Female 1 Flashcards
Mesonephric-like vulvar cyst:
A. Lining.
B. Wall.
C. Contents.
A. Cuboidal or columnar
B. Smooth muscle.
C. Clear fluid.
Ciliated vulvar cyst:
A. Lining.
B. Wall.
A. Ciliated and secretory columnar; may be pseudostratified.
B. No smooth muscle.
Periurethral cyst: Lining.
Transitional epithelium.
Hidradenoma papilliferum:
A. Synonym.
B. Age group.
A. Papillary hidradenoma.
B. Middle age.
Hidradenoma papilliferum: Origins (2).
Apocrine sweat glands.
Ectopic breast tissue.
Hidradenoma papilliferum: Lining.
Luminal layer of columnar or cuboidal cells.
Basal layer of myoepithelial cells.
Herpes viral infection: Histology (4).
“Multinucleation, margination, and molding.”
Ground-glass intranuclear inclusions.
Ballooning degeneration of keratinocytes.
Epidermal necrosis and vesiculation.
Molluscum contagiosum: Cause.
A DNA virus.
Vulvar condyloma: Types of HPV.
6, 11.
Vulvar condyloma: Grading.
Mitotic figures and cytologic atypia:
− Confined to the lower third: VIN 1.
− Present in the middle third: VIN 2.
Vulvar condyloma acuminatum: Behavior (2).
Most lesions regress spontaneously.
Some have progressed to high-grade dysplasia or to carcinoma.
Lichen sclerosus: Relation to squamous-cell carcinoma.
LS is not considered a precancerous condition.
SCC arises in up to 5% of cases of LS in postmenopausal women.
Lichen sclerosus: Treatment.
Topical corticosteroids.
Lichen simplex chronicus vs. squamous-cell hyperplasia.
Squamous-cell hyperplasia is like LSC but without the dermal changes.
Lichen simplex chronicus: Relation to squamous-cell carcinoma.
None known.
The vulvo-gingival syndrome.
Lichen planus involving vulva, vagina, and oral mucosa.
Lichen planus: Histology of advanced disease (2).
Epidermal atrophy.
Postinflammatory hypopigmentation.
Cyst of Bartholin’s duct: Cause.
Obstruction of the duct.
Cyst of Bartholin’s duct:
A. Lining.
B. Contents.
A. Squamous, transitional, or cuboidal.
B. Secretions but no laminated keratin.
Lower Anogenital Squamous Terminology (LAST) terms for ___.
A. Condyloma acuminatum.
B. Bowenoid papulosis.
A. LSIL.
B. HSIL.
Vulvar erythroplasia of Queyrat: Grade.
VIN 3.
Squamous-cell carcinoma of the vulva: Epidemiology.
Young women who smoke and have HPV-associated lesion.
Postmenopausal women without evidence of HPV.
Superficially invasive SCC of the vulva: Criteria (2).
Depth of invasion of more than 1 mm (measured from the base of the nearest dermal papilla).
Less than 2 cm in diameter.
Invasive SCC of the vulva: Criterion.
Depth of invasion is than 1 mm.
Invasive SCC of the vulva: Grading.
Grade 1: No undifferentiated cells; keratin pearls.
Grade 2: Less than half of cells are undifferentiated.
Grade 3: More than half of cells are undifferentiated.
Verrucous carcinoma of the vulva: Synonym.
Giant condyloma of Buschke and Löwenstein.
Warty carcinoma of the vulva:
A. Synonym.
B. Silhouette.
A. Condylomatous carcinoma.
B. Papillary and exophytic.
Warty carcinoma of the vulva: Histology (3).
Fibrovascular fronds.
Many koilocytes.
Irregularly outlined nests of invasive tumor at the base.
Squamous-cell carcinoma of the vulva: Important histologic prognostic factors (4).
Dimensions of tumor
− Thickness.
− Depth of invasion.
− Diameter.
Invasion of lymphatic spaces.
Squamous-cell carcinoma of the vulva: Relation of depth of invasive to nodal status.
Depth of invasion greater than 1 mm imparts a significantly greater risk of involvement of inguinal lymph nodes.
Squamous-cell carcinoma of the vulva: Treatment (2).
Superficially invasive: Wide local excision.
Invasive: Partial or total vulvectomy with inguinal lymph-node dissection.
Malignant melanoma of the vulva: Most common location.
Labia.
Malignant melanoma of the vulva: Clinical appearance.
Up to 35% are amelanotic.
Malignant melanoma of the vulva:
A. Behavior (2).
B. Prognosis.
A. Usually already deeply invasive at diagnosis; frequently recurs locally.
B. About half of patients are dead within 5 years.
Carcinoma of Bartholin’s gland:
A. Age group.
B. Clinical appearance.
A. Older women.
B. May mimic cyst or abscess.
Carcinoma of Bartholin’s gland: Histologic types (5).
