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OBGYN > Gyn Onc > Flashcards

Gyn Onc Flashcards

1
Q

What is gestational trophoblastic neoplasia?

A

a spectrum that includes all neoplasms derived from abnormal placental (trophoblastic) proliferation, most often a benign disease known as hydatidiform mole

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2
Q

What are the key clinical features of gestational trophoblastic neoplasia?

A
  • clinical presentation as pregnancy
  • reliable means of diagnosis by pathognomonic US findings
  • a specific tumor marker known as hCG
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3
Q

What is the difference between gestational trophoblastic neoplasia and hydatidiform mole?

A
  • GTN is a spectrum of neoplasms derived from abnormal placental proliferation which includes hydatidiform mole
  • GTN can arise from pregnancy but most commonly follows a hydatidiform mole
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4
Q

What is a hydatidiform mole?

A

an abnormal proliferation of the syncytiotrophoblast and replacement of normal placental trophoblastic tissue by hydronic placental villi

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5
Q

Hydatidiform Mole

A
  • an abnormal conception, which leads to abnormal proliferation of the syncytiotrophoblast and replacement of normal placental trophoblastic tissue by hydropic placental villi
  • can be complete without identifiable embryonic structures, or partial with some identifiable embryonic tissue
  • complete arise from fertilization of an empty ovum followed by reduplication of the haploid sperm; partial arise from fertilization of a normal ovum by two sperm
  • presents as a pregnancy with a larger-than-expected uterus, exaggerated subjective symptoms of pregnancy, and painless second-trimester bleeding with passage of grape-like masses if not detected sooner
  • fetal heart tones will be absent, US finds a characteristic “snow-storm” appearance without fetal parts, and B-hCG is excessively elevated
  • elevated B-hCG may produce severe nausea and vomiting, hypertension, proteinuria, and clinical hyperthyroidism due to activation of TSH receptors
  • treatment is suction curettage; give Rhgam at the time of uterine evacuation and begin contraception to prevent intercurrent pregnancy
  • patients then require subsequent monitoring of B-hCG to ensure adequate removal, first at 48 hours, then every 1-2 weeks while elevated, and 1-2 months thereafter
  • complete more than partial, poses a risk for choriocarcinoma
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6
Q

What is the difference between a complete and partial hydatidiform mole? How do the two differ in their genesis and karyotype?

A
  • partial are those with some identifiable embryonic structures while complete have none
  • partial are triploid with one haploid set of maternal chromosomes and two haploid sets of paternal chromosomes due to dispermic fertilization of a normal ovum
  • complete are diploid, typically 46,XX, and are entirely of paternal origin since they result from fertilization of a blighted ovum by a haploid sperm that replicates
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7
Q

Compare and contrast complete and partial hydatidiform moles.

A
  • complete have no embryonic tissue while partial have some identifiable embryonic structures
  • complete are diploid due to fertilization of an empty ovum by a haploid sperm that reduplicates while partial are triploid due to dispermic fertilization of a normal ovum
  • complete have diffuse and more severe trophoblastic proliferation and hydropic villi while proliferation is more focal and mild in partial
  • complete are usually diagnosed as a molar gestation while partial are more likely to present as a missed aborption
  • clinically, complete usually have a much larger uterus than expected, co-occur with theca-lutein cysts, and carry a greater risk of malignancy
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8
Q

Pregnancy with severe hypertension prior to 20 weeks gestation is highly suggestive of what?

A

molar pregnancy since the elevated B-hCG is likely to activate TSH receptors and present clinically as hyperthroidism

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9
Q

How are gestational trophoblastic neoplasias classified?

A
  • there are benign forms with hydatidiform moles being the most common and being divided into partial and complete
  • there are malignant forms, including persistent non-metastatic GTN and metastatic GTN
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10
Q

What is persistent gestational trophoblastic neoplasia?

A

a malignant form of GTN which follows any sort of pregnancy and is diagnosed when B-hCG levels do not fall appropriately after these pregnancies

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11
Q

What is an invasive mole?

