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Gyn cancers Flashcards

Mangler breast of vagina

1
Q

what is the most common cause of breast mass

A

Benign fibroadenoma and cyst

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2
Q

what are the majority of vulva cancer

A

squamous cell carcinoma

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3
Q

what is VIN

A

Vulvar intraepithelial neoplasia. Premalignant change characterized by cellular atypic.

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4
Q

What characterize the cellular atypia in VIN

A

Loss of epithelial cell maturation, cellular crowding, nuclear hyperchromatosis and abnormal mitosis

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5
Q

What is median age of VIN

A

40

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6
Q

RFs to VIN

A
  • smoking
  • high risk HPV
  • immunosuppression
  • immunodeficiency
  • Lichen sclerosus (film)
  • Hx of HSV inf
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7
Q

Sx of VIN

A

The 4 P’s

  • Pruritic
  • Papule
  • Patriotic: red/white/blue
  • Parakeratosis (retention of nuclei in stratum corneum)
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8
Q

What makes a suspicious vulvar lesion?

A

Keratotic, pruritic, pigmentet, bleeding mass in postmenopausal women. Lesion not responding to antifungals.

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9
Q

What are the treatment options for VIN ?

A
  • Topical Imiquimod, 5-FU
  • Laser ablation
  • Simple vulvectomy or skinning vulvectomy
  • Split-thickness graft
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10
Q

what are the types of vulvar cancer

A

SCC, malignant melanoma, Bartholins adenocarcinoma, BCC, soft tissue sarcoma

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11
Q

Where is most common location of vulva cancer

A

Labia majora, unifocal (95%)

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12
Q

Where does vulva cancer spread first

A

superficial inguinal LN w a smaller degree of spread via direct extension to vagina, urethra and anus.

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13
Q

Average age of dx in vulva cancer

A

65y ( younger are ass w VIN )

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14
Q

sx of vulva cancer

A

Keratotic, pruritic/ pain , pigmentet, bleeding mass in postmenopausal women. Lesion not responding to antifungals.

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15
Q

dx of vulva cancer

A

Biopsy

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16
Q

How is vulvar carcinoma staged?

A

Using FIGO criteria, surgically using size, invasion, nodal involvement and distant mets

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17
Q

What is the tx of vulvar carcinoma?

A
  • Local excision with inguinal-femoral LN dissection is ToC for primary occurence
  • Stage 1 = ispilateral LN is sufficient
  • Stage 2= modified redical vulvectomy
  • Stage 3 and 4= radical vulvectomy, bilateral inguinofemoral LN and pelvic exenteration. Preop radio and chemo.
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18
Q

What if LAN reveals mets in vulvar carcinoma?

A

Pelvic radiation as adjunct

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19
Q

What is used in recurrence of vulvar carcinoma?

A

secondary excision or chemoradiation

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20
Q

when should first pap be

A

21y, then every 3 y

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21
Q

when should first hpv test be

A

at age 30

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22
Q

when can you discontinue pap

A

At 65 if never had, 3 neg pap i a row, >20y removed from tx for CIN2+, if total hysterectomy if no abnormal paps

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23
Q

Who should you screen w pap annually?

A

Pat w IU DES, HIV, immunecompromised, chronic steroid use

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24
Q

What system is used to classify abnormal epithelial cells found on pap

A

Bethesda

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25
Q

What is ASC- US

A

Atypical squamous cells of undetermined significance

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26
Q

ASC-H

A

Atypical squamous cells cannot exclude high-grade squamous intraepithelial lesion

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27
Q

LSIL

A

Low-grade squamous intraepithelial lesion

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28
Q

HSIL

A

High-grade squamous intraepithelial lesion

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29
Q

SCC

A

Squamous cell carcinoma

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30
Q

AGC

A

Atypical glandular cells

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31
Q

What other than neoplasm may ASC represent

A

Bening inflammatory response to infection or trauma.

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32
Q

Which classifications should you proceed with if >24y, with colposcopy and biopsy

A

LSIL, HSIL, ASC-H

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33
Q

How would you proceed with ASC-US

A

HPV test to determine if colposcopy is indicated or not. Its called reflex testing. If high risk HPV proceed with colposcopy and biopsy.

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34
Q

How to proceed w AGC

A

Colposcopy, high risk HPVtest, and endocervical sampling. Have potential for both cervical and endometial adenocarcinoma

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35
Q

What to do with AGC >35y or those <35y w RF’s for endometrial hyperplasia?

