Benign breast lesions.pptx benign breast lesions

rohitshrivastava97 234 views 88 slides Aug 25, 2024
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About This Presentation

benign breast lesion


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Introduction The breast is a modified skin appendage. Breasts has T wo major structures ( ducts and lobules ), T wo type of epithelium(luminal and myoepithelial), T wo types of stroma interlobular and intralobular) Six to ten major ductal systems originate at the nipple. Their Successive branching eventually leads to the formation terminal duct lobular unit (TDLU).

Normal duct or acinus It has S ingle basally located myoepithelial cell layer (cells with dark, compact nuclei and scant cytoplasm) and A single luminal cell layer (cells with larger open nuclei, small nucleoli, and more abundant cytoplasm).

Lesions of the nipple Nipple adenoma It is the benign proliferation of the glands embedded in a fibrotic stroma. Also k/as florid papillomatosis of the nipple ducts and erosive adenomatosis It is nearly always unilateral, and is often accompanied by serous or bloody discharge from the nipple.

Microscopically, the most common pattern seen is of marked papillomatous changes, often associated with distortion induced by the dense stroma. T here is close interaction of the glandular epithelium of the mammary ducts with the squamous epithelium from the epidermis, resulting in formation of adeno-squamous nests that may be overinterpreted.

Typical polypoid shape of nipple adenoma, as seen in a whole mount section

The complex architectural arrangement can lead to overdiagnosis The continuity with the squamous epithelium of the skin is a characteristic feature of this entity.

High-power view showing usual ductal hyperplasia and necrosis present in a nipple adenoma .

Squamous Metaplasia of Lactiferous Ducts (SMOLD) SMOLD presents clinically as recurrent abscess with or without fistula formation. There is extension of the squamous epithelium of the nipple further than the usual 1–2 mm down the lactiferous ducts. R esulting accumulation of keratinaceous debris leads to duct rupture with consequent inflammatory response.

Patients are often managed with incision and drainage on the presumption of mastitis with abscess formation. The treatment should directed with this clinicopathologic scenario so that the patient may be directed to appropriate management, which is wide excision of the involved duct with a wedge resection of the nipple to eradication of the process.

Keratinizing squamous epithelium extends deep into the ductal system. Metaplastic squamous cells replace the normal glandular lining. High power view demonstrating squamous metaplasia, periductal inflammation and keratin debris in the lumen .

This higher power view demonstrates a proliferation of metaplastic squamous epithelium. This lactiferous duct has been almost completely replaced by squamous epithelium. There is only a small area with glandular epithelial cells

M ammary D uct E ctasia ( Plasma cell mastitis ) Dilatation of one or more larger ducts and filled with inspissated secretions . A ssociated with periductal and interstitial chronic inflammatory changes. The patients may remain asymptomatic or there may be nipple discharge, retraction of the nipple and clinically palpable dilated ducts in the subareolar area.

Microscopically- D ilation of large ducts, A ccumulation of lipid-rich detritus in the lumen and F ibrous thickening of the wall.

If the luminal material escapes from the duct, a florid inflammatory reaction rich in macrophages and plasma cells (“ periductal mastitis ” ). Sometimes, plasma cells are present in impressive numbers and the condition is then termed plasma cell mastitis. In advanced stages, fibrous obliteration of the ducts can occur (“ duct ectasia ”). Occasionally, there may be obliteration of the ducts by fibrous tissue and varying amount of inflammation and is termed obliterative mastitis .

Inflammatory stage of duct ectasia -there is dilation of a large duct, with accumulation of lipid-rich detritus in the lumen and a florid inflammatory reaction rich in macrophages and plasma cells.

FAT NECROSIS It is generally initiated by trauma The condition presents as a well-defined mass with indurated appearance. Grossly, The excised lump has central pale cystic area of necrosis.

F at cells in aspirates from fat necrosis are enlarged and dissociated and t heir cytoplasm is often vacuolated. F at cells in aspirates from the normal breast occur in clusters .

