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Pathophysiology - Endocrine and Reproductive > Clinical and Pathologic Features of Breast Disease > Flashcards

Clinical and Pathologic Features of Breast Disease Flashcards

1
Q

Where can access breast tissue occur? What germ layer is it derived from?

A

Anywhere along the milk line (mammary ridge)
-> from the axilla to the groin

Derived from ectoderm (skin) -> modified sebaceous glands

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2
Q

What is the generally ductular structure of the breast parenchyma?

A

Terminal duct lobular (microscopic) units drain into lobules (macroscopic), which drain into ducts (macroscopic).

The ducts each drain multiple lobules of the breast, and there are about 5-10 ducts which empty into the nipple.

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3
Q

What is the functional unit of the breast and what are the layers of epithelial cells which are present? What is their significance?

A

Terminal duct lobular units

Two layers of cells
1. Luminal cell layer - inner cell layer lining the ducts / lobules, responsible for milk production.

  1. Myoepithliel cell layer - outer cell layer lining the ducts / lobules, contractile function to push milk towards nipple. LOST in cancer (like prostate).
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4
Q

When are the breasts most tender and why?

A

Typically premenstrual

  • > estrogen and progesterone cause development and edema of breast tissue
  • > breast tenderness is worst in late secretory phase of the endometrial cycle
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5
Q

What hormonesdrive the development of the breast during pregnancy?

A
  1. Estrogen
  2. Progesterone
  3. Human placental lactogen (prolactin function, but also growth-hormone like and induces insulin resistance to divert nutrients to baby)
  4. hCG
  5. Prolactin
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6
Q

What do pregnancy tests look for and why?

A

They look for beta subunit of HCG (beta-HCG), because alpha subunit is identical to FSH, LH, and TSH

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7
Q

What happens to the breast tissue during menopause and is this good or bad?

A

Progessive TDLU atrophy and fatty replacement of the stroma

Good thing -> less likely to develop breast cancer if atrophy occurs.

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8
Q

What is gynecomastia and who is it physiologic in?

A

Breast enlargement in males due to increased estrogen relative to testosterone
Physiologic in:
1. Newborns
2. Puberty - usually resolves in 6-12 months
3. Elderly - secondary to decreased testosterone

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9
Q

What are some drug-induced causes of gynecomastia?

A
  1. Marijuana
  2. Cimetidine
  3. Digoxin
  4. Ketoconazole
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10
Q

What are some pathologic non-drug-related causes for gynecomastia and what should be done?

A
  1. Klinefelter syndrome
  2. Cirrhosis (increased estrogen)
  3. Renal failure -> uremia-associated hypogonadism

Should give mammogram to rule out cancer

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11
Q

What is notably absent on histology of gynecomastia?

A

Lobules (there are none in males, they lack acini)

-> ducts and stroma will proliferate

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12
Q

What is the utility of mammography, breast ultrasound, and breast MRI in diagnosis of breast lumps?

A

Mammography - best screening and diagnostic tool

Breast ultrasound - not used for screening, but determines if cyst or solid lump

Breast MRI - adjunctive, should NOT be used instead of mammography / ultrasound

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13
Q

At what age should mammography start?

A

Start at age 40, although now they are starting to suggest 50.

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14
Q

What is the usual cause of acute mastitis and what is happening pathologically?

A

Usually caused by Staphylococcus aureus infection of the breast.

Trauma from early weeks of breast feeding causes cracks / fissures to develop in skin -> invasion of bacteria into breast parenchyma

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15
Q

What are the sequellae of acute mastitis? Treatment?

A

Can lead to acute purulent nipple discharge and erythematous breast. Abscesses may rarely form.

-> heals by fibrosis and scarring

Treatment is continued breastfeeding and antibiotics.

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16
Q

What is periductal mastitis, what is the pathogenesis, and who tends to get it?

A

Painful subareolar mass which occurs as keratinizing squamous metaplasia occurs in the ducts, which causes duct blockage and inflammation. There will be a granulomatous response to spilled keratin, and chronic inflammatory infiltrate.

Occurs in smokers -> have a relative vitamin A deficiency, causing squamous metaplasia

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17
Q

What can periductal mastitis be confused for?

A

Can be confused for breast cancer -> subareolar mass, and nipple is often retracted

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18
Q

What is mammary duct ectasia and what inflammatory infiltrate is seen?

