Breastbenigndisorderspathology 110914231905-phpapp01


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This is a summary of the pathology of the breast.after going through the slide you will have a general concept of Breast

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Breastbenigndisorderspathology 110914231905-phpapp01

  1. 1. Dr.P.Karpagam Kiruba Rajeswari,M.B.B.S,D.C.P., Tutor in Pathology, MAPIMS.
  2. 2. ANATOMY OF BREAST Modified apocrine sweat glands. Breast parenchyma  12 to 20 lobes. 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) Spaces around the lobules and ducts and between the lobes are filled with fatty tissue, ligaments and connective tissue  STROMA
  4. 4. NORMAL HISTOLOGY OF THE BREAST 2 cell types – line ducts & lobules.1. Contractile MYOEPITHELIAL CELLS  lie on the BM  assist in milk ejection during lactation & provides structural support to the lobules2. EPITHELIAL CELLS  Luminal – produce milk. Epithelial & Myoepithelial cells lie on the basement membrane.
  5. 5. NORMAL HISTOLOGY OF THE BREAST2 types of breast STROMA:1. INTERLOBULAR STROMA  Dense fibrous connective tissue + adipose tissue.2. INTRALOBULAR STROMA  Envelopes the acini + hormonally responsive fibroblast – like cells + scattered lymphocytes.
  6. 6. ACUTE MASTITIS First month of breast feeding. Cracks / fissures in the nipple  portal of entry of bacteria. Breast  erythematous,painful,fever +nt. MORPHOLOGY: Staph. Inf. localized area of inflammation. Strep. Inf.  Diffuse, spreading. HPE: Involved breast tissue – necrotic, neutrophil infiltration. Treated with antibiotics, continuous milk expression. Rarely surgical drainage.
  7. 7. PERIDUCTAL MASTITIS Recurrent subareolar abscess/ Squamous metaplasia of lactiferous ducts/ Zuska ds. Painful erythematous subareolar mass. 90% cases – assoc. with smoking  Vit.A def./toxic substances in smoke – alters epithelial differentiation. Recurrent cases – fistula occurs. HPE : Keratinizing squamous metaplasia of ducts. Keratin shed from the cellsplugs the ductal system  dilation & rupture of duct. Periductal tissue  keratin spill  chronic granulomatous inflammatory response. Treatment: En bloc surgical removal of the involved duct, fistula. Antibiotics for secondary bacterial infection.
  8. 8. DUCT ECTASIA 5th – 6th decade, multiparous women. Cl.features: Poorly palpable periareolar mass, thick white secretions from nipple, skin retraction. 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. Eventual fibrosis  skin & nipple retraction. Principal significance produces an irregular palpable mass - mimics the mammographic appearance of carcinoma.
  9. 9. DUCT ECTASIA Dilated duct with surrounding fibrosis and chronic inflammation. Lumen of the duct  eosinophilic secretion & markedly attenuated epithelium.
  10. 10. FAT NECROSIS Cl.features: H/o breast trauma / prior surgery. Painless palpable mass, skin thickening or retraction, a mammographic density, or calcifications. Acute lesions  hemorrhagic + central areas of liquefactive fat necrosis. 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. Proliferating fibroblasts + new vessels + chronic inflammatory cells surround the injured area  Giant cells, calcifications, and hemosiderin appear  focus - replaced by scar tissue.
  11. 11. FAT NECROSIS
  12. 12. GRANULOMATOUS MASTITIS Rare. CAUSES:1. Systemic granulomatous ds. Sarcoidosis, Wegener’s.2. Granulomatous inf. d/t Mycobacteria, Fungi. GRANULOMATOUS LOBULAR MASTITIS – Parous women, confined to lobules, d/t hypersensitivity reactions to the antigens – expressed by the lobular epithelium during lactation.
  13. 13. Benign alterations – in ducts &lobules:Detected by mammography/incidental findings in surgical specimens.Based on the risk of developing Breast Cancer – 3 groups:
  14. 14. FIBROCYSTIC CHANGEMost common benign  Morphology: breast condition. ‘3 principle changes’Primarily affects terminal duct–lobular unit (TDLU). Pathogenesis Obscure – hormones (estrogen) -play a role.Clinical featuresIncidence: 10 – 20 % of adult women.Age : 25 – 45 yrs.Usually bilateral.Vague ‘lumpy’
