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Breast benign disorders pathology

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Breast benign disorders pathology

  1. 1. Dr.P.Karpagam Kiruba Rajeswari,M.B.B.S,D.C.P., Tutor in Pathology, MAPIMS.
  2. 2. ANATOMY OF BREAST <ul><li>Modified apocrine sweat glands . </li></ul><ul><li>Breast parenchyma  12 to 20 lobes . </li></ul><ul><li>Within each lobe – Lactiferous duct - branches repeatedly  leads to no. of terminal ducts  each leads to a lobule  contains multiple acini/alveoli  TDLU (TERMINAL DUCT + LOBULE) </li></ul><ul><li>Spaces around the lobules and ducts and between the lobes are filled with fatty tissue, ligaments and connective tissue  STROMA </li></ul>
  3. 3. LYMPHATIC DRAINAGE OF BREAST
  4. 4. NORMAL HISTOLOGY OF THE BREAST <ul><li>2 cell types – line ducts & lobules. </li></ul><ul><li>Contractile MYOEPITHELIAL CELLS  lie on the BM  assist in milk ejection during lactation & provides structural support to the lobules </li></ul><ul><li>EPITHELIAL CELLS  Luminal – produce milk. </li></ul><ul><li>Epithelial & Myoepithelial cells lie on the basement membrane. </li></ul>
  5. 6. NORMAL HISTOLOGY OF THE BREAST <ul><li>2 types of breast STROMA: </li></ul><ul><li>INTERLOBULAR STROMA  Dense fibrous connective tissue + adipose tissue. </li></ul><ul><li>INTRALOBULAR STROMA  Envelopes the acini + hormonally responsive fibroblast – like cells + scattered lymphocytes. </li></ul>
  6. 10. ACUTE MASTITIS <ul><li>First month of breast feeding. </li></ul><ul><li>Cracks / fissures in the nipple  portal of entry of bacteria. </li></ul><ul><li>Breast  erythematous,painful,fever +nt. </li></ul><ul><li>MORPHOLOGY : Staph. Inf.  localized area of inflammation. </li></ul><ul><li>Strep. Inf.  Diffuse, spreading. </li></ul><ul><li>HPE : Involved breast tissue – </li></ul><ul><li>necrotic, neutrophil infiltration. </li></ul><ul><li>Treated with antibiotics, continuous milk expression. Rarely surgical drainage. </li></ul>
  7. 12. PERIDUCTAL MASTITIS <ul><li>Recurrent subareolar abscess/ Squamous metaplasia of lactiferous ducts/ Zuska ds. </li></ul><ul><li>Painful erythematous subareolar mass. </li></ul><ul><li>90% cases – assoc. with smoking  Vit.A def./toxic substances in smoke – alters epithelial differentiation. </li></ul><ul><li>Recurrent cases – fistula occurs. </li></ul><ul><li>HPE : Keratinizing squamous metaplasia of ducts. Keratin shed from the cells  plugs the ductal system  dilation & rupture of duct. </li></ul><ul><li>Periductal tissue  keratin spill  chronic granulomatous inflammatory response. </li></ul><ul><li>Treatment: En bloc surgical removal of the involved duct, fistula. Antibiotics for secondary bacterial infection. </li></ul>
  8. 13. DUCT ECTASIA <ul><li>5 th – 6 th decade, multiparous women. </li></ul><ul><li>Cl.features: Poorly palpable periareolar mass, thick white secretions from nipple, skin retraction. </li></ul><ul><li>HPE: Dilated ducts filled by granular debris  numerous lipid-laden macrophages, inspissation of breast secretions, marked periductal and interductal ( dense )infiltrate of lymphocytes and macrophages, and variable numbers of plasma cells. </li></ul><ul><li>Eventual fibrosis  skin & nipple retraction. Principal significance  produces an irregular palpable mass - mimics the mammographic appearance of carcinoma. </li></ul>
  9. 14. DUCT ECTASIA <ul><li>Dilated duct with surrounding fibrosis and chronic inflammation. Lumen of the duct  eosinophilic secretion & markedly attenuated epithelium. </li></ul>
