Gyn. Path. 2

Question 1

What is endometrial hyperplasia? Is it invasive?

Answer 1

Non-physiologic, non-invasive proliferation of the endometrium.

Question 2

What causes endometrial proliferation?

How does it present?

Answer 2

Too much estrogen. (and/or not enough progesterone)

Presents as bleeding.

Question 3

What’s an exogenous risk factor for endometrial hyperplasia?

Answer 3

Exogenous estrogens, esp tamoxifen.

Question 4

What are some endogenous risk factors for endometrial hyperplasia?

Answer 4

Ovarian lesions (stromal tumors, PCOS, etc.)
Obesity
Hypertension
Diabetes
Reproductive features like nulliparity etc. (less P4)
Cigarettes

Question 5

Protective factors for endometrial hypeplasia?

Answer 5

Anything that increases progesterone:

Eg. having lots of babies.

Question 6

How is endometrial going to look different, grossly, from a polyp?

Answer 6

Endometrial hyperplasia is going to be diffuse and all over the place, not focal like a polyp.

Question 7

What can you see on an ultrasound of endometrial hyperplasia?

Answer 7

Thickening of the endometrial stripe.

Question 8

Histological features of endometrial hyperplasia? (4 things)

Answer 8

Increased gland-to-stroma ratio.
Irregular gland shape.
Variation in gland size.
Frequent mitoses.

Question 9

What are 2 different axes for classifying endometrial hyperplasia? Which axis is more important?
Which combination is worst?

Answer 9

Simple vs. complex.
No atypia vs. atypia. <- more important.
Complex with atypia is most likely to progress to cancer.

Question 10

What does simple vs. complex refer to in endometrial hyperplasia?

Answer 10

Simple: nice, round glands
Complex: jagged, irregular gland architecture

Question 11

What does atypia mean in the context of endometrial hyperplasia?

Answer 11

Atypia: nuclei look cancerous (open chromatin, prominent nuclei), not in one neat layer at the base of gland epithelium.

Question 12

2 categories of criteria that distinguish endometrial carcinoma from hyperplasia?

Answer 12

Invasion of the myometrial.

Invasion of the stroma.

Question 13

What are 3 histological manifestations of endometrial carcinoma invading the stroma?

Answer 13

Irregular infiltration of glands with altered fibroblastic stroma.
Cribriform glands (confluent, uninterrupted by stroma)
Extensive papillary pattern.

Question 14

What’s in the papillae of the “papillary” pattern of endometrial carcinoma?

Answer 14

A fibrovascular core.

Question 15

What are the two types of endometrial carcinoma? What sets them apart? What are each called based on histology?

Answer 15

Type I: Estrogen dependent. Endometrioid.

Type II: Not estrogen dependent. Serous type or clear cell type.

Question 16

Who does Type I endometrial carcinoma tend to affect?
What is the precursor lesion?
What grade are the cancers, relative to Type II?

Answer 16

Pre-menopausal and peri-menopausal women.
Precursor lesion: Atypical hyperplasia
Cancers tend to be lower grade and indolent.

Question 17

Who does Type II endometrial carcinoma tend to affect?
What is the precursor lesion?
What grade are the cancers usually, relative to Type I?

Answer 17

Post-menopausal women.
Precursor lesion: Intraepithelial carcinoma.
Tends to be higher grade and aggressive.

Question 18

What genetic abnormalities are associated with Type I endometrial carcinomas? (3 things)

Answer 18

PTEN mutation
K-ras mutation
Microsatellite instability

Question 19

What genetic abnormality is associated with Type II endometrial carcinoma?

Answer 19

Loss of p53.

Question 20

Histologic progression of Type II endometrial carcinoma?

Answer 20

Goes straight from intraepithelial carcinoma to papillary growth.

Question 21

What is the clinically relevant threshold for extent of myometrial invasion of endometrial carcinoma? What do you do if that threshold is crossed?

Answer 21

Invasion into 50% the thickness of the wall.

If more than that, sample the lymph nodes.

Question 22

5 year survival rates for endometrial cancer overall?

For localized disease?

Answer 22

75-80% overall. 90% for localized disease.

By stage, Type I and Type II have similar prognoses, but Type I tend to be found at lower stages.

Question 23

What’s the most common type of cervical carcinoma?

Common presentation?

Answer 23

Squamous carcinoma (adenocarcinoma and others are rare)
Abnormal bleeding, post-coital bleeding.

Question 24

What’s the strongest risk factor for cervical squamous carcinoma? (come on, you know this) What specific subtypes are linked with cervical squamous carcinoma?

Answer 24

HPV infection with subtypes 16 and 18

and several other subtypes… but 16 and 18 are most common

Question 25

Micro review: What specific genes in high-risk HPV make them oncogenic?

Answer 25

E6 and E7 (they do a bunch a stuff, including interfering with P53)
Also, high risk integrates, low risk stays in episome.

Question 26

Where in the cervix is usually the first site of pre-neoplastic lesions?

Answer 26

The squamo-epithelial junction / transition zone.

Question 27

What are the 4 different possible results from a pap smear?

Answer 27

Normal
ASC-US: atypical squamous cell of undetermined significance
LSIL: Low-grade squamous intraepithelial lesion (“Low-SIL”)
HSIL: High-grade squamous intraepithlial lesion (“High-SIL”)

Question 28

4 phases of cervical carcinoma progression you can see in cervical biopsy?

Answer 28

Normal
CIN1 - mild dysplasia
CIN3 - severe dysplasia, but no invasion
Microinvasion

Question 29

How many women die a day of cervical carcinoma in the US? In the world?

Answer 29

About 10/day in the US. (better than it used to be, still pretty bad)
About 789/day in the world. (countries with good screening have a lot less mortality)

Question 30

2 gross patterns of invasion of cervical carcinoma?

Answer 30

Invading entire cervix -> “barrel cervix”

Fungating growth, often into vagina.