Uterine Pathology

Front 1

What are the 3 sources of estrogen? What forms are secreted in each?

Back 1

1) Ovary- 17B-estradiol (most potent)
2) Adipose- estrone (2nd)
3) Placenta- estriol

Front 2

What are the 4 sources of progesterone?

Back 2

1) Corpus luteum
2) Placenta
3) Adrenal Cortex
4) Testes

Front 3

1) Estrogen has what effect on uterus?
2) Progesterone?

Back 3

1) Proliferative effect on endometrium; increases myometrial excitability
2) Maintains endometrium to support implantation; decreases myometrial excitability

Front 4

1) What is the regenerative layer of the endometrium?
2) Which pathology is associated with loss of this layer and can lead to secondary amonorrhea?

Back 4

1) Basalis layer
2) Asherman syndrome (due to overaggressive D+G)

Front 5

Which patient population is most at risk for acute endometritis?

Back 5

Women who recently delivered baby (either C-sectional or vaginal) or had an abortion.

Front 6

1)Which pathogen is the most common cause of acute endometritis?
2) Clinical findings of acute endometritis?

Back 6

1) Strep agalactiae (Group B strep)
2) Fever, uterine/abdominal pain, purulent vaginal discharge

Front 7

What histologic finding is necessary to diagnose chronic endometritis?

Back 7

Presence of plasma cells

Endometrium already has resident lymphocytes in the area=>once exposed to pathogen they differentiate to plasma cells

Front 8

1) What are the major pathogens causing chronic endometritis?
2) Which pathogen is specifically involved in chronic endometritis in women w/intrauterine devices?
3) What important complication can arise due to chronic endometritis?

Back 8

1) N. gonorrhea, C. trachomatis
2) Actinomyces israelii
3) Infertility

Front 9

1) How do endometrial polyps present?
2) Development of endometrial polyps is a side effect of which drug?

Back 9

1) Dysfunction uterine bleeding (spotting)
2) Tamoxifen=>has anti-estrogen effect on breast, but slight pro-estrogen effect on endometrium

Front 10

What 3 things may seen on histology of endometriosis?

Back 10

1) Endometrial glands
2) Endometrial stroma
3) Hemosiderin pigment
**Histologic dx made if 2/3 are present**

Front 11

What are the 3 proposed theories on the pathogenesis of endometriosis?

Back 11

1) Retrograde theory- menstrual backflow thru fallopian tubes leads to endometrial tissue implantation outside the uterus. Most likely mechanism
2) Metastatic theory- endometrial differentiation from precursor coelomic epithelium
3) Lymphatic/vascular dissemination theory- explains cases of lung involvement

Front 12

How are endometriosis tissues different than normal, properly located endometrial tissue in the uterus?

Back 12

1) They have increased inflammatory mediators=>PGE2 especially=>explains beneficial effect of COX-2 inhibitors
2) They have higher aromatase activity of the stromal cells=>increased estrogen production=>explains treatment w/aromatase inhibitors

Front 13

How does endometriosis usually present (3)?

Back 13

1) Pain during menstruation
2) Pelvic pain
3) Infertility

Front 14

What are common sites of involvement w/endometriosis (6)?

Back 14

1) Ovary=>Chocolate cyst
2) Pouch of Douglas=>Pain with defecation
3) Uterine ligaments=>Pelvic pain
4) Bladder wall=>Pain with urination
5) Bowel serosa=>Abdominal pain, adhesions
6) Fallopian tube mucosa=>scarring=>infertility, ectopic pregnancy

Front 15

What is the term for endometriosis in soft tissues on gross images?

Back 15

Gun-powder nodules

Front 16

#1 risk factor for developing endometrial hyperplasia?

Back 16

Unopposed estrogen

Front 17

Why do post-menopausal women typically get endometrial hyperplasia?

Back 17

Even though estrogen production by ovaries is significantly decreased in menopause, some peripheral conversion to "other estrogens" (estrone in adipose) leads to unopposed estrogen action on endometrium. Progesterone not made peripherally to balance estrogen.

Front 18

1) Typical presentation of endometrial hyperplasia?
2) Why is obesity a risk factor?

Back 18

1) Post-menopausal uterine bleeding
2) Increased peripheral production of estrone in adipose tissue.

Front 19

What is the most important predictor for progression of endometrial hyperplasia to carcinoma? How does it look on histology?

Back 19

Cellular atypia=> glands are crowded, dysplastic epithelial cells