  10. 15. FAT NECROSIS <ul><li>Cl.features: H/o breast trauma / prior surgery. </li></ul><ul><li>Painless palpable mass, skin thickening or retraction, a mammographic density, or calcifications. </li></ul><ul><li>Acute lesions  hemorrhagic + central areas of liquefactive fat necrosis. </li></ul><ul><li>Subacute lesions - areas of fat necrosis  ill-defined, firm, gray-white nodules containing small chalky-white foci or dark hemorrhagic debris. Central region of necrotic fat cells  intense neutrophilic infiltrate + macrophages. </li></ul><ul><li>Proliferating fibroblasts + new vessels + chronic inflammatory cells surround the injured area  Giant cells, calcifications, and hemosiderin appear  focus - replaced by scar tissue. </li></ul>
  11. 16. FAT NECROSIS
  12. 17. GRANULOMATOUS MASTITIS <ul><li>Rare. </li></ul><ul><li>CAUSES: </li></ul><ul><li>Systemic granulomatous ds.  Sarcoidosis, Wegener’s. </li></ul><ul><li>Granulomatous inf. d/t Mycobacteria, Fungi. </li></ul><ul><li>GRANULOMATOUS LOBULAR MASTITIS – Parous women, confined to lobules, d/t hypersensitivity reactions to the antigens – expressed by the lobular epithelium during lactation. </li></ul>
  13. 19. Benign alterations – in ducts & lobules: <ul><li>Detected by mammography/incidental findings in surgical specimens. </li></ul><ul><li>Based on the risk of developing Breast Cancer – 3 groups: </li></ul>
  14. 20. FIBROCYSTIC CHANGE <ul><li>Most common benign breast condition. </li></ul><ul><li>Primarily affects terminal duct–lobular unit (TDLU). </li></ul><ul><li>Pathogenesis  Obscure – hormones (estrogen) -play a role. </li></ul><ul><li>Clinical features </li></ul><ul><li>Incidence: 10 – 20 % of adult women. </li></ul><ul><li>Age : 25 – 45 yrs. </li></ul><ul><li>Usually bilateral. </li></ul><ul><li>Vague ‘lumpy’ </li></ul><ul><li>Morphology: </li></ul><ul><li>‘ 3 principle changes’ </li></ul>
  15. 21. FIBROCYSTIC CHANGE – CYSTS <ul><li>Dilation & unfolding of </li></ul><ul><li>lobules  small cysts – coalesce  large cysts. </li></ul><ul><li>Unopened cysts  turbid ,semi translucent fluid  brown/blue colour  BLUE – DOME CYSTS. </li></ul><ul><li>Lined by flattened atrophic epithelium/metaplastic apocrine cells ( Abundant granular eosinophilic cytoplasm + round nuclei). </li></ul><ul><li>Calcification – common. </li></ul><ul><li>“ MILK OF CALCIUM” – Mammographers </li></ul><ul><li>Diagnosis – confirmed – disappearance of the cyst after FNAC. </li></ul>
  16. 22. FIBROCYSTIC CHANGE - FIBROSIS <ul><li>Cysts rupture </li></ul><ul><li>Secretory material </li></ul><ul><li>Adjacent stroma </li></ul><ul><li>Chronic inflammation, Fibrosis </li></ul><ul><li>Palpable firmness of the breast </li></ul>
  17. 23. FIBROCYSTIC CHANGE - ADENOSIS <ul><li>Increase in the number of acini per lobule. </li></ul><ul><li>Pregnancy  Normal physiologic adenosis. </li></ul><ul><li>Nonpregnant women  adenosis - focal change. </li></ul><ul><li>Acini – enlarged,not distorted (blunt-duct adenosis). </li></ul><ul><li>Calcifications – occasionally - within the lumens. </li></ul><ul><li>Acini - lined by columnar cells  benign / atypical features ( “flat epithelial atypia”)  Earliest recognizable precursor of epithelial neoplasia </li></ul>
  18. 24. LACTATIONAL ADENOMAS <ul><li>Palpable masses – pregnant/lactating women. </li></ul><ul><li>Normal appearing breast tissue + physiological adenosis + lactational changes. </li></ul><ul><li>Exagerrated focal response to hormones. </li></ul><ul><li>Gross appearance: Well circumscribed mass - distinct lobular configuration, yellowish color, and marked vascularization. </li></ul><ul><li>C/s: Gray / tan. Necrotic changes frequent. </li></ul><ul><li>HPE: Proliferated glands lined by actively secreting cuboidal cells </li></ul>
  19. 26. PROLIFERATIVE BREAST DISEASE WITHOUT ATYPIA <ul><li>Mammographic densities, calcifications, or as incidental findings in specimens from biopsies. </li></ul><ul><li>Found alone/assoc. with non prolif. breast changes. </li></ul><ul><li>Lesions  proliferation of ductal epithelium and/or stroma without cytologic or architectural features suggestive of carcinoma in situ. </li></ul>
