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a_GYNGU > 11/13- Uterine Neoplasms and Pathology > Flashcards

11/13- Uterine Neoplasms and Pathology Flashcards

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
Q

What is seen here?

A

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
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26
Q

What is the risk of progression to cancer with the different types of hyperplasia?

A

(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

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27
Q

How is endometrial hyperplasia without atypia managed in premenopausal and postmenopausal woman?

A

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)
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28
Q

How is endometrial hyperplasia with atypia managed?

A

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
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29
Q

Describe epidemiology of endometrial cancer

  • # __ cancer in women
  • # __ gynecologic cancer
  • Lifetime risk
  • Median age of diagnosis
  • ____% diagnosed before menopause
  • __% under 40 yo
A
  • #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
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30
Q

What is type I vs. type II endometrial cancer?

  • How common
  • Age
  • Histology
  • Hyperplasia present?
  • Prognosis
  • Associations
A

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
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31
Q

What are histologic subtypes of type I and type II endometrial cancer?

A

Type I:

  • Endometrioid adenocarcinoma

Type II:

  • Serous carcinoma
  • Clear cell carcinoma
  • Carcinosarcoma/malignant mixed mullerian tumors
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32
Q

Describe endometrioid adenocarcinoma (type I)

  • ___% of cases
  • Oversall survival
  • Associations
  • Phases
A
  • 75-80% of cases
  • Overall survival 80-90%
  • Associated with obesity and unopposed estrogen
  • Premalignant phase: endometrial hyperplasia (Endometrioid is NOT = to endometrial)
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33
Q

What is seen here?

A

Endometrioid endometrial adenocarcinoma

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34
Q

Describe the FIGO grading system of endometrioid adenocarcinoma

A

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)

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35
Q

What is seen here?

A

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%)
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36
Q

What is seen here?

A

Endometrioid adenocarcinoma, grade 2

  • Still have some glands, but most have fused together to form solid area
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37
Q

What is seen here?

A

Endometrioid adenocarcinoma, grade 3

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38
Q

What is seen here?

A

Endometrioid adenocarcinoma with sqaumous metaplasia

  • Squamous metaplasia is a unique feature of endometrioid carcinomas (helpful in diagnosing adenocarcinoma mets)
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39
Q

Describe serous carcinoma

  • Mode of spread
  • Response to chemo
  • Recurrence risk
  • Microscopic features
  • Genetics
A
  • 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)

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40
Q

What is seen here?

A

Serous carcinoma, solid pattern

  • Very bizarre cells with atypia
  • Some mitotic figures are seen
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41
Q

Describe clear cell carcinoma

  • Type
  • Prognosis
  • Response to chemo
  • Recurrence risk
  • Microscopic features
A
  • 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)
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42
Q

What is seen here?

A

Clear cell carcinoma

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43
Q

Describe carcinosarcoma (Malignant Mixed Mullerian tumor)

  • Prognosis
  • Age group
  • Risks/associations
  • Treated like what
  • Recurrence risk
A
  • Rare with poor prognosis
  • Post-menopausal
  • Previous pelvic radiation
  • Treated like carcinoma not sarcoma
  • High recurrence risk
44
Q

What are features of Malignant Mixed Mullerian tumor?

A
  • 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
Q

What is seen here?

A

Carcinosarcoma

46
Q

What is seen here?

A

Carcinosarcoma/MMMT

47
Q

What are uterine smooth muscle neoplasms (all cards to this point were addressing endometrium; now moving to myometrium)

A
  • Adenomyosis
  • Benign: leiomyomata
  • Malignant: leiomyosarcoma
48
Q

What are signs/symptoms of adenomyosis

A
  • Abnormal uterine bleeding
  • Chronic pelvic pain
  • Dysmenorrhea
  • Dyspareunia
  • Diffuse uterine enlargement (“large boggy uterus”)
49
Q

What is adenomyosis?

  • Presence of what
  • Seen in __% of uteri
  • Co-exist with what
A
  • 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
Q

What is seen here?