Squamous-cell carcinoma.
Adenocarcinoma.
Adenoid-cystic carcinoma.
Transitional-cell carcinoma.
Adenosquamous carcinoma.
Carcinoma of Bartholin’s gland: Immunohistochemistry (2).
Positive:
− CEA in adenocarcinoma.
− S-100 in adenoid-cystic carcinoma.
Carcinoma of Bartholin’s gland: Prognosis (2).
Overall, lymph nodes are involved in up to 40% of cases.
Best prognosis: Adenoid-cystic carcinoma.
Worst prognosis: Adenocarcinoma.
Extramammary Paget’s disease:
A. Presentation.
B. Clinical tool.
A. Often with pruritus.
B. Fluorescein highlights the lesion for excision.
Extramammary Paget’s disease: Origin (2).
Probably represents carcinoma in situ of the sweat ducts.
Not necessarily associated with invasive carcinoma of the vulva.
Extramammary Paget’s disease:
A. Behavior (2).
B. Treatment.
A. Slow progression; often recurs because true extent is difficult to estimate clinically.
B. Wide local excision.
Extramammary Paget’s disease: Clinical appearance.
Red scaly patches with white areas of hyperkeratosis.
Extramammary Paget’s disease: Frequency of underlying adenocarcinoma in the dermis.
10-20%.
Extramammary Paget’s disease: Stains (5).
Positive: CK7, CEA, PAS, mucicarmine, alcian blue.
Granular-cell tumor: Possible confounder.
Pseudoepitheliomatous hyperplasia mimicking SCC.
Angiomyofibroblastoma: Presentation (2).
Painless; clinically resembles cyst of Bartholin’s gland.
Angiomyofibroblastoma: Histology (4).
Hypo- and hypercellular areas.
Thin-walled vessels around which spindle cells congregate.
Edematous or collagenous matrix.
Lymphocytic inflammation.
Angiomyofibroblastoma: Immunohistochemistry (1,1,4).
Positive: Desmin.
Negative: SMA.
Variable: S100, ER, PR, CD34.
Aggressive angiomyxoma vs. angiomyofibroblastoma: Gross pathology.
Aggressive angiomyxoma: Deeper and poorly circumscribed.
Aggressive angiomyxoma: Age group.
Premenopausal women.
Aggressive angiomyxoma: Histology (3).
Benign spindled (myo)fibroblasts in a myxoid stroma.
Medium-sized or large vessels surrounded by collagen and bundles of smooth muscle.
Normal structures may be entrapped.
Aggressive angiomyxoma: Immunohistochemistry (3).
Positive: SMA, ER, PR.
Aggressive angiomyxoma: Behavior.
Locally aggressive; often recurs locally.
Leiomyosarcoma of the vulva: Usual location.
Labium majus.
Leiomyosarcoma of the vulva: Clues to malignancy in a cytologically bland tumor (3).
Infiltrative margins.
Coagulative necrosis.
More than 5 mitotic figures per 10 hpf.
Leiomyosarcoma of the vulva: Behavior (2).
More likely to recur if more than 5 cm in diameter.
May metastasize to lung and liver.
Leiomyosarcoma of the vulva: Treatment.
Wide excision.
Vaginal polyp: Synonyms (2).
Fibroepithelial polyp.
Mesodermal stromal polyp.
Vaginal polyp: Histology.
Resembles ordinary fibroepithelial polyp, but the following could cause confusion with a sarcoma:
− Atypical-appearing myofibroblasts.
− Bizarre multinucleate giant cells.
Vaginal intraepithelial neoplasia:
A. Behavior.
B. Treatment (3).
A. Less than 10% of cases progress to invasive carcinoma.
B. Excision, laser ablation, 5-FU.
Squamous-cell carcinoma of the vagina: Those with low rates of metastasis to lymph nodes (2).
Conventional SCC with less than 3 mm of depth of stromal invasion.
Verrucous carcinoma.
Squamous-cell carcinoma of the vagina: Treatment (2).
Most types: Radiation.
Verrucous carcinoma: Radiation is contraindicated because it can cause transformation to SCC of higher grade.
Vaginal adenosis: Relation to diethylstilbestrol.
Occurs in about 1/3 of women exposed in utero to diethylstilbestrol.
Vaginal adenosis:
A. Presentation.
B. Clinical appearance.
A. Mucoid discharge from the vagina.
B. Red granular spots that iodine does not stain.
Vaginal adenosis: Causes other than diethylstilbestrol (2).
5-FU.
CO₂ laser.
