11/13- Uterine Neoplasms and Pathology Flashcards

(106 cards)

1
Q

From most to least common, rate the gynecologic cancers (3)

A

Uterine > ovarian > cervical cancer

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2
Q

What stage of the uterine cycle are people in anovulation?

A

Proliferative

  • Contributes to hyperplasias and neoplasias
  • No LH burst or movement on to secretory phase
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3
Q

What is seen here? Histologic features?

A

Proliferative endometrium

  • Glands
  • Pseudostratified nuclei
  • Mitosis
  • Stroma
  • Small, plump blue round or spindle cells
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4
Q

What is seen here? Histologic features?

A

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)
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5
Q

What is seen here? Histologic features?

A

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
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6
Q

What is seen here? Histologic features?

A

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)
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7
Q

What hormone is a key factor in endometrial hyperplasia and cancer development? How?

A

Estrogen

  • Proliferative phase is hyper-estrogenic state
  • Estrogen can diffuse across cell memb
  • Activate receptors to promote proliferation of endometrium
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8
Q

What is the theory behind estrogen induced endometrial cancer?

A
  • Cell-acquired DNA mutations occur w/ hyperproliferation
  • Increased probability of random DNA errors
  • Cell cannot correct errors during rapid cell division
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9
Q

What are 6 risk factors for endometrial hyperplasia and cancer?

A
  • 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)
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10
Q

_____ is responsible for 57% of US endometrial cancers

A

Obesity is responsible for 57% of US endometrial cancers

  • Endometrial cancer is the one most strongly associated with obesity
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11
Q

What factors in obesity contribute to the risk of endometrial cancer?

A

Increased endogenous estrogen

  • Adipose cells convert adrenal steroids to estrone
  • Decrease in SHBG, increased bioavailability of estrogens
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12
Q

What is Tamoxifen? What factors of Tamoxifen contribute to the risk of endometrial cancer?

A

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
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13
Q

How does a nulliparous condition affect estrogen exposure?

A
  • 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
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14
Q

Read through these typical presentations of endometrial cancer

A
  • 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
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15
Q

What patients require endometrial sampling for evaluating endometrial cancer?

A

Post-menopausal and irregular vaginal bleeding

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16
Q

What are methods of endometrial sampling for evaluating endometrial cancer? Insufficient modalities?

A
  • Office endometrial biopsy
  • Dilation and curettage

Insufficient:

  • Ultrasound: “endometrial stripe”
  • Pap smear (only sampling cervix, not endometrium)
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17
Q

Describe the diagnostic capabilities of endometrial biopsy for endometrial cancer

A
  • Office endometrial biopsies have a false negative rate of 10%
  • Negative EMB in a symptomatic patient should be followed by a D&C
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18
Q

What is endometrial hyperplasia?

  • What causes it
  • In what age groups
  • Presentation
  • Precancer or benign
A
  • “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 `
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19
Q

What are associated conditions in endometrial hyperplasia?

A
  • 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
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20
Q

How is endometrial hyperplasia classified?

A

Simple hyperplasia

  • With/out atypia

Complex hyperplasia

  • With/out atypia
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21
Q

How is hyperplasia diagnosed? Architecture? Atypia?

A
  • 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
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22
Q

What is seen here?

A

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
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23
Q

What is seen here?

A

Simple endometrial hyperplasia with atypia

  • Glands are somewhat dilated
  • Some branching
  • Cytologically, cells are much larger and rounder; chromatin is more coarse
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24
Q

What is seen here?

