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Breast Disease - Summary
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Breast Disease - Summary Table of all breast conditions organised by history findings, examination findings, investigation findings and management according to Australian guidelines.
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MalignancyInfo History/RF Examination Investigation Management
Breast Ca Most common is adenoCa of the cells lining Lump in the breast Lump as in HOPC – hard Bloods (monitoring) – Lifestyle – lifestyle
Malignant the terminal duct lobular unit Hard consistency consistency, irregular in FBE changes, review/cease
growth of the Epi – most common non-skin malignancy Irregular in shape shape, immobile, may be UEC exacerbating hormonal
stromal and in women, average lifetime risk of Immobile accompanied with pain, nil CMP therapies, regular screening
epithelial cells developing breast Ca is 1 in 8 Ay be accompanied with cyclic associations LFTs
within the Can be classified as: pain, nil cyclic associations Discharge – may be absent CRP/ESR Pharm –
breast tissue Invasive – infiltrating ductal/lobular, or bloody CA-15-3 Carcinoma in-situ –
medullary, mucinous, tubular, papillary Age of Nipples – crusting, tamoxifen
Non-invasive – DCIS, LCIS (more benign) menarche/menopause, ulcerations, erythema, Imaging – Hormone receptor status –
Hormonal – oestrogen +ive, progesterone oestrogen therapies COCP invasion/eversion Mammogram hormone based therapy
+ive, HER2 +ive use, Hx of breastfeeding Skin – dimpling, erythema, Breast U/S – recommended if ER+ - tamoxifen,
ER+, PR+ - +ive prognosis rashes <40y/o anastrozole
HER2+ - -ive prognosis CT or bone scan HER2+ - trastuzumab
All -ive – -ive prognosis Sx – LOW, bone pain (ribs, Women whose cancers
back, humerus), SOB, -ive disease –
possess hormone chemotherapy
cough, changes in bowel Special Tests –
Ax – Genetic mutations (BRCA1/BRCA2) habits, focal neurological receptors have a longer Biopsy (FNA or core
which predisposes to breast + ovarian Ca signs disease-free survival and biopsy) Surgical +/- radiotherapy
(mutations affects <0.1% of population); overall survival than Hormone receptor testing –
hormonal influences – oestrogen may those with early stage Gene expression analyses Breast conserving surgery
stimulate mammary tumours; endogenous RF – women, age – peak
incidence 75-79, oestrogen cancers who are negative (lumpectomy, wide local
(nulliparity, early menarche, late excision, quadrantectomy)
menopause) or exogenous (HRT, oestrogen exposure, early menarche for these receptors. Prevention – aged 50-74 y/o
+ late menopause, HRT, are invited for free Mastectomy (partial,
therapy) simple, modified, radical)
PPx – genetic (loss of tumour suppressor FHx Flow cytometry – used for mammograms every 2yrs;
40+ can get free Reconstructive surgeon
genes such as TP53, BRCA1, BRCA2, RB1 prognosis, not Tx
produces familial syndromes); hormonal – mammogram but not formally
steroid hormone family acts on ErbB, myc, invited, self-examination is no
PI3K/AKT, NFkB, PDGFR, Src and IGF longer recommended
pathways enable uncontrolled cell
growth
Benign tumours
Info History/RF Examination Investigation Management
Benign breast
tumours +
masses
Other breast conditions
Info History/RF Examination Investigation Management
Other breast
conditions
Intraductal papilloma – bloody/serous discharge, main Invasive lobular carcinoma – lines, likely to be present
Buzzwords lactiferous ducts, subareolar breast tissue, not influenced in the opposite breast
Fat necrosis – trauma by hormonal changes Medullary carcinoma – sheets of invasive and
Fibrocystic disease – women of reproductive age, DCIS – cookie cutter appearance, 30% chance of pleomorphic cells, mitotic figures, dense infiltrate of
cystic dilation of terminal ducts, increase in fibrous becoming invasive lymphocytes, hormone receptor -ive, BRCA-1 – highest
stroma, variable proliferation of terminal duct epithelial LCIS – eosinophilic, granular appearance with vacuolated incidence of medullary carcinomas
elements cytoplasm Colloid carcinoma – mucin production, often +ive for
Fibroadenoma – compressed glands, doubles risk of Pagets disease – due to DCIS invading through to the ER/PR