Vaginal adenosis: Most common location.
Upper third of anterior wall of vagina.
Vaginal adenosis: Histology (3).
Usually endocervical-type mucosa, but can be ciliated or endometrial-type.
Mucinous glands in the lamina propria.
Squamous metaplasia in longstanding lesions.
Vaginal adenosis:
A. Behavior.
B. Significance.
A. Usually regresses spontaneously.
B. Rarely associated with clear-cell adenocarcinoma of vagina and cervix.
Clear-cell adenocarcinoma of the vagina: Association (2).
Occurs in very few women who were exposed in utero to DES.
Also occurs in women with no exposure to DES.
Clear-cell adenocarcinoma of the vagina: Typical age of patient.
About 20 years.
Clear-cell adenocarcinoma of the vagina: Patterns of growth (5).
Nodulocystic, solid (most common).
Papillary.
Tubular.
Trabecular.
Clear-cell adenocarcinoma of the vagina: Cytology (3).
The hobnail cell is characteristic.
Other appearances: flat, cuboidal, oxyphilic, signet rings.
Intracellular hyaline and/or psammoma bodies.
Clear-cell adenocarcinoma of the vagina: Associated histologic finding.
Adenosis.
Clear-cell adenocarcinoma of the vagina:
A. Behavior.
B. Likelihood of nodal metastasis.
A. More aggressive than SCC.
B. High if the depth of invasion exceeds 3 mm.
Clear-cell adenocarcinoma of the vagina: Treatment (2).
Early stage: Vaginectomy and hysterectomy.
Late stage: Radiation.
Rhabdomyoma of the vagina:
A. Typical age of patient.
B. Presentation.
A. Middle-aged.
B. Vaginal bleeding, dyspareunia.
Embryonal rhabdomyosarcoma:
A. Most common location.
B. Gross pathology.
A. Anterior wall of vagina.
B. Botryoid.
Embryonal rhabdomyosarcoma: Layers (3).
Superficial: Attenuated squamous mucosa.
Intermediate: Cambium layer consisting of small round (and spindled) blue cells.
Deep: Sparser infiltrate of small round blue cells in a loose stroma.
Embryonal rhabdomyosarcoma: Cytology (3).
Strap cells are helpful but not necessary for the diagnosis.
Cells appear to condense around blood vessels.
Brisk mitotic activity.
Embryonal rhabdomyosarcoma: Immunohistochemistry (4).
Positive: Vimentin, desmin, myogenin, Myo-D1.
Embryonal rhabdomyosarcoma: Behavior (2).
Rapid local invasion; other pelvic organs may be involved at presentation.
Metastasis to lung or bone occurs late.
Müllerian papilloma:
A. Histology.
B. Significance.
A. Papillary tumor with broad fibrovascular cores covered by cuboidal or mucinous epithelium.
B. Clinically similar presentation to that of embryonal RMS.
Papillary adenofibroma of the cervix: Histology.
Similar to phyllodes tumor.
Microglandular hyperplasia: Associations (3).
Oral contraceptives.
Pregnancy.
Postpartum state.
Microglandular hyperplasia: Gross pathology.
Resembles small endocervical polyp; may be multiple.
Microglandular hyperplasia: Histology (3).
Glands are crowded but bland, with no more than 1 mitotic figures per 10 hpf.
Squamous metaplasia and signet-ring cells can be seen.
Inflammatory cells within glands and stroma.
Microglandular hyperplasia: Immunohistochemistry.
Negative: CEA.
Squamous intraepithelial lesion of the cervix: Type most likely to exhibit binucleate cells.
LSIL.
Microinvasive squamous-cell carcinoma of the cervix: Criteria (3).
Depth of invasion is less than 3 mm.
Diameter of invasion is less than 7 mm.
No invasion of vascular spaces.
Microinvasive squamous-cell carcinoma of the cervix: Point from which depth is measured (2).
Most cases: From the basal layer.
Next to a gland: From the top of the gland.
Verrucous carcinoma of the cervix:
A. Association.
B. Behavior.
A. HPV-6 and its subtypes.
B. Rarely metastasizes.
Papillary carcinoma of the cervix: Histology (3).
Papillae lined by several layers of atypical, mitotically active spindle cells.
May show focal squamous differentiation.
Resembles TCC of the genitourinary tract.
Lymphoepithelioma-like carcinoma of the cervix:
A. Cytology of malignant cells.
B. Association.
A. Abundant pink cytoplasm, vesicular nucleus, large nucleolus.
B. Not associated with EBV.
Squamous-cell carcinoma of the cervix: Immunohistochemistry (3).
Positive: Cytokeratin, p63.
Focal: CEA.
