Female 2 Flashcards
Follicular cyst vs. serous cystadenoma.
Follicular cyst: Theca interna layer.
Luteinized follicular cyst of pregnancy:
A. Median size.
B. Histology.
A. 25 cm.
B. Lined by luteinized cells with hyperchromatic, pleomorphic nuclei.
Corpus-luteum cyst: Presentation (3).
Incidental.
Endocrine abnormalities, e.g. hyperestrinism, irregular menstruation.
Rupture and bleeding into the peritoneum.
Corpus-luteum cyst vs. corpus luteum.
The cyst is more than 2 cm in diameter.
Follicular cyst: Syndrome.
McCune−Albright:
− Polyostotic fibrous dysplasia.
− Irregular patches of pigmented skin.
− Endocrine dysplasia.
Hyperreactio luteinalis:
A. Association.
B. Presentation (2).
A. Elevated hCG as in pregnancy, gestational trophoblastic disease.
B. Usually asymptomatic; may cause a mass.
Hyperreactio luteinalis: Gross pathology.
Both ovaries are enlarged by multiple thin-walled cysts filled with blood or serous fluid.
Hyperreactio luteinalis: Histology (2).
Cysts lined by luteinized theca interna with or without granulosa layer.
Ovarian stroma may be edematous.
Hyperreactio luteinalis vs. large luteinized follicular cyst of pregnancy.
The latter is solitary.
Hyperreactio luteinalis: Associated tumor.
Rarely coexists with a pregnancy luteoma.
Polycystic ovarian syndrome: Typical age at presentation.
Third decade.
Polycystic ovarian syndrome: Laboratory abnormalities (2).
Most cases: Increased ratio of LH to FSH.
Some cases: Hyperprolactinemia.
Polycystic ovarian syndrome: Histology (3).
Ovarian cortex: Thickened, collagenous; thick-walled vessels.
Cysts: Follicular cysts in which only the theca interna is luteinized.
Stroma: Nodular luteinization; no corpora lutea or albicantia.
Polycystic ovarian syndrome: Pathogenesis.
Hyperandrogenemia with increased conversion of androstenedione to estrone.
Polycystic ovarian syndrome: Possible effects on the endometrium (2).
Hyperplasia.
Adenocarcinoma.
Stromal hyperthecosis: Typical age at presentation.
Postmenopausal.
Stromal hyperthecosis in premenopausal women: Presentations (2).
More common: − Virilization. − Obesity. − Glucose intolerance. − Hypertension.
Less common: Resembles PCOS.
Stromal hyperthecosis: Gross pathology.
The cut surface of BOTH ovaries contains white or yellow areas.
Stromal hyperthecosis: Histology.
Luteinized cells in the stroma occur singly or in clusters or nodules.
These luteinized cells are not associated with follicles.
HAIR-AN syndrome: Components.
Hyperandrogenemia.
Insulin resistance.
Acanthosis nigricans.
HAIR-AN syndrome: Histology of ovary.
In some cases, there is stromal hyperthecosis + edema and fibrosis.
Stromal hyperplasia: Presentation.
Similar to that of stromal hyperthecosis in premenopausal women.
Stromal hyperplasia: Gross pathology.
Similar to that of stromal hyperthecosis.
Stromal hyperplasia: Histology (2).
Diffuse or vaguely nodular increase in stromal cells.
Minimal collagen.
Stromal hyperplasia vs. ovarian fibroma.
Fibroma:
− Much collagen.
− Larger nuclei.
Stromal hyperplasia vs. low-grade endometrial stromal sarcoma of the ovary (2).
LGESS:
− More mitotic figures.
− Regularly distributed thin-walled vessels.
Massive edema and fibrosis of the ovary:
A. Age group.
B. Presentation.
A. Second decade.
B. Abdominal pain.
Massive edema and fibrosis of the ovary:
A. Laterality.
B. Possible complication.
A. Usually unilateral.
B. Torsion.
Massive edema of the ovary: Gross pathology.
White cut surface with seeping fluid and sometimes with hemorrhage.
Massive edema of the ovary: Histology (3).
Edema of stroma with sparing of outer cortex.
Venous congestion and dilatation of lymphatics.
May contain clusters of lutein cells.
Fibromatosis of the ovary: Gross pathology.
Smooth or lobulated cut surface, sometimes with cysts.
Fibromatosis of the ovary: Histology.
Proliferating spindle cells and collagen surround follicles.
