Non-neoplastic lesions of breast

Dr. Mangala G

LYMPHATIC DRAINAGE

AXILLARY (MOSTLY)

INTERNAL MAMMARY

SUPRACLAVICULAR

Anatomy of

Breast•Lobules•Acini•Lactiferous ducts •Lactiferous sinuses

Histology

• Lobe : (10 in whole breast)• Lobule : (many per lobe)• Acinus/I, Aka Alveolus/I : (Many Per

Lobule)• Duct(s) : INTRA- Or INTER- LOB(UL)AR,

leading to the lactiferous ducts in the nipple

L

O

B

E

LOBULE

One single ACINUS(alveolus)

Epithelial cells

MYO-epithelial cells

Three Normal Phases

• Active: about 50-50 Gland/Stroma ratio• Lactating: Mostly Glands (like thyroid!!!),

>>>50/50• Atrophic: mostly stroma, <<<50/50

At birth• Male and female breasts • Active secretion (transplacental

passage of maternal hormones) bilateral breast enlargement

• Colostrum-like secretion ("witch's milk")

• Recedes several months postpartum

Developmental abnormalitiesAplasia and hypoplasia

• Uncommon – associated with overdevelopment of the contralateral breast• Acquired (irradiation – chest wall tumors)• Unilateral or bilateral amastia (absence of a nipple, breast ducts, pectoralis major muscle) – Sex-linked recessive inheritance

Ectopic breast: Supernumerary breast (from ectopic breast tissue – along the milk lines (midaxillae – normal breasts – medial groin and vulva) • Unilateral axillary breast tissue

Polythelia• Areola and underlying mammary ducts

Aberrant Breast•Beyond the usual anatomic extent (no nipple or areola)

Clinical Presentation

Palpable lump Inflammatory mass Nipple discharge Non-palpable abnormality

Inflammation Acute Mastitis Most clinically important form of mastitis

Breast-feeding cracks/fissures in the nipples bacterial infection (esp. Staph. aureus)

Usually unilateral—acute inflammation in the breast can lead to abscess formation

Treatment = surgical drainage (often under general anesthesia) and antibiotics

    

Recurrent subareolar abscess. When squamous metaplasia extends deep into a duct, keratin becomes trapped and accumulates. If the duct ruptures, the ensuing intense inflammatory response to keratin results in an erythematous painful mass. A fistula tract may burrow beneath the smooth muscle of the nipple to open at the edge of the areola.

Mammary Duct Ectasia 5th and 6th decades Affects mainly large ducts Periductal chronic inflammation destruction and dilation of the ducts

with fibrosis The underlying cause is unknown

Ma Duct Ectasia Contd… Poorly defined periareolar mass; can be

confused clinically/radiologically with carcinoma

Can also present as a thick, cheesy nipple discharge +/- mass

Periductal fibrosis skin retraction

INFLAMMATION Fat Necrosis Uncommon lesion; may be a history of trauma, prior surgical intervention or

radiation therapy

Characterized by a central focus of necrotic fat cells with lipid-laden macrophages

and neutrophils   

INFLAMMATION Chronic inflammation with lymphocytes and

multinucleated giant cells

Major clinical significance is its possible confusion with carcinoma (e.g. fibrosis clinically palpable mass / Ca2+ seen on mammography)

Fibrocystic Disease/Change

• Most common proliferative condition of the breast

• Non-neoplastic lesion• Important because it causes severe

periodic discomfort• One component –atypical

hyperplasia-high risk for cancer• Causes palpable lump-mimicking

cancer

Fibrosis + Cysts = Fibrocystic Disease

Terminology• Term fibrocystic change is preferred than

fibrocystic disease because some of the features are similar to physiological changes

• Terms fibroadenosis & epithelial hyperplasia – changes in 30-45years

• Cystic hyperplasia – changes from 40-45 years

Aetiopathogenesis

Hormonal imbalances

Excess estrogen

Responsiveness of breast tissue to

hormones(focal)

Clinical Features• Age group-30-55yrs

• Incidence-maximum just before menopause, decreases after menopause

• C/F vary with age & underlying pathology

• Gross Morphology:Younger age – Diffuse granularity in one /more segments of

breast - nodules upto 5mmTender,in premenstrual period Menopasual age - Ill defined rubbery mass discrete

swelling indicates cysts, if fibrosis +, lump is firm

Cyst, Gross

Cyst, Microscopic

FIBROCYSTIC CHANGE Contd…

• Histology:– Adenosis– Sclerosing adenosis– Epithelial hyperplasia– Papillomatosis– Cysts– Apocrine metaplasia– Fibrosis

Adenosis -• Increased number of acini/lobules (enlargement

of lobules)• Structurally normal• Lobular stroma increased

• Involves mainly epithelium,but myoepithelium may also be involved

• Correspond to grey-pink nodules on gross and fine nodules felt clinically

Epithelial hyperplasia• Proliferation of epithelial cells in

interlobular,intralobular ducts and acini -> solid mass obliterating lumen

Papillomatosis• Papillae lined by epithelial cells,projecting

into the lumens of dilated ducts/small cysts.• Have fibrovascular cores

Adenosis ↑ acini/lobule

Epithelial hyperplasia

Sclerosing Adenosis

Fibrocystic Changes- 1.Adenosis.2.Papilloma formation3.Epithelial hyperplasia.4.Small cysts

Sclerosing adenosisLobular proliferation

Epithelium involved, myoepithelium more involved

Increased collagen component in the tumour - mimic carcinomas clinically - calcification on mammogram

Cysts Dilatation of acini and terminal ducts Apocrine metaplasia Cysts lined by cells resembling

apocrine sweat glands-large columnar and deeply eosinophilic (pink cell metaplasia)

Fibrosis Related to hormonal imbalance changes in the loose connective tissue of

lobules,denser

Atypical hyperplasia Small ducts,may show abnormalities of

growth, disordered orientation,nuclear pleomorphism,mitotic figures