It can arise in large or small ducts . A central fibrovascular core extends from the wall of a duct. The papillae arborize within the lumen and are lined by myoepithelial and luminal cells. Intraductal papilloma

Features favouring its benignity are:- A hyalinized stroma in broad papillary fibrovascular cores, T he presence of two cell types (epithelial and Myoepithelial), N ormochromatic oval epithelial cell nuclei, S canty mitotic activity, T he presence of foci of apocrine metaplasia , L ack of a cribriform pattern.

Intraductal Papilloma showing complex arborizing architecture S howing dual cell composition, with a well-defined row of myoepithelial cells.

ACUTE MASTITIS AND BREAST ABSCESS Acute pyogenic infection of the breast. Organisms responsible- S taphylococci and S treptococci . Initially a localized area of acute inflammation, if not effectively treated, may cause single or multiple breast abscesses.

GRANULOMATOUS MASTITIS It may occur as a result of the following:- Systemic non-infectious granulomatous disease, Infections e.g. tuberculosis, Silicone breast implants Idiopathic granulomatous mastitis Cystic Neutrophilic Granulomatous Mastitis(CNGM),

Cystic Neutrophilic Granulomatous Mastitis P resence of “cystic” spaces cuffed by neutrophils and a background of lymphocytes, histiocytes, and giant cells. With careful searching, faint rod-like structures may be identified within some of these “cystic” spaces.

Florid Granulomatous Reaction to Silicone Foamy macrophages, foreign body–type multinucleated giant cells, and lymphocytes are present.

FIBROCYSTIC CHANGE

M ost common benign breast condition. P roducing vague ‘lumpy’ breast rather than palpable lump. I ncidence 10-20% in adult women, between 3rd and 5th decades of life . D ecline in incidence after menopause- role of estrogen .

F ibrocystic change of the female breast is characterised by:- Cystic dilatation of terminal ducts. Relative increase in inter- and intralobular fibrous tissue. Variable degree of epithelial proliferation in the terminal ducts.

T he spectrum of histologic changes is divided into two groups: Non-proliferative changes : Simple fibrocystic change. Proliferative changes : Proliferative fibrocystic change.

NON-PROLIFERATIVE FIBROCYSTIC CHANGES Simple fibrocystic change most commonly includes: - F ormation of cysts of varying size, Fibrosis Apocrine metaplasia Calcification Chronic inflammation

Grossly Cysts are usually multifocal and bilateral. They usually contain a cloudy yellow or clear fluid. Some of these cysts have a bluish cast (“ blue dome cysts” of Bloodgood ).

Microscopically , Cyst formation The lining epithelium of cyst is flattened or atrophic. T here is apocrine change or apocrine metaplasia. There is simultaneous epithelial hyperplasia forming tiny intra cystic papillary projections.

Apocrine Metaplasia Cells have Abundant granular eosinophilic cytoplasm with supranuclear vacuoles . The nuclei are round, of medium size and have prominent nucleoli. “ Apocrine snout ”.

Fibrosis There is increased fibrous stroma surrounding the cysts and variable degree of stromal lymphocytic infiltrate.

PROLIFERATIVE FIBROCYSTIC CHANGES Usual Ductal Hyperplasia(UDH) Atypical Ductal Hyperplasia and Atypical Lobular Hyperplasia Columnar Cell Lesions and Flat Epithelial Atypia

Usual ductal hyperplasia M ild (when made up of three or four epithelial cells in thickness) or M oderate to florid (when more pronounced). In florid UDH, the entire lumen is filled by the epithelial proliferation.

UDH:- P resence of oval nuclei with slight overlap giving the cells a streaming appearance. The clefts are preferentially located at the periphery of the duct and there is a lack polarization of cells around the spaces.

Immunohistochemistry , UDH has immunoreactivity for HMW cytokeratin antibodies, in particular for CK 5/6, and estrogen receptors.

Atypical Ductal Hyperplasia ADH has similar cytologic and architectural features to low-grade DCIS, that is, monomorphic cells with ovoid to rounded nuclei and the formation of micropapillae , tufts, fronds, bridges, solid, or cribriform patterns within the involved space, but I ntimately admixed with UDH or S howing only partial involvement of the TDLU.