  15. 15. FIBROCYSTIC CHANGE – CYSTS Dilation & unfolding of lobules  small cysts – coalesce  large cysts. Unopened cysts  turbid ,semi translucent fluid  brown/blue colour  BLUE – DOME CYSTS. Lined by flattened atrophic epithelium/metaplastic apocrine cells (Abundant granular eosinophilic cytoplasm + round nuclei). Calcification – common. “MILK OF CALCIUM” – Mammographers Diagnosis – confirmed – disappearance of the cyst after FNAC.
  16. 16. FIBROCYSTIC CHANGE - FIBROSIS Cysts rupture Secretory material Adjacent stromaChronic inflammation, FibrosisPalpable firmness of the breast
  17. 17. FIBROCYSTIC CHANGE - ADENOSISIncrease in the number of acini per lobule.Pregnancy Normal physiologic adenosis.Nonpregnant women  adenosis - focal change.Acini – enlarged,not distorted (blunt-duct adenosis).Calcifications – occasionally - within the lumens. Acini - lined by columnar cells  benign / atypical features (“flat epithelial atypia”)  Earliest recognizable precursor of epithelial neoplasia
  18. 18. LACTATIONAL ADENOMAS Palpable masses – pregnant/lactating women. Normal appearing breast tissue + physiological adenosis + lactational changes. Exagerrated focal response to hormones. Gross appearance: Well circumscribed mass - distinct lobular configuration, yellowish color, and marked vascularization. C/s: Gray / tan. Necrotic changes frequent. HPE:Proliferated glands lined by actively secreting cuboidal cells
  19. 19. PROLIFERATIVE BREAST DISEASE WITHOUT ATYPIAMammographic densities, calcifications, or as incidental findings in specimens from biopsies.Found alone/assoc. with non prolif. breast changes.Lesions  proliferation of ductal epithelium and/or stroma without cytologic or architectural features suggestive of carcinoma in situ.
  20. 20. MORPHOLOGY – Epithelial hyperplasiaNormal breast ducts & lobules – double layer of epithelial cells  luminal & myoepithelial layers.Epith.hyperplasia Incidental finding - > 2 layers – luminal & myoepithelial cells  fill,distend ducts & lobules.Irregular lumens – periphery of the cellular masses.
  21. 21. Sclerosing Adenosis Palpable mass, a radiologic density, or calcifications. No. of acini per terminal duct - increased to double the number NORMAL found in uninvolved lobules. Normal lobular arrangement - maintained. Acini - compressed and distorted in the central portions of the lesion & characteristically dilated ADENOSIS at the periphery. Myoepithelial cells - prominent.
  22. 22. Complex sclerosing lesion Radial sclerosing lesion (“radial scar”) - commonly occurring benign lesion  forms - irregular masses (mimic invasive carcinoma)mammographically, grossly, and histologically. Central nidus of entrapped glands in a hyalinized stroma with long radiating projections into stroma. Radial scar – misnomer (lesions - not assoc. with prior trauma or surgery)
  23. 23. Papillomas Multiple branching fibro vascular cores, each with a connective tissue axis lined by luminal and myoepithelial cells. Growth - within a dilated duct. Epithelial hyperplasia and apocrine metaplasia - frequently present. Large duct papillomas - solitary, situated in the lactiferous sinuses of the nipple. Small duct papillomas - multiple - located deeper within the ductal system. > 80% of large duct papillomas  nipple discharge. Large papillomas  torsion of stalk  infarction bloody discharge. Intermittent blockage and release of normal breast secretions or irritation of the duct by the papilloma  Non bloody discharge. Others  + nt as small palpable masses, or as densities or calcifications seen on mammograms
  24. 24. Atypical ductal/lobular hyperplasia  Cellular proliferation -resembles carcinoma in situ - but lacks sufficient qualitative orquantitative features for diagnosis as carcinoma.
  25. 25. ATYPICAL DUCTAL HYPERPLASIA Found in Bx specimens – done for calcifications,mammographic densities,palpable masses. Relatively monomorphic proliferation of regularly spaced cells, sometimes with cribriform spaces.Limited in extent, only partially filling ducts. 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. 26. ATYPICAL LOBULAR HYPERPLASIA Proliferation of cells  the cells do not fill or distend more than 50% of the acini within a lobule. 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 A population of monomorphic small, lobular cells lie between the ductal round, loosely cohesive cells partially fill basement membrane and a lobule. Some intracellular lumens can overlying normal ductal epithelial be seen cells.