A

a complete mole that invades the myometrium without any intervening endometrial stroma as seen on a histologic sample

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12
Q

Choriocarcinoma

A
  • a malignant germ cell tumor composed of cyto- and syncytiotrophoblasts
  • mimics placental tissue but villi are absent
  • it spreads via the hematogenous route early (makes sense because the usual function of trophoblasts is to establish fetal blood flow) and goes to the lungs
  • high B-hCG is characteristic and may lead to theca lutein cysts in the ovary or hyperthyroidism (since the a subunit of B-hCG resembles that of FSH, LH, and TSH)
  • it arises as a complication of gestation (following hydatidiform mole, normal pregnancy, ectopic pregnancy spontaneous abortion, etc.) or as a spontaneous germ cell tumor
  • when it arises from the gestational pathway it tends to respond well to chemotherapy; but those that arise spontaneously do not
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13
Q

What should be done if abnormal bleeding continues for more than 6 weeks after pregnancy?

A

patient should be evaluated with hCG levels to exclude a new pregnancy or gestational trophoblastic neoplasia

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14
Q

What is nonmetastatic persistent GTN and how is it treated?

A
  • it is a persistence of GTN following any sort of pregnancy, which is malignant but not yet metastatic
  • treated with single-agent chemotherapy such as MTX or actinomycin D
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15
Q

How is metastatic GTN classified?

A
  • it is divided into good- and poor-prognosis disease
  • a short interval from the antecedent pregnancy (less than 4 months), pretherapy hCG levels less than 40,000, no brain or liver metastases, no antecedent term pregnancy, and no prior chemotherapy are all indicative of good prognosis
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16
Q

Which HPV types are low-risk and which are high-risk?

A
  • low-risk are 6 and 11

- high-risk are 16, 18, 31, and 33

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17
Q

Low-risk HPV is associated with what diseases?

A

condylomata acuminata, aka genital warts, and with low-grade squamous intraepithelial lesions (LSILs)

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18
Q

What are the internal and external cervical os?

A
  • the internal os is the upper part of the cervix that opens into the endometrial cavity
  • the external os is the lower part that opens into the vagina
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19
Q

What is the ectocervix and what is the endocervix?

A
  • the ectocervix is the exterior portion of the cervical canal
  • the endocervix is the interior cervical canal
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20
Q

Describe the cervical epithelium.

A
  • the ectocervix is lined by stratified, non-keratinizing squamous epithelium
  • the endocervix is lined by a columnar epithelium
  • the squamocolumnar junction is where the two different epithelia meet
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21
Q

What is the clinical significance of the squamocolumnar junction?

A

it is where the epithelium of the ectocervix and endocervix meet and is clinically important because it is where almost all cervical neoplasias arise

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22
Q

Where is the squamocolumnar junction of the cervix located?

A
  • during childhood, the SCJ is located just inside the external os
  • during puberty, hormones and acidification cause a metaplasia that causes the SCJ to evert to a position on the enlarged cervical surface
  • this metaplasia is known as transformation zone and the area between the original SCJ and new SCJ is known as the transformation zone
  • during perimenopause, the new SCJ recedes upward into the endocervical canal, out of direct visual contact
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23
Q

What is the transformation zone of the cervix?

A

it is the area between the original squamocolumnar junction just inside the external os and the active squamoucolumnar junction which changes throughout reproductive life

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24
Q

What is a nabothian cyst?

A
  • a benign cyst that arises from the normal metaplasia within the transformation zone of the cervix
  • during this metaplasia, glands within the columnar epithelium may become trapped by squamous epithelium, forming the cyst
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25
Q

What are koilocytes?

A

cervical epithelial cells with shrunken, withered, raisin-like nuclei, indicative of cells infected by HPV without integration of the viral DNA into the host genome

26
Q

What are the risk factors for cervical neoplasia?

A
  • more than one sexual partner, past STD, or early first intercourse
  • male partner who has had a partner with cervical cancer
  • smoking
  • HIV, organ transplant, immunosuppression
  • diethylstilbestrol exposure
  • infrequent or absent cervical cytology screening tests
27
Q

How are epithelial cervical neoplasias classified?