Squamous-cell carcinoma of the cervix: Poor prognostic factor.
Overexpression of p21 in large-cell keratinizing and in non-keratinizing SCCs.
Glassy-cell carcinoma of the cervix: Histology (4).
Discrete cell borders.
Ground-glass cytoplasm.
Large nucleoli.
Many mitotic figures.
Invasive squamous-cell carcinoma of the cervix: Treatment.
Radical hysterectomy with or without adjuvant chemotherapy.
Adenocarcinoma in situ of the cervix: Presentation (2).
Usually asymptomatic and incidentally discovered.
Adenocarcinoma in situ of the cervix: Associations (4).
HPV-18.
Obesity.
Hypertension.
Progesterone-containing OCPs.
Adenocarcinoma in situ of the cervix: Histology (4).
High ratio of nucleus to cytoplasm.
Nuclear atypia.
Cellular stratification.
Mitotic figures, apoptotic bodies.
Adenocarcinoma in situ of the cervix: Most common types (3).
Endocervical.
Intestinal.
Endometrioid.
Immunohistochemistry for CEA in the endocervix.
Absent in normal endocervical glands.
Usually present in mucinous adenocarcinomas.
Adenocarcinoma in situ of the cervix: Immunohistochemistry (3).
Positive: p16, CEA, vimentin.
Microinvasive adenocarcinoma in situ of the cervix: Criteria (2).
Depth of invasion is less than 5 mm.
Diameter of invasion is less than 7 mm.
Microinvasive adenocarcinoma in situ of the cervix: Point from which depth is measured.
From the basement membrane.
Adenocarcinoma in situ of the cervix: Treatment.
Cervical conization.
Invasive adenocarcinoma of the cervix: Age group.
Fourth and fifth decades.
Invasive adenocarcinoma of the cervix: Histologic types (8).
Mucinous: Endocervical, intestinal, signet-ring-cell.
Endometrioid.
Minimal-deviation.
Well-differentiated papillary-villoglandular.
Clear-cell.
With features of carcinoid tumor.
Invasive adenocarcinoma of the cervix: Criterion of mixed type.
At least two histologic types each make up at least 10% of the tumor.
Minimal-deviation adenocarcinoma of the cervix: Histology (4).
Cytologically bland glands.
Irregular contours and variable size.
Infiltration deep (more than 5 mm) into the cervix.
May elicit stromal desmoplasia.
Papillary-villoglandular adenocarcinoma of the cervix: Age group.
Third and fourth decades.
Papillary-villoglandular adenocarcinoma of the cervix: Histology (4).
Complex branching papillae.
Stratified columnar lining: endocervical, endometrial, or intestinal.
Cytologically bland.
May invade deeply.
Clear-cell adenocarcinoma of the cervix: Association.
DES in some cases.
Clear-cell adenocarcinoma of the cervix: Patterns of growth (5).
Solid, tubulocystic (most common).
Papillary.
Tubular.
Trabecular.
Clear-cell adenocarcinoma of the cervix: Histology.
Similar to that of clear-cell adenocarcinoma of the vagina.
Cervical adenocarcinoma with features of carcinoid tumor: Significance (2).
Rarely causes paraneoplastic syndromes.
Unresponsive to the usual therapy.
Invasive adenocarcinoma of the cervix: Grading.
Moderately differentiated: Glands make up 10-50% of the tumor.
Endometrioid adenocarcinoma of the cervix vs. direct extension of endometrial adenocarcinoma (3).
Direct extension of endometrial adenocarcinoma:
− Clinical history.
− No HPV.
− No endocervical adenocarcinoma in situ.
Invasive adenocarcinoma of the cervix: Importance of size (2).
Less than 1 cm: Unlikely to metastasize.
More than 5 cm: Radiation therapy.
Adenosquamous carcinoma of the cervix: Histopathology.
Poorly differentiated SCC + high-grade adenocarcinoma.
Neuroendocrine tumors of the cervix:
A. Presentation.
B. Gross pathology.
A. Paraneoplastic syndromes sometimes.
B. Often ulcerated.
Neuroendocrine tumors of the cervix: Type of HPV.
HPV-18 has been detected.
Neuroendocrine tumors of the cervix: Treatment.
Radical hysterectomy.
Bilateral dissection of pelvic and periaortic lymph nodes.
Radiation if nodes are positive.
Metastases to the cervix: Most common origins (3).
Ovary.
Breast.
Endometrium.
Cervical vs. endometrial origin of adenocarcinoma: Immunohistochemistry.
Cervical origin: CEA, CDX2 (mucinous types), p16.
Endometrial origin: Vimentin.
Acute endometritis: Associations (3).
Pelvic inflammatory disease (#1).
Intrauterine contraceptive device.