Atypical ductal hyperplasia . Proliferative ductal lesion with monomorphic cells and cribriform architectural pattern .

Atypical Ductal Hyperplasia A TDLU with a predominantly cribriform proliferation of monomorphic epithelial cells. T he low-grade nuclear atypia and the polarization around the cribriform spaces.

Atypical Lobular Hyperplasia ALH is monomorphic proliferation of atypical epithelial cells with round nuclei and indistinct nucleoli. The cells are dys-cohesive and often have intracytoplasmic lumina. Difference is <50% of the TDLU is expanded by the atypical proliferation in ALH, >50% of the TDLU expanded by the atypical proliferation in LCIS .

Atypical Lobular Hyperplasia. There is expansion of the lobules by a monomorphic proliferation of atypical epithelial cells with round nuclei and indistinct nucleoli. The cells are dys -cohesive and often have intracytoplasmic lumina .

Flat Epithelial Atypia FEA is characterized by a single or stratified layer of columnar to cuboidal cells with low nuclear grade atypia and loss of polarization with respect to the basement membrane. There is variable dilatation of the acini of the affected TDLUs, with smooth, rather than irregular, contours. Apical snouts can be prominent. The lumens of the acini contain granular secretions and/or calcifications .

The acini of the TDLU are variably dilated and the spaces lined by a stratified layer of monomorphic cuboidal cells.

The spaces are dilated and lined by a stratified layer of cuboidal cells with low-grade cytologic atypia .

Columnar Cell Lesions C olumnar cell change and columnar cell hyperplasia refer to these same architecturally “flat” lesions but without the cytologic atypia . It is these two lesions in which the lining epithelial cells are most recognizably columnar with elongated nuclei oriented perpendicular to the basement membrane.

The acini of the TDLU are variably dilated and the spaces lined by a layer of columnar epithelial cells .

Prognostic Significance No or mild UDH ( non-proliferative changes ): no increased risk for subsequent invasive carcinoma. Moderate or florid UDH ( proliferative disease without atypia ): 1.5–2 times the risk. ADH or ALH ( atypical hyperplasia ): 4–5 times the risk. DCIS or LCIS: 8–10 times the risk.

Fibroadenoma

Fibroadenoma is a benign tumour of fibrous and epithelial elements. It is the most common benign tumour of the female breast. M/C age of presentation 15 to 30 years of age. Clinically, appears as a solitary, discrete, freely mobile nodule within the breast.

Grossly , T ypical fibroadenoma is a small (2-4 cm diameter), solitary, well encapsulated, spherical or discoid mass. The cut surface is firm, grey-white, slightly myxoid and may show slit-like spaces formed by compressed ducts.

Microscopically , F ibrous tissue comprises most of a fibroadenoma. The arrangements between fibrous overgrowth and ducts may produce two types of patterns. These are intracanalicular and pericanalicular patterns: ” .

Intracanalicular pattern W hen the connective tissue invaginates into the glandular spaces so that it appears to be within them. M ay appear as cords of epithelial elements surrounding masses of fibrous stroma. ”

Peri canalicular pattern W hen the regular round or oval configuration of the glands is preserved. C haracterised by encircling masses of fibrous stroma around the patent or dilated ducts.

Numerous clusters of epithelial cells and myoepithelial cells in the background. Under higher magnification, the complexity of the multilayered cluster is evident.

M orphologic variants of fibroadenomas T ubular adenoma . If the tumour is predominantly composed of closely-packed ductular or acinar proliferation and fibrous tissue element in the tumour is scanty .

L actating adenoma If an adenoma is composed of acini with secretory activity, S een during pregnancy or lactation.

Juvenile fibroadenoma U ncommon variant. It is larger and rapidly growing mass seen in adolescent girls. In this particular lesion the pericanalicular growth pattern predominates; florid hyperplasia is often seen as part of the epithelial component.

