GYN CA Flashcards

(88 cards)

1
Q

vulvar intraepithelial neoplasm

A

VIN- cellular atypia contained w/in the epithelium. characterized by loss of epithelial cell maturation, cellular crowding, nuclear hyperchromatosis an abnormal mitosis

VIN I (mild), VIN II moderate, VIN III, severe depends on depth

20% have coexistent invasive CA penetrating basement membrane.

correlated w/ HPV infection- other risks: cigarette and immune compromised

2 forms: young-> aggressive multifocal assoc HPV; older focal, slow to invade NOT HPV

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2
Q

VIN affects

Dx?

A

premenopausal women 75% w/ HPV, median age 40; risk HPV 16 and 18, cigarettes, immunodeficiency

Dx: asymptomatic so need thorough inspection for masses, ulcers, color changes; pruritus/irritation, palpable abnormality, perineal burning, dysuria (not responsive to antifungel)

biopsy lisions that appear flat/raised, red/white

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3
Q

Tx of VIN

A

depends of degree of disease

spontantous regression

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4
Q

Pagets disease of the vagina- extramammary pages dieases

Dx?

A

uncommon apocrine gland neoplasia affecting the anogenital areas of women and men

Ages 50-80 in caucasion

recurs locally w/ minimal invasion , 20% coexistent adenocarciona(mets common then)

Dx: chronic inflam changes: hyperemic, sharp demarcations, thickened, puritic, velvety red lesions-> eczematous and scar to white plaques

most common in Pts > 60y but symptoms of vulvar pruritus and vulvodynia precede by years - Biopsy

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5
Q

Tx of Pagets disease of the vulva

A

wide local excision in absence of invasion; fatal if spreads to the nodes
r/o adenocarciona
high recurrence rate may require maple local lesions

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6
Q

Cancers of vulva

A

arise from skin, glandular tissue subq, mucosa

Most common- squamous cell (87%); malignant melanoma (6%), bartholins adenocarcinoma (4%), basal (

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7
Q

Dx and staging of vulvar CA

A

annula exam finds vulvual parities, pain and bleeding, vulvar mass(fleshy, nodular, warty)
-> unifocal lesion 90% on labia majora; Dx w/ biopsy; 20% have secondary neoplasia (cervical)

surgically staged based on size, invasion, nodal and mets; radical local excision w/ inguinal-femoral lymph node dissection; 25% no palpable nodes and can use sentinel node biopsy

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8
Q

Tx of vulvar CA

A

complete pelvic exam prior, wide local excision w/ inguinal lymph node dissection is Tx of choice.

Stage 1 disease - ipsilateral lymphadenectomy sufficient. II- modified radical vulvectomy; II and IV - radical vulvectomy, bilateral inguino-femoral lymph node dissection and pelvic execration

PreOP radiation and chemo
5yr survival = 75%
Melanoma- Lymphadenectomy rarely preformed- depth is key, METS = 100% mortality
Squamous - + inguinal lymph node = prognosis, >3 bad

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9
Q

preinvasive disease of vagina - vaginal intraepithelial neoplasm (VAIN)

A

premalignant lesion but much less common than VIN or CIN

VAIN 1- limited to epithelium, II -thicker, III- involves> 2/3 epithelium and full thickness abnormalities (carcinoma in situ)

most common as multiracial lesion in vaginal apex associated w/ CIN, cervical CA, condyloma and Hx of HPV
Peak incidence mid-late 40s w/ 50-90% coexistent or prior neoplasia

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10
Q

Dx of VAIN and Tx

A

almost always symptomatic
maybe d/c or poistcoital spotting. Dx due to Pap smear- persistently abnormal paps but no cervical neoplasia

annual pap smears if high grade CIN and hysterectomy to look for VAIN
colposcopy and biopsy

Tx: local excision or laser (r/o invasive), Intravaginal 5 FU is helpful w/ multifocal lesions and immunosuppression

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11
Q

CA of the vagina

A

rare - only 1-2% of malignanies of gyn, secondary more common than primary
squamous most common, adenocarciona, sarcomas and melanomas

clear cell adenocarcinoma in 1970s w/ DES

squamous - ulcerated, nodular, posterior wall and upper 1/3 of vagina; spread lymphatic to inguinal nodes and deep pelvic or direct extension; hematogenous spread potential

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12
Q

Dx and Tx of vaginal CA

A

10% asymptomatic - pruritis, post meno bleeding, positcoital spoting, watter/blodd d/c; can have urinary and GI symptoms
May be diagosed w/ persistent paps abnormal

Squam complicated w/ involved local structures - need pre-op imaging, cystoscope, proctosigmoidoscopy, IVP to assess spread

2cm or lower 2/3rds vagina get external nd internal radiation alone

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13
Q

Dx and Tx of vaginal CA

A

10% asymptomatic - pruritis, post meno bleeding, positcoital spoting, watter/blodd d/c; can have urinary and GI symptoms
May be diagosed w/ persistent paps abnormal

Squam complicated w/ involved local structures - need pre-op imaging, cystoscope, proctosigmoidoscopy, IVP to assess spread

2cm or lower 2/3rds vagina get external and internal radiation alone

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14
Q

Dx and Tx of vaginal CA

A

10% asymptomatic - pruritis, post meno bleeding, positcoital spoting, watter/blodd d/c; can have urinary and GI symptoms
May be diagosed w/ persistent paps abnormal

Squam complicated w/ involved local structures - need pre-op imaging, cystoscope, proctosigmoidoscopy, IVP to assess spread