Pregnancy.
Causes of neutrophils in the endometrium (4).
Normal endometrium
− Late secretory.
− Menstrual.
− Early proliferative.
Acute endometritis.
Chronic endometritis: Associations (2).
Intrauterine device.
Compression by a uterine leiomyoma.
Chronic endometritis: Histology (5).
Plasma cells.
Glands in various phases.
Focal glandular crowding.
Glandular epithelium may show mild cytologic atypia.
Stromal cells may be spindled.
Endometrial polyp: Pharmacological cause.
Tamoxifen.
Endometrial polyp:
A. Most common location.
B. Origin.
A. Uterine fundus.
B. Basalis.
Endometrial polyp: Mutation.
inv(6) in some polyps.
Adenomyomatous polyp.
An endometrial polyp with much muscle in the stroma.
Atypical polypoid adenomyoma: Location.
Lower uterine segment.
Atypical polypoid adenomyoma: Histology (2).
Irregularly shaped glands in a smooth-muscle stroma.
No desmoplasia; few or no mitotic figures.
Atypical polypoid adenomyoma: Cytology (2).
Epithelium is atypical but not markedly so.
Squamous metaplasia and central necrosis may be seen.
Endometrial hyperplasia: Risk factors (3).
Obesity.
Nulliparity.
Increased estrogen (whether endogenous or exogenous).
Endometrial hyperplasia: Genetic association.
Inactivation of PTEN.
Endometrial hyperplasia: Relation of diagnosis to phase.
Hyperplasia is most often diagnosed in the proliferative phrase, rarely in the secretory phase.
Endometrial hyperplasia: Simple vs. complex.
Simple: Rounded glands.
Complex: Branched glands, never cribriform.
Endometrial hyperplasia: Clinically most important diagnostic information.
Presence of absence of atypia is more important than simple vs. complex architecture.
Endometrial hyperplasia: Additional histologic finding.
Squamous metaplasia.
Endometrial hyperplasia vs. endometrial adenocarcinoma (3).
Endometrial adenocarcinoma:
− Cribriform structures and back-to-back glands.
− Desmoplastic stroma.
− Cytologic atypia may be no worse than in hyperplasia with atypia.
Endometrial hyperplasia: Treatment (2).
Trial of progestin.
Persistent hyperplasia: Hysterectomy.
Endometrial intraepithelial carcinoma:
A. Median age at presentation.
B. Significance.
A. 60 years.
B. Likely precursor lesion of uterine serous carcinoma.
Endometrial intraepithelial carcinoma: Histology (3).
Occurs on the surface endometrium, including the surfaces of polyps.
Markedly atypical nuclei with prominent nucleoli as in invasive serous carcinoma.
Adjacent endometrium is usually atrophic.
Endometrial intraepithelial carcinoma: Immunohistochemistry (2).
Positive: p53.
Ki-67 shows high proliferative index.
Endometrial carcinoma: Basic types (2).
Type I: Preceded by endometrial hyperplasia; associated with unopposed estrogen.
Type II: Preceded by endometrial intraepithelial carcinoma.
Endometrioid endometrial carcinoma: Grading.
Grade 2: Solid areas make up 5-50% of the tumor.
Marked nuclear atypia and mitotic figures increase the grade by one.
Endometrial adenocarcinoma with squamous differentiation (2).
Squamous areas may be benign or malignant; prognosis is not affected either way.
Squamous areas are ignored when assigning grade.
Villoglandular adenocarcinoma of the endometrium: Histology (2).
Short papillae lined by low-grade cells.
Papillae lined by high-grade cells should be called serous carcinoma.
Secretory adenocarcinoma of the endometrium:
A. Association.
B. Histology (3).
A. Hormonal therapy.
B. Resembles secretory endometrium; tumor cells are of low grade and contain glycogen; glands contain secretions.
Ciliated carcinoma of the endometrium.
Contains ciliated cells; usually low grade.
Serous carcinoma of the endometrium: Histology (2).
Markedly pleomorphic cells lined thick and thin papillae.
Psammoma bodies occur in 30% of cases.
Types of endometrial carcinomas that are of high grade (grade 3) by definition.
Serous and clear-cell.
Clear-cell carcinoma of the endometrium:
A. Patterns of growth (4).
B. Cytology.
A. Papillary, glandular, solid, mixed.
B. Pleomorphic cells and hobnail cells filled with glycogen.
Mucinous adenocarcinoma of the endometrium: Diagnosis.
More than half of the tumor cells show mucinous differentiation.
Squamous-cell carcinoma of the endometrium:
A. Diagnosis.
B. Association.
A. Cervical SCC must be excluded.
B. Squamous metaplasia of the endometrial lining (ichthyosis uteri).
Mixed carcinoma of the endometrium: Diagnosis.