A

Endometrial biopsy

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36
Q

What should you do with a woman >30 with neg. pap and pos. HPV?

A

Screen w pap and HPV in a year

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37
Q

What abnormalities are you looking for in colposcopy

A

Acetowhite epithelium, mosaicism/cobblestone, punctated vessels, abnormal vessel geography (hairpin loops or arboreta)

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38
Q

What do you do w abnormality on colposcopy

A

biopsy to get histology

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39
Q

What are the histologic results from biopsy of cervix

A

Classified based on depth of invasion. CIN1, 2, and 3. (cervical intraepithelial neoplasia)

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40
Q

What is done w CIN1

A

Repeat pap 6m x 2, or repeat HPV test in 1 year

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41
Q

What is done w CIN 2 or CIN1 that persist for >2y

A

Cryotherapy or surgical excision. Alt. to CIN2 is observation w colposcopy and pap every 6 months for 24months

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42
Q

CIN 3

A

LEEP (loop electrical excision procedure) is the most common. Also Lets (large loop excision of the transformational zone) Before was cold-knife conization used (CKC).

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43
Q

What to do w CIN that involve endocervix

A

CKC or two stage LEEP

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44
Q

What to do w CIN that are large, multifocal or involving vagina?

A

Laser conization. Allow for more precise removal of only abnormal tissue and removal of less normal cervix

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45
Q

What are the SE of cervical excision procedures?

A

Cervical stenosis, cervical insuffisiency, infection, or bleed

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46
Q

What is the follow up from surgical excision of cervix

A

Every 6m w repeat pap and colposcopy for 1y. If results remain normal, pat can return to routine screen for at least 20y

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47
Q

What are the risk factors of cervical cancer?

A
  • early intercourse
  • early childbearing
  • high risk partners
  • multiple partners
  • low SES
  • hx of STI
  • smoking
  • immunodeficiency
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48
Q

Sx of cervical cancer

A
  • early is asx
  • postcoital bleed
  • abnormal bleed
  • pelvic pain or pressure
  • rectal or UT sx
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49
Q

What are the findings on PE w speculum w cervical cancer

A

Friable, bleeding cervical lesion which invade other parts of vagina

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50
Q

What are PE findings w bimanual w cervical cancer

A

Cervical mass, invasive lesion to upper vagina, cul de sac or adnexa

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51
Q

how to dx cervical cancer

A

biopsy is required. Ct to confirm and define extent of disease

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52
Q

How is cervical cancer staged?

A

FIGO clinical staging (as the only gyn cancer!!). Involves the invasion into adjacent structures and metastases. Used methods are XR, cystoscopy, proctoscopy, IVP and barium enema. CT and MRI for extent, not stage. If one stage has been assigned it does not change based on intraoperative findings.

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53
Q

What is stage 1 in cervical cancer?

A

Confined to cervix, a is microscopic, b is gross.

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54
Q

stage 0 in cervical ca

A

Cervical carcinoma in situ.

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55
Q

stage 2 in cervical ca

A

spread beyond cervix, but not to pelvic wall, b is parametrial involvement

56
Q

stage 3 in cervical ca

A

spread to pelvic wall (3b), lower 1/3 of vagina, or caused hydronephrosis of a kidney

57
Q

stage 4 in cervical ca

A

spread beyond true pelvis or involves mucosa of the bladder and or the rectum

58
Q

how is the tx of cervical cancer classified

A

Preinvasive disease= 0-1a1
Early disease= 1a2 to 2a
Advanced disease = 2b-4

59
Q

tx of preinvasive disease of cervical cancer (0-1a to 1)

A

CKC or simple hysterectomy

60
Q

tx of early disease in cervical cancer (1a1 to 2a)

A

Radical hysterectomy or radiation

61
Q

tx of advanced disease in cervical cancer (2b to 4)

A

Chemoradiation. External beam radiation, cisplatin-based chemo and intracavitary radiation.

62
Q

what to do w cervical cancer after radio and recurrence?

A

Pelvic excenteration

63
Q

what is the incidence of endometrial carcinoma

A

most common gyn cancer, 4th common cancer in women overall.