A

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)
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25
What is seen here?
**Complex endometrial hyperplasia with atypia** - A lot of branching of the glands; can't tell one from another. All seem to be connected - See baseline gland in bottom right (basal nuclei, no atypia) - Other nuclei are very different
26
What is the risk of progression to cancer with the different types of hyperplasia?
(Penny, nickel, dime, quarter) - Simple without atypia: 1% - Complex without atypia: ~5% - Simple with atypia: 10% - Complex with atypia: 25% NOTE: atypia more significant than simple vs. complex; simple with atypia \> complex without atypia
27
How is endometrial hyperplasia without atypia managed in premenopausal and postmenopausal woman?
Premenopausal, if no atypia on biopsy: - Provera or - Mirena IUD or - OCPs - Resample every 3-6 mo Postmenopausal, if no atypia on biopsy - Provera or Mirena - Resample every 3-6 mo - Hysterectomy if disease persists or bleeding (or if want from the start)
28
How is endometrial hyperplasia with atypia managed?
Desires fertility or not surgical candidate: - Dilation and curettage - Progestin therapy or Mirena IUD - Rebiopsy every 3 mo If completed childbearing (or later biopsy comes back positive) - Hysterectomy
29
Describe epidemiology of endometrial cancer - #\_\_ cancer in women - #\_\_ gynecologic cancer - Lifetime risk - Median age of diagnosis - \_\_\_\_% diagnosed before menopause - \_\_% under 40 yo
- **#4** cancer in women (#7 cancer COD) - **#1 gynecologic** cancer - Lifetime risk: **3%** - Median age of diagnosis = **61 yo** - **20-25%** diagnosed before menopause - **5%** under 40 yo
30
What is type I vs. type II endometrial cancer? - How common - Age - Histology - Hyperplasia present? - Prognosis - Associations
**Type I (90%)** - Hyperestrogenism - Younger age - Endometrioid histology - Hyperplasia present - Low grade - Good prognosis - Obesity - Lynch syndrome **Type II (10%)** - Not associated with estrogen - Older age - Other histologies (not endometrioid) - Hyperplasia absent - High grade - Poor prognosis
31
What are histologic subtypes of type I and type II endometrial cancer?
**Type I:** - Endometrioid adenocarcinoma **Type II:** - Serous carcinoma - Clear cell carcinoma - Carcinosarcoma/malignant mixed mullerian tumors
32
Describe endometrioid adenocarcinoma (type I) - \_\_\_% of cases - Oversall survival - Associations - Phases
- **75-80%** of cases - Overall **survival 80-90%** - Associated with **obesity** and **unopposed estrogen** - Premalignant phase: endometrial hyperplasia (Endometrioid is NOT = to endometrial)
33
What is seen here?
Endometrioid endometrial adenocarcinoma
34
Describe the FIGO grading system of endometrioid adenocarcinoma
Recall, grading is based on histology! (Staging is based on size/spread) **- Grade 1**: 5% or less of solid growth pattern (non-squamous) **- Grade 2**: 6-50% of solid pattern (non-squamous); lost glandular histology **- Grade 3:** \>50% solid pattern (non-squamous)
35
What is seen here?
**Endometrioid adenocarcinoma, grade 1** - Back to back glands with no intervening stroma but most of glands are still tubular - Very little solid component (under 5%)
36
What is seen here?
**Endometrioid adenocarcinoma, grade 2** - Still have some glands, but most have fused together to form solid area
37
What is seen here?
**Endometrioid adenocarcinoma, grade 3**
38
What is seen here?
**Endometrioid adenocarcinoma with sqaumous metaplasia** - Squamous metaplasia is a unique feature of endometrioid carcinomas (helpful in diagnosing adenocarcinoma mets)
39
Describe serous carcinoma - Mode of spread - Response to chemo - Recurrence risk - Microscopic features - Genetics
- Type II (high grade) - Mode of spread more like ovarian cancer with extra-uterine spread, even with minimal invasion - Typically chemosensitive (very mitotically active) - High recurrence risk _Microscopic features:_ - Glandular, papillary, and solid architectures - Diffuse marked atypia\*, pleomorphism, and increased mitosis - Giant cells, psammoma bodies TP53 mutations NOTE: anolagous to high grade serous carcinoma of the ovary (there is no analogous form of the low grade ovarian serous carcinoma)
40
What is seen here?
**Serous carcinoma, solid pattern** - Very bizarre cells with atypia - Some mitotic figures are seen
41
