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Endocrine and Reproductive Systems > P- Breast and Pregnancy Pathology > Flashcards

P- Breast and Pregnancy Pathology Flashcards

1
Q

Describe the etiology, clinical features and histopathology of acute mastitis.

What is treatment?

A

Etiology- complications of nursing, bacterial

Clinical - red tender breasts that may develop abcesses

Histopathology - neutrophils/necrotic tissue in duct lumen. Other architecture is fine.

Treat with antibiotics and drainage of the abscess

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2
Q

Describe the etiology, clinical features and histopathology of duct ectasia.

A

Etiology - unknown

Clinical - unilateral thickening of breast tissue [may mimic cancer**]

Histopathology- dilated ducts filled with necrotic debris surrounded by periductal plasma cell inflammation

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3
Q

Describe the etiology, clinical features and histopathology of traumatic fat necrosis.

A

Etiology - trauma of some sort [often forgotten/unnoticed]

Clinical - unilateral irregular node [may mimic cancer]

Pathology: fat necrosis [foamy histiocytes eating up lipid]

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4
Q

What age would you notice fibrocystic disease {FCD}? What is the clinical presentation?

A

FCD is very common and presents in women 20-40 years old with lumpy breasts

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5
Q

What are the 2 main divisions of fibrocystic disease?

Which puts you at an increased risk for carcinoma?

A
  1. Non-proliferative = no increased risk of carcinoma

2. Proliferative = increased risk for developing carcinoma [mild to moderate risk]

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6
Q

How does non-proliferative fibrocystic disease present grossly?
Histologically?

A

Grossly :

  • rubbery white nodules from fibrosis
  • “blue dome” cysts
  • cystic cavities

Histology:

  • fibrosis and cysts
  • apocrine metaplasia [enlarged really pink cytoplasm on the epithelium]
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7
Q

What are the 2 prominent features proliferative FCD presents with on histologically?

Which one puts you at a greater risk for carcinoma development?

A
  1. Epithelial hyperplasia in varying degrees
    - usual ductal hyperplasia
    - atypical ductal hyperplasia
    - atypical lobular hyperplasia

** epithelial hyperplasia increases the risk of cancer

  1. Sclerosing adenosis
    - lobular proliferation of small tubules
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8
Q

When you are looking at the histology of a breast mass, you notice a lot of epithelial hyperplasia where the cells are mixed up and swirling around. What type of FCD is this?

A

Usual ductal hyperplasia in proliferative FCD

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9
Q

Describe the pathology of sclerosing adenosis.

A

Lobular proliferation of small tubules

A lot of fibrosis squeezes the acinar units, so it must be viewed on low powe

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10
Q

What are the 3 main benign breast tumors?

A
  1. fibroadenoma
  2. intraductal papilloma
  3. phyllodes tumors [rare]
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11
Q

A patient under the age of 30 presents with a well-circumscribed, mobile, firm nodule that feels like a marble.
What is the most likely diagnosis and what would you see grossly/histologically?

A

Fibroadenoma which is grossly white with little clefts [glands]

On histology you would see :

  1. benign glands
  2. fibrous stroma
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12
Q

A patient presents with serous or bloody discharge. You are able to palpate a small sub-areolar tumor. What benign lesion could this be?
How does it look grossly/histologically?

A

It sounds like intraductal papilloma

Grossly it looks like a clamshell with cauliflower papilloma growing out of it

Histologically:
papillary growth in the lactiferous ducts

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13
Q

In phyllodes tumors the ________ is benign and the __________ is malignant.
What size are these tumors?

A

These tumors can range from small to massive and can be benign or malignant.

The epithelium is benign and the stroma is malignant.

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14
Q

You are examining a slide of tissue from a breast mass. You see:

  1. hypercellular stroma growing in a leaf-like pattern
  2. glands

What is this tumor likely to be? What is the prognosis/behavior of the tumor?

A

Fibrous and glandular makes you think fibroadenoma HOWEVER the leaf-like pattern of the stroma and hypercellularity lets you know that it is actually PHYLLODES tumor.

Benign and low grade malignant are likely to recur.

High grade malignant is likely to recur and metastasize

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15
Q

What is the relative incidence of carcinoma in the female breast?

A

1/8 women in the USA will get breast cancer [#1 cancer] -about 200,000
It is the #2 cause of cancer deaths in women [1 is lung] - about 40,000

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16
Q

What are the 6 biggest risk factors for the development of invasive breast carcinoma?