A
  • can be atypical squamous cells, either of undetermined significance or without ability to exclude HSIL
  • LSIL, which encompasses HPV infection, mild dysplasia, or CIN I
  • HSIL, which encompasses CIN 2 and CIN 3, carcinoma in situ, and moderate or severe dysplasia but is still a precursor lesion
  • invasive squamous carcinoma
28
Q

Describe colposcopy with directed biopsy.

A
  • a method for further evaluation of an abnormal cervical cytology test
  • the cervix is washed with a 3-4% acetic acid solution, which dehydrates cells, causing those with large nuclei (dysplasia or HPV-infected) to appear white
  • this is visualized with a binocular stereomicroscope with a green filter that helps also identify abnormal vasculature
  • directed biopsy is performed on areas with white epithelium, abnormal vascular patterns, or punctate lesions, which are most commonly seen around the squamocolumnar junction
29
Q

What is required for a colposcopy to be considered satisfactory?

A

the entire squamocolumnar junction and the entire margins of abnormal areas must be visualized

30
Q

What is an endocervical curettage?

A
  • a method for evaluating an abnormal cervical cytology test when colposcopy is not able to visualize all the necessary components
  • involves using a small curette to collect cells from the endocervical canal and then using an endocervical brush to retrieve additional cells dislodged in the curette specimen
31
Q

How are women with atypical squamous cells of undetermined significance (ASC-US) on cytology managed?

A

the preferred next step is HPV testing
- if HPV testing is negative, repeat co-testing in 3 years
- if testing is positive, colposcopy is indicated
another acceptable approach is to repeat cytology 1 year later
- if it is negative, no further management is required and routine screening is sufficient
- if positive and shows ASC or a more severe lesion, then colposcopy is indicated

32
Q

How do recommendations for management of ASC-US differ in women age 21-24?

A
  • perform reflex HPV testing: if negative, continue routine screening; if positive, repeat cytology in 12 months
  • if repeat cytology is negative, finds ASC-US, or finds LSIL, repeat cytology again in 12 months; routine to normal screening if this three total tests show this
  • if follow-up cytology shows progression to ASC-H, AGC, or HSIL, perform colposcopy
33
Q

How are women with low-grade squamous intraepithelial lesions (LSILs) on cytology managed?

A
  • if HPV testing is negative, monitor the patient closely with repeat cotesting in 12 months; if repeat testing shows ASC or more or HPV testing is positive, perform colposcopy
  • if HPV testing isn’t performed, is positive, or the patient has a past history of ASC-US with positive HPV testing, perform colposcopy
34
Q

Why do women age 21-24 have different options for management of abnormal cytology findings?

A
  • because ASC and LSIL are more common in younger women and the likelihood of spontaneous regression in this population is higher
  • furthermore, HPV DNA testing is more likely to be positive, so using it as a triage method is less useful
35
Q

Describe cervical cancer screening recommendations.

A
  • perform cytology every three years beginning at age 21
  • add reflex HPV testing at 30 and perform cytology every five years as long as results are normal
  • discontinue cytology at 65 years of age if the patient has no history of CIN 2 or higher
36
Q

How should a cytology finding of HSIL be managed?

A

because CIN 2 or 3 is likely with HSIL cytology findings, immediate treatment with LEEP is the preferred management

37
Q

How is ASC-H found on cytology further evaluated?

A

with colposcope

38
Q

What is the recommendation for managing the following cervical cytology findings?

  • ASC-US
  • ASC-H
  • AGC
  • LSIL
  • HSIL
A
  • ASC-US: perform HPV testing or repeat cytology in one year, and if positive, perform colposcopy
  • ASC-H: perform colposcopy
  • AGC: perform colposcopy, HPV testing, and ECC; add endometrial sampling if the women is over 25 or has risk for endometrial neoplasia
  • LSIL: perform HPV testing or repeat cytology in one year, and if positive, perform colposcopy
  • HSIL: treat with LEEP
39
Q

What are the two types of cervical atypic?

A

atypical squamous cells and atypical glandular cells

40
Q

What is the recommendation for AGC findings on cervical cytology?

