Breast Flashcards
Plasma-cell mastitis: Clinical appearance.
May evolve into a hard mass that, together with axillary lymphadenopathy, can mimic carcinoma.
Plasma-cell mastitis: Inflammatory changes (2).
Extensive lymphoplasmacytic infiltrate.
Xanthomatous reaction sometimes.
Plasma-cell mastitis: Epithelial changes (2).
Hyperplasia, necrosis.
Plasma-cell mastitis: Special stains.
Negative: GMS, PAS, AFB.
Subareolar abscess:
A. Surgical association.
B. Clinical appearance.
A. Reduction mammoplasty.
B. Can mimic that of inflammatory carcinoma.
Subareolar abscess: Causes (5).
Staphylococcus.
Streptococcus.
Bacteroides.
Proteus.
Mycobacterium tuberculosis.
Subareolar abscess: Epithelial changes (2).
Squamous metaplasia of ducts.
Keratin plugs in lactiferous ducts.
Plasma-cell mastitis: Typical patient.
Woman who has stopped lactating years ago.
Granulomatous mastitis:
A. Etiology.
B. Clinical appearance.
A. Unknown.
B. Hard mass that may mimic carcinoma.
Granulomatous mastitis: Histology (2).
Granulomatous inflammation of lobules.
Giant cells, plasma cells, and eosinophils accompany the granulomas.
Granulomatous mastitis vs. sarcoidosis.
Sarcoidosis: Noncaseating, naked granulomas that are usually found between the lobules.
Granulomatous mastitis: Behavior.
May recur and require many excisions.
Fat necrosis: Clinical appearance.
May mimic carcinoma clinically and on mammogram.
Fat necrosis: Later histologic changes (3).
Fibroblasts and collagen deposition.
Scar.
Calcification (“eggshell calcifications”) on mammogram.
Diabetic mastopathy: Typical patient.
Premenopausal woman with diabetes of the first type.
Diabetic mastopathy:
A. Clinical appearance (2).
B. Mamographic appearance.
A. Hard, mobile mass; often bilateral.
B. Nonspecific.
Diabetic mastopathy: Histology (3).
Densely fibrotic, keloid-like stroma.
Lymphocytes around small vessels, lobules, ducts.
Calcifications may be visible.
Juvenile hypertrophy:
A. Age of patient.
B. Mammographic appearance.
A. Less than 16 years.
B. Benign.
Juvenile hypertrophy: Histology (2).
Proliferation of ducts and connective tissue but not of lobules.
May resemble gynecomastia.
Juvenile hypertrophy: Genetics.
Most cases are sporadic.
Cases with PTEN mutation are more likely to turn malignant.
Granular-cell tumor:
A. Typical location.
B. Mammographic appearance.
A. Upper inner quadrant.
B. Mimics carcinoma.
Granular-cell tumor: Immunohistochemistry (2,1).
Positive: S100, CEA.
Variable: CD68.
Granular-cell tumor: Electron microscopy (2).
Many lysosomes.
Myelin figures.
Granular-cell tumor: Morphologic differential diagnosis (4).
Apocrine carcinoma.
Metastatic renal-cell carcinoma.
Metastatic melanoma.
Metastatic alveolar soft-part sarcoma.
Granular-cell tumor: Treatment.
Ya gotta cut it all out, or it might come back.
Fibrocystic changes: Histologic components (5).
Cysts.
Stromal fibrosis.
Apocrine metaplasia.
Sclerosing adenosis.
Epithelial hyperplasia without atypia.
Fibrocystic disease: Risk of carcinoma.
Sclerosing adenosis and florid ductal hyperplasia without atypia: Slightly increased risk.
All other changes: No increase in risk.
Columnar-cell lesions: Types (3).
Columnar-cell change.
Columnar-cell hyperplasia.
Flat epithelial atypia.
Columnar-cell lesions: Histologic location.
Terminal ductal-lobular units.
Columnar-cell change: Histology (4).
Dilated acini.
Bland, mitotically inactive cells.
Up to two layers of epithelium.
Apocrine snouts and luminal secretions may be visible.
Columnar-cell hyperplasia: Histology (2).
More than two layers of epithelium.
Papillae.
Flat epithelial atypia: Histology.
Essentially columnar-cell change or columnar-cell hyperplasia with cytologic atypia.
Nuclei are round and no longer oriented perpendicular to the basement membrane.
Columnar-cell lesions: Immunohistochemistry (4,3).
Positive: ER, PR, bcl-2, LMW-CK.
Negative: p53, Her-2, HMW-CK.
Columnar-cell change: Genetics.
Loss of 16q.