Describe clear cell carcinoma - Type - Prognosis - Response to chemo - Recurrence risk - Microscopic features
- Type II - Rare with poor prognosis - Typically resistant to chemotherapy (not many mitoses) - High recurrence risk (like all type II carcinomas) _Microscopic features:_ - Tubulocystic, papillary, and solid architectures - Focal marked atpia, pleomorphism\* - Can have clear or eosinophilic cytoplasm - Relative lack of mitosis\* (distinguishes from serous carcinoma)
42
What is seen here?
Clear cell carcinoma
43
Describe carcinosarcoma (Malignant Mixed Mullerian tumor) - Prognosis - Age group - Risks/associations - Treated like what - Recurrence risk
- Rare with poor prognosis - Post-menopausal - Previous pelvic radiation - Treated like carcinoma not sarcoma - High recurrence risk
44
What are features of Malignant Mixed Mullerian tumor?
- Carcinoma and sarcoma features - Polypoid masses, usually occupying entire endometrial cavity - Epithelial component : endometrioid, serous, clear cell, undifferentiated, squamous, mixed - Stromal component: * **Homologous** (undifferentiated sarcoma, endometrial stromal sarcoma, leiomyosarcoma) * **Heterologous** (rhabdomyosarcoma, chondrosarcoma, osteosarcoma, liposarcoma) * may have poorer prognosis
45
What is seen here?
Carcinosarcoma
46
What is seen here?
Carcinosarcoma/MMMT
47
What are uterine smooth muscle neoplasms (all cards to this point were addressing endometrium; now moving to myometrium)
- Adenomyosis - Benign: leiomyomata - Malignant: leiomyosarcoma
48
What are signs/symptoms of adenomyosis
- Abnormal uterine bleeding - Chronic pelvic pain - Dysmenorrhea - Dyspareunia - Diffuse uterine enlargement ("large boggy uterus")
49
What is adenomyosis? - Presence of what - Seen in \_\_% of uteri - Co-exist with what
- Not a true neoplasm - Presence of endometrial glands and stroma within myometrium * Endometriosis was this outside of the endometrial cavity - Seen in up to **20%** of uteri - Co-exist with endometriosis (same pathogenesis)
50
What is seen here?
Adenomyosis - Many cystic, dilated cavities - Microscopically these are endometrial glands surrounded by endometrial stroma - Often filled with blood (functional glands)
51
What is seen here?
Adenomyosis - Top left: normal endometrium (proliferative phase) - Myometrium glands surrounded by stroma
52
What are signs/symptoms of Leiomyoma?
- Asymptomatic - Heavy abnormal uterine bleeding - Pelvic pain or pressure: “bulk symptoms” - Reproductive dysfunction/infertility - Enlarged irregular shaped uterus - Pelvic mass
53
What are features of leiomyoma (gross and histologic)?
Benign smooth muscle neoplasms within myometrium - Sharply circumscribed, firm, gray white nodules - Submucosal, intramural, subserosal - Bland spindle cells (no atypia); look just like myometrium - Very few mitoses - Degenerative changes (hyaline/ischemic necrosis, never tumor necrosis)
54
What is seen here?
Leiomyoma - Submucosal (below wall, in cavity), intramural (within wall), and subserosal (protruding out into serosa of uterine cavity) all seen - Central ischemia and necrosis
55
What is seen here?
Leiomyoma
56
Describe uterine sarcomas - Incidence - ___ are 2% of cases * Prognosis - Other types
- Extremely rare 1. **Leiomyosarcoma** * 2% of cases * Usually incidental finding after hysterectomy * Poor prognosis 2. **Endometrial stromal sarcoma** 3. **Adenosarcoma**
57
Describe leiomyosarcoma - Benign or malignant - Gross and cytologic features - Met capacity - Prognosis
Malignant smooth muscle neoplasms that arise de novo (don't come from leiomyomas) - Fleshy, bulky masses that invade the uterine wall/ protrude into lumen _Histologically:_ - Marked cytologic atypia - Tumor necrosis - Frequent mitoses Metastasize hematogenously to lung, bone and brain - Poor prognosis
58
What is seen here?
Leiomyosarcoma
59
What are the histologic features seen here? What do they indicate?
**Leiomyosarcoma** - Top left: **tumor necrosis** * Abrupt transition to pink necrosis - Top right: **atypia** * Very bizarre, large cells; some small - Bottom left: **increased mitosis** - Bottom right: **vascular invasion** (over lymphatic, because they are sarcomas)
60
What are endometrial cancer treatments?
- Surgery - Adjuvant Treatment * Radiation * Chemotherapy * Hormonal therapy
61
What is removed in surgical staging?
