Breast Flashcards

1
Q

Plasma-cell mastitis: Clinical appearance.

A

May evolve into a hard mass that, together with axillary lymphadenopathy, can mimic carcinoma.

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2
Q

Plasma-cell mastitis: Inflammatory changes (2).

A

Extensive lymphoplasmacytic infiltrate.

Xanthomatous reaction sometimes.

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3
Q

Plasma-cell mastitis: Epithelial changes (2).

A

Hyperplasia, necrosis.

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4
Q

Plasma-cell mastitis: Special stains.

A

Negative: GMS, PAS, AFB.

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5
Q

Subareolar abscess:

A. Surgical association.
B. Clinical appearance.

A

A. Reduction mammoplasty.

B. Can mimic that of inflammatory carcinoma.

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6
Q

Subareolar abscess: Causes (5).

A

Staphylococcus.

Streptococcus.

Bacteroides.

Proteus.

Mycobacterium tuberculosis.

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7
Q

Subareolar abscess: Epithelial changes (2).

A

Squamous metaplasia of ducts.

Keratin plugs in lactiferous ducts.

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8
Q

Plasma-cell mastitis: Typical patient.

A

Woman who has stopped lactating years ago.

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8
Q

Granulomatous mastitis:

A. Etiology.
B. Clinical appearance.

A

A. Unknown.

B. Hard mass that may mimic carcinoma.

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9
Q

Granulomatous mastitis: Histology (2).

A

Granulomatous inflammation of lobules.

Giant cells, plasma cells, and eosinophils accompany the granulomas.

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10
Q

Granulomatous mastitis vs. sarcoidosis.

A

Sarcoidosis: Noncaseating, naked granulomas that are usually found between the lobules.

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11
Q

Granulomatous mastitis: Behavior.

A

May recur and require many excisions.

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12
Q

Fat necrosis: Clinical appearance.

A

May mimic carcinoma clinically and on mammogram.

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13
Q

Fat necrosis: Later histologic changes (3).

A

Fibroblasts and collagen deposition.

Scar.

Calcification (“eggshell calcifications”) on mammogram.

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14
Q

Diabetic mastopathy: Typical patient.

A

Premenopausal woman with diabetes of the first type.

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15
Q

Diabetic mastopathy:

A. Clinical appearance (2).
B. Mamographic appearance.

A

A. Hard, mobile mass; often bilateral.

B. Nonspecific.

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16
Q

Diabetic mastopathy: Histology (3).

A

Densely fibrotic, keloid-like stroma.

Lymphocytes around small vessels, lobules, ducts.

Calcifications may be visible.

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17
Q

Juvenile hypertrophy:

A. Age of patient.
B. Mammographic appearance.

A

A. Less than 16 years.

B. Benign.

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18
Q

Juvenile hypertrophy: Histology (2).

A

Proliferation of ducts and connective tissue but not of lobules.

May resemble gynecomastia.

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19
Q

Juvenile hypertrophy: Genetics.

A

Most cases are sporadic.

Cases with PTEN mutation are more likely to turn malignant.

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20
Q

Granular-cell tumor:

A. Typical location.
B. Mammographic appearance.

A

A. Upper inner quadrant.

B. Mimics carcinoma.

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21
Q

Granular-cell tumor: Immunohistochemistry (2,1).

A

Positive: S100, CEA.

Variable: CD68.

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22
Q

Granular-cell tumor: Electron microscopy (2).

A

Many lysosomes.

Myelin figures.

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23
Q

Granular-cell tumor: Morphologic differential diagnosis (4).

A

Apocrine carcinoma.

Metastatic renal-cell carcinoma.

Metastatic melanoma.

Metastatic alveolar soft-part sarcoma.

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24
Q

Granular-cell tumor: Treatment.

A

Ya gotta cut it all out, or it might come back.

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25
Q

Fibrocystic changes: Histologic components (5).

A

Cysts.

Stromal fibrosis.

Apocrine metaplasia.

Sclerosing adenosis.

Epithelial hyperplasia without atypia.

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26
Q

Fibrocystic disease: Risk of carcinoma.

A

Sclerosing adenosis and florid ductal hyperplasia without atypia: Slightly increased risk.

All other changes: No increase in risk.

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27
Q

Columnar-cell lesions: Types (3).

A

Columnar-cell change.

Columnar-cell hyperplasia.

Flat epithelial atypia.

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28
Q

Columnar-cell lesions: Histologic location.

A

Terminal ductal-lobular units.

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29
Q

Columnar-cell change: Histology (4).

A

Dilated acini.

Bland, mitotically inactive cells.

Up to two layers of epithelium.

Apocrine snouts and luminal secretions may be visible.

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30
Q

Columnar-cell hyperplasia: Histology (2).

A

More than two layers of epithelium.

Papillae.

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31
Q

Flat epithelial atypia: Histology.