Fibroma vs. fibromatosis.
In ovarian fibroma, there are no follicles.
Pregnancy luteoma: Typical patient.
Black multipara in her third or fourth decade.
Pregnancy luteoma: Possible presentation (2).
Mother: Hirsutism, virilization.
Infant: Virilism.
Pregnancy luteoma: Gross pathology (3).
Multiple in half of cases.
Bilateral in one third of cases.
Yellow-brown or gray on cut surface.
Pregnancy luteoma: Architecture.
Well-circumscribed nodules in a sparse stroma.
Pregnancy luteoma: Cytology.
Nuclei: Round; may be hyperchromatic; may show moderate mitotic activity.
Cytoplasm: Polygonal, abundant, eosinophilic, granular.
Pregnancy luteoma vs. luteinized thecoma (2).
Pregancy luteoma:
− Related to pregnancy.
− Contains no lipid.
Pregnancy luteoma vs. lipid-poor steroid tumor.
Lipid-poor steroid tumor
− Rarely bilateral.
− More mitotic activity.
Endometriosis: Inflammatory reaction.
Histiocytes, pseudoxanthoma cells.
Endometriosis vs. endometrioid cystadenoma.
Endometrioid cystadenoma: No endometrial stroma.
Endometriosis: Benign histologic variations (2).
Hyperplasia, metaplasia.
Ovarian malignancy associated with endometriosis:
A. Risk factor.
B. Most common types (2).
A. Hyperestrogenic state.
B. Endometrioid carcinoma of the ovary, clear-cell carcinoma of the ovary.
Follicular cyst: Layers.
Luminal: Granulosa cells (small and dark).
Basal: Theca interna cells (large and pale).
Benign ovarian serous tumors: Types (5).
Cystadenoma.
Papillary cystadenoma.
Surface papilloma.
Adenofibroma.
Cystadenofibroma.
Benign ovarian serous tumors: Lining cells.
Typically resemble those of the Fallopian tube; may also be columnar secretory cells.
Ovarian serous cystadenoma vs. epithelial inclusion cyst.
Inclusion cyst: Less than 1 cm in diameter.
Simple cyst.
Term used when it is unclear whether a structure is a follicular cyst or a serous cystadenoma.
Rete cystadenoma:
A. Origin.
B. Histology.
A. Rete ovarii.
B. Nonciliated epithelial lining; smooth muscle and hilus cells in the wall.
Serous borderline tumor:
A. Synonym.
B. Age group.
A. Atypical proliferative serous tumor.
B. 30-60 years of age.
Serous borderline tumor: Histology (2).
Complex papillae with hierarchical branching.
No destructive stromal invasion.
Serous borderline tumor: Implants (3).
Consist of proliferating epithelium with complex glands, resembling the tumor in the ovary.
Not regarded as metastasis.
Present in peritoneum or in lymph nodes.
Serous borderline tumor: Immunohistochemistry (2).
Positive: WT-1.
Usually weak or negative: p53.
Micropapillary serous carcinoma: Histology.
Micropapillae
− Long and thin; no hierarchical branching.
− No fibrovascular core (by definition).
− Arise from edematous true papillae that do not invade the stroma.
Micropapillary serous carcinoma: Classification.
Regarded as a serous borderline tumor and as a low-grade carcinoma.
Serous borderline tumor: Treatment.
Tumors confined to the ovary: Surgical excision cures more than 95% of patients.
Ovarian carcinomas of type 1:
A. Stage at presentation.
B. Behavior.
A. Usually stage 1.
B. Slow-growing and usually retain low grade.
Ovarian carcinomas of type 1:
A. Histology.
B. Genetics.
A. Analogous to that of cystadenomas and borderline tumors.
B. Mutations in KRAS/BRAF are more common than mutations in TP53.
Ovarian carcinomas of type 1: Examples (5).
Serous carcinoma (grade 1).
Mucinous, endometrioid, and clear-cell carcinomas.
Transitional-cell carcinomas.
Ovarian carcinomas of type 2:
A. Stage at presentation.
B. Behavior (2).
A. Usually high stage.
B. Arises de novo; aggressive behavior.
Ovarian carcinomas of type 2: Genetics.
Mutations in TP53 are much more common than mutations in KRAS/BRAF.
Ovarian carcinomas of type 2: Examples (2).
Serous carcinoma (grade 2 or grade 3).
Carcinosarcoma.
Low-grade ovarian serous carcinoma: Gross pathology (2).