Adenosis: Potentially misleading histologic features (4).
Florid adenosis: Focal necrosis, infarction.
Sclerosing adenosis: Growth around nerves.
Microglandular adenosis: Absence of myoepithelial cells (even by IHC), loss of lobular pattern.
Microglandular adenosis: Additional histologic features (3).
Extension around normal epithelial structures and sometimes into the fat.
Bland cells; rare mitotic figures.
PAS-positive eosinophilic secretions.
Atypical microglandular adenosis.
Consists of typical adenosis + areas of more complex structure and cytologic atypia.
Microglandular adenosis: Immunohistochemistry (4,2).
Positive: Cytokeratin, S100, cathepsin D, collagen IV.
Negative: EMA, ER.
Microglandular adenosis vs. infiltrating tubular carcinoma (4).
Tubular carcinoma:
− Angular ducts.
− Stroma is rich in fibroblasts instead of hypocellular.
− No eosinophilic secretions.
− Usually expresses EMA and ER.
Adenosis: Risk of carcinoma.
Slightly increased.
Radial sclerosing lesion: Types.
Radial scar: Less than 1 cm in diameter.
Complex sclerosing lesion: At least 1 cm in diameter.
Radial sclerosing lesion: Radiography.
Center: Dense radiolucency.
Periphery: Radiating linear densities.
Radial sclerosing lesion: Histology.
Center: Collagenous scar with fibrosis and elastosis.
Periphery: Entrapped ducts with epithelial layer, myoepithelial layer, and basement membrane.
Radial sclerosing lesion: Infiltration (2).
Can infiltrate around nerves.
Should not infiltrate into the adjacent fat.
Radial sclerosing lesion: Relation to carcinoma (3).
May be confused mammographically and pathologically with carcinoma.
Carcinoma may arise in it.
May be associated with a increased risk of carcinoma.
Solitary intraductal papilloma:
A. Location.
B. Presentation.
A. Subareolar mass.
B. Serous or bloody discharge from the nipple.
Multiple papilloma: Location.
Peripheral breast tissue.
Intraductal papilloma: Myoepithelial layer.
Present but may be focally absent.
Intraductal papilloma: Possible types of metaplasia (5).
Apocrine.
Squamous.
Mucinous.
Clear-cell.
Sebaceous.
Intraductal papilloma: Confounding histologic features (2).
Sclerosis of cores with entrapment of ductal epithelium.
Infarction due to torsion of the papillae.
Atypical intraductal papilloma.
Intraductal papilloma containing ADH or DCIS.
Intraductal papilloma: Myoepithelial markers (6).
S100.
Calponin.
p63.
SMA.
Smooth-muscle-myosin heavy chain.
CD10.
Intraductal papilloma vs. atypical intraductal papilloma: Immunohistochemistry (2).
ER
− Papilloma without atypia: Expressed by only a minority of cells.
− Atypical papilloma: Expressed diffusely in areas of ADH and DCIS.
High-molecular-weight cytokeratins
− Papilloma without atypia: Expressed.
− Atypical papilloma: Not expressed in areas of ADH and DCIS.
Intraductal papilloma vs. encapsulated papillary carcinoma.
Papillary carcinoma: No myoepithelial cells.
Intraductal papilloma: Risk of carcinoma.
Increased with all types, solitary and multiple, with or without atypia.
Intraductal papilloma: Mutation.
Loss of heterozygosity at 16p13 in papillomas with florid hyperplasia.
Intraductal papilloma: Favorable histologic feature.
Apocrine metaplasia.
Florid papillomatosis of the nipple:
A. Presentation.
B. Clinical appearance.
A. Serous or bloody discharge.
B. Ulceration, erythema, and scaling of the nipple.
Florid papillomatosis of the nipple: Basic histology.
Florid ductal hyperplasia.
Florid papillomatosis of the nipple: Patterns of growth (4).
Sclerosing papillomatosis.
Papilloma.
Adenosis.
Mixed proliferative.
Florid papillomatosis of the nipple: Myoepithelial cells.
May be inconspicuous or absent in sclerosing lesions.
Florid papillomatosis of the nipple: Variation.
Areas of ADH, DCIS, or invasive carcinoma within the papillomatosis.
Florid papillomatosis of the nipple: Immunohistochemistry of the epithelial cells.
Positive: Cytokeratin 34βE12.
Florid papillomatosis of the nipple: Association with carcinoma.
Carcinoma is present or occurs later in 10% of cases.
Florid papillomatosis of the nipple: Treatment.
Complete excision, usually including the nipple.
Pseudoangiomatous stromal hyperplasia: Patients (2).