A

Essentially columnar-cell change or columnar-cell hyperplasia with cytologic atypia.

Nuclei are round and no longer oriented perpendicular to the basement membrane.

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32
Q

Columnar-cell lesions: Immunohistochemistry (4,3).

A

Positive: ER, PR, bcl-2, LMW-CK.

Negative: p53, Her-2, HMW-CK.

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33
Q

Columnar-cell change: Genetics.

A

Loss of 16q.

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34
Q

Adenosis: Potentially misleading histologic features (4).

A

Florid adenosis: Focal necrosis, infarction.

Sclerosing adenosis: Growth around nerves.

Microglandular adenosis: Absence of myoepithelial cells (even by IHC), loss of lobular pattern.

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35
Q

Microglandular adenosis: Additional histologic features (3).

A

Extension around normal epithelial structures and sometimes into the fat.

Bland cells; rare mitotic figures.

PAS-positive eosinophilic secretions.

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36
Q

Atypical microglandular adenosis.

A

Consists of typical adenosis + areas of more complex structure and cytologic atypia.

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37
Q

Microglandular adenosis: Immunohistochemistry (4,2).

A

Positive: Cytokeratin, S100, cathepsin D, collagen IV.

Negative: EMA, ER.

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38
Q

Microglandular adenosis vs. infiltrating tubular carcinoma (4).

A

Tubular carcinoma:

− Angular ducts.
− Stroma is rich in fibroblasts instead of hypocellular.
− No eosinophilic secretions.
− Usually expresses EMA and ER.

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39
Q

Adenosis: Risk of carcinoma.

A

Slightly increased.

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40
Q

Radial sclerosing lesion: Types.

A

Radial scar: Less than 1 cm in diameter.

Complex sclerosing lesion: At least 1 cm in diameter.

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41
Q

Radial sclerosing lesion: Radiography.

A

Center: Dense radiolucency.

Periphery: Radiating linear densities.

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42
Q

Radial sclerosing lesion: Histology.

A

Center: Collagenous scar with fibrosis and elastosis.

Periphery: Entrapped ducts with epithelial layer, myoepithelial layer, and basement membrane.

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43
Q

Radial sclerosing lesion: Infiltration (2).

A

Can infiltrate around nerves.

Should not infiltrate into the adjacent fat.

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44
Q

Radial sclerosing lesion: Relation to carcinoma (3).

A

May be confused mammographically and pathologically with carcinoma.

Carcinoma may arise in it.

May be associated with a increased risk of carcinoma.

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45
Q

Solitary intraductal papilloma:

A. Location.
B. Presentation.

A

A. Subareolar mass.

B. Serous or bloody discharge from the nipple.

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46
Q

Multiple papilloma: Location.

A

Peripheral breast tissue.

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47
Q

Intraductal papilloma: Myoepithelial layer.

A

Present but may be focally absent.

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48
Q

Intraductal papilloma: Possible types of metaplasia (5).

A

Apocrine.

Squamous.

Mucinous.

Clear-cell.

Sebaceous.

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49
Q

Intraductal papilloma: Confounding histologic features (2).

A

Sclerosis of cores with entrapment of ductal epithelium.

Infarction due to torsion of the papillae.

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50
Q

Atypical intraductal papilloma.

A

Intraductal papilloma containing ADH or DCIS.

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51
Q

Intraductal papilloma: Myoepithelial markers (6).

A

S100.

Calponin.

p63.

SMA.

Smooth-muscle-myosin heavy chain.

CD10.

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52
Q

Intraductal papilloma vs. atypical intraductal papilloma: Immunohistochemistry (2).

A

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.

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53
Q

Intraductal papilloma vs. encapsulated papillary carcinoma.

A

Papillary carcinoma: No myoepithelial cells.

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54
Q

Intraductal papilloma: Risk of carcinoma.

A

Increased with all types, solitary and multiple, with or without atypia.

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55
Q

Intraductal papilloma: Mutation.

A

Loss of heterozygosity at 16p13 in papillomas with florid hyperplasia.

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56
Q

Intraductal papilloma: Favorable histologic feature.

A

Apocrine metaplasia.

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57
Q

Florid papillomatosis of the nipple:

A. Presentation.
B. Clinical appearance.

A

A. Serous or bloody discharge.

B. Ulceration, erythema, and scaling of the nipple.

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58
Q

Florid papillomatosis of the nipple: Basic histology.

A

Florid ductal hyperplasia.

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59
Q

Florid papillomatosis of the nipple: Patterns of growth (4).

A

Sclerosing papillomatosis.

Papilloma.

Adenosis.

Mixed proliferative.

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60
Q

Florid papillomatosis of the nipple: Myoepithelial cells.

A

May be inconspicuous or absent in sclerosing lesions.

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61
Q

Florid papillomatosis of the nipple: Variation.

A

Areas of ADH, DCIS, or invasive carcinoma within the papillomatosis.