64
Q

RFs for endometrial cancer

A
  • high dose menopausal estrogen
  • obesity x 2-4
  • nulliparity
  • (early menarche)
  • late menopause
  • PCOS, chronic anovulation
  • Tamoxifen
  • DM 2 > 1
  • HT
  • endometrial hyperplasia
  • (gallbladder disease, Lynch sd)
  • (white, higher ses, older age, north american or northern europe)
65
Q

What is type 1 endometrial cancer

A

The estrogen dependent neoplasm (adenocarcinoma)

  • Unnopposed estrogen present
  • Slow growing
  • Atypical hyperplasia, proliferation of gladular cells
  • Endometroid histology, well differentiated
  • Low grade
  • favorable Px
  • (superficial, young pat, PTEN, KRAS)
66
Q

What is type 2 endometrial cancer

A

The estrogen independent cancer. Serous and clear cell

  • Rapid growth
  • Atrophic epithelium as precursor
  • High grade
  • Deep invasion
  • relatively old
  • p53, her2/neu
67
Q

Protective factors for endometrial cancer

A
  • OCP
  • Progestin contraceptives
  • Smoking
  • Exercise, healthy diet
  • High parity
  • Pregnancy
  • HRT
68
Q

sx in endometrial cancer

A

Most common sx is abnormal bleed. In premeno: menorrhagia, intermenstrual bleed. Postmen: any bleed. In advanced ds: pelvic pain, pelvic mass and WL

69
Q

how to dx endometrial cancer

A
  • Postmeno: TVS w endometrial thickness >4mm, EMB or D&C if bleed persist
  • Premeno: biopsy all women >45y w persisten abnormal bleed
  • If EMB cannot be done: D&C
  • If EMB show atypical hyperplasia or necrosis do D&C
  • Labs: hCG, CBC, TFTs, pap, FSH(menopause), prolactin
  • CA-125 is done preop
  • US: fibroids, adenomyosis, polyps, hyperplasia
70
Q

How is endometial cancer staged

A

W FIGO surgical staging. Previous clinically. Pathologic confirmation of extent of disease progression

71
Q

Stage 1 and 2 in endometrial cancer and tx

A

1- conficed to corpus uteri
2- invade cervical stroma, not extend beyond uterus
tx: Total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH-BSO). Pelvic and para-aortic LN sampling. If high risk then radiation. If grade 3 tumor, papillary serous or clear cell histology or enlarged LN should use radiation (even if confined to uterus)

72
Q

Stage 3 and 4 in endometrial cancer anc tx

A

3- Local or regional spread of tumor (A serous B vagina,parametrial C pelvic, para-aotic LN)
4- mets to bladder, bowel or beyond
tx: TAH-BSO, pelvic and para-aortal LN sampling. Additional radiation.

73
Q

How to tx advanced and recurrent endometrial cancer

A

Chemo, but not yet determined the best regimen

TAP (taxol/paclitaxel, adriamycin/doxorubicin, platinum/cisplatin)

74
Q

high risk features in endometrial cancer

A
  • > 50% myometrial invasion
  • papillary serous or clear cell tumor
  • grade 3 tumor (>50% solid growth)
  • large tumor (>2cm or filling cavity)
  • spread beyond the uterine fundus (stage 3 or 4)

Confers higher risk of recurrence and lower survival rate

75
Q

how to follow up on endometral cancer

A

PE w speculum and rectovaginal exam every 3m for 3y. 2 x a year next 2 years. If w/o recurrent disease, followed anually .

76
Q

What are the risks of taking tamoxifen?

A
  • Endometrial hyperplasia and cancer
  • invasive carcinoma
  • uterine sarcoma
  • endometrial polyps
77
Q

Why do you get carcinomatous ileus from ovarian cancer?

A

It spreads through peritoneal fluid, and leads to ascites in the abdomen. It can lead to malnutrition, slow starvation, cachexia and death.

78
Q

what are the rfs to ovarian cancer

A
  • BRCA1> BRCA2
  • Lynch 2
  • Family history of ovarian cancer
  • Personal history of breast cancer
  • hx of long uninterupted ovulation: early menarche, late menopause, infertility, nulliparity, delayed childbearing
  • High diatary fat
  • Talc powder use on perineum, asbestos
  • Higher incidence in whites
79
Q

Which ovarian cancers are more common in girls and young adults?

A

Nonepithelial (germ cell and sex stromal tumors)

80
Q

What are the protective factors of ovarian cancer?

A
  • Multiparity
  • Breastfeeding
  • OCP
  • Chronic anovulation
  • Tubal ligation
  • Hysterectomy
81
Q

What are the sx of ovarian cancer?

A
  • usually asx until advanced
  • abd distention, bloating
  • vague abd pain
  • early satiety
  • Nausea, anorexia, indigestion
  • pelvic pressure, ventral hernia
82
Q

What may be the findings on PE w ovarian cancer?