Bilateral in 80% to 90% of cases.
More than 90% of tumors are in advanced stage.
Low-grade ovarian serous carcinoma: Histology (3).
Papillae with infiltration of ovarian stroma.
Psammoma bodies
− Present in most well-differentiated tumors.
− May exceed the epithelial component (“psammocarcinoma”).
High-grade ovarian serous carcinoma: Origin.
Fimbriae of Fallopian tubes.
High-grade ovarian serous carcinoma: Gross pathology (2).
Bilateral in about 65% of cases.
May be mostly cystic (if well-differentiated) or solid.
High-grade ovarian serous carcinoma: Architecture (2).
Desmoplastic invasion of stroma.
Few papillae; mostly solid growth.
High-grade ovarian serous carcinoma: Cytology.
High-grade nuclei with atypical mitotic figures.
Cellular budding and stratification.
High-grade ovarian serous carcinoma: Additional finding.
Serous tubal intraepithelial carcinoma in the Fallopian tube.
Serous ovarian carcinomas: Immunohistochemistry (5,1).
Positive: Cytokeratin, EMA, vimentin, CA125, WT-1.
Negative: CEA.
Retiform Sertoli-Leydig cell tumor of the ovary:
A. Age group.
B. Presentation.
A. First decade.
B. May cause virilization.
Retiform Sertoli-Leydig cell tumor of the ovary: Histology (2).
Bland cells with scant cytoplasm line tubules and cysts.
Other types of Sertoli-Leydig cell tumor usually coexist.
Proportion of ___ ovarian tumors that are benign.
A. Serous.
B. Mucinous.
A. 70%.
B. 75-85%.
Benign ovarian mucinous tumors: Histology (2).
Endocervical- or intestinal-type epithelium.
May contain Paneth cells.
Benign ovarian mucinous tumors: Immunohistochemistry.
Positive: CK7.
Mucinous cystadenoma vs. mucin-secreting serous cystadenoma.
In a serous tumor, any mucin is apical only.
Follicular cyst: Special stain.
Reticulin stains demonstrates network around thecal cells but not about granulosa cells.
Follicular cyst: Age group.
Occur most often in the reproductive years but can appear at any age.
Benign ovarian mucinous tumors: Associated tumors (4).
Dermoid cyst.
Appendiceal mucoceles.
Pseudomyxoma peritonei.
Brenner tumors.
Pseudomyxoma peritonei: Associated tumors (2).
Appendiceal tumor.
Mucinous ovarian tumor.
Mucinous borderline tumors: Possible laboratory abnormality.
Elevated serum inhibin.
Mucinous borderline tumors: Types.
Endocervical-type: Less common, more likely to be bilateral, smaller.
Intestinal-type: More common, less likely to be bilateral, larger.
Mucinous borderline tumor vs. benign mucinous tumor (4).
Borderline mucinous tumor:
− More crowding of structures.
− More nuclear atypia.
− More nuclear stratification.
− More mitotic activity.
Mucinous carcinoma of the ovary: Possible laboratory findings (4).
Elevated
− CEA.
− CA19-9.
− CA125.
− Inhibin.
Mucinous carcinoma of the ovary: Laterality.
Less than 20% are bilateral.
Mucinous carcinoma of the ovary: Immunohistochemistry (3,2).
Positive: CK7, CK20, CEA.
Negative: Vimentin, WT-1.
Krukenberg’s tumor: Origin (2).
Stomach (#1).
Breast.
Krukenberg’s tumor vs. mucinous carcinoma of the ovary.
Krukenberg’s tumor:
− Usually bilateral.
− Contains signet-ring cells.
Mucinous carcinoma of the ovary: Prognosis.
Five-year-survival rate is about 40%.
Endometrioid tumors of the ovary: Types.
Carcinoma (most tumors).
Benign tumors (rare).
Borderline tumors (rare).
Endometrioid tumors of the ovary: Laboratory finding.
Elevated serum CA125.
Endometrioid carcinoma of the ovary: Laterality.
About 30% of tumors are bilateral.
Endometrioid tumors of the ovary: Histology (3).
Benign: Usually adenofibromatous.
Borderline: Usually adenofibromatous; squamous morules often.
Malignant: Stromal invasion; squamous morules often.
Clear-cell tumors of the ovary: Types.
Carcinoma (most tumors).
Benign tumors (rare).
Borderline tumors (rare).
Clear-cell tumors of the ovary: Risk factors (2).