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62
Q

Florid papillomatosis of the nipple: Immunohistochemistry of the epithelial cells.

A

Positive: Cytokeratin 34βE12.

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63
Q

Florid papillomatosis of the nipple: Association with carcinoma.

A

Carcinoma is present or occurs later in 10% of cases.

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64
Q

Florid papillomatosis of the nipple: Treatment.

A

Complete excision, usually including the nipple.

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65
Q

Pseudoangiomatous stromal hyperplasia: Patients (2).

A

Woman of childbearing age.

Man with gynecomastia.

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66
Q

Pseudoangiomatous stromal hyperplasia: Gross pathology.

A

Well circumscribed and typically encapsulated.

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67
Q

Pseudoangiomatous stromal hyperplasia: Histology.

A

Myofibroblasts line slitlike spaces.

Densely collagenous stroma.

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68
Q

Pseudoangiomatous stromal hyperplasia: Differential diagnosis.

A

Low-grade angiosarcoma.

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69
Q

Pseudoangiomatous stromal hyperplasia: Treatment.

A

Wide local excision with clear margins.

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70
Q

Adenoma: Types (3).

A

Tubular.

Lactating.

Apocrine.

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71
Q

Tubular adenoma: Histology.

A

Densely packed ductal structures composed of a single layer of bland epithelial cells surrounded by myoepithelial cells.

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72
Q

Lactating adenoma: Histologic changes related to pregnancy (2).

A

Less secretion (than in adenomas resected postpartum).

Tendency toward infarction.

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73
Q

Adenoma: Association with carcinoma.

A

No increased risk of subsequent carcinoma.

Carcinoma can arise in an adenoma.

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74
Q

Fibroadenoma: Pharmacologic association.

A

Cyclosporine.

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75
Q

Giant fibroadenoma.

A

A fibroadenoma that is larger than 5 cm or that weighs more than 500 g.

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76
Q

Fibroadenoma vs. phyllodes tumor (3).

A

Phyllodes tumor:

− Leaflike architecture.
− May show cytologic atypia.
− May show increased mitotic activity.

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77
Q

Juvenile fibroadenoma.

A

Occurs in young girls.

More stromal cellularity than in typical fibroadenoma.

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78
Q

Fibroadenoma: Association with breast cancer.

A

No association if

− Fibroadenoma is not complex.
− There is no family history of breast cancer.

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79
Q

Fibroadenoma: Malignancies that can arise in it (3).

A

Lobular carcinoma in situ (#1).

Invasive lobular carcinoma.

Invasive ductal carcinoma.

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80
Q

Fibroadenoma: Treatment.

A

Rarely recurs if incompletely excised.

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81
Q

Phyllodes tumor: Age group.

A

Fifth and sixth decades.

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82
Q

Phyllodes tumor: Behavior.

A

Aggressive; frequently recurs.

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83
Q

Phyllodes tumor: Epithelial component (2).

A

Ductal epithelium similar to that of fibroadenoma.

Squamous metaplasia may occur.

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84
Q

Phyllodes tumor: Mesenchymal component.

A

Cellularity tends to be greatest around the ducts.

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85
Q

Phyllodes tumor: Metaplasia of the mesenchymal component.

A

Osseous, cartilaginous, fatty, or muscular.

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86
Q

Benign phyllodes tumor: Histology (5).

A

Fewer than 5 mitotic figures per 10 hpf.

Minimal pleomorphism.

No necrosis.

Discrete margins.

Cellularity may vary.

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87
Q

Malignant phyllodes tumor: Stromal overgrowth.

A

At least 10 microscopic fields without epithelium.

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88
Q

Malignant phyllodes tumor: Other histologic features (4).

A

More than 5 mitotic figures per 10 hpf.

Nuclear pleomorphism.

Necrosis.

Infiltrative margins.

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89
Q

Phyllodes tumor vs. carcinosarcoma.

A

Carcinosarcoma: Malignant epithelial and stromal components are separate from each other.

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90
Q

Phyllodes tumor: Metastasis (2).

A

Hematogenous dissemination to lungs, pleura, bones.

Usually only the sarcomatous component is represented.

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91
Q

Phyllodes tumor: Genetics (3).

A

+1q.

Overexpression of p53.

Complex karyotypic abnormalities.

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92
Q

Atypical ductal hyperplasia: Definition.

A

No more than 3 mm in diameter

− or −

No more than two duct spaces involved.

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93
Q

Atypical ductal hyperplasia vs. DCIS (4).

A

ADH:

− Smaller.
− More nuclear overlap.
− Less distinct cell membranes.
− Irregular (not “punched-out” secondary lumens).

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94
Q

Ductal carcinoma in situ: Variants (4).

A

Comedocarcinoma.

Cribriform.

Solid.

Micropapillary.