A

Adenomyosis

  • Many cystic, dilated cavities
  • Microscopically these are endometrial glands surrounded by endometrial stroma
  • Often filled with blood (functional glands)
51
Q

What is seen here?

A

Adenomyosis

  • Top left: normal endometrium (proliferative phase)
  • Myometrium glands surrounded by stroma
52
Q

What are signs/symptoms of Leiomyoma?

A
  • Asymptomatic
  • Heavy abnormal uterine bleeding
  • Pelvic pain or pressure: “bulk symptoms”
  • Reproductive dysfunction/infertility
  • Enlarged irregular shaped uterus
  • Pelvic mass
53
Q

What are features of leiomyoma (gross and histologic)?

A

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
Q

What is seen here?

A

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
Q

What is seen here?

A

Leiomyoma

56
Q

Describe uterine sarcomas

  • Incidence
  • ___ are 2% of cases
  • Prognosis
  • Other types
A
  • Extremely rare
    1. Leiomyosarcoma
  • 2% of cases
  • Usually incidental finding after hysterectomy
  • Poor prognosis
  1. Endometrial stromal sarcoma
  2. Adenosarcoma
57
Q

Describe leiomyosarcoma

  • Benign or malignant
  • Gross and cytologic features
  • Met capacity
  • Prognosis
A

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
Q

What is seen here?

A

Leiomyosarcoma

59
Q

What are the histologic features seen here? What do they indicate?

A

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
Q

What are endometrial cancer treatments?

A
  • Surgery
  • Adjuvant Treatment
  • Radiation
  • Chemotherapy
  • Hormonal therapy
61
Q

What is removed in surgical staging?

A
  • Uterus
  • Cervix
  • Bilateral Fallopian tubes and ovaries
  • Lymph node dissection
  • Pelvic
  • Para-aortic
  • Washings? (not really anymore)
  • Omentectomy?
62
Q

What supplies blood to the uterus?

A
  • Uterine arteries (from internal iliac?)
  • Gonadal arteries
  • More…
63
Q

Describe FIGO surgical staging of endometrial cancer

A
  • 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
Q

When do you know stage of endometrial cancer?

A

Only after surgery for staging

  • STAGE IS NOT GRADE
  • Stage = location/spread
  • Grade = histological features
65
Q

What adjuvant treatment is helpful considering the fact that endometrial cancer is commonly confined?

A

Radiation

66
Q

Describe adjuvant therapy for stage I disease

  • __% of patients have stage I disease
  • 5 yr cure rates of __%
  • Prognosis

When is adjuvant therapy considered?

A

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
Q

Describe the benefits and indications for the different adjuvant treatments:

  • Radiation
  • Chemotherapy
  • Hormonal therapy
A
  • 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
Q

What is the 5 yr survival for the different stages of endometrial cancer?

A
  • Stage I (73%): 86%
  • Stage II (12%): 66%
  • Stage III (12%): 44%
  • Stage IV (3%): 16%
69
Q

What are the survival rates by histologic type:

  • Endometrioid
  • Adenosqumous
  • Mucinous
  • Clear cell
  • Papillary serous
A
  • Endometrioid: 80%
  • Adenosqumous: 79%
  • Mucinous: 73%
  • Clear cell: 63%
  • Papillary serous: 54%
70
Q

Why is there no screening for endometrial cancer?

A
  • 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
Q

What are relevant genetic syndromes for endometrial cancer?

  • __% of endometrial cancer is hereditary
A
  • 5% of endometrial cancer is hereditary
  • Most present as part of the Lynch II or hereditary non-polyposis colorectal cancer (HNPCC) syndrome
72
Q

What cancers are people with Lynch syndrome predisposed to?

A
  • Ovarian
  • Uterine (endometrial)
  • Colorectal

Also: stomch, pancreas, uroepithelial, biliary tract, brain, small bowel

73
Q

Describe Lynch syndrome (HNPCC)

  • Incidence
  • Genetic mechanism
  • Lifetime risk of endometrial cancer in women
A
  • 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
Q

What are the screening guidelines for Lynch syndrome (when is it done)?

