Breast Pathology Flashcards
what are the methods of breast cytopathology
FNA
fluid
nipple discharge
nipple scrape
what are the stages of breast FNA cytology
C1 - Unsatisfactory C2 - Benign C3 - Atypia, probably benign C4 - Suspicious of malignancy C5 - Malignant
why is breast FNA not done as much now
as if malignant cant tell if invasive or in situ
what are the diagnostic forms of breast histopathology
needle core biopsy
vacuum assisted biopsy (large volume of sample)
skin biopsy
incisional biopsy of mass
what are the therapeutic modalities of breast histopathology
vacuum assisted excision
excisional biopsy of mass
resection of cancer
what are the types of breast cancer resection
wide local excision- conserves breast
mastectomy
what are the stages of needle core biopsy
B1 - Unsatisfactory / normal B2 - Benign B3 - Atypia, probably benign B4 - Suspicious of malignancy B5 - Malignant B5a - carcinoma in situ B5b - invasive carcinoma
what is breast carcinoma in situ
still in ducts (removal of tissue can be curative)
what test is necessary for invasive breast carcinoma
minimum of axiallry node sampling
what are the developmental abnormalities of the breast
hypoplasia
juvenile hypertrophy (grow lots in short amount of time)
accessory breast tissue/ nipple
what are the non neoplastic benign breast diseases
gynaecomastia fibrocystic change hamartoma fibroadeonoma sclerosing lesions: -sclerosis adenosis -radial scar/ complex sclerosing adenosis
what is gynaecomastia
breast development in males
ductal growth without lobular development (dont get acini)
how many lacteriferous ducts at the nipple
15-20
what are the inflammatory breast diseases
fat necrosis (common after trauma) duct ectasia (ducts get dilated and blocked) acute mastitis/ abscess
what are the benign breast tumours
phyllodes tumour (spectrum to benign to malignant- most benign) intraduct papilloma (benign to malignant, rarely invasive)
what are the causes of gynaecomastia
exogenous (happens in newborns, self limiting)/ endogenous hormones
cannabis
prescription drugs
liver disease
how does liver disease cause gynaecomastia
metabolism of cholesterol based hormones disrupted excess of oestrogen based hormones
what age group get fibrocystic change in breast
20-50, majority 40-50
very common
what causes fibrocystic change
menstrual abnormalities (esp anovulatory cycles, prolonged osterogenic stimulation)
early menarche
late menopause
what is the usual outcome for breast fibrocystic change
resolves/ diminished after menopause
what is the presentation of fibrocystic change
smooth discreet lumps (cysts) sudden pain (ruptures/ bleeding of cysts) cyclical pain incidental finding screening often bilateral
what is the pathology of fibrocystic change
cysts;
- 1mm- several cm
- blue domed with pale fluid (not blood filled, this would be red flag)
- usually multiple
- associated with other benign changes
intervening fibrosis
what type of seceretory cells line the ducts
merocrine
what is the histology of fibrocystic change
cysts:
- thin walled, may hive fibrotic wall
- lined by apocrine epithlium
intervening fibrosis
what is metaplasia
The change from one fully differentiated cell type to another fully differentiated cell type
what is the management of fibrocystic change
exclude malignancy
reassure
excise if necessary
what cell change is happening in fibrocystic change
metaplasia- not pre cursor lesion/ neoplastic
what is a hamartoma
circumscribed lesion composed of cell types normal to the breast but present in an abnormal proportion or distribution
(not excised unless causing problem)
what is the usual patient group for a fibroadenoma
common (17%)
commoner in african women
usually solitary, 10% multiple
can get multiple recurring
what is the presentation of a fibroadenoma
peak incidence in 3rd decade
screening
painless, firm, discrete, mobile mass (breast mouse)
what does a fibroadenoma look like on USS
solid
what is the pathology of a fibroadenoma
circumscribed rubbery grey/ white colour biphasic tumour/ lesion (two components in equal proportion) : epithelium, stroma localised hyperplasia proliferation of intralobular stroma
what is the management for a fibrodenoma
diagnose
reassure
excise
what is sclerosing adenosis associated with
fibrocystic change
what is the pathology of sclerosing lesions
benign, disorderly proliferation of acini and stroma
can cause a mass or calicifcation
may mimic carcinoma- hard to diagnose
what is the presentation of sclerosing adenosis
pain, tenderness or lumpiness/ thickening