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95
Q

Ductal carcinoma in situ: V

A

E

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96
Q

Comedocarcinoma:

A. Nuclei.
B. Associated histologic feature.

A

A. High-grade (grade III).

B. Retrograde cancerization of lobules.

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97
Q

Cribriform DCIS: Nuclei (4).

A

Monotonous.

May show mild or moderate atypia.

Few mitotic figures.

Areas of necrosis may be seen.

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98
Q

Solid DCIS: Nuclei (2).

A

Intermediate grade.

Otherwise similar to those of cribriform DCIS.

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99
Q

Micropapillary DCIS: Histology (3).

A

False papillae are regularly distributed within the duct.

Minimal cytologic atypia.

Extensive involvement of the breast.

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100
Q

Ductal carcinoma in situ: Immunohistochemistry (4).

A

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.

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101
Q

Ductal carcinoma in situ: Low-grade.

A

Minimal nuclear pleomorphism.

No necrosis.

102
Q

Ductal carcinoma in situ: Intermediate-grade.

A

Minimal nuclear pleomorphism + necrosis

− or −

Moderate nuclear pleomorphism without necrosis.

103
Q

Ductal carcinoma in situ: High-grade.

A

Marked cytologic atypia + necrosis.

High mitotic rate.

104
Q

Ductal carcinoma in situ involving lobules vs. lobular carcinoma in situ (3).

A

DCIS:

− Cells are larger and more pleomorphic.
− Cell borders are more distinct.
− No intracytoplasmic mucin.

105
Q

Atypical ductal carcinoma: Association with carcinoma.

A

Fourfold to fivefold risk.

106
Q

Mammographic appearance of ___.

A. Atypical lobular hyperplasia.
B. Lobular carcinoma in situ.

A

Nonspecific calcifications.

107
Q

Atypical lobular hyperplasia and lobular carcinoma in situ: Laterality.

A

Much more often bilateral and multifocal than DCIS.

108
Q

Atypical lobular hyperplasia: Histology (3).

A

Bland cells fill lobules but do not distend them.

Only one lobular unit is involved and usually less than half of the acini.

Usually no intracytoplasmic mucin droplets (signet-ring cells).

109
Q

Lobular carcinoma in situ: Histology (3).

A

Bland cells expand the lobules.

May exhibit pagetoid spread into the adjacent ducts.

Signet-ring cells are often visible.

110
Q

Pleomorphic LCIS: Cytology.

A

Nucleoli are more conspicuous, and nuclei are considered grade III.

111
Q

Conventional LCIS: Immunohistochemistry (2,3).

A

Variable: ER, PR.

Negative: Her-2, p53, E-cadherin.

112
Q

Pleomorphic LCIS: Immunohistochemistry (3,2).

A

Positive: Her-2, GCDFP-15, p53.

Negative: ER, PR.

113
Q

Lobular neoplasia in situ.

A

Term that includes both atypical lobular hyperplasia and lobular carcinoma in situ.

114
Q

Atypical lobular hyperplasia and lobular carcinoma in situ: Treatment (2).

A

Diagnosed on needle biopsy: Excision.

Diagnosed on excision: Close follow-up and hormonal therapy.

115
Q

Atypical lobular hyperplasia and lobular carcinoma in situ: Most important mutated gene.

A

CDH1 (E-cadherin).

116
Q

Atypical lobular hyperplasia and lobular carcinoma in situ: Association with carcinoma (3).

A

Subsequent carcinoma may develop in either breast.

Any type of invasive carcinoma can occur.

LCIS: Up to tenfold risk.

117
Q

Infiltrating ductal carcinoma: Risk factors (5).

A

Family history.

Early menarche.

Late menopause.

Nulliparity or first parturition after age 30.

Obesity.

118
Q

Infiltrating ductal carcinoma: Genes associated with increased risk (5).

A

BRCA1 (chromosome 17), BRCA2 (chromosome 13): Up to 85% lifetime risk.

p53: Li-Fraumeni syndrome.

ATM, even in carriers.

PTEN.

119
Q

Infiltrating ductal carcinoma: Most important predictor of prognosis.

A

The status of the lymph nodes.

120
Q

Infiltrating ductal carcinoma: Grade I (3).

A

Ducts make up 75% of the tumor.

Relatively bland cells.

Rare mitotic figures.

121
Q

Infiltrating ductal carcinoma: Grade II (4).

A

Tubules are present but make up less than 75% of the tumor.

Twofold to threefold variation in size of cells.

Moderate nuclear pleomorphism.

Moderate mitotic activity.

122
Q

Infiltrating ductal carcinoma: Grade III (4).

A

No tubules.

Greater than threefold variation in size of cells.

Marked nuclear pleomorphism.

High mitotic activity; atypical mitotic figures.

123
Q

Infiltrating ductal carcinoma: Expression of ER and PR.

A

Grades I and II: Usually both are expressed.

Grade III: Usually neither is expressed.