A
  • Solid, fixed irregular mass
  • Ascites
  • mets to umbilicus= Sister Mary Joseph nodule
  • Meigs sd= ovarian tumor, ascites and right hydrothorax
83
Q

How to dx ovarian cancer?

A
  • Primary diagnostic tool is pelvic US
  • CT and MRI can assist in dx and delieate spread
  • CA-125, AFP, LDH, hCG titers can be used for monitoring
  • Barium enema and IVP for mets dx
84
Q

How to stage ovarian cancer?

A

Surgically w TAHBSO w omenectomy, pap of diaphragm , peritoneal washing and sampling of pelvic and para-aortic LN.
1- confined to ovary (A=1 ovary, B=2 ovaries, C= capsule rupture, ascites)
2- ovary + pelvic extention (uterus, tubes, ascites)
3- ovary + peritoneal mets
4- distant mets

85
Q

what are the types of ovarian cancers

A

Epithelial cell tumors, germ cell tumors and sex stromal tumors (unclassified: lipid cell tumor and sarcoma)

86
Q

what are the types of epithelial tumors

A

Serous, (cystadenoma, cystadenocarcinoma) , mucinous, endometroid, clear cell, Brenner and undifferetiated

87
Q

which marker can be used to track epithelial cell ovarian cancer? ‘

A

CA- 125, (CAT)

88
Q

what are the tx of epithelial ovarian cancer?

A

TAHBSO, omenectomy, cytoreduction and bilateral pelvic and para-aortic LN sampling. Chemo w carboplatin and paclitaxel, both IV and intraperitoneal.

89
Q

what are the types of germ cell ovarican cancers?

A
  • mature cystic teratoma (dermoid cyst), most common
  • immature teratoma (M)
  • dysgerminoma (M)
  • choriocarcinoma (placental tissue) (M)
  • embryoynal carcinoma (M)
  • endodermal sinus tumor/ Yolksac tumor
  • Monoderm teratoma
  • Polyembryoma (M)
  • Mixed germ cell tumor
90
Q

what tumor markers can you use in ovarian germ cell tumors?

A
  • Dygerminoma = LDH
  • Endodermal sinus tumor (yolksac) = AFP
  • Choriocarcinoma = hCG
91
Q

tx of GCT

A
  • Dermoid cys= cystectomy or oophorectomy
    For all other GCT:
  • Unilateral salpingo-oophorectomy if fertility is desired
  • If childbearing is complete, or ca is bilateral= TAHBSO
  • Multiagent chemo (except immature teratoma, dysgerminoma) = BEP (bleomycin, etoposide and cisplatin)
92
Q

What is seen in histology of granulosa theca cell ovarian cancer

A

Resemble fetal ovary, produce estrogen. Have coffe bean nucei in small clusters arranged around central cavity. This is known as Call Exner bodies

93
Q

What does Sertolo Leydig cell ovarian cancer resemble?

A

Fetal testes. Produce testosterone and other androgens

94
Q

What is ass. w sexcord ovarian tumor, the fibroma ?

A

Ascites, Meigs sd

95
Q

What are sx of granulosa theca cell tumor?

A

It produce estrogen and inhibinA/B. Feminization, precocious puberty, menstrual irregularity, secondary amenorrrhea or postmeno bleed. May be endometrial hyperplasia or cancer

96
Q

what are the sx of sertoli leydic cell tumor?

A

Produce testo and androgens. Can cause virilizing effects as breast atrophy, hirsutism, deepened voice, acne, clitoromegaly, receding hairline

97
Q

tx of sex cord tumor

A

Usual tx is unilateral salpingo-oophorectomy. In women w complete childbearing TAHBSO. No chemo or radio!

98
Q

what are epithelial ovarian tumor?

A

From ovary surface epithelium, primitive mesoderm. Slow growing. Usually advanced at disease. Ass w BRCA and CA 125. Serous cyst adenocarcinoma is the most common malignant tumor.

99
Q

what are germ cell ovarian tumor?

A

From cells destined to become eggs, primordial germ cell. Most common ovarian neoplasm >20y. Rapid growing, but usually at stage 1 at dx. Are x3 more common in black and asian compared to caucasian.

100
Q

what are sex cord/stromal tumor

A

From hormone producing cells or cells making up interstitium of the ovary. Age of onset is variable, usually btw 40-70. Granulosa-theca cell and Sertoli-Leydig cell tumors produce estrogen and testo/androgens. Low-grade malignancy, usually unilateral.