A
  1. family history [1st degree relative]
  2. increased length of reproductive cycle
  3. nulliparity or primagravidas over 35
  4. obesity
  5. exogenous estrogens [more than the amount in birth control]
  6. previous breast or endometrial cancer
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17
Q

What is the effect of family history on breast cancer risk?

A

Familial breast cancer is 5-10% of invasive breast cancers.
BRCA1, BRCA2 and p53 [Li Fraumeni)

The patients tend to be younger with bilateral involvement

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18
Q

What is the purpose of mammography?

A

It helps detect early, non-palpable insitu and invasive masses by guiding core or open biopsy to the area of concern.

concerning areas are:

  1. irregular radiodensities
  2. microcalcifications
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19
Q

What are the 2 non-invasive carcinomas?

Which is more prevalent?

A
  1. ductal carcinoma in situ [80%]

2. lobular carcinoma in situ [20%]

20
Q

What are the 5 invasive carcinomas of the breast?

Which 2 are the most serious?

A

Invasive cancers are the majority of breast carcinomas (70-85%)

  1. invasive ductal carcinoma
  2. invasive lobular carcinoma
  3. tubular/cribriform carcinoma
  4. medullary carcinoma
  5. colloid carcinoma

1 & 2 are the most aggressive

21
Q

What are the pathological characteristics of high grade ductal carcinoma in situ?

A
  1. high grade nuclei with pleomorphism, mitotic activity

2. comedonecrosis - pus-filled areas of necrotic cancer cells [like the white stuff from a white head]

22
Q

What is the prognosis of high grade ductal carcinoma in situ?

A

After lumpectomy = 40% recurrence/invasion

Lumpectomy + radiation = <10% recurrence

23
Q

What is the pathology of low grade ductal carcinoma in situ?

What is the prognosis of low grade ductal carcinoma in situ?

A
  1. low grade nuclei - bland cells
  2. cribriform [cookie cutter spaces]
  3. papillary pattern

Prognosis is <10% recurrence or invasion after lumpectomy AND radiation

24
Q

Describe the gross and histological appearance of Paget’s disease of the breast.
What is the prognosis?

A

Pagets = DCIS [ductal carcinoma in situ] that has spread to the skin of the nipple.

Grossly it is an ulcerated, fissured, and oozing nipple with an underlying mass.

Histology: malignant ductal cell invasion of the epidermis that looks like little tumor pockets

Prognosis depends on the stage of the underlying tumor

25
Q

How does lobular carcinoma in situ present clinically?

What is the histology?

A

It presents in pre-menopausal women as multifocal, bilateral lesions.

Histology: expansion and filling of the acini of a lobular unit with uniform, bland cells

26
Q

How do LCIS and DCIS differ in their relationships to cancer?

A

LCIS is a MARKER of increased risk for breast cancer and not a precursor lesion of invasive carcinoma like DCIS.

In patients with LCIS, 30% will get carcinoma but it can be lobular or ductal and in the same or opposite breast. That is why it is a marker and not a precursor lesion.

27
Q

What are the exceptions to LCIS being a marker? [when is LCIS a precursor lesion]

A
  1. more pleiomorphic nuclei than normal LCIS
  2. signet ring cells
  3. involved ducts showing central necrosis and behaving more like DCIS
28
Q

What is treatment for LCIS?

A
  1. bilateral mastectomy [rarely, and prob not warranted]
  2. tamoxifen if it has PR or LR
  3. watch and follow-up
29
Q

What is the most common type of invasive carcinoma in the breast?

A

80% are invasive ductal carcinomas

30
Q

What is the clinical presentation of infiltrating ductal carcinoma?
What is the gross and histological pathology?

A

It presents as a rock hard mass [stony desmoplasia] that is irregular, fixed to adjacent structures and causes dimpling/retraction.

Gross: scar-like [scirrhous carcinoma]

Histology:

  1. infiltrating malignant ductal cells
  2. variable gland formation
  3. desmoplastic stroma
31
Q

What is the incidence of invasive lobular carcinoma compared to invasive ductal carcinoma?
How does it present clinically?
What is the gross and histologic appearance?

A

It is much less common than infiltrating ductal carcinoma [10% compared to 80%]

Clinically: multricentric and bilateral that may be similar to infiltrating ductal carcinoma but with distant mets [peritoneum, ovary, endometrium, meninges, GI]\

Gross: rubbery –> stone hard

Histology:

  1. infiltrating individual low grade malignant cells
  2. glands align in a single file line
32
Q

Where can invasive breast carcinomas spread?