ER is expressed and PR is lost in about 10-15% of tumors.

124
Q

Infiltrating ductal carcinoma: Expression of Her-2.

A

More common in tumors of higher grade.

125
Q

Infiltrating ductal carcinoma: Other immunohistochemistry (5).

A

Positive: CK8/18, CK19, CK7, EMA, E-cadherin.

126
Q

Infiltrating ductal carcinoma: Mutated genes (2).

A

RAS, Her-2.

127
Q

Infiltrating ductal carcinoma: Importance of concurrent DCIS.

A

Tumors in which more than 25% is DCIS have a worse prognosis.

128
Q

Infiltrating ductal carcinoma: Mutations that affect prognosis (2).

A

Expression of Her-2 and mutation of p53 bring a worse prognosis.

129
Q

Infiltrating ductal carcinoma: Cytogenetic effect on prognosis.

A

Increased S-phase fraction.

130
Q

Infiltrating lobular carcinoma: Classic pattern of growth.

A

Single cells or single files of cells in a sclerotic background, often growing concentrically around ducts.

131
Q

Infiltrating lobular carcinoma: Other patterns of growth (5).

A

Solid.

Tubulolobular.

Alveolar.

Apocrine.

Pleomorphic.

132
Q

Infiltrating lobular carcinoma: Immunohistochemistry.

A

Variable: ER, PR, Her-2.

133
Q

Infiltrating lobular carcinoma: Cytogenetics (2).

A

Classic: Loss of 16q, gain of 1p.

Pleomorphic: Overexpression of Her-2 and p53, loss of ER and PR.

134
Q

Infiltrating lobular carcinoma: Metastasis (4).

A

More likely than invasive ductal carcinoma to metastasize to bone marrow, ovary, serosal surfaces, CSF.

135
Q

Triple-negative carcinoma:

A. Frequency.
B. Epidemiology.

A

A. Accounts for 10-17% of all breast carcinomas.

B. More common in premenopausal women.

136
Q

Triple-negative carcinoma: Histology (4).

A

Most tumors are high-grade ductal carcinomas of no specific type.

Geographic necrosis.

Squamous metaplasia.

May undergo focal sarcomatoid change.

137
Q

Triple-negative carcinoma: Immunohistochemistry (6).

A

Most triple-negative carcinomas exhibit the basal-like phenotype, thus expressing

− CK 5/6, CK14, CK17.
− EGFR.
− SMA, p63.

138
Q

Triple-negative carcinoma: Related types of breast cancer (2).

A

Basal-like breast cancers.

BRCA1-related breast cancers.

139
Q

Triple-negative carcinoma: Metastasis.

A

Hematogenous, mainly to lungs and brain, less often to lymph nodes and bones.

140
Q

Medullary carcinoma: Gross pathology.

A

Firm and may be well circumscribed, sometimes even with a distinct capsule.

141
Q

Medullary carcinoma: Histology (5).

A

Syncytial growth.

High-grade nuclei.

Many mitotic figures.

Brisk lymphoplasmacytic response.

Well-defined, pushing borders.

142
Q

Medullary carcinoma: Incompatible histologic features (2).

A

Invasion of surround fat.

Glandular or ductal structures.

143
Q

Medullary carcinoma: Immunohistochemistry (3,1,3).

A

Positive: CK5/6, p53, Ki-67.

Often positive: EGFR.

Negative: ER, PR, Her-2.

144
Q

Medullary carcinoma: Genetics.

A

Often associated with mutation in BRCA1.

145
Q

Medullary carcinoma: Flow cytometry.

A

Tumor cells are often aneuploid or polyploid.

146
Q

Medullary carcinoma: Behavior.

A

Better prognosis.

Less likely to metastasize to axillary lymph nodes.

147
Q

Mucinous carcinoma:

A. Synonym.
B. Mammographic appearance.

A

A. Colloid carcinoma.

B. Well-circumscribed mass (also on gross examination).

148
Q

Mucinous carcinoma: Histology (2).

A

Lakes of mucin surround groups of infiltrating tumor cells.

Cells form sheets or clusters but usually form no glands.

150
Q

Mucinous carcinoma: Histologic subtypes.

A

Type A: Paucicellular, no neuroendocrine differentiation.

Type B: Hypercellular, neuroendocrine differentiation.

151
Q

Mucinous carcinoma: Immunohistochemistry (2,2,1).

A

Positive: CK7, neuroendocrine markers (in Type B).

Usually positive: ER, PR.

Negative: Her-2.

152
Q

Mucinous carcinoma: Flow cytometry.

A

Cells of pure mucinous carcinoma are usually diploid.

153
Q

Mucinous carcinoma vs. mucocele-like tumor.

A

Mucocele-like tumor: Mucous lakes are lined by benign epithelium and contain no floating clusters of cells.

154
Q

Mucinous carcinoma: Prognosis.