A

perform colposcopy, HPV testing, and ECC; add endometrial sampling if the women is over 25 or has heightened risk for endometrial neoplasia

41
Q

What methods are available for ablation of cervical dysplasia?

A

cryotherapy, laser ablation, electrofulguration, or cold coagulation

42
Q

What is LEEP?

A

an excisional method for treating cervical neoplasia that relies on electrosurgical energy

43
Q

What parts of the cervix are excised when treating cervical neoplasia with excision rather than ablation?

A

a cone-shaped specimen is removed from the cervix, including the SCJ, all identified lesions on the ectocervix, and a portion of the endocervical canal

44
Q

When is excisional therapy preferred over ablative therapy for cervical intraepithelial neoplasia?

A

excisional is preferred…

  • if endocervical curettage is positive
  • if the colposcopy is unsatisfactory
  • if there is a substantial discrepancy between the screening cervical cytology and the histologic data from biopsy and ECC
45
Q

Cervical Cancer

A
  • most cases are squamous cell while adenocarcinoma makes up only a small percentage of cases
  • the average age of diagnosis is about 50 years old and CIN precedes invasive carcinoma by about 10 years
  • the key risk factor is high-risk HPV infection; secondary risk factors include smoking and immunodeficiency
  • symptoms most often include watery vaginal discharge, intermittent spotting, and postcoital bleeding
  • may invade through the anterior uterine wall into the bladder, blocking the ureters and causing hydronephrosis with post renal failure; a common cause of death in these patients
  • staging is based on histologic assessment and on physical and laboratory examination; surgical findings guide treatment but do not affect staging
  • treatment options include surgery (conization, hysterectomy, and/or lymph node dissection) radiation therapy, and chemotherapy (usually cisplatin)
  • after treatment, patients should have follow-up every four months for two years, and then every six months until 5 years post-treatment
  • recommend cervical cytology annually for the patient’s lifetime and CXRs annually for the first 5 years
46
Q

What are the guidelines for administration of the HPV vaccine?

A
  • recommended for boys and girls age 11-12 but as early as 9 years old
  • if the first dose is given before age 15, then a second is needed 6 to 12 months later
  • if the first dose is given after age 15, a second is needed 1-2 months later and a third 6 months after the first
47
Q

Uterine Leiomyoma

A
  • a hormonally responsive (to estrogen) benign tumor derived from the smooth muscle of the myometrium
  • most are intramural but can be subserosal or submucosal
  • presents with abnormal uterine bleeding, namely progressively heavier and longer menstrual flow, a progressive increase in pelvic pressure, and secondary dysmenorrhea
  • if they grow significantly they may even apply pressure to the ureters as they cross the pelvic brim, leading to hydroureter and hydronephrosis
  • patients may experience a dull, intermittent, low midline cramping pain if a submucosal leiomyoma becomes pedunculate and prolapses through the internal os
  • diagnosed based on physical exam and imaging studies; usually felt as a large, midline, irregular-contoured mobile pelvic mass with a solid quality
  • hysteroscopy, hysterosalpingography, saline infusion US, and exploratory surgery may also be necessary
  • treatment is usually conservative and directed toward the symptoms; progestin supplementation and prostaglandin synthetase inhibitors control dysmenorrhea and menstrual flow while estrogen antagonists can reduce fibroid size
  • surgical treatment may include a myomectomy or hysterectomy
  • uterine artery embolization is a newer treatment
48
Q

What differentiates a subserosal, submucosal, and intramural leiomyoma?

A
  • subserosal are just below the uterine serosa
  • submucosal are just below the endometrium
  • intramural are in the muscular wall
49
Q

Leiomyosarcoma

A
  • a uterine malignancy
  • most often seen in postmenopausal patients presenting with a rapidly enlarging uterine mass, postmenopausal bleeding, unusual vaginal discharge, and pelvic pain
50
Q

What surgical options are available for the treatment of uterine leiomyomas?

A
  • myomectomy can be used if the patient has a rapidly enlarging asymptomatic mass, symptoms are not well controlled medically, or the mass is causing hydronephrosis and the patient wishes to remain fertile
  • hysterectomy is the definitive treatment but should only be used in symptomatic women who have completed childbearing
51
Q

Describe uterine artery embolization?

