for stage 1 (confined to ovary)
“borderline”: 95% Carcinoma: 66% (but only one half of cases present as stage 1) |
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Pseudomyxoma Peritoneii
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Recently shown that this phenomenon is ALWAYS due to a GI primary (usually appendiceal) with metastases to both ovaries and the peritoneum
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Endometrial tumors
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Epithelium looks just like benign proliferative endometrium
Coexistent endometriosis with 10-20% of tumors Sometimes tumor is obviously arising within an endometriotic cyst Still, most of the time there is no demonstrable endometriosis, and tumors presumably arise from surface epithelium |
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Borderline endometrial tumors
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Glands become crowded and have more complex architecture
Basically, looks like complex atypical hyperplasia of the endometrium, but in the ovary NO INVASION Very, very rare |
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Endometroid carcinoma
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Gross
Cystic or solid Often hemorrhagic Rare or no papillary formations Microscopic features Identical to endometrioid tumors of the uterus Grade them the same way Usually well-differentiated Often foci of squamous metaplasia Helps differentiate from GI met |
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Clear cell tumors
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Benign and borderline tumors are extremely rare
Only 7.4 % of ovarian malignancies Carcinomas bilateral in less than 10% Though to be a variant of endometrioid Frequent association with endometriosis Occasional origin in endometriotic cysts Frequently mixed with endometrioid Gross Spongy, often cystic Not very distinctive Microscopic Architecture Papillary (often with hyalinized cores Tubular-cystic Solid sheets |
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Cytologic features of Clear cell
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Large cells
Prominent cell borders Hobnailing Cytoplasm clear or oxyphilic May contain hyaline globules; PAS+ May contain mucin or fat Clear cytoplasm due to glycogen |
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Brenner Tumors
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Usually unilateral and benign
Borderline and malignant types exist, but are very rare Often incidental finding Gross firm, white to yellow Usually 2-10 cm Microscopically: solid and cystic nests of urothelial-like cells embedded in abundant, dense stroma |
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MMMT
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Less than 1% of ovarian neoplasms
Gross: generically malignant Fleshy, necrotic, hemorrhagic Microscopically, a mixture of carcinoma and sarcoma (older term= carcinosarcoma) Carcinoma type is always GYN: serous, endometrioid, squamous or clear cell Sarcoma type is often not GYN Commonly chondrosarcoma, osteosarcoma, rhabdomyosarcoma Evidence suggests these are really carcinomas at heart, with divergent differentiation Prognosis is terrible |
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Metastasis of Ovarian cancer
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Most common sites of spread
Contralateral ovary Peritoneal cavity (especially serous tumors) Para-aortic and pelvic lymph nodes Liver “Sister Joseph’s nodule”=umbilical metastasis, sometimes the presenting feature |
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Germ Cell tumors
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95% are benign (mature teratomas)
Affect predominantly children/young adults More likely to be malignant the younger the patient Not always pure: 8% are mixed types Highly chemoresponsive these days Overall disease-free survival rates are over 95% |
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Dysgerminoma
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1-2 % of primary ovarian neoplasms
80% of patients <30 y/o Analogous to seminoma of testis Gross: Often fairly large Smooth surface, often lobulated Fleshy, solid cut surface |
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Cytology of dysgerminoma
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Uniform round cells
Nuclei Round Prominent nucleoli Cytoplasm Clear to finely granular Contains glycogen (PAS+) Prominent cell membranes 6-8% have scattered syncytiotrophoblastic cells-hCG positive |
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Clinical aspects of dysgerminoma
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May metastasize to contralateral ovary, retroperitoneal nodes, peritoneal cavity
Treatment: oophorectomy and chemo (+/- RT) If it recurs, does so quickly 80% of recurrences within 2 years Survival rate (for pure, encapsulated dysgerminoma): 95% |
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Yolk Sac tumor
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AKA Endodermal Sinus Tumor
Most patients are < 30 y/o Gross: generic malignant appearance Microscopic: extremely (painfully) variable, with many patterns and subtypes described Often patterns are mixed Scary types resemble endometrioid carcinoma, hepatocellular carcinoma Regardless of pattern, almost always contain intracytoplasmic and extracellular hyaline, PAS-D+ droplets, which are usually AFP-positive Serum elevation of AFP |
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PagF of yolk sac tumors
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Elusive Schiller Duval Bodies. Diagnostic if present
These are a layer germ cells around a central vein. These are surrounded by a cavitating lesion just like a glomerulus |