  20. 27. MORPHOLOGY – Epithelial hyperplasia <ul><li>Normal breast ducts & lobules – double layer of epithelial cells  luminal & myoepithelial layers. </li></ul><ul><li>Epith.hyperplasia  Incidental finding - > 2 layers – luminal & myoepithelial cells  fill,distend ducts & lobules. </li></ul><ul><li>Irregular lumens – periphery of the cellular masses. </li></ul>
  21. 28. Sclerosing Adenosis <ul><li>Palpable mass, a radiologic density, or calcifications. </li></ul><ul><li>No. of acini per terminal duct - increased to double the number found in uninvolved lobules. </li></ul><ul><li>Normal lobular arrangement - maintained. </li></ul><ul><li>Acini - compressed and distorted in the central portions of the lesion & characteristically dilated at the periphery. </li></ul><ul><li>Myoepithelial cells - prominent. </li></ul>NORMAL ADENOSIS
  22. 29. Complex sclerosing lesion <ul><li>Radial sclerosing lesion (“radial scar”) - commonly occurring benign lesion  forms - irregular masses (mimic invasive carcinoma)mammographically, grossly, and histologically. </li></ul><ul><li>Central nidus of entrapped glands in a hyalinized stroma with long radiating projections into stroma. </li></ul><ul><li>Radial scar – misnomer (lesions - not assoc. with prior trauma or surgery) </li></ul>
  23. 30. Papillomas <ul><li>Multiple branching fibro vascular cores, each with a connective tissue axis lined by luminal and myoepithelial cells. </li></ul><ul><li>Growth - within a dilated duct. </li></ul><ul><li>Epithelial hyperplasia and apocrine metaplasia - frequently present. </li></ul><ul><li>Large duct papillomas - solitary, situated in the lactiferous sinuses of the nipple. </li></ul><ul><li>Small duct papillomas - multiple - located deeper within the ductal system. </li></ul><ul><li>> 80% of large duct papillomas  nipple discharge. </li></ul><ul><li>Large papillomas  torsion of stalk  infarction  bloody discharge. </li></ul><ul><li>Intermittent blockage and release of normal breast secretions or irritation of the duct by the papilloma  Non bloody discharge. </li></ul><ul><li>Others  + nt as small palpable masses, or as densities or calcifications seen on mammograms </li></ul>
  24. 31. <ul><li>Atypical ductal/lobular hyperplasia  Cellular proliferation - resembles carcinoma in situ - but lacks sufficient qualitative or quantitative features for diagnosis as carcinoma. </li></ul>
  25. 32. ATYPICAL DUCTAL HYPERPLASIA <ul><li>Found in Bx specimens – done for calcifications,mammographic densities,palpable masses. </li></ul><ul><li>Relatively monomorphic proliferation of regularly spaced cells, sometimes with cribriform spaces. Limited in extent, only partially filling ducts. </li></ul>Duct is filled with a mixed population of cells  oriented columnar cells at the periphery and more rounded cells within the central portion. Some of the spaces - round and regular, the peripheral spaces - irregular and slitlike  Highly Atypical.
  26. 33. ATYPICAL LOBULAR HYPERPLASIA <ul><li>Proliferation of cells  the cells do not fill or distend more than 50% of the acini within a lobule. </li></ul><ul><li>Atypical lobular hyperplasia  also involves contiguous ducts through pagetoid spread ( discrete intraepidermal proliferation of cells occurring singly/ nests at all levels of the epidermis) in which atypical lobular cells lie between the ductal basement membrane and overlying normal ductal epithelial cells. </li></ul>A population of monomorphic small, round, loosely cohesive cells partially fill a lobule. Some intracellular lumens can be seen

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