Endometriosis.
Malignant clear-cell tumor: Nulliparity.
Clear-cell tumors of the ovary: Histology (3).
Benign: Usually adenofibromatous; mature glands.
Borderline: Usually adenofibromatous; atypical glands.
Malignant: Stromal invasion.
Clear-cell tumors of the ovary: Stains (2).
Positive: PAS (diastase sensitive), cytokeratin.
Clear-cell carcinoma of the ovary: Appearances of cells (5).
Hobnail.
Flat.
Signet-ring.
Clear.
Oxyphilic.
Clear-cell carcinoma of the ovary: Additional cytologic features (3).
Inconspicuous nucleoli.
Many abnormal mitotic figures.
Hyaline globules.
Clear-cell carcinoma of the ovary: Patterns of growth (4).
Papillary.
Tubulocystic.
Solid.
Mixed.
Transitional-cell tumors of the ovary:
A. Synonym.
B. Types (3).
A. Brenner tumors.
B. Benign (most cases), borderline, malignant.
Benign transitional-cell tumor of the ovary: Cytology (2).
Nucleus: Grooved.
Cytoplasm: Pale.
Benign transitional-cell tumor of the ovary: Architecture (3).
Well-defined nests and trabeculae of transitional epithelium.
Cysts lined by glandular epithelium.
Densely fibrotic stroma.
Borderline transitional-cell tumor of the ovary: Cytology.
More necrosis, more mitotic activity than in benign tumor.
Borderline transitional-cell tumor of the ovary: Architecture.
Nests are poorly defined.
Transitional-cell carcinoma of the ovary: Cytology (3).
More pleomorphism.
More mitotic activity.
Occasional necrosis.
Transitional-cell carcinoma of the ovary: Architecture (2).
Destructive stromal invasion.
Some single tumor cells.
Transitional-cell tumors of the ovary: Immunohistochemistry (2).
Positive: CK8/18.
Negative: CK20.
Benign transitional-cell tumor vs. mucinous cystadenoma.
Mucinous cystadenoma: No transitional cells.
Transitional-cell tumors of the ovary: Associated tumors (4).
Dermoid cyst.
Struma ovarii.
Carcinoid tumor.
Mucinous cystadenoma.
Transitional-cell carcinoma of the ovary: Prognosis.
Poor unless unilateral.
Malignant mixed müllerian tumor of the ovary: Epithelial component (2).
Serous or endometrioid carcinoma.
There may be bizarre tumor cells.
Malignant mixed müllerian tumor of the ovary: Mesenchymal component (6).
Homologous
− Endometrial stromal sarcoma.
− Fibrosarcoma.
− Leiomyosarcoma.
Heterologous
− Chondrosarcoma.
− Rhabdomyosarcoma.
− Osteosarcoma.
Malignant mixed müllerian tumor of the ovary vs. immature teratoma (3).
Immature teratoma
− First and second decades of life.
− Contains immature neuroectodermal tissue.
− Cartilage is immature rather than chondrosarcomatous.
Malignant mixed müllerian tumor of the ovary: Behavior.
Early metastasis to omentum, pelvic organs, liver.
Most common ovarian sex cord−stromal tumor.
Fibroma.
Ovarian fibroma: Genetic association.
Basal-cell-nevus syndrome.
Ovarian fibroma: Nongenetic associations.
Meigs’ syndrome: Ascites, hydrothorax, ovarian fibroma.
No hormonal association (nonfunctioning tumor).
Ovarian fibroma:
A. Laterality.
B. Size.
A. The vast majority are bilateral.
B. Most are greater than 3 cm; if less than 1 cm, it is a fibromatosis nodule.
Ovarian fibroma: Cytology (2).
Bland spindle cells, often in a storiform pattern, with few mitotic figures.
A minor sex-cord component (tubules) may be present.
Ovarian fibroma: Stroma.
Hyalinized and often exhibits intercellular edema.
Thecoma: Clinical types.
Classic: Postmenopausal women.
Luteinized: Younger patients, estrogenic, can cause endometrial hyperplasia and carcinoma.
Thecoma: Laterality.
Most are unilateral.
Classic thecoma: Histology (3).
Plump, lipid-laden, haphazardly arranged spindle cells.
Hyaline plaques may be present.
Granulosa cells make up less than 10% of the tumor.
Luteinized thecoma: Histology.
Theca cells and spindle cells are luteinized (much clear or pink cytoplasm; central, round nucleus).