- Uterus - Cervix - Bilateral Fallopian tubes and ovaries - Lymph node dissection * Pelvic * Para-aortic - Washings? (not really anymore) - Omentectomy?
62
What supplies blood to the uterus?
- Uterine arteries (from internal iliac?) - Gonadal arteries - More...
63
Describe FIGO surgical staging of endometrial cancer
- **Stage I**: confined to uterus - **Stage II:** cervix involved - **Stage III:** uterine serosa, adnexa, positive cytology, vaginal mets, pelvic/aortic node mets - **Stage IV:** bladder, bowel, inguinal node, distant mets e.g lung
64
When do you know stage of endometrial cancer?
Only after surgery for staging - STAGE IS NOT GRADE * Stage = location/spread * Grade = histological features
65
What adjuvant treatment is helpful considering the fact that endometrial cancer is commonly confined?
Radiation
66
Describe adjuvant therapy for stage I disease - \_\_% of patients have stage I disease - 5 yr cure rates of \_\_% - Prognosis When is adjuvant therapy considered?
Stage I disease – **70%** of patients are stage I – 5 year cure rates approach **85-90%** – Majority of women are **cured with surgery alone**. Consideration of adjuvant therapy for patients with **high risk features:** - Histology - Grade of tumor - Stage/LN status - Age - Depth of invasion
67
Describe the benefits and indications for the different adjuvant treatments: - Radiation - Chemotherapy - Hormonal therapy
- **Radiation**: reduces risk of local recurrence, but does not affect overall survival - **Chemotherapy**: administered in pts with extremely high risk for recurrence or with extrauterine disease - **Hormonal therapy**: indicated in pts desiring fertility or are poor surgical candidates * Recommend hysterectomy after childbearing
68
What is the 5 yr survival for the different stages of endometrial cancer?
- **Stage I** (73%)**:** 86% - **Stage II** (12%): 66% - **Stage III** (12%)**:** 44% - **Stage IV** (3%)**:** 16%
69
What are the survival rates by histologic type: - Endometrioid - Adenosqumous - Mucinous - Clear cell - Papillary serous
- Endometrioid: 80% - Adenosqumous: 79% - Mucinous: 73% - Clear cell: 63% - Papillary serous: 54%
70
Why is there no screening for endometrial cancer?
- Precursors of Type I cancers are symptomatic - Type II cancers have no currently recognized premalignant phase Most cases are detected early due to symptoms (e.g. abnormal uterine bleeding) - No inexpensive, accurate, noninvasive screening test exists - Not indicated in asymptomatic women **unless have Lynch syndrome**
71
What are relevant genetic syndromes for endometrial cancer? - \_\_% of endometrial cancer is hereditary
- **5%** of endometrial cancer is hereditary - Most present as part of the **Lynch II** or hereditary non-polyposis colorectal cancer (**HNPCC**) syndrome
72
What cancers are people with Lynch syndrome predisposed to?
- Ovarian - Uterine (endometrial) - Colorectal Also: stomch, pancreas, uroepithelial, biliary tract, brain, small bowel
73
Describe Lynch syndrome (HNPCC) - Incidence - Genetic mechanism - Lifetime risk of endometrial cancer in women
- Incidence: **1/200-1000** - Mutation in mismatch repair gene * MLH1, MSH2, MSH6, PMS2 - Women with HNPCC have **40-60%** lifetime risk for **endometrial cancer** - Early onset cancers
74
What are the screening guidelines for Lynch syndrome (when is it done)?
* Endometrial or colon CA **\<50 yo** * Endometrial or colon CA **with** synchronous or metachronous colon **or other Lynch associated tumor at any age** * Endometrial or colon CA and **first-degree relative with Lynch assoc tumor \<50 yo** * Endometrial or colon CA at **any age with ≥ 2 first-degree or second-degree relatives** with Lynch assoc tumors regardless of age * Specific colorectal CA (ie. Crohn-like lymphocytic reaction, peritumoral lymphocytes, etc.)
75
What screening should be done in Lynch patients for endometrial cancer?
– **Endometrial biopsy every 1–2 years**, beginning at age **30-35 years** – Keeping a **menstrual calendar** and evaluating abnormal uterine bleeding – Consider **prophylactic surgery @ 35-40 yo** or when childbearing complete
76
What screening should be done in Lynch patients for colon cancer?
– Colonoscopy **every 1–2 years**, beginning: * age **20-25** years, or * **2–5 years before the earliest** cancer diagnosis in the family, whichever is earlier
77
What are protective factors against endometrial cancer? What can be done to decrease risk?
