inflammatory breast

acute mastitis.....1st month in breastfeeding...cracks and fissures in

nipples..staph aureus + strep...acute inflm + abcess form

periductal mastitis...abcess...fistula formation under nipple....smoking+tobaccoo

use+zuska diseases..keratinizing squamous metaplasia of lacteferous
ducts....keratin sheds

Mammary duct actesia..5th or 6th decade +multiparous+thick white nipple

scretions+skin retraction+dilation of ducts+ periductal and interductal tissue
contains dense infiltrates of lymphocytes and macrophages, and variable numbers of
plasma cells + granulomatous inflammation forms around cholesterol deposits

Fat Necrosis.... hemorrhagic and contain central areas of liquefactive fat necrosis
+firm, gray-white nodules containing small chalky-white foci or dark hemorrhagic
debris.giant cells, calcifications, and hemosiderin

Lymphocytic mastopathy.. collagenized stroma surrounding atrophic ducts and

lobules+ most common in women with type 1 (insulin-dependent) diabetes or
autoimmune thyroid disease

GRANULOMATOUS MASTITIS+granulomatous inflammation is confined to the lobules,

suggesting that it is caused by a
hypersensitivity reaction to antigens expressed by lobular epithelium during
lactation.

Benign epithelial lesions

(1) nonproliferative breast changes, (2) proliferative breast

disease, and (3) atypical hyperplasia

NONPROLIFERATIVE BREAST CHANGES (FIBROCYSTIC CHANGES)

three principal morphologic changes: (1) cystic change, often with

apocrine metaplasia; (2) fibrosis; and (3) adenosis.

cysts contain turbid, semi-translucent fluid that produces a brown or blue color
(blue-dome cysts)+�Milk of calcium� is a term mammographers use to describe
calcifications that line the bottom of a rounded cyst
fibrosis by cystic rupture
Adenosis. Adenosis is defined as an increase in the number of acini per lobule. A
normal physiologic adenosis occurs during pregnancy..columner epith

PROLIFERATIVE BREAST DISEASE WITHOUT ATYPIA

proliferation of ductal epithelium and/or stroma without cytologic or

architectural features suggestive of carcinoma in situ
Epithelial Hyperplasia
presence of more than two cell layers. The additional cells consist of both luminal
and myoepithelial cell types that fill and distend ducts and lobules.

Sclerosing Adenosis.

number of acini per terminal duct is increased to at least double

the number found in uninvolved lobules+acini are compressed and distorted in the
central portions of the lesion but characteristically dilated at the periphery
stromal fibrosis may completely compress the lumens
Complex Sclerosing Lesion

have components of sclerosing adenosis, papillomas, and epithelial hyperplasia

radial scar irregular central mass with long radiodense projections. not
associated with prior trauma or surgery

Papillomas.
Papillomas are composed of multiple branching fibrovascular cores, each having a
connective tissue axis lined by luminal and myoepithelial cells
Large duct papillomas are usually solitary and situated in the lactiferous sinuses
of the nipple.
Small duct papillomas are commonly multiple and located deeper within the ductal
system.Intraductal papilloma. A central fibrovascular core extends from the wall of
a duct

PROLIFERATIVE BREAST DISEASE WITH ATYPIA

includes atypical ductal hyperplasia and atypical lobular hyperplasia

lacking sufficient qualitative or quantitative features for diagnosis as carcinoma

Atypical ductal hyperplasia

monomorphic proliferation of regularly spaced cells,sometimes with cribriform
spaces
duct is filled with a mixed population of cells consisting of oriented columnar
cells at the periphery and more rounded cells within the central portion

Atypical lobular hyperplasia is defined as a proliferation of cells identical to

those of lobular
carcinoma in situ (LCIS, described later), but the cells do not fill or distend
more than 50% of
the acini within a lobule+ pagetoid spread monomorphic small,round, loosely
cohesive cells partially fill a lobule

CLINICAL SIGNIFICANCE OF BENIGN EPITHELIAL CHANGES

tell risk factor for developing carcinoma

Risk reduction can be achieved by bilateral prophylactic mastectomy or treatment
with estrogen antagonists, such as tamoxifen.

Carcinoma of the Breast

Risk factor
age average 61+peak 75-80
Age at Menarche.
Women who reach menarche when younger than 11 years of age have a 20% increased
risk+late menupause
Age at First Live Birth
First-Degree Relatives with Breast Cancer
Atypical Hyperplasia.
Estrogen Exposure.
Postmenopausal hormone replacement therapy increases the risk of breast cancer
Breast Density.
High breast radiodensity is a strong risk factor for developing cancer
Radiation Exposure
Carcinoma of the Contralateral Breast or Endometrium
diet+obesity+exercise+breastfeeding

Mutations in BRCA1 and BRCA2 account for the majority of cancer attributable to
single mutations and about 3% of all breast cancers
 Mutations in BRCA1 also markedly increase the risk of developing
ovarian carcinom
BRCA1-associated breast cancers are commonly poorly differentiated, have �medullary
features� (a syncytial growth pattern with pushing margins and a lymphocytic
response), and do
not express hormone receptors or overexpress HER2/neu (the so-called �triple
negative�
phenotype
BRCA1 ....trip;e negative
BRCA2....ER +ve
, decreased expression of BRCA1 and CHEK2 is common in
sporadic cancers

f Carcinogenesis and Tumor Progression

e proliferative changes, which may stem from the loss of growthinhibiting signals,
aberrant increases in pro-growth signals, or decreased apoptosis the ability to
drive neo-angiogenesis The final step of carcinogenesis, the transition of
carcinoma in situ to invasive carcinoma, is the most important

The most likely cell type of origin for the majority of carcinomas is the ER-
expressing luminal
cell, since the majority of cancers are ER-positive and precursor lesions, such as
atypical
hyperplasias, are most similar to this type of cell ER-negative carcinomas may
arise from ER-negative myoepithelial cells