Week 4 - BREAST Flashcards

Inflammations, Benign Tumors, Breast Cancer, Others

1
Q

What level is the nipple at?

A

T4

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2
Q

What are the common draining lymph nodes of the breast and why?

A
  • apical axillary
  • lateral axillary
  • pectoral axillary

lesions are more common in the upper outer quadrant

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3
Q

Outline breast anatomy

A
  • modified sweat glands
  • lobes and lobules of gland
  • glands –> lactiferous ducts
  • ducts enlarge beneath nipple to form lactiferous sinus –> individually open on nipple (6-10)
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4
Q

Outline age changes in breast

A

Puberty

  • less glands
  • more fibrous tissue

Adult (lactating)

  • plenty of glands (esp. during lactation)
  • fibro-fatty

Menopause

  • atrophy of glands
  • fat
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5
Q

What is congenital aplasia of the breast known as?

A

Turners

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6
Q

Where are accessory/ectopic breasts seen?

A

along the milk line

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7
Q

What is the most common breast disorder?

A

Inflammation

*mastitis –> acute lactational common (bacteria)

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8
Q

What is the commonest proliferative condtion of the breast?

A

Fribrocystic disease/change

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9
Q

What is the commonest benign and malignant neoplasm of the breast?

A

benign –> fibroadenoma

malignant –> carcinoma + DCIS

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10
Q

Clinically, what is the commonest cause of breast lumps?

A
  • **fibrocystic changes (hormone-induced) –> 40%
  • no disease = 30%
  • cancer = 10%
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11
Q

What is likely Dx of a single mobile breast lump in young adult?

A

fibroadenoma

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12
Q

What is likely Dx of an ill-defined lump(s) or cyclical pain?

A

fibrocystic change

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13
Q

What is likely Dx of a firm lump +/- tethering (fixed)?

A

carcinoma
25-35yrs = familial
35-55yrs = sporadic

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14
Q

What is the cause of clear/purulent discharge vs bloody discharge?

A

clear/pus –> inflammation (duct ectasia)

bloody –> duct papilloma

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15
Q

What is the difference between non-lactational and lactational acute mastitis?

A

non-lactational –> central, periductal, rare

lactational –> periphery, common

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16
Q

What is the etiology of acute lactational mastitis?

A
  • first few weeks after delivery
  • crack in nipple (entry point)
  • S. aureus/Strep. pyogenes
  • localised inflammation, swelling, erythema + pus (periphery)
  • enlarged axillary LNs
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17
Q

What are the causes of chronic mastitis?

A
  • granulomatous (TB, silicone implants)
  • traumatic fat necrosis (chronic granuloma, radial scar)
  • diabetic mastopathy (DM1 lymphocytic inflamm)
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18
Q

What is a multiparous woman?

A

having borne more than one child

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19
Q

Who is affected more commonly by duct ectasia?

A
  • chronic inflammatory condition
  • later age >50yrs
  • multiparous women
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20
Q

What is the etiology of duct ectasia?

A

-inpissation of breast secretions (drying of milk) within ducts –> chronic inflammation

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21
Q

What are the features of duct ectasia?

A
  • duct obstruction/destruction, dilatation –> inflammation, fibrosis with fat globules (obstructed milk) + foamy macrophages in lumen
  • periareolar mass with white, cheesy nipple discharge
  • recurrent abscess/fistula
  • scarring with nipple inversion may mimic carcinoma

*similar to bronchiectasis in lung (plenty of pus)

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22
Q

What is microscopy of duct ectasia?

A
  • dilated ducts

- plenty of surrounding inflammatory cells

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23
Q

What is fat necrosis and what is the typical cause?

A
  • uncommon, chronic scarring of breast
  • usually following trauma, surgery, biopsy –> fat necrosis granulomatous inflammation –> scarring and calcification
  • *mimics carcinoma**
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24
Q

Why is there cyclical pain/discomfort in fibrocystic disease/change?

A
  • hormone sensitive

- estrogen-induced hyperplasia of glands + stroma

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25
Q

What re the 2 major types of fibrocystic disease/change?

A
  1. non-proliferative (low grade)
    - cystic dilatation of ducts + fibrosis
  2. proliferative (high grade)
    - epithelial proliferation** –> higher chance of malignant transformation (DCIS –> carcinoma)
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26
Q

What are the gross and microscopic features of fibrocystic diasease/change?

A

Gross:
-grey, white scar tissue with cysts; multiple irregular nodules

Micro:
-fibrosis, cysts, hyperplastic/dilated glands

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27
Q

What is sclerosing adenosis?

A
  • fibrocystic disease (proliferative type) –> epithelial proliferation
  • sometimes epithelial proliferation forms multiple glandular structures with dense fibrous stroma
  • clinical and biopsy findings mimic carcinoma
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28
Q

What is blue dome cyst?

A

when one of the cysts in fibrocystic disease becomes very large –> blue dome cyst

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29
Q

What is the pathogenesis of fibrocystic disease?