A

Inflammation with DILATION of subareolar ducts

-> chronic inflammatory infiltrate with plasma cells and macrophages is seen on biopsy

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19
Q

What is the classical presentation of mammary duct ectasia and what can it be confused with?

A

Presents as periareolar mass with “green-brown” nipple discharge due to inflammatory debris.

Happens in post-menopausal women, so easily confused with breast cancer.

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20
Q

What is primary granulomatous mastitis and what causes it?

A

Type IV hypersensitivity reaction in the breast lobules of unknown cause.

Not due to infection (i.e. TB) or sarcoidosis, etc

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21
Q

What benign entity is most likely to mimic breast cancer both clinically and on mammography? What is its pathogenesis?

A

Fat necrosis

  • > trauma leads to formation of a hard mass which is necrotic
  • > dystrophic calcification (due to saponification) allows it to be seen on mammography
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22
Q

What will patients present with clinically in fat necrosis and what will biopsy show? Treatment?

A

Present clinically with a benign lump, often with skin retraction. Patients often remember no traumatic event.

Biopsy shows necrotic fat cells and giant cells (inflammatory infiltrate lining fat cells)

Treatment is NSAIDs

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23
Q

What is the single most common change in the premenopausal breast and what is the cause? What age group is susceptible?

A

Fibrocystic changes -> older premenopausal women (>35 years).

Thought to be due to abnormal hormonal response / sensitivity

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24
Q

What is the typical presentation of fibrocystic changes? How many cysts are there typically?

A

Breast pain, swelling, and tenderness which is associated with areas of nodularity, induration, and gross cysts

  • > vague irregularity of breast tissue, especially upper outer quadrant
  • > often multifocal and bilateral
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25
Q

How does a fibrocystic change generally appear grossly? Are the lesions benign or malignant?

A

Appears to have a blue-dome appearance on gross exam. Represents a fluid-filled ductal proliferation which forms scarring and fibrosis around an obstructed duct. The duct then erodes into a blood vessel -> bleeding into cyst = BLUE DOME.

They are benign, but may be associated with increased risk of developing breast cancer in BOTH breasts

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26
Q

What is a non-proliferative fibrocystic lesion and is it associated with increased risk of cancer? What non-carcinogenic chnage is associated with it?

A

Cyst with fibrous stroma, and some degree of cystic dilatation of terminal ducts.

Often has apocrine cell metaplasia associated with it (eosinophilic blebbing at epithelial surface), but NO increased risk of cancer

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27
Q

What two lesions are associated with roughly 2x risk of breast cancer as fibrocystic changes? How will the lumens look on the ductal one?

A
  1. Usual ductal hyperplasia - excess benign cells lining ducts-> lumens will appear irregular (indicates benign), a type of proliferative change
  2. Sclerosing adenosis - adenosis = glands, sclerosing = fibroblasts, this is a normal looking hyperplasia of acini with intermixed fibrosis. Often becomes calcified (confusable on mammogram)
28
Q

What fibrocystic lesions are at greater risk (4-5x) of progressing to breast cancer? How will the lumens of the ductal one appear?

A
  1. Atypical ductal hyperplasia - lumens within the proliferated ducts appear more round than usual ductal hyperplasia, and cells are monomorphic / atypical
  2. Lobular hyperplasia - increased number of cells lining each lobule, look like “marbles in a petri dish” acini
29
Q

What is the most common benign neoplasm of the breast, and who tends to get it?

A

Fibroadenoma, usually in premenopausal women <35

30
Q

What is the growth pattern of fibroadenoma and does it increase your risk for cancer?

A

Small, well-circumscribed mass, usually solitary. Includes fibrous component with proliferative intralobular duct connective tissue, and a gland component.

It is estrogen-sensitive, so iti grows during pregnancy and prior to menstruation.

No increased risk of cancer.

31
Q

How is physiologic vs nonphysiologic nipple discharge determined?

A

Physiologic - bilateral, non-bloody, from multiple ducts, and due to stimulation

Pathologic - unilateral, from a single duct, bloody, and often spontaneous -> requires biopsy

32
Q

What is lactation vs galactorrhea and some causes?

A

Lactation - milk production in association with breastfeeding, appropriate. Occurs up to 2 years after breast feeding

Galactorrhea - Milk production outside lactation (i.e. breastfeeding). Common causes include drug-induced (i.e. neuroleptic drugs, cimetidine, birth control pills), prolactinoma, or nipple stimulation

33
Q

What is the most common cause of serous or blood nipple discharge? How can you tell if it’s benign or malignant

A

Intraductal papilloma
-> papillary growth into a large duct, typically under the areola.

