GYN Malignancies Flashcards

1
Q

Name the 3 most common gynecologic malignancies in the order of prevalence.

A
  1. adenocarcinoma of the endometrium
  2. epithelial ovarian cancer
  3. squamous cell carcinoma of the cervix
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2
Q

What are the risk factors of endometrial cancer?

A

atypical hyperplasia
unopposed estrogen
obesity

nulliparous
late menopause
diabetes
HTN

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3
Q

Contrast type 1 and type 2 endometrial cancers

A

type 1 is estrogen related, type 2 is estrogen unrelated
type 1 occurs in younger patients, type 2 in older patients
type 1 are typically heavier, type 2 thinner
type 1 is usually low grade, type 2 high grade (aggressive)
type 1 more curable/ longer pre-cancer phase, type 2 potential basis (lynch)
type 1 often have PTEN and KRAS mutations, type 2 often have p53 mutations

type 1 has an endometriod histology and type 2 has serous histology

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4
Q

What is the histologic appearance of type 1 cancers?

A

endometrial hyperplasia- increased glandular tissue and increasingly less regular architecture (cribriform- back to back)

nuclei become larger, rounder and nucleoli are more prominent

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5
Q

What is the histologic appearance of endometrial carcinoma type 2?

A

instead glands there is papillary structure, malignant cells line the surface of glands with a high N/C ratio and more pleomorphism

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6
Q

Who needs an endometrial biopsy to rule out endometrial cancer?

A

any one with post menopausal bleeding
perimenopausal inter menstrual bleeding
bleeding with history of involution

postmenopausal women with Pap test

thickened endometrial stripe via sonography

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7
Q

What are different surgical techniques that are used to control endometrial cancer based on pathology present?

A

can include peritoneal cytology, TAH/BSO, pelvic and aortic lymph node dissection

purpose of procedure:
defines extent of disease
minimizes over/under treatment
min. increases perioperative morbidity/mortality
decreases over rx risk and cost
allows comparison of therapeutic results
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8
Q

Wha is the usual treatment for endometrial cancer regarding adjuvant postoperative therapy?

A

whole pelvic radiation and vaginal cuff boost, mostly for stage II + and with nodal involvement

can reduce recurrence by up to 50% with 25-30d treatment

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9
Q

What are risk factors for ovarian cancer?

A
increased age (post-menopausal)
family history
infertility/ low parity
uninterrupted ovulation
personal cancer history, esp. breast cancer

decreased risk: OCPs, pregnancy, tubal ligation, breast feeding

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10
Q

Serious tumor is generated from which ovarian precursor?

A

surface epithelial cells (represents 65-70% of tumors)

*note many “ovarian” epithelial carcinomas are thought to arise form the fibrillated end of the uterine tube

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11
Q

Contrast the mutations found in low and high grade epithelial ovarian cancer.

A

low grade: KRAS, BRAF, PTEN, B-catenin

high grade p53

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12
Q

Is CA125 a reliable screen for ovarian cancer?

A

although CA125 is elevated in most advanced epithelial ovarian cancers it has poor sensitivity and poor specificity and is only used in screening high risk population (increase pre-test probability)

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13
Q

What is the optimal therapy for ovarian cancer?

A

(aggressive surgery yields best survival results-optimal cytoreduction)

TAH and BSO +/- infra colic omentectomy, peritoneal samples from pelvis, gutters and diaphragm surfaces, pelvic and aortic lymph node dissection for staging

in younger women, reproductive conservation may be appropriate

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14
Q

When is chemotherapy recommended for ovarian cancer?

A

all patients should receive a taxmen and a platinum, 73% will respond although many women with advanced disease will experience recurrence

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15
Q

What are important points for follow up of ovarian cancer/

A

recto-vaginal pelvic exam and CA125/3-4mo for 2 years
discuss HRT, diet and exercise and continue general health maintenance (mammography, pap smear, bone density, CRC, cholesterol etc.)

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16
Q

What are risk factors for cervical cancer?

A
early age of intercourse
number of sexual partners
smoking- ability to fight HPV infection
lower SES
high-risk male partner
other sexually transmitted diseases
17
Q

What percent of cervical cancers world wide contain HPV?

A

99.7% contain integrated HPV DNA; most likely to infect the squamocolumnar junction of the cervix

18
Q

How does HPV initiate oncogenesis?

A

HPV E6 and E7 interfere with the normal action of p53 and RB E2F; causes cell to NOT undergo apoptosis (p53) and skip growth arrest (RB)

19
Q

What are qualities of cervical cells that have become metaplastic?

A

low grade dysplastic cells: larger nucleus, more course chromatin, halo around the nucleus (contains HPV particles)

20
Q

What is the defining feature of cervical squamous cell CARCINOMA?

A

basal invasion through the epithelium

21
Q

Summarize key reasons why cervical cancer screening works.

A

sampling the cervix is relatively non-invasive
natural progression of cancer is slow
changes can be recognized microscopically
changes can be treated before invasion
Pap test is relatively inexpensive
HPV testing is integrated into screening in patients over 29yo

22
Q

What is the most classic sign of cervical cancer?

A

post-coital bleeding

also: foul vaginal discharge, abnormal bleeding, pelvic pain, unilateral leg swelling or pain, pelvic mass, gross cervical lesion

23
Q

What modalities are used in cervical cancer staging?

A
general physical exam
recto-vaginal pelvic exam
CXR
cystoscopy and proctoscopy
IVP- intravenous pyelogram or CT
24
Q

What is the mainstay of treating advanced cervical cancer?

A

chemoradiation: 4-5 weeks, 2 or more implants, especially concurrent with cisplatin based chemo (radio sensitizer)