A

Better than that of infiltrating ductal carcinoma of no special type.

155
Q

Tubular carcinoma:

A. Most common age at presentation.
B. Mammographic appearance.
C. Gross appearance.

A

A. Fourth decade.

B. May be undetectable.

C. Firm, stellate, sclerotic.

156
Q

Tubular carcinoma: Cytology.

A

Bland; rare mitotic figures.

157
Q

Tubular carcinoma: Histology

A

Small, angulated tubules in a dense stroma.

May infiltrate into adjacent fat.

158
Q

Tubular carcinoma: Histologic requirement.

A

Pure tubular carcinoma: Essentially 100% of the tumor has tubular architecture.

159
Q

Tubular carcinoma: Immunohistochemistry (1,2).

A

Usually positive: ER.

Negative: Her-2, EGFR.

160
Q

Papillary carcinoma: Cytology.

A

Degree of atypia is typically not helpful in distinguishing between papillary carcinoma and benign papillary lesions.

161
Q

Mucinous carcinoma: Histologic requirement.

A

Extracellular mucin must make at least half of the tumor.

162
Q

Papillary carcinoma: Histology

A

Distended duct containing many complex papillary fronds.

163
Q

Papillary carcinoma: Incompatible features (2).

A

Complete layer of myoepithelial cells.

Apocrine metaplasia.

164
Q

Infiltrating papillary carcinoma: Histologic requirement.

A

There must be unequivocal infiltration of extracapsular stroma.

165
Q

Papillary carcinoma: Immunohistochemistry (2,2).

A

Positive: ER, PR.

Negative: Her-2, HMWCK.

166
Q

Papillary carcinoma vs. benign papillary lesions: Immunohistochemistry.

A

CEA: Most papillary carcinomas express it; benign papillary lesions do not.

167
Q

Invasive papillary carcinoma: Behavior.

A

Rarely spreads to lymph nodes.

168
Q

Metaplastic carcinoma: Types.

A

Biphasic: Carcinomatous and sarcomatous component.

Monophasic: Sarcomatous only.

169
Q

Metaplastic carcinoma: Histology of the carcinomatous component (2).

A

Most often poorly differentiated ductal carcinoma.

Squamous-cell carcinoma.

170
Q

Metaplastic carcinoma: Histology of the sarcomatous component (2).

A

Most often bone or cartilage.

Fibromatosis-like metaplastic carcinoma may be a low-grade variant.

171
Q

Metaplastic carcinoma: Histology of metastatic deposits.

A

Adenocarcinoma, metaplastic components,or both.

172
Q

Metaplastic carcinoma: Immunohistochemistry of the carcinomatous component (3).

A

Positive: Cytokeratin, EMA, vimentin.

173
Q

Metaplastic carcinoma: Immunohistochemistry of the sarcomatous component (3).

A

Positive: p63, vimentin, cytokeratin (focal).

174
Q

Metaplastic carcinoma: Prognostic markers.

A

Usually triple-negative.

175
Q

Metaplastic carcinoma: Effect of type of metaplasia on prognosis.

A

Chondroid or osseous: Worse prognosis.

Squamous: No effect on prognosis.

176
Q

Papillary carcinoma: Mutations (2).

A

Loss of heterozygosity of 16q23.

Loss of heterozygosity at locus of TP53.

177
Q

Secretory carcinoma: Mean age at presentation.

A

25 years.

178
Q

Secretory carcinoma: Histology (3).

A

Bland cells form back-to-back ducts.

Abundant eosinophilic cytoplasm.

Intracellular and extracellular PASD-positive secretions.

179
Q

Secretory carcinoma: Immunohistochemistry (4).

A

Positive: CEA, EMA, S-100, α-lactalbumin.

180
Q

Secretory carcinoma: Prognostic markers.

A

ER and PR are often not expressed.

181
Q

Secretory carcinoma: Electron microscopy.

A

Many membrane-bound secretory granules lined by microvilli.

182
Q

Secretory carcinoma: Mutation.

A

t(12;15)(p13;q35) :: ETV6−NTRK3.

183
Q

Secretory carcinoma vs. lactating adenoma (2).

A

Lactating adenoma:

− Sharply circumscribed.
− Retains myoepithelial cells.

184
Q

Secretory carcinoma: Prognosis.

A

Better than that of ductal carcinoma of no special type.

185
Q

Apocrine carcinoma: Mammographic appearance.

A

Similar to that of typical infiltrating ductal carcinoma.

186
Q

Apocrine carcinoma: Histology (3).

A

Apocrine cells forming nests, sheets, glands.

More pleomorphic nuclei and large nucleoli than in benign apocrine cells.

Architecture of intraductal apocrine carcinoma is similar to that of typical IDC.

187
Q

Apocrine carcinoma: Histologic requirement.

A

All or nearly all of the tumor cells are apocrine.