Can see two layers of cells to know it’s not malignant.

34
Q

What neoplasm should be suspected if what was presumed to be a fibroadenoma does not regress after menopause? What is its growth pattern?

A

Phyllodes tumor

  • > fibroadenoma-like (both proliferations of glands and stroma) but has an overgrowth of the “fibrous” mesenchymal component of the tumor
  • > They have a very cellular stroma -> sarcomatous type tumor (stroma can be very ugly, much less benign looking than fibroadenoma).
  • > characteristic “leaf-life” projections of fibrous tissue on biopsy
35
Q

What is the pattern of spread of phyllodes tumor and what must be done to deal with them? Are they benign or malignant?

A

Usually benign, and must be resected with wide margins (like pleomorphic adenoma) to prevent recurrence.

If they become malignant (rare) they will spread by blood rather than lymph nodes due to being a sarcoma.

36
Q

What are the risk factors for malignant breast cancer?

A

All the risks for increased / nonstop estrogen exposure as before, + atypical hyperplasia type fibrocystic change (5x risk)

  • Late age to first child boon
  • Early menarche / late menopause
  • Fat intake / obesity
  • FHx of breast cancer, or BRCA/BRCA2 mutations
  • Hormone replacement therapy
37
Q

What cancers are BRCA1 / BRCA2 associated with?

A

BRCA1 - medullary breast carcinoma especially, + serous carcinoma of the ovary and fallopian tube
>80% lifetime risk of Breast cancer

BRCA2 - Most associated with breast carcinoma in males

38
Q

Do masectomies eliminate your risk of breast cancer in BRCA if you have bilateral removal?

A

No -> reduces it by about 90%. There is still a small risk becuase breast tissue sometimes extends into the axilla / subcutaneous tissue of the chest wall

39
Q

In what area does most breast cancer arise and where does it commonly spread to?

A

Most arises in the upper outer quadrant of the breast (where the breast tissue is)

Spreads to BONE, lung, liver, and brain

40
Q

What is stage 0 ductal breast cancer also known as? What are its two grades?

A

Ductal carcinoma in situ

Low Grade DCIS - looks like atypical ductal hyperplasia, no central necrosis, atypical ductal cells fill ducts but don’t invade basement membrane

High Grade DCIS - comedocarcinoma

41
Q

What is comedocarcinoma? Will both layers of epithelial cells be present?

A

High grade DCIS -> necrosis and dystrophic calcification seen in the center of the ducts. Cells are atypical but still in situ because bounded by basement membrane.
-> picked up easily via mammography due to calcifications

Yes, both layers of epithelial cells will be present until tissue invasion occurs

42
Q

What does lobular carcinoma in situ (LCIS) resemble and how is it usually discovered?

A

Resembles atypical lobular hyperplasia -> difference is in the amount of hyperplasia

It is usually discovered via incidental biopsy, because it lacks clinical and mammographic signs (no mass or calcifications)

43
Q

Is LCIS usually solitary? How is it treated?

A

It is often multifocal and bilateral

Treated as a super risk factor, as risk of cancer is usually for invasive DUCTAL carcinoma.

Observe closely and give tamoxifen hormonal therapy. (ER antagonist as breast, agonist at bone/uterus)

44
Q

Do in situ breast carcinomas usually present with masses?

A

No! That’s why you typically have to screen for them via mammography. Lobular carcinoma in situ does not (as you just saw), and ductal carcinoma does not because it’s limited to the ducts and has not invaded the stroma to make it firm.

Mass -> likely invasive carcinoma

45
Q

What is Paget disease and what will it look like on the patient? Is this DCIS or invasive cancer?

A

Extension of neoplastic adenocarcinoma cells through the ducts to involve the skin of the nipple

Appears as ulceration and erythema of the nipple

It can be either DCIS or invasive adenocarcinoma

46
Q

How will Paget disease appear histologically? How should you manage it?

A

Similar to extramammary Paget disease
-> “Paget cells” clear cytoplasm in the epidermis, either singly or in clusters.

Patient generally needs biopsy with removal of the lump since it’s almost always associated with underlying carcinoma when in the breast

47
Q

What is the most common type of breast cancer? How does it present classically on the outside and with a mammogram?

A

Invasive ductal carcinoma.