Thecoma: Stains (2).
Positive: Reticulin (fibers surround cells), inhibin.
Thecoma vs. stromal hyperthecosis.
Stromal hyperthecosis: Almost always bilateral.
Adult granulosa-cell tumor: Age of peak incidence.
Fifth decade.
Adult granulosa-cell tumor: Possible hormonal manifestations (3).
Uterine bleeding.
Endometrial hyperplasia.
Endometrial carcinoma.
Adult granulosa-cell tumor: Acute complication.
Rupture and bleeding into the peritoneum.
Adult granulosa-cell tumor: Classic pattern.
Microfollicular.
Adult granulosa-cell tumor: Variant appearances of granulosa cells (2).
Luteinized.
Large, dark nuclei; sometimes multinucleate.
Adult granulosa-cell tumor: Features of diffuse and sarcomatoid patterns (5).
Less differentiation.
Few Call-Exner bodies.
More nuclear pleomorphism.
More mitotic activity.
Spindle cells.
Adult granulosa-cell tumor: Other patterns (5).
Trabecular.
Insular.
Macrofollicular.
Watered-silk.
Gyriform.
Adult granulosa-cell tumor: Immunohistochemistry (3,1).
Positive: Inhibin, calretinin, vimentin.
Often positive: CD56.
Adult granulosa-cell tumor: Prognosis (2).
May recur decades later.
Stage I: Ten-year survival rate is 80-90%.
Juvenile granulosa-cell tumor: Age group.
First three decades of life.
Juvenile granulosa-cell tumor vs. adult granulosa-cell tumor: Cytology (3).
The cells of juvenile granulosa-cell tumor
− Lack nuclear grooves.
− Have more cytoplasm.
− Are often luteinized.
Juvenile granulosa-cell tumor: Additional cytologic features (2).
There may be nuclear atypia.
There may be frequent mitotic figures.
Juvenile granulosa-cell tumor vs. adult granulosa-cell tumor: Contents of follicles.
JGCT: Mucicarmine-positive secretions.
AGCT: Basement-membrane matter.
Juvenile granulosa-cell tumor: Prognosis.
Usually good; excision cures some.
Sclerosing stromal tumor of the ovary: Age of peak incidence.
Second decade.
Sclerosing stromal tumor of the ovary: Histologic components.
Pseudo-lobules.
Thin-walled vessels.
Sclerosing stromal tumor of the ovary: Cells of pseudo-lobules (2).
Fibroblasts.
Vacuolated, lipid-laden cells.
Sclerosing stromal tumor of the ovary: Stroma of pseudo-lobules.
Edematous or densely collagenous (sclerosing).
Sclerosing stromal tumor of the ovary: Immunohistochemistry (2).
Positive: Inhibin, vascular markers.
Sertoli-cell tumor of the ovary: Age of peak incidence.
Second decade.
Sertoli-cell tumor of the ovary: Function.
Usually nonfunctioning but can be androgenic or estrogenic.
Sertoli-cell tumor of the ovary: Cytology (2).
Most tumors: Similar to benign Sertoli cells.
Some tumors: Large, lipid-rich Sertoli cells.
Sertoli-cell tumor of the ovary: Architecture (3).
Tubules filled with neoplastic Sertoli cells.
Fibrous or hyalinized stroma.
No Leydig cells.
Sertoli-cell tumor of the ovary: Immunohistochemistry (2,1).
Positive: Cytokeratin, inhibin.
Negative: EMA.
Sertoli-cell tumor of the ovary: Prognosis.
Excellent if well differentiated.
Regarded as a low-grade malignancy.
Sertoli-Leydig cell tumor of the ovary: Age group.
Any age, but especially in the second decade.
Sertoli-cell tumor of the ovary: Endocrine effect.
Virilization or hirsutism due may be seen in half of patients.
Sertoli-cell tumor of the ovary: Possible hematologic manifestation.
Erythrocytosis due to androgens.
Juvenile granulosa-cell tumor: Histology (3).
Sheets of cells and immature follicles.
Sertoli-cell tumor of the ovary: Histology of well-differentiated tumor.
Similar to that of Sertoli-cell tumor, but with clusters of Leydig cells in the stroma.
Sertoli-cell tumor of the ovary: Histology of tumor of intermediate differentiation (4).
Cellular nodules in a fibrous or edematous stroma.
Sertoli cells form tubules, clusters, and cords.