At least two different types of carcinoma, at least 10% of each.
Undifferentiated carcinoma of the endometrium: Histologic types (3).
Small-cell.
Giant-cell.
Spindle-cell.
Endometrial carcinoma: Immunohistochemistry (4).
Positive: Vimentin.
Negative: CEA.
Most serous and clear-cell carcinomas lack ER and PR and express p53.
Adenofibroma of the endometrium: Histology (3).
Resembles fibroadenoma of the breast.
Often contains cysts and papillae.
Fewer than 4 stromal mitotic figures per 10 hpf.
Adenofibroma of the endometrium: Treatment.
Hysterectomy.
Adenosarcoma of the endometrium: Mitotic rate.
More than 5 stromal mitotic figures per 10 hpf.
Adenosarcoma of the endometrium: Gross pathology.
Solitary sessile polypoid mass, often large.
Adenosarcoma of the endometrium: Histology.
Resembles phyllodes tumor of the breast.
Adenosarcoma of the endometrium: Stromal cells (2).
More densely aggregated around cystlike spaces and along clefts.
At least 4 mitotic figures per 10 hpf.
Adenosarcoma of the endometrium: Epithelial cells.
Usually endometrioid, but other types are possible.
Adenosarcoma of the endometrium: Third histologic element (2).
Sex cord−like cells are epithelial, have foamy cytoplasm, and are arranged in trabeculae, insulae, or tubules.
Present in 5% of tumors.
Adenosarcoma of the endometrium: Heterologous elements.
Rhabdomyosarcoma more often than chondrosarcoma.
Adenosarcoma of the endometrium vs. carcinosarcoma.
In adenosarcoma, only the mesenchymal component is malignant.
Carcinosarcoma of the endometrium: Synonyms (2).
Metaplastic carcinoma.
Malignant mixed müllerian (or mesodermal) tumor.
Carcinosarcoma of the endometrium: Association.
Pelvic radiation therapy.
Carcinosarcoma of the endometrium: Epithelial component.
Endometrial adenocarcinoma, any type.
Carcinosarcoma of the endometrium: Mesenchymal component (2).
Homologous: May resemble fibrosarcoma, leiomyosarcoma, endometrial stromal sarcoma.
Heterologous: Rhabdomyosarcoma, chondrosarcoma, osteosarcoma, others.
Carcinosarcoma of the endometrium: Immunohistochemistry (3).
Epithelial component: Positive for CK8/18.
Endometrial stromal sarcoma: Positive for CD10.
Heterologous components: As expected.
Carcinosarcoma of the endometrium:
A. Histology of metastasis (2).
B. Site of metastasis.
A. Epithelial early; mesenchymal (with or without epithelial) layer.
B. Lungs.
Adenomyosis: Diagnosis.
Endometrial glands must be at least 2 mm deep to the basalis.
Endometrial adenocarcinoma involving adenomyosis vs. invasive endometrial adenocarcinoma.
Endometrial adenocarcinoma involving adenomyosis:
− Malignant glands are surrounded by endometrial stroma.
− No desmoplasia.
Uterine leiomyoma: Permissible and impermissible gross findings (3,2).
Permissible: Cystic degeneration, hyalinization, calcification.
Impermissible: Extensive hemorrhage, coagulative necrosis.
Uterine leiomyoma: Impermissible histologic finding.
Coagulative necrosis.
Epithelioid uterine leiomyoma: Variants (3).
Clear-cell.
Plexiform.
Leiomyoblastoma.
Plexiform epithelioid uterine leiomyoma: Histology.
Rows and columns of epithelioid cells separated by fibrous stroma.
Leiomyoblastoma: Histology (3).
Eccentric nuclei.
Granular pink cytoplasm.
Hyalinization.
Symplastic leiomyoma: Histology.
Otherwise typical leiomyoma that contains scattered or focally clustered bizarre giant cells.
Intravascular leiomyomas.
Intravenous leiomyomatosis: Leiomyomas follow the myometrial veins beyond the uterus but do not metastasize.
Benign metastasizing leiomyoma.
Uterine leiomyoma: Mitotic rate.
Usually no more than 5 per 10 hpf.
Exception: Mitotically active leiomyoma can have up to 20 per 10 hpf, but the histology is otherwise typical.
Uterine leiomyoma: Immunohistochemistry (5).
Positive: Desmin, caldesmon, SMA.
Often positive: ER, PR.
Leiomyoma: Electron microscopy (3).
Actin filaments.
Dense bodies.
Incomplete basal lamina.
Uterine leiomyoma: Types regarded as having uncertain malignant potential (4).
