🔥 Inflammatory conditions
−- mastitis Acute infection of breast tissue
- Erythema, firmness, pain — often during lactation
- Most common pathogen: S. aureus
- Abscess formation possible (acute + chronic inflammation)
- Clinical mimic: inflammatory carcinoma (both painful)
- fat necrosis Post-traumatic or post-surgical
- Palpable mass or calcifications on mammography
- Histology: necrotic fat, chronic inflammation, hemosiderin, fibrosis, calcification
- ⚠️ Inflammatory carcinoma: peau d'orange, erythema, warm — biopsy to differentiate from mastitis.
🌀 Fibrocystic changes
−- Very common, benign; reproductive age; upper outer quadrant
- Classified into nonproliferative vs proliferative (risk stratification)
| Nonproliferative | Proliferative |
|---|---|
| Fibrosis, cysts (blue-domed), apocrine metaplasia, microcalcifications | Ductal hyperplasia (± atypia), sclerosing adenosis, atypical lobular hyperplasia |
- Relative risk for breast cancer:
- No increase: fibrosis, cysts, apocrine metaplasia, adenosis
- 1.5–2× : sclerosing ductal hyperplasia, papillomas
- 4–5× : atypical ductal or lobular hyperplasia
- Distinction from carcinoma:
- Fibrocystic: often bilateral, multiple nodules, menstrual variation, may regress with pregnancy
- Carcinoma: usually unilateral, single mass, no menstrual variation, does not regress with pregnancy
- Microscopic key: myoepithelial layer preserved in sclerosing adenosis (vs carcinoma)
🟢 Benign neoplasms
−- Fibroadenoma most common benign tumor in women <35
- Round, mobile, rubbery mass; cleft-like spaces on cut section
- Proliferation of stroma, ducts, lobules
- Phyllodes tumor (cystosarcoma phyllodes) — age 50s
- Can be benign or malignant; local recurrence common, metastasis low
- Increased stromal cellularity, clefts, stromal overgrowth, irregular margins
- Intraductal papilloma
- Classic: bloody nipple discharge
- Papillary growth within lactiferous ducts; myoepithelial layer preserved
🔴 Malignant neoplasms
−- Breast carcinoma — most common cancer in women (US), 1 in 9; 2nd most common cause of cancer death
- Risk factors:
- Age, prolonged estrogen exposure (early menarche, late menopause, nulliparity, obesity, exogenous estrogens)
- Proliferative fibrocystic changes (atypical hyperplasia)
- First-degree relative; hereditary (BRCA1/2, TP53)
- DCIS and LCIS: preinvasive; myoepithelial layer preserved
- Untreated DCIS → 35% invasive (same quadrant)
- LCIS → 35% invasive (either breast, lobular or ductal)
- Most common location: upper outer quadrant
- Gross: stellate, white-tan, gritty mass; may cause nipple retraction, skin dimpling, fixation
| Histologic type | Key features | ER/PR / HER2 |
|---|---|---|
| Invasive ductal (NOS) | Most common (>80%); duct formation, desmoplastic stroma | 70% ER+ ; 30% HER2+ |
| Invasive lobular | Single-file pattern; multifocal/bilateral | ~50% ER+ ; HER2- |
| Mucinous (colloid) | Clusters floating in mucin; better prognosis | ER+ ; HER2- |
| Tubular | Excellent prognosis; rarely metastasizes | ER+ ; HER2- |
| Medullary | Syncytial groups, lymphocyte response; better prognosis | ER- ; HER2- |
| Inflammatory | Dermal lymphatic invasion; peau d'orange; poor prognosis | variable |
- Paget disease of nipple — ulceration, crusting, fissuring; intraepidermal Paget cells (clear halo)
- Prognostic factors: axillary node status (sentinel biopsy), size, grade, ER/PR, HER2/neu (trastuzumab target)
- Markers for monitoring metastatic disease: CA 15-3, CA 27.29, CEA
- ⚠️ HER2/neu overexpression → more aggressive; trastuzumab response. All invasive cancers tested for ER/PR and HER2.
⚥ Gynecomastia
−- Unilateral or bilateral benign male breast enlargement
- Causes (androgen–estrogen imbalance):
- Physiologic: newborns, puberty, elderly
- Pathologic: cirrhosis, Klinefelter, prolactinoma
- Drugs: spironolactone, ketoconazole
- Histology:
- Ductal epithelial hyperplasia
- Ductal elongation and branching
- Periductal fibroblast proliferation
- Increased vascularity
Altered androgen/estrogen → ductal proliferation → gynecomastia