What is the prognosis based on?

A

Spread to:

  1. axillary lymph node
  2. internal mammary lymph nodes
  3. lungs, bone liver

Prognosis:

  1. STAGE is most important
  2. <2cm is usually a good prognosis
  3. The more lymph mets, the worse prognosis
  4. histologic grade and type affect prognosis
33
Q

In addition to staging and grade of the tumor, what 5 other pathologic features and markers affect the prognosis of breast cancer?

A
  1. ER-PR [tamoxifen]
  2. Her2 [herceptin]
  3. DNA ploidy
  4. proliferative rate
  5. p53
34
Q

What do each of the following prognostic markers mean?

  1. ER/PR
  2. Her2
  3. Ki67
A
  1. treat with tamoxifen
  2. treat with herceptin
  3. marker of proliferation
35
Q

List the 4 molecular subtypes of invasive breast carcinoma from best to worst prognosis.

A
  1. Luminal A [ER/PR +, Her2 - , low Ki67]
  2. Luminal B [ER/PR +, Her2 +/-, high Ki67
  3. Triple Neg/Basal-like = all negs with ck5/6 and EGFR +
  4. Her2 [ER/PR -, Her2 +]
36
Q

What are 5 factors that lead to gynecomastia?

A

Hormonal imbalance that leads to hyperestrogenism

  1. puberty
  2. old age
  3. klinefelter’s 47xxy
  4. leydig tumor cells
  5. cirrhosis
37
Q

What is toxemia in pregnancy?
What is the cause?
When does it usually present?
What is therapy?

A
  1. pre-ecclampsia = hypertension, proteinuria, edema
  2. ecclampsia = hypertension, proteinuria, edema, DIC, convulsions

It is caused by abnormal placentation and placenta ischemia.
It presents in the first pregnancy, last trimester

Therapy: bed rest, antihypertensives, induce delivery

38
Q 
Define ectopic pregnancy.
What is the most common site of implantation?
What are the predisposing factors?
What are possible outcomes?
What are the methods of detection?
A

It is when the fetus implants and grows in a location other than the uterus.

The most common site is the fallopian tubes [90%]

Predisposing factors: PID

Outcomes: hemorrhage, rupture, spontaneous regression

Methods of detection:

  1. hCG, ultrasound, laparoscopy
  2. severe abdominal pain
  3. endometrial biopsy [lack of chorionic villi = ectopic pregnancy and rules out uterine pregancy]
39
Q

How do complete and incomplete hydatidiform moles differ in their clinical presentation?

A

Complete :

  1. bleeding
  2. enlarged uterus
  3. HCG markedly elevated
  4. vesicles on US

Incomplete:

  1. uterus NOT enlarged
  2. HCG less elevated
  3. clinical Dx of missed or spontaneous abortion
40
Q

How do complete and incomplete hydatidiform moles differ in their gross appearance ?

A

Complete - bunch of bloody grapes

Incomplete - missed or spontaneous abortion, may have fetal parts [no clusters]

41
Q

How do complete and incomplete hydatidiform moles differ in histologic appearance?

A

Complete:

  1. villi with hydropic swelling
  2. trophoblastic proliferation

Incomplete:

  1. some villi enlarged
  2. focal trophoblastic proliferation
42
Q

How do complete and incomplete hydatidiform moles differ in cytogenetics?

A

Complete:

  • 46XX or XY
  • empty egg fertilized with 1 or 2 sperm

Incomplete

  • TRIPLOID
  • egg fertilized by 2 haploid or 1 diploid sperm
43
Q

How do complete and incomplete hydatidiform moles differ in prognosis?

A

Complete - 10% develop invasive moles, 2.5% choriocarcinoma

Incomplete - rarely followed by choriocarcinoma

44
Q

What is the most common precursor lesion of gestational choriocarcinoma?

A
  1. hydatidiform moles [50%]

Followed by:

  1. abortion
  2. normal pregnancy
  3. ectopic pregnancy
45
Q

What is seen histologically for gestational choriocarcinoma?

A

[just like in testicular choriocarcinoma]

  1. malignant syncitial and cytotrophoblasts
  2. no villi
  3. hemorrhage
46
Q

How does gestational choriocarcinoma spread?
What is treatment?
What is the prognosis?

A

It spreads by direct and hematogenous spread

Treatment: surgery and chemo

Prognosis -100% cure

Endocrine and Reproductive Systems (27 decks)

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