A
  • 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
Q

What screening should be done in Lynch patients for endometrial cancer?

A

– 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
Q

What screening should be done in Lynch patients for colon cancer?

A

– 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
Q

What are protective factors against endometrial cancer? What can be done to decrease risk?

A
  • Decrease circulating estrogen levels
  • Weight loss/exercise
  • Smoking
  • Combined estrogen/progesterone therapy
  • Prior OCP use
78
Q

What are the classifications of Gestational Trophoblastic Disease (GTD) and Gestational Trophoblastic Neoplasia (GTN)

A

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
Q

Describe the incidence of the different types of GTD/GTN

A
  • 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
Q

What are risk factors for molar pregnancy?

A
  • 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
Q

What are signs/symptosm of molar pregnancy?

  • Early
  • Late
  • Labs
A

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
Q

What is seen here?

A

US appearance of molar pregnancy

  • “Bag of grapes”
  • See many vesicles
83
Q

How does a molar pregnancy develop?

A

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
Q

Compare and contrast partial and complete mole:

  • Karyotype
  • Fetal tissue
  • Progression
  • Metastatic potential
  • Associations
  • Risk of GTN
A

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
Q

Describe gross and microscopic features of a partial hydatidiform mole

A

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
Q

What is seen here?

A

Partial mole

  • Mostly abnormal but some normal villi
  • Trophoblastic hyperplasia
  • Can get inclusions of trophoblasts into uterus due to convolution
87
Q

What are gross and microscopic features of complete hydatidiform moles?

A

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
Q

What is seen here?

A

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
Q

What are treatment options for hydatidiform mole?

A
  • 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
Q

How is GTN diagnosed?

A
  • 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
Q

Describe choriocarcinoma

  • Local or invasive
  • Method of spread
  • Clinical presentation
  • Response to chemo
  • More common after complete or partial mole
A
  • 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
Q

What is the most common GTN after non-molar pregnancy?

A

Choriocarcinoma

  • 50% - complete moles
  • 25% - previous abortions
  • 22% - normal pregnancies
  • 3% - ectopic pregnancies
93
Q

What are gross and microscopic features of choriocarcinoma?

A

Gross

  • Soft, fleshy
  • Extensive hemorrhage and necrosis

Microscopic

  • Proliferating syncytiotrophoblasts and cytotrophoblasts
  • Abundant mitoses
94
Q

What is seen here?

A

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
Q

What are the most common sites of metastasis for Gestational Trophoblastic Neoplasia?

A
  • 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
Q

Describe staging of GTN

  • What else should be evaluated?
A
  • 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
Q

What are some risk factors considered for GTN?

A
  • 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
Q

How is GTN managed?

  • What determines which treatment is chosen
A

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
Q

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
A

(:

100
Q

What is the most common gyn cancer in the US?

  • Which is the most fatal?
A
  • Most common = uterine (endometrial) cancer
  • Most fatal = ovarian
101
Q

What is the risk of endometrial cancer with:

  • Complex hyperplasia with atypia
  • SImple hyperplasia
  • Complex hyperplasia without atypia?
A
  • Complex hyperplasia with atypia: 28%
  • Simple hyperplasia: 1%
  • Complex hyperplasia without atypia: 3%
102
Q

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

A

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
Q

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

A. Grade 2 endometrioid endometrial adenocarcinoma

B. Choriocarcinoma

C. Leiomyosarcoma-proliferation of spindle cells; see glands here, so not this

D. Endometrial polyp

104
Q

Case cont’d)

What is your next step in treatment recommendations?

A. Observation

B. Chemotherapy

C. Surgery

D. Radiation therapy

A

A. Observation

B. Chemotherapy

C. Surgery- treatment of choice if done with fertility and can be operated on

D. Radiation therapy

105
Q

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?

A

There is no good screening test for uterine cancer

106
Q

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

A. Bad luck

B. Hereditary breast and ovarian cancer

C. MEN 1

D. HNPCC syndrome

a_GYNGU (17 decks)

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