A
  • a method for selectively embolizing the uterine artery with polyvinyl alcohol particles to cause an acute infarction of a targeted leiomyoma
  • may cause acute post-embolization pain and fever, delayed infection, or delayed passage of necrotic fibroid tissue
  • not considered a viable option in patients who desire future childbearing
52
Q

What is MRI-guided focused ultrasound surgery?

A

a treatment option for leiomyosarcoma which delivers concentrated ultrasound energy to raise the temperature and cause coagulative necrosis

53
Q

What is the most common gynecologic cancer?

A

endometrial carcinoma

54
Q

What are the kinds of endometrial hyperplasia?

A
  • hyperplasia without atypia can be simple, in which case both glandular and stromal elements proliferate and there is very little association with endometrial carcinoma
  • hyperplasia without atypia can be complex, in which there is a proliferation of primarily glandular elements only; glands appear back-to-back and it represents a true intraepithelial neoplastic process
  • hyperplasia with atypia which is a precursor lesion to endometrial carcinoma
55
Q

What ultrasound finding is consistent with endometrial hyperplasia or carcinoma?

A

an endometrial thickness over 4 mm in a postmenopausal patient

56
Q

What are risk factors for endometrial hyperplasia and cancer?

A
  • long-term use of estrogen replacement therapy
  • tamoxifen use
  • obesity
  • nulliparity or history of infertility
  • early menarche, late menopause
57
Q

Endometrial Hyperplasia

A
  • risk factors are related to exposure to estrogen
  • the hallmark is abnormal uterine bleeding
  • diagnosis is made by endometrial sampling and D&C is used to exclude the possibility of coexistent endometrial cancer afterwards
  • classified as simple without atypia, complex without atypia, or with atypia
  • simple without has very little association with cancer, complex without has a weak association as it is a true intraepithelial neoplastic process, and with atypia is a precursor lesion with a strong association to cancer
  • medical therapy includes progestins and is first-line, but hysterectomy is definitive therapy and recommended after a patient has completed childbearing
58
Q

How do progestins help treat endometrial hyperplasia?

A
  • alter the enzymatic pathways which convert estradiol to weaker estrogens
  • decrease the number of estrogen receptors on endometrial glandular cells
  • thin the endometrium and induce stromal decidualization
59
Q

Endometrial Polyps

A
  • a hyperplastic protrusion of endometrium
  • most commonly seen in perimenopausal or immediately postmenopausal women
  • most often caused by tamoxifen, which has weak pro-estrogenic effects on the endometrium
  • presents with abnormal uterine bleeding
  • rarely demonstrate malignant change but polyps in postmenopausal women or those who are taking tamoxifen are more likely to be associated with endometrial carcinoma
60
Q

Endometrial Cancer

A
  • most cases are seen in postmenopausal women presenting with postmenopausal bleeding
  • most are adenocarcinomas but there can be a squamous epithelium coexisting with the glandular components
  • type I, endometrioid, are more common, caused by exposure to unopposed estrogen, tend to be low-grade, and have a favorable prognosis
  • type II, non-endometrioid, are less common, said to be estrogen-independent and arise spontaneously, arise from an atrophic endometrium, and have a less favorable prognosis
  • diagnosis is made based on endometrial sampling; preoperative CA-125 can be helpful in advanced disease
  • the single most important prognostic factor is histologic grade while depth of myometrial invasion is second most
  • hysterectomy is the primary treatment; surgical staging requires concurrent BSO, lymph node dissection, and peritoneal washing
61
Q

Uterine Sarcoma

A
  • arise from the myometrium or endometrial stroma
  • progressive uterine enlargement in the postmenopausal period is often indicative; other symptoms include postmenopausal bleeding, pelvic pain, and vaginal discharge
  • surgical removal is the most reliable method for diagnosis
  • virulence is directly related to the number of mitotic figures and degree of cellular atypia found on histology
  • staging is surgical and based on the same criteria as endometrial adenocarcinoma

OBGYN (21 decks)

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