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Embryonal Carcinoma
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In the ovary, usually seen in combination with other tumor types
Morphology: Sheets and nests of large, primitive, malignant cells Poorly defined cell borders Occasional suggestion of gland formation, but no well-defined glands High mitotic activity Frequent syncytiotrophoblastic cells Serum markers HCG often elevated, due to syncytiotrophoblast cells or admixed choriocarcinoma AFP usually elevated, even if not mixed with YST (but levels not as high as in YST) |
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Prognosis of YST and Embryonal Carcinoma
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Both are very aggressive tumors and prognosis was once dismal
With current chemotherapy, much better, and most patients can be cured completely |
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Choriocarcinoma
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Most are of gestational origin, in which case the ovarian tumors are almost always mets from a uterine primary
Non-gestational tumors of germ cell origin are rare, and usually a component of a mixed germ cell tumor Appearance Mixture of cytotrophoblast and syncytiotrophoblast Characteristically hemorrhagic |
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Prognosis of Choriocarcinoma
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Prognosis for gestational type of tumor is good; these are very chemosensitive
Prognosis for a pure non-gestational (germ cell) tumor is horrible Prognosis is pretty good if part of a mixed germ cell tumor |
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Teratoma
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Usually cystic (“Mature Cystic Teratoma”)
20% of all ovarian neoplasms Most common ovarian tumor in childhood Composed of any number of adult tissues Skin and hair always Teeth common Anything can happen Intracystic nodule (“Rokitansky’s protuberance”) is usually the most interesting part in terms of variety of tissue |
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Beware !
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Malignant transformation can occur (2%)
Most common is squamous carcinoma |
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Monodermal teratoma
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Tumor consists solely of one type of adult tissue
Most famous is “struma ovarii”, a tumor of mature thyroid tissue Looks and acts like normal thyroid tissue |
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Immature malignant teratoma
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Mixture of embryonal and adult tissues
Immature component is most often neuroepithelial Sometimes the tumor is all or almost all one type of malignant tissue Thorough sampling is necessary, because prognosis depends on the amount of immature tissue present (grading schemes dependent on this) |
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Sex Cord Stromal Tumors
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Comprise about 5% of ovarian neoplasms
Granulosa Cell Tumor Thecoma/Fibroma (accounts for ½ of all sex cord stromal tumors) Sertoli-Leydig Cell Tumor Others |
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Granulosa Cell tumor
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1-2% of all ovarian tumors, 95% of all granulosa cell tumors
Gross Usually solid and encapsulated, but may be partially to completely cystic Solid gray to yellow cut surface Hemorrhage is common |
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Adult granulosa Cell tumor
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Architecture is highly variable
Multiple growth patterns described Most “famous” is the microfollicular pattern displaying characteristic Call-Exner bodies Cytologic features are distinctive Longitudinal nuclear grooves (“coffee-bean”) May not be in all cells |
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Clinical Behavior of Granulosa Cell Tumors
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All have malignant potential
Often spread or recur after many (10-20) years May produce estrogen In prepubertal patients, may result in precocious puberty In adult women, can result in endometrial hyperplasia/carcinoma |
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Fibroma/Thecoma
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Considered together because they are not really distinct, but parts of a morphologic continuum (“fibrothecoma”)
Benign spindle cell lesions Variable lipid content Thecomas may have hormonal manifestations (estrogenic or androgenic) Fibromas may be associated with ascites +/- right sided pleural effusion (Meig’s syndrome) |
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Sertoli/Leydig Cell tumors
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Recapitulate testicular structures/development
Often masculinizing Very variable histologic appearance, from well-formed tubules of Sertoli cells admixed with islands of Leydig cells to poorly-differentiated/sarcomatoid tumors |
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Metastases to the Ovary
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About 7% of ovarian masses presenting as ovarian primaries turn out to be metastases
Common sources Stomach Colon Appendix Breast Uterus Lung Skin (melanoma) |
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Krukenberg Tumor
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Usually bilateral
Diffuse infiltration of ovary by signet ring cells with intracellular mucin Most common primary is stomach, but may also be breast, colon, appendix |