- Decrease circulating estrogen levels * Weight loss/exercise * Smoking - Combined estrogen/progesterone therapy - Prior OCP use
78
What are the classifications of Gestational Trophoblastic Disease (GTD) and Gestational Trophoblastic Neoplasia (GTN)
_Gestational Trophoblastic Disease (GTD)_ - Hydatidiform mole (complete, partial) _Gestational Trophoblastic Neoplasia (GTN)_ - Invasive mole - Choriocarcinoma - Placental site trophoblastic tumor (PSTT) - Epithelioid trophoblastic tumors (ETT)
79
Describe the incidence of the different types of GTD/GTN
- Molar pregnancy * 1/600 therapeutic abortions * 1/1500 pregnancies * 1/120 in Asia - Gestational choriocarcinoma: 1/20-40,000 - PSTT and ETT are RARE
80
What are risk factors for molar pregnancy?
- **Prior** molar pregnancy - Extremes of **age** (\< 20, \>40) - **History** of multiple prior SAB and infertility - Dietary factors * **Vitamin A** or **carotene deficiency** * Diet **low in animal fat** - **Asian**, American Indian, Hispanic, African ancestry
81
What are signs/symptosm of molar pregnancy? - Early - Late - Labs
_Early clinical symptoms:_ - Vaginal bleeding/pelvic pain or pressure - Excessive uterine size for gestational age - Hyperemesis - Spontaneous abortions _Late clinical symptoms:_ (since diagnostic techniques are better, don't see these too much) - Pre-eclampsia in 1st TM - Hyperthryoidism * B-hCG has anologous component to TSH; may cause hyeprthyroidism - Ovarian theca lutein cysts * Large ovarian masses due to hyperstimulation from excess hCG _Labs:_ - **Increased B-hCG** * Very high levels in complete * Modest in partial
82
What is seen here?
US appearance of molar pregnancy - "Bag of grapes" - See many vesicles
83
How does a molar pregnancy develop?
**Dispermic fetilization of maternal egg (partial mole)** - Results in triploid pregnancy (69, XXX/XYY/XXY) **Dispermic fertilization of empty ovum (complete mole)** - Results in diploid pregnancy Recall: - Maternal chromosomes account for fetal growth - Patenal chromosomes account for placental growth
84
Compare and contrast partial and complete mole: - Karyotype - Fetal tissue - Progression - Metastatic potential - Associations - Risk of GTN
_Partial mole:_ - 69XXY, 69 XXX - Fetal tissue **present** - **1-4%** -\> persistant tumor - **Rarely** (0.1%) metastatic - **NOT** associated with choriocarcinoma - Risk of **GTN is 1-3%** _Complete mole_ - 46XX, XY - Fetal tissue **absent** - **15-20%** -\> local uterine invasion - **5%** metastasis - Risk of **GTN is 20%**
85
Describe gross and microscopic features of a partial hydatidiform mole
_Grossly:_ - Some grape-like vesicles - Fetus may be present _Microscopy:_ - Dual villous population, some enlarged and some normal - Less trophoblastic hyperplasia compared to complete moles - Trophoblastic inclusions
86
What is seen here?
**Partial mole** - Mostly abnormal but some normal villi - Trophoblastic hyperplasia - Can get inclusions of trophoblasts into uterus due to convolution
87
What are gross and microscopic features of complete hydatidiform moles?
_Gross:_ - Grape-like vesicles fill the uterus _Microscopy:_ - Abnormality involves all the villi - Enlarged and scalloped - Central cisterns - **Circumferential** trophoblastic hyperplasia (in normal pregnancy, if present, it is polar)
88
What is seen here?
**Complete mole** - **Top left**: all villi enlarged and very atypical - **Top right**: exuberant trophoblastic hyperplasia; circumferential - **Bottom right**: central cistern (center degenerates due to large size and forms empty space)
89
What are treatment options for hydatidiform mole?
- **Suction curettage: treatment of choice** - **Hysterectomy** * If pt desires surgical sterilization * Reduces likelihood of requiring chemo for malignant sequelae - Follow **hCG levels** **weekly** until normal x 3wks, then **monthly** for 6-12 mo * Risk of GTN \< 1% if hCG normalizes - **Contraception**: for minimum of 1 yrs (since monitoring hCG levels)
90
How is GTN diagnosed?
* **Plateau of HCG** that lasts for 4 measurements over a period of **3 weeks** * **Rise of 10%+** in HCG over ≥ 2 weeks * HCG level remains **elevated for 6 months** or more * **Histologic** diagnosis of choriocarcinoma
91
Describe choriocarcinoma - Local or invasive - Method of spread - Clinical presentation - Response to chemo - More common after complete or partial mole