A

-excess estrogens and sensitivity to estrogens –> hormone-induced hyperplasia of glands/stroma

30
Q

What are the differences between benign and malignant breast neoplasms?

A

Benign:

  • round, smooth, soft/rubbery, mobile
  • multiple (FCD)
  • young <35y
  • painful
  • no lymph nodes/no wt. loss
  • fibroadenoma (stromal)
  • ductal papilloma (epithelial)

Malignant:

  • irregular, rough, hard/gritty, fixed
  • single
  • old >35y
  • painless
  • lymph nodes/wt. loss
  • radiating scar (characteristic); nipple retraction/oedema
  • ductal carcinoma
31
Q

What are the 2 types of fibroadenoma?

A
  1. simple fibroadenoma
    - solitary, few (<5/breast), multiple (>5/breast)
    - <5cm round, well demarcated capsulated nodules
  2. giant fibroadenoma (>5cm)
    - juvenile (<20yrs, benign)
    - adult –> phyllodes tumour (benign to malignant)
32
Q

What are gross and microscopic features of simple fibroadenoma?

A

Gross:
-well demarcated, mobile, round/nodular, capsulated, <5cm

Micro:

  • atrophic, compressed slit like flat glands in loose fibrous stroma
  • capsule
33
Q

What is the difference between simple and giant fibroadenoma?

A

simple:

  • tumour of stroma
  • <5cm (small/round), mobile
  • compressed, flat slit-like glands
  • atrophic glands

giant:

  • tumour of gland and stroma
  • > 5cm (large/round), non mobile
  • can be malignant (in adults - 15%)
  • “leaf-like” clefts and slits
  • hypercellular, branching glands + stroma
34
Q

What are the gross and microscopic features of intraductal papilloma?

A

Gross:

  • solitary, intraductal papillary proliferation
  • sub areolar lump with bloody discharge

Micro:

  • benign papillary proliferation of lactiferous duct epithelium
  • stalk + papillae
35
Q

What is the prognosis of intraductal papilloma?

A

-recurrent but v rare risk of metastases

36
Q

What happens to fibroadenomas in pregnancy vs. menopause?

A

pregnancy –> increases due to hormones

menopause –> regresses/calcifies

37
Q

True or False?

OCP is a known risk factor for BrCa

A

True

38
Q

What is the majority of malignant breast cancers?

A

ductal carcinomas

39
Q

What is the etiology of breast carcinoma?

A
  1. hormone
    - increased estrogen/estrogen therapy (OCP)
    - long duration between menarche and menopause
    - decreased progesterone
  2. environment
    - obesity, high fat diet
    - smoking, alcohol, radiation
    - atypical hyperplasia
  3. genetics
    - FHx (familial in 12%)
    - early menarche/late menopause
    - increased HER2/NEU (20%) - bad
    - increased RAS + MYC
    - decreased BRCA1 (50%) + BRCA2 (30%)
40
Q

What is the normal appearance of a duct?

A
  • luminal cells - columnar epithelial
  • myoepithelial contractile cells
  • basement membrane
  • stromal cells
41
Q

What is the pathogenesis of breast cancer?

A
  • proliferation of luminal epithelial cells in response to etiological factors (hormone, environment, genetics)
  • loss of apotosis/genome instability/loss of growth inhibition –> atypical hyperplasia
  • dysplasia occurs –> when it fills the while duct but BM still intact (carcinoma insitu)
  • invasive carcinoma once it ruptures/spreads through BM

*RF’s –> hyperplasia –> dysplasia –> DCIS –> ca.

42
Q

What are the IDC genetic subtypes?

A
  1. luminal A** commonest
    - ER +, PR +, HER2 -
  2. luminal B
    - ER +, PR +, HER2, +
  3. HER2+
    - ER -, PR -, HER2 +
  4. Basal like
    - ER -, PR -, HER2 -
43
Q

What is low grade vs high grade IDC?

A

low grade = luminal types = ER/PR +

high grade = basal-like = familial –> “triple negative”

44
Q

How can we tell if there is invasion or just carcinoma in situ?

A

-immunohistochemistry special stain for myoepithelial cells will indicate intact myoepithelial cells, and thus intact BM –> therefore DCIS/LCIS

45
Q

What are the different morphologies of DCIS?

A
  1. cribiform –> multiple cavities
  2. comedo –> central necrosis (high grade)
  3. Paget’s disease –> DCIS spreads to skin to form eczematous patches
46
Q

Commonest genetic mutation causing familial breast cancer is?

A

BRCA1 gene loss (50%)

47
Q

What can happen to nipple in breast carcinoma?

A

skin tethering/puckering due to radiating fibrous tissue–> pulls nipple inside (nipple retraction)

48
Q

Why are malignant tumours of the breast fixed/immobile?

A

-scar tissue gets attached to muscles/bones/surrounding tissue

49
Q

What is the mammographic appearance of breast carcinoma?