Sertoli cells have darker nuclei and less cytoplasm than benign Sertoli cells.
Leydig cells form clusters.
Sertoli-cell tumor of the ovary: Histology of poorly differentiated tumor (2).
Diffuse pattern of densely packed pleomorphic spindle cells.
Many mitotic figures.
Sertoli-cell tumor of the ovary: Heterologous elements (3).
Not seen in well-differentiated SLCT.
Most common: Benign mucinous epithelium of gastrointestinal type.
Others: Immature skeletal muscle and/or immature cartilage.
Retiform Sertoli-cell tumor of the ovary: Histology (3).
Similar to that of well-differentiated SLCT, with the addition of
− Tubules and cysts of rete testis−type epithelium.
− Other patterns of SLCT elsewhere in the tumor.
Sertoli-cell tumor of the ovary: Immunohistochemistry.
Positive for inhibin.
Sertoli-cell tumor of the ovary: Associated tumor.
Rare association with botryoid embryonal rhabdomyosarcoma of the cervix.
Sex-cord tumor with annular tubules: Syndrome.
One third of tumors are associated with Peutz-Jeghers syndrome.
Sex-cord tumor with annular tubules: Architecture.
Simple (ring-shaped) and complex (interconnecting rings) tubules surround hyaline matter.
Sex-cord tumor with annular tubules: Cytology.
Cells lining the tubules have much pale cytoplasm; the nuclei face the periphery of the ring.
Sex-cord tumor with annular tubules: Histologic feature associated with syndrome.
Peutz-Jeghers syndrome: Tubules may be calcified.
Sex-cord tumor with annular tubules: Behavior.
One fourth of cases are malignant; lymphatic spread is typical.
Sex-cord tumor with annular tubules: Classification.
Considered a sex cord−stromal tumor that can differentiate toward granulosa-cell tumors or Sertoli-cell tumors.
Gynandroblastoma: Histology.
Contains at least 10% of each:
− Granulosa-cell component.
− Sertoli-cell component.
Gynandroblastoma: Behavior.
Almost always benign.
Stromal luteoma:
A. Classification.
B. Behavior.
A. Steroid-cell tumor.
B. Benign.
Stromal luteoma: Architecture.
Nodules of lutein cells confined to the ovarian stroma.
Stromal luteoma: Cytology.
Nucleus: Small, round, with prominent nucleolus.
Cytoplasm: Eosinophilic, lipid-poor.
Leydig-cell tumor:
A. Synonym.
B. Presentation.
A. Hilus-cell tumor.
B. Classically androgenic but can be estrogenic.
Leydig-cell tumor: Histology.
Variable arrangements of Leydig cells.
The cells contain the eosinophilic crystalloids of Reinke.
Leydig-cell tumor: Immunohistochemistry.
Positive: Inhibin.
Dermoid cyst: Rule of 15.
Bilateral in 15% of cases.
Usually less than 15 cm in diameter.
Dermoid cyst: Histology.
All three germ layers are typically represented, i.e. not just skin.
Malignant transformation of dermoid cyst:
A. Frequency.
B. Type of malignancy.
C. Typical patient.
A. Less than 3%.
B. Squamous-cell carcinoma.
C. Postmenopausal woman.
Mature solid teratoma: Age group.
First and second decades.
Mature solid teratoma: Histology.
Same as that of dermoid cyst except that it is solid.
Dysgerminoma:
A. Frequency.
B. Associations.
A. Most common malignant germ-cell tumor of the ovary.
B. Ovarian dysgenesis; pregnancy.
Dysgerminoma: Possible laboratory findings (2).
Elevated LDH.
Elevated hCG.
Dysgerminoma: Histology.
Resembles seminoma.
Dysgerminoma: Immunohistochemistry (2).
Positive: PLAP.
Negative: Cytokeratin (usually), EMA.
Dysgerminoma: Metastasis.
Occurs late:
− Initially by the lymphatics.
− Later by the blood vessels to liver, lungs, bone.
Yolk-sac tumor: Age of peak incidence.
Second and third decades.
Yolk-sac tumor, glandular variant: Histology (2).
Intestinal and endometrioid types exist.
Hepatoid cells in the glandular lumens may mimic squamous morules.
Yolk-sac tumor: Immunohistochemistry (3).
Positive: AFP, α₁-antitrypsin, creatine kinase.
Yolk-sac tumor, hepatoid variant vs. hepatoid carcinoma (2).