* Highly **invasive** * **Hematogenous** spread * Clinical presentation usually due to **bleeding** from metastatic site * Highly **chemosensitive** * More common after **complete** mole rather than partial mole
92
What is the most common GTN after non-molar pregnancy?
**Choriocarcinoma** * 50% - complete moles * 25% - previous abortions * 22% - normal pregnancies * 3% - ectopic pregnancies
93
What are gross and microscopic features of choriocarcinoma?
_Gross_ - Soft, fleshy - Extensive hemorrhage and necrosis _Microscopic_ - Proliferating syncytiotrophoblasts and cytotrophoblasts - Abundant mitoses
94
What is seen here?
**Choriocarcinoma** - Channels of blood between tumor cells - Large cells forming syncytium (sheet); join to form multinucleated cells; synctiotrophoblast in periphery - Smaller cells are cytotrophoblasts (center)
95
What are the most common sites of metastasis for Gestational Trophoblastic Neoplasia?
- **Lung** (80%) - Vagina (30%) - Pelvis (20%) - Brain (10%) - Liver (10%) These mets have a tendency to bleed; DON'T biopsy to confirm (could bleed to death)
96
Describe staging of GTN - What else should be evaluated?
- **Stage I**: confined to uterus - **Stage II**: outside uterus but confined to genital structures - **Stage III**: metastasized to lung with/out genital structure involvement - **Stage IV**: all other metastatic sites Stage should be followed by **sum of risk factors** - Affects therapy
97
What are some risk factors considered for GTN?
- Age - Antecedent pregnancy resulting in term, abortion, or mole (more risk with term) - Interval - Pretreatment serum hCG (lower = lower risk) - Tumor size - Met sites - Number of mets - Prior failed chemotherapy
98
How is GTN managed? - What determines which treatment is chosen
Usually highly chemosensitive - _Single agent chemotherapy_ * **Methotrexate** or **actinomycin D** * **Stage I** disease or risk factor score **0-6** - _Combo chemotherapy_ * **EMA-CO, EMA-EP** * **Stage IV** disease or risk factor score **7+** * PSTT, ETT
99
Key points to remember: - Endometrial = Uterine (location description) - Endometrioid DOES NOT = endometrial - Stage DOES NOT = grade - Adenomyosis and leiomyoma DO NOT cause postmenopausal bleeding * Do NOT dismiss unusual vaginal bleeding
(:
100
What is the most common gyn cancer in the US? - Which is the most fatal?
- Most **common** = **uterine** (endometrial) cancer - Most **fatal** = **ovarian**
101
What is the risk of endometrial cancer with: - Complex hyperplasia with atypia - SImple hyperplasia - Complex hyperplasia without atypia?
- Complex hyperplasia with atypia: **28%** - Simple hyperplasia: **1%** - Complex hyperplasia without atypia: **3%**
102
58 yo healthy female preset to the EC with vaginal spotting for 3 days. You order a pelvic US that shows uterine fibroids. What do you tell the pt? A. No worries. Bleeding is due to fibroids B. It's ok to have bleeding sometimes, as long as it's not heavy C. You need a pelvic exam and an endometrial biopsy
FIBROIDS NEVER CAUSE BLEEDING IN POST-MENOPAUSAL PATIENT A. No worries. Bleeding is due to fibroids B. It's ok to have bleeding sometimes, as long as it's not heavy **C. You need a pelvic exam and an endometrial biopsy**
103
Endometrial biopsy returns with the following pathology. What is your diagnosis? A. Grade 2 endometrioid endometrial adenocarcinoma B. Choriocarcinoma C. Leiomyosarcoma D. Endometrial polyp
**A. Grade 2 endometrioid endometrial adenocarcinoma** B. Choriocarcinoma C. Leiomyosarcoma-proliferation of spindle cells; see glands here, so not this D. Endometrial polyp
104
Case cont'd) What is your next step in treatment recommendations? A. Observation B. Chemotherapy C. Surgery D. Radiation therapy
A. Observation B. Chemotherapy **C. Surgery**- treatment of choice if done with fertility and can be operated on D. Radiation therapy
105
40 yo female with BMI 39 wants to be tested for uterine cancer because her best friend's mom just died of uterine cancer. No irregular menstrual Sx. What do you tell her?
There is no good screening test for uterine cancer
106
35 yo recently dx with endometrial cancer and has 1 uncle and father with colon cancer and 1 aunt with ovarian cancer. She likely has: A. Bad luck B. Hereditary breast and ovarian cancer C. MEN 1 D. HNPCC syndrome
A. Bad luck B. Hereditary breast and ovarian cancer C. MEN 1 **D. HNPCC syndrome**