188
Q

Apocrine carcinoma: Immunohistochemistry (1,1,1).

A

Positive: CEA.

Often positive: Androgen receptor.

Negative: S100.

189
Q

Apocrine carcinoma: Prognostic markers.

A

ER and PR are variable expressed.

190
Q

Apocrine carcinoma: Special stain.

A

PAS-positive, diastase-resistant.

191
Q

Apocrine carcinoma: Behavior.

A

Similar to that of invasive ductal carcinoma of no special type.

192
Q

Adenoid-cystic carcinoma: Location.

A

Periareolar or subareolar.

193
Q

Adenoid-cystic carcinoma: Histology (3).

A

No perineural invasion.

May show squamous differentiation or sebaceous features.

Otherwise similar to AdCC of the salivary gland.

194
Q

Adenoid-cystic carcinoma: Grading.

A

Grade I: None of the tumor is solid.

Grade II: No more than 30% of the tumor is solid.

Grade III: More than 30% of the tumor is solid.

195
Q

Adenoid-cystic carcinoma: Immunohistochemistry (2).

A

Positive: Myoepithelial markers, CK7.

196
Q

Adenoid-cystic carcinoma: Prognostic markers.

A

ER and PR are usually not expressed.

197
Q

Adenoid-cystic carcinoma vs. invasive cribriform carcinoma (3).

A

Invasive cribriform carcinoma:

− No dual-cell population.
− No basement-membrane-like matter.
− Negative: S-100, SMA.

198
Q

Adenoid-cystic carcinoma: Behavior.

A

Much less aggressive than other mammary carcinomas.

Much less aggressive than AdCC of the salivary gland.

199
Q

Adenoid-cystic carcinoma: Mutation.

A

Alterations of chromosome 6q.

200
Q

Inflammatory carcinoma: Histology (2).

A

Usually an infiltrating ductal carcinoma, high-grade or poorly differentiated.

Tumor within dilated dermal lymphatics.

201
Q

Inflammatory carcinoma: Immunohistochemistry (2).

A

Positive: p53, E-cadherin.

202
Q

Inflammatory carcinoma: Prognostic markers.

A

Positive: Her-2.

Negative: ER, PR.

203
Q

Inflammatory carcinoma: Histologic requirements (2).

A

Invasive mammary carcinoma.

Tumor in the dermal lymphatics.

204
Q

Inflammatory carcinoma: Treatment.

A

Chemotherapy.

Mastectomy.

Radiation.

205
Q

Inflammatory carcinoma: Prognosis.

A

60% are dead within 5 years.

206
Q

Inflammatory carcinoma: Mutated genes (3).

A

Her-2.

RhoC.

LIBC/WISP3.

207
Q

Paget’s disease of the nipple: Association with carcinoma (2).

A

Usually accompanies concurrent carcinoma in the same breast, but rarely occurs without it.

Carcinoma is usually intraductal, often with an infiltrating component.

208
Q

Paget’s disease of the nipple: Cytology.

A

Nucleus: Large, with large nucleus.

Cytoplasm: Abundant, pale, vacuolated, may contain intracytoplasmic lumens.

209
Q

Paget’s disease of the nipple: Architecture.

A

Cells may occur individually are form clusters or glandlike structures.

210
Q

Paget’s disease of the nipple: Special stains.

A

Positive (50-60% of cases): Mucicarmine, PAS.

211
Q

Paget’s disease of the nipple: Immunohistochemistry (5,2).

A

Positive: CK7, EMA, CEA, AR, p53.

Negative: HMWCK, S100.

212
Q

Paget’s disease of the nipple: Prognostic markers (2).

A

Positive: Her-2, ER.

213
Q

Paget’s disease of the nipple: Treatment (2).

A

Mastectomy, whether or not a breast mass has been identified.

Tamoxifen may be used in premenopausal women with positive lymph nodes.

214
Q

Hemangioma: Typical location.

A

Perilobular breast tissue.

215
Q

Hemangioma: Most frequent type.

A

Cavernous.

216
Q

Hemangioma vs. low-grade angiosarcoma: Possibly helpful immunohistochemical stain.

A

Ki-67.

217
Q

Infantile hemangioma.

A

Associated with

− Decreased expression of Hox-A5.
− Immunopositivity for GLUT1.

218
Q

Angiosarcoma: Mean age at presentation.

A

Fourth decade.

219
Q

Angiosarcoma: Associations (2).

A

Irradiation.

Pregnancy.

220
Q

Angiosarcoma, low-grade: Histology (4).

A

Recognizable vascular channels with little or no endothelial tufts or papillary fronds.

Hyperchromatic nuclei without significant pleomorphism.

Few or no mitotic figures.

221
Q

Angiosarcoma, intermediate-grade: Histology (3).

A

Endothelial tufts and papillary fronds create focal hypercellular areas.

Moderate nuclear pleomorphism.

