11/13- Uterine Neoplasms and Pathology Flashcards
(106 cards)
From most to least common, rate the gynecologic cancers (3)
Uterine > ovarian > cervical cancer
What stage of the uterine cycle are people in anovulation?
Proliferative
- Contributes to hyperplasias and neoplasias
- No LH burst or movement on to secretory phase
What is seen here? Histologic features?

Proliferative endometrium
- Glands
- Pseudostratified nuclei
- Mitosis
- Stroma
- Small, plump blue round or spindle cells
What is seen here? Histologic features?

Early secretory endometrium
- Progesterone causes secretory changes (starts in base)
- Base has tiny vacuoles; gives “piano key” appearance
- Day 16-18 of menstrual cycle (right after ovulation)
What is seen here? Histologic features?

Mid secretory endometrium
- Secretions become supra-nuclear; secreted into lumen (in the center)
- Stromal cells acquire abundant cytoplasm, pinker, (pseudo-decidualization); becomes “cushiony”
- Spiral arterioles become prominent
What is seen here? Histologic features?

Late secretory endometrium with onset of menstruation
- Tiny blue nests of stromal cells; stromal breakdown
- See glands breaking down
- Endometrium undergoes ischemia (vessels constrict and you see a lot of bleeding)
What hormone is a key factor in endometrial hyperplasia and cancer development? How?
Estrogen
- Proliferative phase is hyper-estrogenic state
- Estrogen can diffuse across cell memb
- Activate receptors to promote proliferation of endometrium
What is the theory behind estrogen induced endometrial cancer?
- Cell-acquired DNA mutations occur w/ hyperproliferation
- Increased probability of random DNA errors
- Cell cannot correct errors during rapid cell division
What are 6 risk factors for endometrial hyperplasia and cancer?
- Age (most important!)
- Early menarche, late menopause
- Race
- Highest in non-Hispanic white females
- Higher mortality in African American women
- Unopposed estrogen exposure
- Estrogen replacement (no progestin)
- Early menarche/late menopause
- Nulliparity
- Insulin resistance
- Obesity (10x risk)
- Nulliparity
- Tamoxifen use
- FHx
- Infertility
- PCOS
- Estrogen producing ovarian tumors (granulosa cell tumors)
_____ is responsible for 57% of US endometrial cancers
Obesity is responsible for 57% of US endometrial cancers
- Endometrial cancer is the one most strongly associated with obesity
What factors in obesity contribute to the risk of endometrial cancer?
Increased endogenous estrogen
- Adipose cells convert adrenal steroids to estrone
- Decrease in SHBG, increased bioavailability of estrogens
What is Tamoxifen? What factors of Tamoxifen contribute to the risk of endometrial cancer?
Selective estrogen receptor modulator
- Breast: estrogen antagonist
- Uterus: estrogen agonist
Trials found:
- NSABP B-14 trial: 7.5x rate of endo CA
- Carcinogenic potential of tamoxifen on the endometrium is clearly established but mechanism is not known
- Current recommendations are for EMB for vaginal bleeding; no need for routine screening with US or EMB
- Benefits of the med outweigh the risks
How does a nulliparous condition affect estrogen exposure?
- There are potential hormonal factors during pregnancy and lactation that represent a period of reduced exposure to unopposed estrogen (missing in nulliparity)
- Higher risk for endometrial cancer
Read through these typical presentations of endometrial cancer
- 63 yo with BMI 32 who presents 4 month history of postmenopausal bleeding
- 46 yo with BMI 43 who presents with irregular heavy vaginal bleeding for past 5 years
- 39 yo with BMI 27 who presents with prolonged menses for the past 6 months and family history of colon and endometrial cancer
What patients require endometrial sampling for evaluating endometrial cancer?
Post-menopausal and irregular vaginal bleeding
What are methods of endometrial sampling for evaluating endometrial cancer? Insufficient modalities?
- Office endometrial biopsy
- Dilation and curettage
Insufficient:
- Ultrasound: “endometrial stripe”
- Pap smear (only sampling cervix, not endometrium)
Describe the diagnostic capabilities of endometrial biopsy for endometrial cancer
- Office endometrial biopsies have a false negative rate of 10%
- Negative EMB in a symptomatic patient should be followed by a D&C
What is endometrial hyperplasia?
- What causes it
- In what age groups
- Presentation
- Precancer or benign
- “Overgrowth” of endometrium secondary to prolonged unopposed estrogen
- Seen in adolescents through menopause
- Presents with abnormal uterine bleeding
- Considered precursor to “Type 1” endometrial cancer `
What are associated conditions in endometrial hyperplasia?
- Anovulatory cycles in teens
- Granulosa cell tumors of the ovary
- Unopposed estrogen (women with a uterus should not, as a rule, ever receive estrogen therapy alone without progesterone)
- Tamoxifen
How is endometrial hyperplasia classified?
Simple hyperplasia
- With/out atypia
Complex hyperplasia
- With/out atypia
How is hyperplasia diagnosed? Architecture? Atypia?
- Hyperplasia: shift of gland:stroma ratio > 2:1
- Architecture:
- Simple: dilated glands with minimal branching
- Complex: complex glandular branching
- Atypia: enlargement and rounding of nuclei, coarse chromatin and irregular nuclear contours as compared to the patient’s normal endometrium
What is seen here?

Simple endometrial hyperplasia without atypia
- Some branching, but not too much; most glands are just dilated
- Cytology of glands look very much like proliferative endometrium
What is seen here?

Simple endometrial hyperplasia with atypia
- Glands are somewhat dilated
- Some branching
- Cytologically, cells are much larger and rounder; chromatin is more coarse
What is seen here?

Complex endometrial hyperplasia without atypia
- Glands are very blanched (complex)
- Glands getting crowded and hard to distinguish
- Still cells are not very different form baseline epithelium (similar to proliferative endometrium)




