Malignant Changes Malignant changes in fibroadenomas are found in only 0.1% of cases. The malignant change usually involves the epithelial component, and the large majority are in situ lesions.

PHYLLODES TUMOUR (CYSTOSARCOMA PHYLLODES) Cystosarcoma phyllodes is an uncommon bulky breast tumour with leaf-like gross appearance ( phyllodes =leaf-like) having an aggressive clinical behaviour. Most patients are between 30 to 70 years of age.

T he tumour resembles a giant fibroadenoma. Phyllodes tumour can be classified into benign, borderline and malignant on the basis of histologic features of stromal cells.

Grossly , T he tumour is generally large, 10-15 cm in diameter, round to oval, bosselated, and less fully encapsulated than a fibroadenoma. The cut surface is grey-white with cystic cavities, areas of hemorrhages, necrosis and degenerative changes

The tumor showing typical appearance of the cut surface. The tumor has undergone extensive infarction.

Histologically, T he phyllodes tumour is composed of an extremely hypercellular stroma, accompanied by benign ductal structures. Thus, phyllodes tumour resembles fibroadenoma except for marked stromal overgrowth.

The histologic criteria considered to distinguish benign, borderline and malignant categories of phyllodes tumour are based on following cellular features of stroma: frequency of mitoses; cellular atypia; cellularity; and infiltrative margins.

“ B enign ”:- The stromal component has a fibroblastic appearance with little or mild stromal cell atypia and few mitoses (<5 per 10 high-power fields). Malignant phyllodes tumors have a high degree of stromal cellularity, marked stromal cell nuclear atypia, numerous mitoses (≥10 per 10 high-power fields), and a greater imbalance in the distribution of glands in the stroma.

Benign Borderline Malignant Stromal atypia Mild Moderate Marked Stromal cellularity Mildly increased, can be focal Moderately increased, can be focal Marked and diffusely increased Stromal overgrowth Absent Absent or very focal Present Mitotic count  <5/10 HPF or < 2.5/mm² 5 - 9/10 HPF or 2.5 - < 5/mm² ≥ 10/10 HPF or ≥ 5/mm² Tumour border Well defined Well defined or focally permeative Diffusely permeative Malignant heterologous elements Absent Absent Presence directly upgrades to malignant category

B enign phyllodes tumour , showing cleft-like spaces and condensation of stromal cells under the epithelium.

Malignant phyllodes tumour with liposarcomatous differentiation of the neoplastic stromal component.

Complex sclerosing lesion (radial scar). This is a group of breast lesions characterized by a generally small size, stellate shape, and a central fibro-elastotic core, with variable degree of epithelial proliferation and distortion. Microscopically, the connective tissue center is densely fibrotic or fibro-elastotic. Basophilic elastic tissue may be seen in the walls of obliterated ducts and the stroma.

S mall ducts and glands are embedded within the stroma that appear disorganized due to the distortion caused by the fibrosis. B ut these are still composed of both epithelial and myoepithelial cell. A t the periphery of the “radial spokes” are larger duct-like structures that may be dilated and/or may exhibit UDH.

Typical stellate shape of radial scar. Benign ductular structures are entrapped in the central fibro-elastotic stroma .

Gynaecomastia E nlargement of the male breast resulting from hypertrophy and hyperplasia of both glandular and stromal components. It presents as button like subareolar enlargement. Micro scopically there is an increase in the dense collagenous connective tissue associated with epithelial hyperplasia of the duct lining. Lobule formation is almost never observed .

Microscopically, T he ducts show a variable degree of epithelial hyperplasia and are surrounded by a prominent edematous stroma, which results in a typical “ halo ” effect. The microscopic changes are related to the duration of the gynecomastia. Cases of short duration have a prominent hyperplastic epithelial component, with micropapillary (“gynecomastoid”) architecture, and stromal edema, Cases of long duration have prominent stromal fibrosis.

References ROSAI AND ACKERMAN’S SURGICAL PATHOLOGY Eleventh Edition . Koss’ Diagnostic Cytology AND ITS HISTOPATHOLOGIC BASES.

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