Epithelioid.
Symplastic.
Intravenous.
Any leiomyoma with more than 5 mitotic figures per 10 hpf in a woman over 35 years of age.
Uterine leiomyosarcoma: Treatment.
Surgery and radiation.
Uterine leiomyosarcoma: Variants (2).
Epithelioid.
Myxoid.
Endometrial stromal nodule: Histology (3).
Cells resemble those of endometrial stroma.
Usually no more than 10 mitotic figures per 10 hpf.
Evenly spaced thin-walled vessels.
Endometrial stromal nodule: Border.
Pushing.
Endometrial stromal nodule: Possible additional histologic findings (2).
Small foci of necrosis.
Structures resembling sex cords.
Endometrial stromal nodule: Immunohistochemistry (2,2).
Positive: CD10, vimentin.
Negative: SMA, desmin.
Endometrial stromal nodule: Prognosis.
Cured by excision.
Low-grade endometrial stromal sarcoma: Gross pathology.
Wormlike masses within the myometrium represent intravascular invasion.
Low-grade endometrial stromal sarcoma: Histology (4).
Similar to that of endometrial stromal nodule, except that LGESS shows
− Infiltrative growth.
− Lymphovascular invasion.
− Mitotic rate of 10-20 per 10 hpf.
Low-grade endometrial stromal sarcoma:
A. Treatment.
B. Prognosis.
A. TAH-BSO.
B. May recur years later.
High-grade endometrial stromal sarcoma: Gross pathology.
Infiltration is more diffuse, rarely wormlike.
High-grade endometrial stromal sarcoma: Histology (5).
Thin-walled vessels are unevenly distributed.
May show heterologous differentiation.
Usually no epithelioid foci.
Frequent lymphovascular invasion.
Coagulative necrosis.
High-grade endometrial stromal sarcoma: Cytology (3).
Some cells may retain resemblance to endometrial stromal cells.
Pronounced cytologic atypia, sometimes with bizarre cells.
Usually more than 10 mitotic figures per 10 hpf.
High-grade endometrial stromal sarcoma: Immunohistochemistry (1,2,2).
Positive: Vimentin.
Negative: SMA.
Focal: Cytokeratin, CD10.
Endometrial stromal sarcoma: Best criterion for assigning grade.
Degree of cytologic atypia.
High-grade endometrial stromal sarcoma: Treatment.
Same as for leiomyosarcoma.
High-grade endometrial stromal sarcoma: Prognosis.
Most patients are dead within 5 years.
Endosalpingosis: Age group.
Reproductive age.
Endosalpingosis:
A. Origin.
B. Association.
A. Secondary müllerian system.
B. Atypical proliferative serous tumors.
Endosalpingosis:
A. Sites.
B. Histology (2).
A. Pelvic peritoneum covering pelvic organs.
B. Variably sized glands lined by a single layer fallopian tubal epithelial cells; may contain psammoma bodies.
Atypical endosalpingosis: Histology.
Endosalpingosis with cellular stratification and atypia.
Trophoblastic cells: Cytology (3).
Cytotrophoblasts: Small, mononuclear, pale or clear cytoplasm, distinct cell borders.
Syncytiotrophoblast: Large, multinucleate, opaque cytoplasm with vacuoles.
Intermediate trophoblast: Medium-sized, mononuclear, opaque cytoplasm without vacuoles, indistinct cell borders.
Trophoblastic cells: Positive immunohistochemical stains (3).
All trophoblasts: Cytokeratin.
Syncytiotrophoblasts: hCG.
Intermediate trophoblasts: hPL.
Exaggerated placental site: Synonym.
Exaggerated implantation site.
Exaggerated placental site: Histology (4).
Intermediate trophoblasts and syncytiotrophoblasts invade the myometrium.
Intermediate trophoblasts may invade the spiral arterioles.
Chorionic villi may be present.
Mitotic figures are rare.
Placental-site nodule: Laboratory finding.
Serum hCG is usually normal.
Placental-site nodule: Histology (3).
Mostly intermediate trophoblasts; rare syncytiotrophoblasts.
Extensive hyalinization.
Collapsed vascular lumens in the center of the mass.
Placental-site nodule:
A. Putative origin.
B. Treatment.
A. Unresorbed involuted placental site.
B. None needed.
Normal chorionic villi: Histology (3).
Little or no edema.
Polar trophoblastic proliferation.
No scalloping of villous borders.
Complete hydatidiform mole: Timing.
Occurs in the second trimester.
Complete hydatidiform mole: Possible consequences (3).
Persistent gestational trophoblastic disease.
Another complete mole.
Choriocarcinoma.
Complete hydatidiform mole: Histology (4).
All villi are abnormal.
