PATHOLOGY - PowerPoint Presentation

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PATHOLOGY FEMALE GENITAL SYSTEM Part 4 Noushin Afshar Moghaddam (MD/professor of Pathology/Shahid Beheshti University)

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SURFACE EPITHELIALTUMOR (Surface epithelial stromal tumor)

GERM CELL TUMORSEX CORD – STROMAL TUMORMETASTATIC TUMOR

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OVARIAN TUMORS

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Overall frequency

15-20%Proportion of malignant ovarian tumors 3-5% Age group affected 0-25+ years

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GERM CELL TUMOR

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The younger the patient , the greater is the likelihood of malignancyOver 90% of germ cell tumors are

benign cystic teratoma

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GERM CELL TUMORS

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TERATOMADYSGERMINOMA

ENDODERMAL SINUS TUMOR ( Yolk sac tumor)CHORIOCARCINOMA

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GERM CELL TUMORS

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Mature cystic Teratoma (

Dermoid cyst) Dermoid cyst with malignant Transformation Immature Teratoma (Malignant teratoma)Specialized Teratoma

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TERATOMA

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5cm – 10 cmFound incidentally on abdominal radiographs or scan

For unknown reasons , sometimes produce infertilityTorsion in 10% - 15%, producing an acute surgical emergency

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Mature cystic teratoma

(Dermoid cyst)

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Ovary, mature cystic teratoma

These cystic tumors contain hair and sebaceous material and often have a protuberant nodule (Rokitansky protuberance) that contains numerous types of tissues, including brain, bone, and even teeth.

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Mature cystic Teratoma

(Dermoid cyst)

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Mature cystic Teratoma

(

Cartilage tissue

)

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Dermoid cyst with malignant Transformation (SCC)

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Early in life , the mean age 18 years

Predominantly solid with areas of necrosisParticularly ominous are the foci of Neuroepithelial differentiation

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Immature (Malignant) Teratoma

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Immature Teratoma

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Struma OvariiCarcinoid

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Specialized Teratoma

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Thyroid tissue in mature teratoma (Struma Ovarii)

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2nd – 3rd decadesOccur with gonadal dysgenesis

80% – 90% unilateralCounterpart of testicular seminomaSolid, large to small gray masses

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Dysgerminoma

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ovarian dysgerminoma

pale brown appearance of the parenchyma, along with some central collagenous scar

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Sheets or cords of large cleared cells separated by scant fibrous strands Stroma may contain lymphocytes and occasional granuloma.

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Dysgerminoma

Morphologic features

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Dysgerminoma

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All malignantonly one third aggressive and spread

all radiosensitive with 80% cure

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Dysgerminoma

Behavior

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First three decades of life Unilateral

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Choriocarcinoma

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Metastasizes early and widely Primary focus may disintegrate ,leaving only“mets”.

In contrast to placental tumors ,ovarian primaries are resistant to chemotherapy .

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Choriocarcinoma

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Often small , hemorrhagic focus two types epithelium :

cytotrophoblast syncytiotrophoblast

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Choriocarcinoma

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Choriocarcinoma

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SURFACE EPITHELIALTUMOR (Surface epithelial stromal tumor)

GERM CELL TUMORSEX CORD – STROMAL TUMORMETASTATIC TUMOR

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OVARIAN TUMORS

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GRANULOSA CELL TUMORTHECOMA (THECA CELL TUMOR)

FIBROMA SERTOLI CELL TUMOR LEYDIG CELL TUMOR

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SEX CORD – STROMAL TUMOR

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Most postmenopausal

at any age Unilateral

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Granulosa

-theca cell tumor

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tiny or large gray to yellow (with cystic spaces )

Composed of mixture of cuboidal granulosa cells in cords, sheets or strandsGranulosal elements may recapitulate ovarian follicle called Call-Exner bodies .

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Granulosa

cell tumor

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May elaborate large amounts of estrogen (from thecal elements) may promote e

ndometrial or breast carcinoma Granulosa element may be malignant (5% to 25%)Granulosa-Theca Tumor

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Granulosa cell tumor

with Call- Exner body

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tiny or large yellow (with cystic spaces )

Composed of spindled or plump lipid-laden plump theca cells.

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Theca cell tumor

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Thecoma of the ovary

Plump theca cells

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Thecoma

Fat stain

Plump lipid-laden theca cells.

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Solid gray fibrous cells in fibroma

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Fibroma

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fibrothecoma

firm and scar-like may be hormonally active if the thecoma component predominates

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Fibroma

of the ovary

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Most hormonally inactive About 40% ,for obscure reasons ,produce ascites and hydrothorax (

Meigs’ syndrome). Rarely malignant .

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Fibroma

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All ages Unilateral

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Sertoli-Leydig cell

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Usually small gray to yellow-brown

solid Recaps development of testis with tubules, or cords and plump pink Sertoli cells.

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Sertoli-Leydig cell

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masculinizing or defeminizing Uncommonly malignant.

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Sertoli-Leydig cell

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Primaries are:

breast lung ,and gastrointestinal tract (Krukenberg tumors)

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Metastases to ovary

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Older ages Mostly bilateral

Usually solid gray-white masses up to 20 cm in diameter .Anaplastic tumor cells ,cords, glands, dispersed through fibrous background Cells may be “signet ring” mucin-secreting.