Yolk-sac tumor, hepatoid variant:
− Less nuclear atypia.
− Accompanied by other types of YST.
Embryonal carcinoma: Age of peak incidence.
First decade.
Embryonal carcinoma: Laboratory finding.
Elevated hCG.
Embryonal carcinoma: Histology (2).
Similar to that of testicular embryonal carcinoma.
Also contains syncytiotrophoblasts.
Embryonal carcinoma: Immunohistochemistry (2,1).
Positive: PLAP (syncytiotrophoblasts), cytokeratin.
Negative: EMA.
Polyembryoma:
A. Age group.
B. Possible laboratory findings (2).
A. Children, young adults.
B. Elevated AFP, elevated hCG.
Polyembryoma: Histologic components (3).
Embryoid bodies representing various stages of development.
Syncytiotrophoblasts sometimes.
Fibrous or edematous stroma.
Polyembryoma: Histology of mature embryoid body (4).
Embryonic disk:
− Columnar ectoderm.
− Cuboidal endoderm.
Amniotic cavity.
Yolk sac.
Extraembryonic mesenchyme.
Polyembryoma: Most commonly associated germ-cell tumor.
Teratoma (mature or immature).
Polyembryoma:
A. Behavior (2).
B. Treatment.
A. Invades locally and metastasizes distantly.
B. Excision and chemotherapy.
Choriocarcinoma: Age group.
Children and young adults.
Choriocarcinoma: Presentation (2).
Children: Isosexual precocious puberty.
Adults: Signs of ectopic pregnancy.
Choriocarcinoma: Cytology.
Cytotrophoblasts: Distinct cells borders; single vesicular nucleus with large nucleus.
Syncytiotrophoblasts: Indistinct cell borders; many hyperchromatic nuclei.
Choriocarcinoma: Locations of cells.
Cytotrophoblasts in the center, syncytiotrophoblasts surround it.
Choriocarcinoma: Immunohistochemistry (4).
Positive: Cytokeratin, hCG, hPL, PLAP.
Choriocarcinoma vs. other germ-cell tumors.
Other germ-cell tumors: No cytotrophoblasts.
Choriocarcinoma: Spread.
Hematogenous, lymphatic, and local spread.
Immature teratoma: Age at peak incidence.
Second and third decades.
Immature teratoma: Intraoperative finding.
Half of cases show capsular perforation with adhesion to adjacent structures.
Immature teratoma: Components.
Ectodermal: Primitive neural tissue, e.g. rosettes.
Mesodermal: Cartilage, muscle, mesenchyme.
Endodermal: Tubules lined by columnar epithelium.
Immature teratoma: Grade 0.
All tissues are mature.
No mitotic activity.
Immature teratoma: Grade 1.
Minor immature component.
Slight mitotic activity.
Immature teratoma: Grade 2.
Moderate immature component.
Moderate mitotic activity.
Immature teratoma: Grade 3.
Much immature tissue.
High mitotic activity.
Immature teratoma: Grade 4.
The teratoma takes over the woman, converting her to a slimy, creeping mass of immature tissue.
Immature teratoma: Spread.
Peritoneal implantation: Most common.
Lymphatic.
Hematogenous: Rare.
Immature teratoma:
A. Prognosis.
B. Treatment.
A. Poor for grades 2 and 3.
B. Surgery and chemotherapy.
Monodermal teratoma: Examples (2).
Struma ovarii.
Carcinoid tumor.
Struma ovarii: Presentation (3).
Usually asymptomatic.
Can cause mass-related symptoms.
Can cause thyrotoxicosis.
Struma ovarii:
A. Gross pathology.
B. Histology.
A. Green-brown cut surface; solid and/or cystic.
B. Mature thyroid tissue that can undergo oxyphilic and other benign changes.
Carcinoid tumor of the ovary: Presentation.
The carcinoid syndrome happens occasionally.
Carcinoid tumor of the ovary: Gross pathology.
Most carcinoids occur with other teratomatous elements:
− Dermoid cyst (most often).
− Mucinous cystic teratoma.
− Mature solid teratoma.
Carcinoid tumor of the ovary: Histology.
The insular pattern is the most common.
Gonadoblastoma:
A. Typical patient.
B. Presentation.
A. Phenotypic female with 46,XY or 45,X.
B. Virilization sometimes.
Gonadoblastoma: Gonad.
May be ambiguous, e.g. abdominal or inguinal testis, streak gonad.