A
  • mammographic density (white areas)
  • more white areas = more risk of malignancy
  • > 75% density = 4-fold increased risk
  • dusty calcification
  • radial scar
50
Q

What are the gross and microscopic features of IDC?

A

Gross:

  • hard, gritty
  • dense fibrous tissue with radiating folds

Micro:

  • pleomorphic cells forming irregular ducts
  • collagen stroma
51
Q

True or False?

HER2 is good, ER/PR is bad

A

FALSE

ER/PR is good, HER2 is bad

52
Q

What are the features of lobular carcinoma?

A
  • multifocal, bilateral, familial
  • small cells, uniform cluster
  • NO tubule/duct formation
  • “indian file” (single cell lines between collagen bundles)
  • LCIS = precancer stage
  • typically ER/PR -, HER2/neu +
  • E-cadherin neg. (unlike IDC)
53
Q

What are the features of medullary carcinoma?

A
  • <3% (rare)
  • high grade, better prognosis (plenty of lymphocytes within tumour)
  • expansile* (no skin tethering)
54
Q

What are the features of inflammatory carcinoma?

A
  • clinically erythematous breast (mistaken for mastitis)

- dermal lymphatic obstruction –> inflammatory-like appearance, yet NO significant inflammation

55
Q

Which breast cancer can males get?

A
  • 1%
  • ONLY ductal carcinoma
  • males have NO lobules*
56
Q

What is Paget’s disease?

A
  • spreading of cancer cells from DCIS along ducts –> peri areolar skin –> eczematous reaction
  • micro –> clusters of malignant cells in superficial epidermis
57
Q

What is peu-de Orange and how does it occur?

A
  • orange-skin appearance in breast cancer lymphoedema
  • tumor cells/emboli within lymphatic vessels –> obstruction –> lymphoedema

*exacerbated by radiation –> radiation kills malignant cells –> lymphangitis –> more obstruction

58
Q

How can breast cancer spread?

A

direct:
-chest wall, muscles, bones

lymphatics:
-axillary

haematogenous:
-CNS/brain, liver, bone, lungs

59
Q

What is gynecomastia and the causes of it?

A
  • breast enlargement in men
  • *estrogen excess –> klinefelter’s, hyperthyroidism, pituitary/adrenal tumours, testicular failure, drugs
  • liver failure/cirrhosis, lung cancer, testicular cancer
  • diethylstilbestrol Tx. for prostate ca.
  • drugs –> spironolactone, H2 antagonists (peptic ulcer), neuroactive agents
60
Q

What is microscopy of gynecomastia?

A
  • duct + stromal hyperplasia
  • NO acini or lobules

*reason why male breast cancers are only DUCTAL carcinomas

61
Q

How is a breast lump diagnosed?

A
  • history first*
  • mammography
  • US
  • fine needle aspiration biopsy (FNA)
  • core/needle biopsy
  • excision biopsy
  • special molecular tests on biopsy –> immunoperoxidase (HER2, PR, ER); molecular techniques - gene detection (BRCA)

TRIPLE ASSESSMENT

62
Q

What is triple assessment?

A

Diagnostic methods for BrCa:

  1. clinical assessment
  2. imaging
  3. biopsy
63
Q

What is a mammogram?

A
  • low radiation x-ray of breast (0.4mSv c.f. 3-8 X-ray)
  • light compression by plates to stabilise/spread interior structures
  • detects v. fine fibrosis/calcification (<100microm)
  • reveals a lump 1-2yrs before palpable
  • more for those at risk or Sx.
64
Q

Compare breast cytology for normal breast vs malignancy

A

normal:
-uniform cells, v few, regular, cohesive

malignancy:
-plenty cells, haemorrhagic, pleomorphic, necrotic

65
Q

What Tx. is used for HER2+ breast cancer pts.?

A

herceptin (trastuzumab)

*HER2+ BrCa grow quickly and spread more than others (poor prognosis)

66
Q

Compare BRCA1 and BRCA2

A

BRCA1:

  • 52% of genetic type
  • young age
  • high grade, necrosis
  • triple negative***
  • FHx ovarian, prostate, pancreas Ca.
  • chromosome 17q

BRCA2:

  • 32% of genetic type
  • not specific
  • low grade, NOS type, scarring (schirrous)
  • ER+***
  • FHx of male breast ca (ovary/prostate also)
  • chromosome 13q
67
Q

What contrast is used in PET scan and what does it show?

A
  • radiolabelled glucose by IV

- high metabolic rate cells (cancer cells) –> 3D view of cancer spread over body

68
Q

Fibroadenoma is a tumour of..?

A

intralobular stroma

69
Q

What is microscopy of DCIS?

A
  • dilated ducts, epithelial proliferation –> CRIBIFORM = commonest type
  • intact wall (myoepithelial cells)
  • no infiltration
70
Q

What is microscopy of IDC?

A
  • pleomorphic cells forming irregular ducts
  • dense fibrous stroma
  • DCIS at periphery (if present suggests cancer has gone through DCIS stage)
  • radiating scars of collagen tissue