101
Q

what is fallopian tube cancer?

A

Lumen w papillary growth of solid tumor arising from the mucosa. Bilateral 10%. Occur at any age, most 55-60. Extremely rare. More common w caucasian, BRCA1/2, nulliparity, infertility. Progression similar to ovarian cancer, peritoneal spread and ascites.

102
Q

Sx of fallopian tube cancer

A
  • Typically asx
  • Classic triad of Latzko: profuse watery discharge, pelvic pain, pelvic mass
  • Hydrops tubae profulens (intermittent hydrosalpinx): Pressure induced discharge, watery or bloody tinged color. Result in shrink of adnexal mass.
  • Low back pain
103
Q

dx of fallopian cancer

A

Almost never dx preoperatively. On US adnexal mass or ascites. Elevated CA-125. Cervical cytology rarely positive.

104
Q

tx of fallopian cancer

A

Surgically staged. TAHBSO, omenectomy, cytoreduction, peritoneal cytology, retroperitoneal LN sampling. Adjuctive chemo IV or IV+intraperitoneal w carboplatin and paclitaxel. CA-125 and CT for monitoring.

105
Q

concerning findings in US regarding pelvic mass(ovarian)

A

Size >8cm, solid or cystic and solid, nodular, papirllary, multilocular thick >2mm, present in solid component, bilateral, ascites, peritoneal mass, lymphadenopathy.

106
Q

What is gestational trophoblastic disease?

A

Abnormal proliferation of trophoplastic (placental) tissue. Result form abnormal fetal cells.
Divided into molar pregnancy, persistent/invasive mole, choriocarcinoma and placental site trophoblastic tumpr (PSTT)

107
Q

what is begign GTD?

A

Molar pregnancy or hydatidiform moles. May be complete or partial. Complete mole have higher malignant potential.

108
Q

what are the rfs of GTD

A
  • Previous molar pregnancy
  • Extremes of age
  • Diet: low in betacarotene, folic acid and animal fat
  • smoking
  • nulliparity
  • infertility
  • blood group A
  • spontaneous abortions
  • OCP
109
Q

what is thought to be the MoA in complete mole

A

Empty egg gets fertilized by sperm. Sperm replicates inside egg, making it typically 46XX.

110
Q

what is the placental abnormality in complete mole?

A

Characterized by noninvasive trophoblastic proliferation ass w diffuse swelling of chorionic villi. This hydropic degeneration will give it the appearance of grape-like vesicles filling the uterus. Absence of fetus. Syncytiotrophoblast produce hCG.

111
Q

What gives the sx in complete mole?

A

Extremely high levels of hCG. The alpha subunit can be found in LH, FSH and TSH, and the mole may act at a homolog to these, stimulating large theca lutein cyst >6cm. May result in hyperthyroidism and cause hyperemesis gravidarum, and early preeclampsia.

112
Q

clinical presentation of complete mole

A
  • heavy/irregular bleed is most common sx
  • cherry-like cluster per vagina
  • irritability, photophobia, nervousness, anorexia, tremor(hyperthyroidism)
  • N/V (hyperemesis gravidarum)
  • uterus larger than expected
  • pre-eclamptic signs, HT and swelling. If <20 w it is pathognomonic for molar pregnancy!
113
Q

how to dx molar pregnancy, complete mole

A
  • extremely high cHG (>100 000)
  • Pelvic US: Snow storm, bilateral theca lutein cyst >6cm
  • Definitive dx w patologic examination of tumor
114
Q

what is tx of complete mole?

A
  • Immediate D&C under general anesthesia
  • Preop: CBC, CMP, PT/PTT, TFT, maternal typing
  • Given antiHT, and BB, IV oxytocin ang RhoGAM if Rh-neg
115
Q

how is follow-up on complete molar pregnancy after tx

A
  • Quatitative hCG after 48hrs postop
  • hCH every week for 3 weeks
  • Every months for 6months
  • Should normalize within 14 weeks. A plateau or rise in hCG during monitoring, or elevated hCG after 6m is a sign of persistent/invasive disease
116
Q

What is an incomplet or partial mole?

A

Formed whem a noraml ovum is fertilized by 2 sperms simultaneously. Result in triploid karyotype w 69XXY. Placenta is characterized by focal hydroptic vili and trophoblastic hyperplasia primarly of the cytotrophoblast. Ass w presence of a fetus w multiple anomalies. Much lower malignancy potential than complete mole.