Gonadoblastoma: Histology (3).
Nests consisting of seminoma-like germ-cell tumor with admixed Sertoli cells or granulosa cells.
Lutein or Leydig cells in the stroma between the nests.
May be calcified or hyalinized.
Hypercalcemic small-cell carcinoma: Age at peak incidence.
Second decade.
Hypercalcemic small-cell carcinoma: Cytology (4).
Small cells with fine chromatin and scant cytoplasm.
Large cells with hyperchromatic nucleus and much cytoplasm.
Necrosis and brisk mitotic activity.
May show focal mucinous differentiation.
Hypercalcemic small-cell carcinoma: Architecture.
May form small follicle-like structures containing eosinophilic matter.
Hypercalcemic small-cell carcinoma: Immunohistochemistry (3).
Negative: Neuroendocrine markers, inhibin, CEA.
Metastasis to the ovary: Relative frequency.
Less than 10% of ovarian tumors.
Metastasis to the ovary: Most common primary sites (4).
Gynecological tract (#1).
Intestine.
Stomach.
Breast.
Krukenberg tumor: Definition.
Any metastatic signet-ring tumor to the ovary (not just gastric).
Metastasis to the ovary: Frequency of bilaterality.
About 70%.
Metastasis to the ovary: Most common locations within the ovary.
Cortex and hilum.
Metastatic signet-ring tumor to the ovary vs. primary ovarian mucinous adenocarcinoma with signet rings (2).
Primary tumor:
− Typically unilateral.
− Signet rings are usually a minor component.
Acute and chronic salpingitis: Leading causes (3).
Sexually transmitted infections: Chlamydia, Neisseria.
Curettage.
Placement of IUD.
Granulomatous salpingitis: Causes (2).
Infectious agents: TB, parasites, Actinomyces.
Systemic diseases: Crohn’s, sarcoidosis.
Chronic salpingitis: End stage.
Hydrosalpinx.
Chlamydial salpingitis: Histologic clue.
Hyperplasia of lymphoid follicles.
Tubal endometriosis vs. physiologic extension of endometrial tissue into the tube.
Endometriosis involves serosa and subserosa.
Physiologic extension involves the mucosa only.
Endometrial colonization of the fallopian tube.
Physiologic extension with occlusion of the tubal lumen by endometrial tissue.
Salpingitis isthmica nodosa:
A. Age group.
B. Significance.
C. Cause.
A. Third and fourth decades.
B. Can lead to ectopic pregnancy.
C. Unknown.
Salpingitis isthmica nodosa: Gross pathology (2).
Nodules within the wall of the isthmus of the fallopian tube.
Often bilateral.
Salpingitis isthmica nodosa: Histology (2).
Nests or cysts of tubal epithelium, surrounded by muscular layer.
Connections to the tubal lumen can be demonstrated.
Tubal ectopic pregnancy: Risk factors (4).
Chronic salpingitis (#1).
Congenital abnormalities of the tube.
Salpingitis isthmica nodosa.
Endometriosis.
Tubal ectopic pregnancy: Most common site.
Ampulla.
Adenomatoid tumor of the fallopian tube: Patterns of growth (4).
Adenomatoid, glandular: Most common.
Solid.
Cystic.
Adenomatoid tumor of the fallopian tube: Immunohistochemistry (5).
Positive: Cytokeratin, vimentin, EMA, calretinin, WT-1.
Most common ___ tumor of the fallopian tube.
A. Epithelial.
B. Mesenchymal.
A. Papilloma.
B. Leiomyoma.
Epithelial papilloma of the fallopian tube: Histology.
Branching fibrovascular stalk.
Single layer of nonciliated columnar or oncocytic epithelium.
Epithelial papilloma of the fallopian tube vs. adenomatous hyperplasia.
In adenomatous hyperplasia the epithelium shows
− Stratification and disordered arrangement of cells.
− Cytologic atypia.
− Occasional mitotic figures.
Most common malignancy of the fallopian tube.
Metastatic.
Carcinoma of the fallopian tube: Age group.
Postmenopausal women.
Carcinoma of the fallopian tube: Significance of serous tubal intraepithelial carcinoma.
It is a precursor of ovarian serous carcinoma.
Carcinoma of the fallopian tube: Invasive types (4).
Serous (#1).
Mucinous, endometrioid, clear-cell.
Carcinoma of the fallopian tube: Intraoperative findings (2).
Often bilateral.
Nearly always invasive.