becoming invasive; oestrogen will cause rapid growth, skin, halo cells Tubular carcinoma – proliferation of spindly stromal
staghorn appearance Invasive ductal carcinoma – nests, outer quadrant of cells
breasts, nipple retraction, axillary lymphadenopathy
, Phyllodes tumour – hypercellular, sarcomatous stroma, Clinical Px – symptomology fluctuates with menstrual
abundant mitoses, large >4c, can be benign (epithelial) cycle
or malignant (parenchymal) Hx – bilateral breast pain/heaviness, swelling,
***Estrogen receptor expression is increased but gene is lumpiness, nipple discharge, but only 50% have
not mutated Sx
***HER 2 staining is due to gene amplification Ex – tender, firm, rubbery, circumscribed mobile
mass
Benign Breast Disease Dx – U/S shows circumscribed cyst that resolved after
aspiration, 50% will show histological changes on
Non-proliferative lesions – characterised by fibrous microscopy Fat Necrosis
and cystic changes Mx – usually self-limiting, iodine may help improve pain – Pseudo-mass that usually develops after trauma
Lesions do not ↑ risk of breastCa may drain cyst with FNA Ax – trauma
Occur in aged 30-50 and after hormone- Pathology – irregular steatocytes, loss of peripheral
replacement therapy Tx nuclei, intracellular amorphic necrotic material, lipid-
Clinical Px – mobile masses, clinical features vary with laden macrophages
menstrual cycle Clinical Px – Hx of breast trauma (e.g seatbelt in MVA),
Breast pain – may be bilateral Hx of surgical reduction or augmentation, firm mass with
Focal areas of nodularity or cysts (outer quad) irregular borders
Nipple discharge is described as Dx – triple test
“straw-like”/brown/green U/S – indistinct margins and solid mass
Mammogram – indistinct margins +/-
Proliferative Lesions (Without Atypia) – refers to cell calcifications
hyperplasia, which may or may not ↑ risk of breast Ca Biopsy – fat necrosis under microscope
Atypical Hyperplasia – usually involves the ducts or Fibroadenomas Mx – self-limiting
lobules Tumour of fibrous and glandular tissue, classified as:
Cells lose their apical-basal orientation – causes ↑ risk of Giant - >10cm Intraductal Papilloma
breastCa Juvenile – in pts b/w 10-18 y/o Refers to a benign growth within the ductal system that
Complex – contains proliferative changes such is usually well-circumscribed, polyploid and haemorrhagic
as sclerosing adenosis, duct epithelial Epi – relatively rare, with incidence 2-3%
hyperplasia or calcification Pathology – arises within large cystic ducts as multiple
Epi – 2nd most common benign breast lesion; fertile papillae, arranged in complex arborising pattern +
<40 y/o, pregnant F and those receiving oestrogen Tx vascular tissue core
Ax – cause is unknown, but may be hormone dependent Clinical Px – nipple discharge, nipple retraction, mass
Pathology – shows fibroblastic proliferation + usually small (<3cm) and well-circumscribed, not always
palpable on Ex
compressed glands/ducts ⇢ ducts may attain a
Dx – triple test
staghorn appearance
U/S – dilated ducts with oval mass
Clinical Px – mass that ↑ in size during pregnancy or
Mammogram – often negative for disease
with oestrogen Tx
Biopsy – papillary growth pattern
Hx – often ASx other than palpable mass
Mx – microdochectomy (removal of a breast duct),
Ex – defined, smooth, rubbery mobile mass
excision
Dx – triple test is usually performed:
Fibrocystic Breast Disease Prognosis – may progress to atypia or DCIS if left
U/S – solid, oval/round circumscribed mass
Formation of cystic, non-cancerous breast lumps untreated
Biopsy – epithelial (glandular) and stromal and
Epi – most common benign breast disease, most fibrous changes
common in F aged 20-50y/o Mx – serial observation, excise if symptomatic
Ax – exact cause not known, but due to hormonal Prognosis - ↑risk of breast Ca if complex, adjacent
influence on breast tissue, causing some cells to grow atypia present or strong FHx of breastCa
and differentiate abnormally, resulting in cysts
Iodine def as a RF
Pathology – variable sized/dilated ducts, may rupture
and cause inflammation – foamy macrophages,
cholesterol clefts, fibrosis
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