117
Q

what are the associated anomalies in a partial mole fetus?

A

IUGR, hydrocephalus, syndactyly

118
Q

what is the levels of hcg in partial mole, and why

A

hCG will be normal, or slightly elevated. It is because the cytotrophoblast does not produce hCG

119
Q

What is the presentation of partial mole?

A

Usually as an spontaneous abortion in late 1st or early 2nd TM. Dx at routine US. PE unremarkable, may be less size for the date of fetus.

120
Q

dx of partial mole

A
  • Quantitative hCG is normal for pregnancy
  • Pelvic US: 1) fetus w anomalies, or gestational sac 2) low amniotic fluid 3) enlarged placenta w “swiss cheese” appearance
121
Q

how to follow up on partial mole

A
  • Quatitative hCG after 48hrs postop
  • hCH every week for 3 weeks
  • Every months for 6months
  • Should normalize within 8 weeks. A plateau or rise in hCG during monitoring, or elevated hCG is a sign of persistent/invasive disease
122
Q

tx of partial mole

A

D&C as in complete mole

123
Q

what is malignant GTD?

A

Named bc local invasion and metastasis. Devided into persistent/invasive mole, choriocarcinoma and PSTT. 50% occurs months-years after molar pregnancy(persistient), 25 occur after misscariage, EAB, ectopic pregnancy(choriocarcinoma). The last 25% occur after normal pregnancy (choriocarcinoma) .

124
Q

how is malignant GTD classified?

A

Nonmetastatic if confined to uterus, or metastatic if progress beyond uterus. Metastatic can also be devided into good px and bad px, depending on length of tome since pregnancy, hCH level, brain/liver mets, type of antecedent pregnancy.

125
Q

what is persistant/invasive mole

A

Almost always occuring after evacuation on molar pregnancy. Clinical presentation w hx of molar pregnancy and hCG rise or plateau. Most common sx is abnormal uterine bleed.

126
Q

how to dx invasive mole

A

hCG levels and pelvic US. Cornerstone of dx.

127
Q

tx of invasive mole

A
  • if plateau hCG and no mets, can consider new D&C
  • if nonmetastatic: methotrexate or actinomycin-D
  • w mets: single chemo w methotrexate, actinomycin-D or etoposide
128
Q

how to follow up on invasive mole after tx

A

Monitor weekly hCG until normal for 3w. Then monthly for 1 year. Use barrier contraception until hCG is normal. Hormonal contraception w 1y of normal hCG. Avoid pregnancy 1yr after finishing chemo

129
Q

what is choriocarcinoma in GTD

A

Malignancy of placental tissue, pure epithelial tumor. Gestational is most common. Histology shows sheets of anaplastic cytotrophoblast and syncytotrophoblast in absence of chorionic villi. Mets tend to be highly vascular and bleed easily.

130
Q

presentation of choriocarcinoma in GTD

A
  • late postpartum bleed >6-8w
  • At metastatic stage
  • Lung mets: cough, dyspnea, resp.distress, hemoptysis
  • CNS mets: headache, dizziness, spaceoccupying lesion sx
  • PE: uterine enlargement, signs of metastatic disease, vaginal mass, bilateral theca lutein cyst, neuro sx
131
Q

how to dx choriocarcinoma GTD

A

hCG, pelvic US. Appropriate imaging for mets

132
Q

tx of choriocarcinoma GTD

A

stage 1- methotraxate
stage 2-4- methotrexate, actinomycin D, etoposide
Follow-up w hCG until normal 3wks, monthly hCG for a year.

133
Q

what is PSTT

A

Placental site trophoblastic tumor. Extremely rare, arise from placental implantation site. Intermediate cytotrophoblast infiltrate the myometrium and invade blood vessels. Histologically the tumors are characterized w ansence of villi, and proliferation of intermediate trophoblast and excessive production of hPL

134
Q

what is sx of PSTT

A

Persistent vaginal bleed. May occur weeks to years after an antecendent pregnancy. PE may show enlarged uterus

135
Q

Dx of PSTT

A

Haw low cHG. may use serum hPL. Pelvid US: uterine mass, both cystic and solid components.

136
Q

tx of PSTT

A

Not sensitive to chemo. ToC is hysterectomy w multiagent chemo given 1 w after surgery to prevent recurrent disease.
Chemo: EMA/CO (etopomide, methotrexate, actinomycin/ cyclophosphamide, vincristine)

Gyn/OB (4 decks)

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