Woman of childbearing age.
Man with gynecomastia.
Pseudoangiomatous stromal hyperplasia: Gross pathology.
Well circumscribed and typically encapsulated.
Pseudoangiomatous stromal hyperplasia: Histology.
Myofibroblasts line slitlike spaces.
Densely collagenous stroma.
Pseudoangiomatous stromal hyperplasia: Differential diagnosis.
Low-grade angiosarcoma.
Pseudoangiomatous stromal hyperplasia: Treatment.
Wide local excision with clear margins.
Adenoma: Types (3).
Tubular.
Lactating.
Apocrine.
Tubular adenoma: Histology.
Densely packed ductal structures composed of a single layer of bland epithelial cells surrounded by myoepithelial cells.
Lactating adenoma: Histologic changes related to pregnancy (2).
Less secretion (than in adenomas resected postpartum).
Tendency toward infarction.
Adenoma: Association with carcinoma.
No increased risk of subsequent carcinoma.
Carcinoma can arise in an adenoma.
Fibroadenoma: Pharmacologic association.
Cyclosporine.
Giant fibroadenoma.
A fibroadenoma that is larger than 5 cm or that weighs more than 500 g.
Fibroadenoma vs. phyllodes tumor (3).
Phyllodes tumor:
− Leaflike architecture.
− May show cytologic atypia.
− May show increased mitotic activity.
Juvenile fibroadenoma.
Occurs in young girls.
More stromal cellularity than in typical fibroadenoma.
Fibroadenoma: Association with breast cancer.
No association if
− Fibroadenoma is not complex.
− There is no family history of breast cancer.
Fibroadenoma: Malignancies that can arise in it (3).
Lobular carcinoma in situ (#1).
Invasive lobular carcinoma.
Invasive ductal carcinoma.
Fibroadenoma: Treatment.
Rarely recurs if incompletely excised.
Phyllodes tumor: Age group.
Fifth and sixth decades.
Phyllodes tumor: Behavior.
Aggressive; frequently recurs.
Phyllodes tumor: Epithelial component (2).
Ductal epithelium similar to that of fibroadenoma.
Squamous metaplasia may occur.
Phyllodes tumor: Mesenchymal component.
Cellularity tends to be greatest around the ducts.
Phyllodes tumor: Metaplasia of the mesenchymal component.
Osseous, cartilaginous, fatty, or muscular.
Benign phyllodes tumor: Histology (5).
Fewer than 5 mitotic figures per 10 hpf.
Minimal pleomorphism.
No necrosis.
Discrete margins.
Cellularity may vary.
Malignant phyllodes tumor: Stromal overgrowth.
At least 10 microscopic fields without epithelium.
Malignant phyllodes tumor: Other histologic features (4).
More than 5 mitotic figures per 10 hpf.
Nuclear pleomorphism.
Necrosis.
Infiltrative margins.
Phyllodes tumor vs. carcinosarcoma.
Carcinosarcoma: Malignant epithelial and stromal components are separate from each other.
Phyllodes tumor: Metastasis (2).
Hematogenous dissemination to lungs, pleura, bones.
Usually only the sarcomatous component is represented.
Phyllodes tumor: Genetics (3).
+1q.
Overexpression of p53.
Complex karyotypic abnormalities.
Atypical ductal hyperplasia: Definition.
No more than 3 mm in diameter
− or −
No more than two duct spaces involved.
Atypical ductal hyperplasia vs. DCIS (4).
ADH:
− Smaller.
− More nuclear overlap.
− Less distinct cell membranes.
− Irregular (not “punched-out” secondary lumens).
Ductal carcinoma in situ: Variants (4).
Comedocarcinoma.
Cribriform.
Solid.
Micropapillary.
Ductal carcinoma in situ: V
E
Comedocarcinoma:
A. Nuclei.
B. Associated histologic feature.
A. High-grade (grade III).
B. Retrograde cancerization of lobules.
Cribriform DCIS: Nuclei (4).
Monotonous.
May show mild or moderate atypia.
Few mitotic figures.
Areas of necrosis may be seen.
Solid DCIS: Nuclei (2).
Intermediate grade.
Otherwise similar to those of cribriform DCIS.
Micropapillary DCIS: Histology (3).
False papillae are regularly distributed within the duct.
Minimal cytologic atypia.
Extensive involvement of the breast.
Ductal carcinoma in situ: Immunohistochemistry (4).
Her-2/neu: More often positive in high-grade tumors.
Ki-67: Positive in more than 20% of cells of high-grade tumors.
ER and PR: More often positive in low-grade tumors.
Laminin and type IV collagen: Positive.