asymptomatic
age 20-70
is there a risk of malignancy in sclerosing adenosis
is benign
negligible risk of carcinoma
what is the presentation of a radial scar
wide age range, common
incidental finding
mammographically detected
what is the pathology of a radial scar
radial scar= 1-9mm complex sclerosing lesions= >10mm stellate architecture central puckering radiating fibrosis
what is the histology of a radial scar
fibroelastic core
radiating fibrosis containing distorted ductules
fibrocystic change
epithelial proliferation
how risky are radial scars
Mimic carcinoma radiologically
Probably not premalignant per se
Often show epithelial proliferation
In situ or invasive carcinoma may occur within these lesions
what is the treatment for a radial scar
excise/ sample extensively by vacuum biopsy
what causes fat necrosis of the breast
local trauma (seat belt injury, often no Hx) warfarin therapy
what is the pathology of fat necrosis
damage and disruption of adipocytes
infiltration by acute inflammatory cells
foamy macrophages
subsequent fibrosis and scarring
distorts breast causing dimpling or nipple indrawing
what is the management for fat necorsis
confirm diagnosis
exclude malignancy
what are the clinical features of duct ectasia
affects sub-areolar ducts pain acute episodic inflammatory changes bloody and/ or purulent discharge fistulation nipple retraction and distortion
what is duct ectasia associated with
smoking
what is the pathology of duct ectasia
sub areolar duct dilation
periductal inflammation
periductal fibrosis
scarring and distortion
what is the management of duct ectrasia
Treat acute infections
Exclude malignancy
Stop smoking
Excise ducts
what are the main causes of acute mastitis/ abscess
duct ectasia:
- mixed organisms
- anaerobes
lactation
- staph aureus
- strep pyogenes
what is the management for acute mastitis/ abscess
antibiotics
percutaneous drainage
incision and drainage
treat underlying cause
what are the clinical features of a phyllodes tumour
40-50
slow growing unilateral breast mass
what is the pathology of a phyllodes tumour
biphasic tumour
stromal overgrowth
behaviour depends on stromal features (benign, borderline, malignant): prone to local recurrence if not adequately excised
rarely metastasise
what are the breast papillary lesions
intraduct papilloma
nipple adenoma
encapsulated papillary carcinoma
what is the presentation on an intraduct papilloma
age 35-60 nipple discharge +/- blood asymptomatic at screening: -nodules -calcification
what is the pathology of intraduct papilloma
sub areolar ducts
2-20 mm diameter
papillary fronds containing a fibrovascular core
covered by myoepithelium and epithelium
epithelium may show proliferative activity (usual type hyperplasia, atypical ductal hyperplasia, ductal carcinoma in situ)
what is breast angiosarcoma associated with
previous x ray therapy
what makes a phyllodes tumour malignant
sarcomatous stromal component
what cancers spread to breast
carcinoma: -bronchial -ovarian serous carcinoma -clear cell carcinoma of kidney malignant melanoma soft tissue tumours -leiomysarcoma
what cell type does breast carcinoma arise from
breast epithelial cells
arises in glandular epithelium of the terminal duct lobular unit
(technically an adenocarcinoma but call carcinoma)
what are the precursor lesions for breast carcinoma
(epithelial proliferations) intraductal: -epithelial hyperplasia usual type -columnar cell change (+/- atypia) -aytpical ductal hyperplasia -ductal carcinoma in situ lobular: -lobular in situ neoplasia (atypical lobular hyperplasia, lobular carcinoma in situ)
what are the features of in situ carcinoma
confined within BM of acini and ducts
cytologically malignant but non invasive
non obligate precursor of invasive carcinoma (not all will progress)
classified into lobular or ductal
what are the types of lobular in situ neoplasia
atypical lobular hyperplasia (<50% of lobule involved)
lobular carcinoma in situ (>50% of lobule involved)
what are the histological characteristics of lobular in situ neoplasia
small intermediate sized nuclei solid proliferation intra-cytoplasmic lumen/ vacuoles oestrogen receptor positive E-cadherin negative (CDH1 gene, immunohistochemistry)
what are the clinical features of lobular in situ neoplasia
frequently multifocal and bilateral
incidence decreases after menopause (ER positive)
not palpable or visible grossly
usually an incidental finding, may calcify- mammography
what is the significance of lobular in situ neoplasia