Central cisternae (acellular spaces).
Irregular, diffuse circumferential proliferation of trophoblasts.
No fetal parts, no nucleated red blood cells.
Complete hydatidiform mole: Histology (2).
Positive: p53.
Focally positive: p57.
Complete hydatidiform mole: Cytogenetics.
Usually 46,XX.
Sometimes 46,XY.
Sometimes triploid.
Complete hydatidiform mole: Origin.
All chromosomes come from the sperm.
Complete hydatidiform mole: Treatment (2).
Complete evacuation.
Chemotherapy may be indicated if hCG is still elevated at day 60.
Partial hydatidiform mole: Possible consequences (2).
Persistent gestational trophoblastic disease.
Negligible risk for choriocarcinoma.
Partial hydatidiform mole: Histology (4).
Only some villi are abnormal.
Edematous villi with irregular, scalloped borders.
Proliferation of trophoblast is focal instead of circumferential.
Nucleated red blood cells may be visible.
Partial hydatidiform mole: Immunohistochemistry (2).
p53: Weaker staining than in complete mole.
p57: More diffuse standing than in complete mole.
Partial hydatidiform mole: Cytogenetics.
69,XXX or 69,XXY: Dispermatic fertilization.
Complete vs. partial hydatidiform mole: Uterine size.
Complete: Large for gestational age.
Partial: Small for gestational age.
Complete vs. partial hydatidiform mole: Serum hCG.
Complete: Persistently elevated.
Partial: Slightly elevated.
Complete vs. partial hydatidiform mole: Trophoblastic proliferation.
Complete: Circumferential.
Partial: Focal.
Invasive hydatidiform mole: Gross pathology.
Invasion of myometrium or beyond.
Invasive hydatidiform mole: Histology.
Similar to that of complete (or partial) mole, up with invasion of myometrium or of myometrial vascular spaces.
Invasive hydatidiform mole vs. placenta accreta.
Placenta accreta (increta, percreta):
− Normal villi without molar change.
− No villi in the blood vessels.
Invasive hydatidiform mole: Behavior (2).
Can cause uterine rupture.
Hydronic villi may be embolized to lungs and brain but usually regress spontaneously.
Invasive hydatidiform mole: Treatment.
Chemotherapy.
Invasive hydatidiform mole vs. choriocarcinoma.
Choriocarcinoma has no chorionic villi.
Since invasive mole and choriocarcinoma both cause persistently elevated hCG after evacuation of molar pregnancy, and both respond to chemotherapy, tissue diagnosis is not often required for treatment.
Invasive hydatidiform mole: Antecedent.
Usually a complete mole.
Gestational choriocarcinoma: Histology (3).
No chorionic villi.
Cytotrophoblasts mixed with syncytiotrophoblasts or with intermediate trophoblasts.
Necrosis, mitosis, pleomorphism, vascular invasion.
Gestational choriocarcinoma: Sites of metastasis (5).
Early: Vagina, lung.
Later: Brain, bone marrow, liver.
Gestational choriocarcinoma: Treatment.
Responds well to chemotherapy.
Placental-site trophoblastic tumor: Associations.
Usually follows normal pregnancy or missed abortion (rather than a molar pregnancy).
Placental-site trophoblastic tumor: Effects on the uterus (2).
Enlargement.
Perforation sometimes.
Placental-site trophoblastic tumor: Laboratory finding.
Mildly but persistently elevated serum hCG.
Placental-site trophoblastic tumor: Behavior.
Most examples are considered benign.
Placental-site trophoblastic tumor: Predominant cell.
Intermediate trophoblast.
Placental-site trophoblastic tumor: Histology.
Infiltration between bundles of myometrial smooth muscle.
Vascular invasion and replacement of vascular walls.
Deposition of fibrinoid matter in and around vascular walls.
Placental-site trophoblastic tumor: Indicators of poor prognosis (5).
High cellularity.
High mitotic index.
Marked necrosis.
Local spread.
Distant metastasis.
Placental-site trophoblastic tumor: Immunohistochemistry (2).
hPL: Diffuse expression, reflecting predominance of intermediate trophoblasts.
hCG: Focal.
Placental-site trophoblastic tumor vs. choriocarcinoma (2).
Choriocarcinoma:
− Very high serum hCG.
− No fibrinoid matter in and around blood vessels.
Placental-site trophoblastic tumor: Putative pathogenesis.
Dysregulation of intermediate trophoblasts.
Placental-site trophoblastic tumor: Possible extrauterine complication.
Hematuria, proteinuria, eosinophilic deposits in the glomerular capillaries.
Placental-site trophoblastic tumor: Treatment.
Malignant examples do not respond to chemotherapy.