Presents as a firm, fibrous, rock-hard mass with dimpling of the skin or retraction of the nipple due to desmoplasia.

Often has a characteristic stellate shape on mammogram with little tentacles reaching out -> ductal proliferations going everywhere.

48
Q

What are the four main subtypes of invasive ductal carcinoma?

A
  1. Tubular carcinoma
  2. Mucinous carcinoma
  3. Medullary carcinoma
  4. Inflammatory carcinoma
49
Q

What is the most classic subtype of invasive ductal carcinoma? Prognosis?

A

Tubular carcinoma - well-differentiated tubules that lack myoepithelial cells -> good prognosis

50
Q

What is mucinous carcinoma? Prognosis?

A

Invasive ductal carcinoma characterized by abundant extracellular mucin

“Cells are stuck in mucus so they can’t go anywhere” - good prognosis -> rarely metastasizes

51
Q

What is medullary carcinoma / who gets it?

A

Invasive ductal carcinoma with large, high-grade cells associated with lymphocytes / plasma cells

-> good prognosis, in BRCA1 carriers

52
Q

What characterizes inflammatory carcinoma grossly and microscopically and what is it also called?

A

Characterized by carcinoma in dermal lymphatics

-> also called “peau d’orange” from thickened, erythematous, orange-peel like rough skin surface

53
Q

What is inflammatory breast carcinoma often mistaken for? What is the prognosis?

A

Often mistaken for mastitis or Paget disease

Prognosis is very poor -> (has already spread into lymphatics)

54
Q

How does invasive lobular carcinoma appear histologically?

A

Appears as an orderly row of cells “single file” pattern due to being discohesive.

  • > will not form glands
  • > minimal desmoplasia
55
Q

Does lobular carcinoma present with a mass? What is the most common mutation?

A

Typically does not present with a mass due to lack of desmoplasia. Often radiographically silent for this reason as well.

Negative for E-cadherin -> allows cells to become discohesive and line up single file.

56
Q

What are the most prognostically important and useful factors for breast carcinoma?

A

Important - Presence of distant metastases -> greatest effect on prognosis

Useful - spread to axillary lymph nodes (given distant metastasis is rare at presentation)

57
Q

What is the method of assessing axillary lymph nodes for metastasis?

A
  1. Sentinal lymph node biopsy -> biopsy the first lymph node that drains the mass in the region.
  2. If metastases are contained, axillary lymph node dissection (ALND) must be performed to remove 2-3 levels of lymph nodes.
58
Q

What is adjuvant therapy vs neoadjuvant therapy?

A

Adjuvant therapy - chemotherapy given after surgical removal of cancer

Neoadjuvant therapy - chemotherapy prior to surgery.

59
Q

What agents are used to treat ER+ breast cancer by inhibiting peripheral conversion of androgens to estrogens? Name them.

A

Aromatase inhibitors:

Anastrozole, Letrozole, Exemestane

-> “An astronaut Lets his Ex smell his aroma”

60
Q

What is the SERM (selective estrogen receptor modulator) used for breast cancer and how does it work? Does it increase your risk of any cancers?

A

Tamoxifen - antagonizes estrogen receptor at breast, but agonizes at uterus and bone
-> increased risk for endometrial cancer

61
Q

What does trastuzumab target?

A

The HER2/neu receptor -> an epidermal growth factor receptor (EGFR) which is an oncogene overexpressed in some breast cancers

62
Q

Why does being a black woman afford you a poor prognosis in breast cancer?

A

You are more likely to give triple negative cancer (ER-, progesterone receptor -, and HER2/neu-) -> no therapies will work

63
Q

What is the most common type of male breast cancer and what are the presenting symptoms?

A

Invasive ductal carcinoma (males have few lobules)

Symptoms: skin and chest fixation more common (desmoplasia has less breast tissue to work with)

  • > subareolar mass is common
  • > nipple discharge may be present
64
Q

What are the risk factors for male breast cancer?

A

Hyperestrogenic states: Klinefelter syndrome.

BRCA2

65
Q

What is the difference between ductal and lobular breast cancer?

A

Ductal -> cells differentiate into duct-like structures
Lobule -> cells differentiate into lobule-like structures before becoming single-file when they are invasive

They are derived from the same precursor cells, carcinoma is just named based on the shapes that they form. I.e. you could have a ductal carcinoma derived from the lobules of the terminal duct lobular unit.

Pathophysiology - Endocrine and Reproductive (27 decks)

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