Few mitotic figures.

222
Q

Angiosarcoma, high-grade: Histology (5).

A

More endothelial tufts and papillae.

Marked nuclear pleomorphism.

Many mitotic figures, often atypical.

Necrosis.

Blood lakes.

223
Q

Angiosarcoma: Expression of cytokeratins.

A

Present in up to 35% of epithelioid angiosarcomas.

224
Q

Angiosarcoma, high-grade:

A. Epidemiology.
B. Prognosis.

A

A. Younger patients.

B. Poor.

225
Q

Angiosarcoma: Treatment.

A

Total mastectomy.

Axillary dissection is not indicated.

226
Q

Postmastectomy angiosarcoma: Association.

A

Status post mastectomy with or without irradiation.

227
Q

Postmastectomy angiosarcoma:

A. Frequency.
B. Timing.

A

A. Occurs in less than 0.45% of patients after mastectomy.

B. Occurs around 10 years after mastectomy.

228
Q

Postmastectomy angiosarcoma: Histology (5).

A

High-grade angiosarcoma in a densely collagenous background.

Changes of chronic lymphedema:
− Epidermal hyperplasia.
− Subcutaneous edema.
− Fibrosis.
− Proliferation of small vessels.
229
Q

Postmastectomy angiosarcoma vs. postirradiation angiosarcoma (2).

A

Postirradiation angiosarcoma:

− Occurs within the irradiated area.
− Occurs within 5 years after irradiation.

230
Q

Postmastectomy angiosarcoma: Treatment.

A

Amputation and chemotherapy.

231
Q

Postmastectomy angiosarcoma: Prognosis.

A

Most patients are dead within 2 years.

232
Q

Gynecomastia: Associated non-neoplastic diseases (4).

A

Cirrhosis.

Renal failure.

Chronic pulmonary disease.

Klinefelter’s syndrome.

233
Q

Gynecomastia: Associated neoplasms (4).

A

Germ-cell tumors.

Large-cell carcinoma of the lung.

Some gastric cancers.

Some renal cancers.

234
Q

Gynecomastia: Associated drugs (5).

A

Cimetidine.

Spironolactone.

Protease inhibitors.

Ethanol.

Anabolic steroids.

Others.

235
Q

Gynecomastia: Architecture.

A

Cribriform or micropapillary pattern is typical.

236
Q

Gynecomastia: Stromal changes (2).

A

Fibrosis.

Pseudoangiomatous stromal hyperplasia sometimes.

237
Q

Gynecomastia: Association with carcinoma.

A

None.

238
Q

Gynecomastia: Treatment (3).

A

Treatment of the causative disease.

Tamoxifen in early stage.

Surgery.

239
Q

Carcinoma of the male breast: Genetic risk factors (2).

A

Genes of high penetrance such as BRCA2.

Klinefelter’s syndrome.

240
Q

Carcinoma of the male breast: Other risk factors (5).

A

Hyperthyroidism.

Obesity.

Damage to liver.

Damage to testicles.

Damage to chest wall.

241
Q

Carcinoma of the male breast: Peak age at diagnosis.

A

71 years.

242
Q

Carcinoma of the male breast: Presentation.

A

Painless mass.

243
Q

Carcinoma of the male breast: Typical histology.

A

Infiltrating ductal carcinoma.

DCIS is rare.

244
Q

Carcinoma of the male breast: Immunohistochemistry (4).

A

Variable: ER, PR, AR, Her-2.

245
Q

Carcinoma of the male breast: Main differential diagnosis.

A

Metastatic carcinoma of the prostate gland.

246
Q

Carcinoma of the male breast:

A. Frequency of metastasis to axillary lymph nodes.
B. Sites of distant metastasis (3).

A

A. About 50% at presentation.

B. Lungs, bones, CNS.

247
Q

Metastasis to the ___ breast: Leading primary sites.

A. Female.
B. Male.

A

A. The other breast.

B. The prostate.

248
Q

Primary vs. metastatic tumor in the breast: Stromal change.

A

Elastosis is more common in primary breast cancer.

249
Q

Primary vs. metastatic tumor in the breast: Epithelial change.

A

Calcification is more common in primary breast cancer.

250
Q

Primary breast carcinoma vs. metastatic melanoma: Immunohistochemical pitfalls (2).

A

Melanoma can express cytokeratin and EMA.

Breast carcinoma can express S100.

251
Q

Primary breast carcinoma vs. metastatic ovarian carcinoma: Immunohistochemistry (3,1).

A

Ovarian carcinoma

− Positive: WT-1, CA125, mesothelin.
− Negative: GCDFP-15.

252
Q

Primary breast carcinoma vs. metastatic gastric carcinoma: Immunohistochemistry (2).

A

Gastric carcinoma tends to express CDX2 and CD20.

253
Q

Metastasis to the breast: Prognosis.

A

Death usually within 2 years.