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Metastases to ovary

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Krukenberg tumor

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Krukenberg tumor

Desmoplastic stroma

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Krukenberg Tumor

Signet ring cell

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No symptoms or signs until they are well advanced.Ovarian tumors of surface cell origin are usually asymptomatic until they become large enough to cause local pressure symptoms: pain

gastrointestinal complaints urinary frequency

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CLINICAL CORRELATIONS FOR ALL OVARIAN TUMOR

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about 30% of all ovarian neoplasms are discovered incidentally on routine gynecologic examination.Smaller masses, particularly dermoid cysts, sometimes become twised on their pedicles

torsion:- producing severe abdominal pain -an acute abdomen.

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CLINICAL CORRELATIONS FOR ALL OVARIAN TUMOR

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Fibromas and malignant serous tumors often cause ascites.The latter resulting from metastatic seeding of the peritoneal cavity, so that tumor cells can be identified in the ascitic fluid

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CLINICAL CORRELATIONS FOR ALL OVARIAN TUMOR

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Screening detection methods are being developedlimited value in discovering ovarian cancers while they are still curable

Among the many markers that have been explored, elevated serum levels of CA 125 been reported in 75% to 90% of women with epithelial ovarian cancer

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CLINICAL CORRELATIONS FOR ALL OVARIAN TUMOR

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undetectable in up to 50% of patients with cancer limited to the ovary

elevated in a variety of benign conditions, as well as nonovarian cancersIt is most valuable as a screening test in asymptomatic postmenopausal women because of the low incidence of confounding variables

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CA125

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great value in monitoring response to therapy

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CA125

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InflammationsEctopic pregnancy

EndometriosisRare primary tumors

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Fallopian tubes

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ChlamydiaMycoplasma homonis

ColiformsGonococciStreotococci and staphylococci ( In postpartum setting)

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Fallopian tubes Inflammations

(Salpingitis )

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Almost always in combination

of T.B endometritis

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T.B salpingitis

Tuberculosis

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Ectopic Pregnancy (EP)Gestational Trophoblastic Disease (GTD)

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Diseases of Pregnancy

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fertilized ovum implants outside of the uterine fundus

1% of pregnanciesa tubal ectopic pregnancy may proceed for several weeks, but the enlargement can rupture the tube and lead to acute, life-threatening bleeding, often about 6 weeks after a previous menstrual period.

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Ectopic pregnancy (EP)

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A positive pregnancy test)

Ultrasoundculdocentesis with presence of bloodDiagnosis of ectopic pregnancy

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Fallopian tubes (Tubal pregnancy) =90%

ovaries abdominal cavityintrauterine portion of the oviducts(interstitial pregnancy)Most common sites

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Inflammation tumors

IUD may increase the riskIn 50% 0f the cases no anatomic causecause

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About 1 in 150 pregnancies results in ectopic implantation

Most cannot be sustained at

extrauterine

sites.

   

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In 50% of the cases endometrium shows hypersecretory with deciduas changes

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Ectopic pregnancy

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Fallopian tube, ectopic pregnancy - Gross

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tubal epithelium at the right, with rupture site and chorionic

villi

at the lower left.

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Hydatidiform mole

Complete Partial Choriocarcinoma

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Gestational trophoblastic disease

(GTD)

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Normal chorionic

villi

Cytotrophoblasts

and

syncytiotrophoblast

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1 to 1.5 per 2000 pregnanciesMost common before age 20 and after age 40 years

the uterus is large for dates, but no fetus is present HCG levels are markedly elevated

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Complete Hydatidiform mole

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Patients with a hydatidiform mole are often large for dates

hyperemesis gravidarum more frequentlyPatients may present with bleeding, and may pass some of the grape-like villiThe patient is then followed with serial HCG levels

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The grape-like

villi

of a

hydatidiform

mole are seen here.

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Real Grape

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Hydropic swelling of chorionic villiAvascular villi

Proliferation of trophoblasts

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Complete Hydatidiform mole

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Complete Hydatidiform mole

             

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In this

hydatidiform

mole there is atypical

trophoblastic

proliferation, but

villi

are still present

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10% Invasive2% - 3% Choriocarcinoma

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Complete Hydatidiform mole

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occurs when two sperms fertilize a single ovum

The result is triploidy (69 XXY)Only some of the villi are grape- likea fetus can be present rarely survives past 15 weeks

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PARTIAL MOLE(Microscopy)

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PARTIAL MOLE(Microscopy)

In partial moles, some

villi

(as seen here at the lower left) appear normal, whereas others are swollen.

There is minimal

trophoblastic

proliferation.

                  

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Feature Complet mole partial Mole

____________________________________________________________ karyotype 46,XX(46,XY) Triploi(69,XXY) villous edema All villi somevilli Trophoblast Diffuse; Focal; slight proliferation circumferential Atypia Often present Absent Serum hCG Elevated Less elevated hCG in tissue ++++ + Behavior 2% choricocarcinoma Rare____________________________________________________________

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FEATURES OF COMPLETE VERSUS

PARTIAL HYDATIDIFORM MOLE

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GestationalNon – Gestational (of Germ cell origin in ovary, testis,…)

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Choriocarcinoma

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1 in 30000 pregnancies in USA1 in 2000 pregnancies in Asian and African countries

Much less common than hydatidiform mole

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Choriocarcinoma

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50% after Complete Hydatidiform

mole 25% after an abortion22.5% after normal pregnancies2.5% after Ectopic pregnanciesRare after partial mole

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Choriocarcinoma

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Villi are not present

there is a proliferation of bizarre trophoblastic cellsvery aggressive marked HCG levelsHalf of choriocarcinomas arise in preceding hydatidiform molesChoriocarcinoma

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The END