15-10% have higher grade lesion on open diagnostic biopsy
higher risk of invasive carcinoma
is itself a true precursor lesion
what is the management for lobular in situ neoplasia
if discovered on core biopsy- excision/ vacuum biopsy to exclude higher grade lesions
if discovered on vacuum or excision biopsy- follow up with annual mmg for 5 years
what is the risk of intrdauctal proliferations
risk of progression to invasive carcinoma
what are the histological features of ductal carcinoma in situ
arises in TDLU
unicentric (single duct system)
Calcification (formed by cell necrosis) can be picked up on screening before it is palpable
cytologically malignant epithelial cells
confined within BM of duct
may involve lobules
may involve nipple skin- Pagets
what is pagets disease of the nipple
high grade DCIS extending along ducts to reach the epidermis of the nipple
STILL IN SITU
how is DCIS classified
cytological grade
histology
presence of necrosis
what is the significance of DCIS
risk as true precursor of invasive carcinoma
what is the management for DCIS
diagnosis
surgery
adjuvant radiotherapy
chemoprevention- endocrine therapy
what is microinvasive carcinoma
DCIS with invasion of <1mm beyond the BM
what is the management for microinvasive carcinoma
(treat as high grade DCIS as low risk of mets)
surgery
adjuvant radio
chemoprevention
what are the grades of ductal carcinoma in situ
low, intermediate and high
what is the pathway of ductal epithelial proliferations
normal hyperplasia of usuall type atypical ductal hyperplasia ductal carcinoma in situ invasive carcinoma
when does breast carcinoma become invasive
when is breaches BM >1mm and infiltrates normal tissue
microinvasion <1mm
what is the peak age group for breast cancer
50-70
what are the risk factors for breast carcinoma
age early menarche late first birth nulliparity not breastfeeding late menopause endogenous hormones exogenous hormones (OCP, HRT) previous breast disease (environment/ genetics stay same) geography (western europe, australia/ new zealand, north europe, north america) increase BMI (oestrogen levels) low physical activity alcohol fatty diet (NSAID lower risk) smoking genetics
does risk of breast cancer reduce after stopping OCP or HRT
yes
pretty much back to normal after 5-10 years
what genetic cancer syndromes cause breast cancer
BRCA 1 and 2 TP53 cowdens peutz-jeghers syndrome ataxia telengiectasia
what are the differences in BRCA 1 and 2
1- breast, ovarian, bowel prostate
2- breast (inc male), ovarian, prostate, pancreatic
what can be done prophylatically in breast cancer genetic syndromes
MRI (doesnt work for BRCA 1)
surgery
what are breast cancers usually like in BRCA 1 and 2
high grade without a precursor
what is the current trend in breast cx mortality rate
going down
10 year survival 78%
what is the 2nd commonest cause of cancer death in women
breast cx
what is the lifetime risk of breast cx
1 in 8
what is the natural Hx of invasive breast carcinoma
local invasion (breast stroma, skin, muscles of chest wall) lymphatics blood born (esp ER +ve tumour)- bone, liver, brain, lungs, abdo viscera, female genital tract
what nodes to majority of breast cancers spread to
axillary
small percent go to internal mammary
what are the typeso f hormone receptor expressing invasive breast cancers
oestrogen receptor (ER)- if +ve will respond to anti oestrogen therapy (oophrectomy, tamoxifen (blocks receptor), aromatase inhibitors (letrozole, stops production), GnRh antagonists (goserilin, induces menopause in younger women)
progesterone receptor (PR)
HER2- human epidermal growth factor receptor 2 - responds to trastuzamab
what is the most common type of invasive breast carcinoma
ductal (aka no special type) 70%
lobular 10% more less common ones
what is tumour grade a measure of
tumour differentiation
high grade= poorly differentiated= poor prognosis
how is breast carcinoma graded
tubular differentiation
nuclear pleomorphism
mitotic activity
what does a triple negative breast cancer mean
does express a hormone receptor, wont respond to hormonal therapy, need chemo
how is breast cancer stages
Direct invasion of adjacent tissues T0 - T4 Local tumour growth (size of tumour and extent of involvement of adjacent structures) Lymphatic spread N0 - N3 Regional lymph nodes Blood-borne spread M0 - M1 Distant metastasis
what are the predictive and prognostic factors for invasive breast carcinoma
ER (PgR)
HER 2
histopathology
clinical factor
notting predictive index (diameter, grade, lymph node status)