2cm or lower 2/3rds vagina get external and internal radiation alone

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15
Q

number one killer gyn cancer world wide

A

cervical CA in the developing world

endometrial in the US

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16
Q

CIN - cervical intraepithelia neoplasia

A

premalignant changes in the cervical epithelium that can progress to cervical CA
severity depends on portion of epithelium showing disordered growth and development
-> changes start at basal layer and can expand

CIN 1- lower 1/3; II = lower 2/3rds; III = >2/3 and can expand full thickness of epithelium (Carcinoma in situ)

CIN most commonly occurs during menarche and after pregnancy w/ estrogen simulation of transformation zone

HPV primary cause = 6 and 11 lowest on but 90% condylomas; 16, 18, 31 and 45 high risk onc

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17
Q

Epidem of CIN

A

most commonly diagnosed in 20s (25-35); mtpl and early exposure to HPV, early childbearing, low SES

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18
Q

Dx and screenof CIN

A

asymptomatic, use Pap to sample transformatin zone (squamous-> columnar). Sample the endocervical and ectocervical cells of external os and also endocervical canal w/ city brush

all women >21 start screen at 21, test q3y; >30 can expand to 5 yr w/ HOV co-test; stop age 65-70y if 3 or > normal paps and no CIN 2-3 in past 20y

total hysterectomy can stop unless not CIN2-3, normal 3x can also stop

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19
Q

Abnormal pap smears classes -6

A

HPV cell changes -> nuclear enlargement, multi nucleation, hyperchromasia, pweinuclear cytoplasmic clearing

ASC-US: Atypical squamous cells if undetermined significance
ASC-H: Atypical squad cells - cannot exclude high grade
LSIL: low grade squamous intraepithelial lesion
HSIL: sigh grade squamous intraepithelial lwsion
SCC: squamous cell carcinoma
AGC: Atypical glandular cells

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20
Q

Atypical squamous cells in CIN

A

benign inflame response to infection/trauma -> preinvasive (10-15%);
ASC- H should have colposcopy;
ASC:US should have HPV testing(reflex) -> colposcopy

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21
Q

who gets colposcopy

an additional endometrial biopsy?

A

ASC-H, LSIL, HSIL, AGC

Atypical glandular cells also get endometrial biopsy if >35 of

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22
Q

Screen of 30y/o for HPV and pap w/ only + HPV how does screening change

A

repeat both HPV and pap n 1 yr; depending on result get colposcopy, sputtered and HPV 16 or 18 is positive get a colposcopy

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23
Q

HPV test for high risk lesions (ASC-H, LSIL, HSIL)

A

not done for always high risk HPV types

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24
Q

time course of + paps

A

epithelial abnormalities will regress over 6m-2y, some abnormalities persist at current level, others progress to more serious lesions

ASC and LSIL represent transient infection, HSIL more likely to persost

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25
colposcopy may visulaizw
acetowhite epithelium, mosaicism, punctiations, atypical vessels where they should be biopsy CIN ->1, 2, or3
26
TX of CIN1
repeat cytology q6months for 1 yr, or high risk HPV in 1 yr | Persistent for 2y then offer LEEP
27
TX of CIN2
LEEP procedure or repeat pap+ clop q6m for 2 yrs in young women
28
Tx of CIN3
LEEP procedure or large loop excision of transformation zone; traditionally cold knife conization lesions w/ endocervic TX w/ CKC or 2 stage LEEP to allow more endocervix removed
29
F/u of LEEP and conization
can have cervical stenosis, cervical insufficiency, infection or bleeding persistence rate of II or III is 4% w/ recurrence 10-15% f/u pap q6m w/ pap and repeat pap and colposcopy at 1 yr; normal can return to normal screening for 20yrs
30
Cervical CA
squamous cell - 80% w/ mets by direct extension Adenocarcinoma 20% (clear cell one type) 11000 annually w/ Dx at 53 usually and High risk 16. 18, 31 and 45 cervical CA is AIDS defining
31
clinical manifestations and diagnosis of cervical CA
Usually asymptomatic, most commonly postcoital bleeding if symptoms watery d/c, pelvic pain/pressure, rectal/urinary tract, friable/bleeding cervical lesion, bimanual mass Pap smears do NOT dx CA- need tissue biopsy, need a colposcopy and biopsy
32
TX of CIN1
repeat cytology q 6months for 1 yr, or high risk HPV in 1 yr Persistent for 2y then offer LEEP
33
clinical manifestations and diagnosis of cervical CA
Usually asymptomatic, most commonly postcoital bleeding if symptoms watery d/c, pelvic pain/pressure, rectal/urinary tract, friable/bleeding cervical lesion, bimanual mass Pap smears do NOT dx CA- need tissue biopsy, need a colposcopy and biopsy
34
Cervical CA staging
clinically staged vs surgically staged. Evaluation of invasion into adjacent structures and med - ising exam under anesthesia, CXR, cystoscope, proctoscope, IVP, barium enema -> MRI/CT cannot be used to determine stage; Once a stage has been assigned it does not change based on intraoperative findings and progression 1- confined to cervix(90% survival; II not to pelvic side walls to lower 1/3 vagina(75%); III - walls and L vagina(45%); IV beyond the pelvis, local invasion and METS(20%)
35
Tx of cevical CA
stage 0 and I - simple hysterectomy or cold knife cone; Early: Stage 1a-IIa needs radiation or radical hysterectomy(bilateral pelvic node), parametric, upper vaginal cuff, uterosacral/cardinal ligment local vasc Advance: IIb-IV - chemoradiation w/ both external beam and intracavitary w/ cisplatin based chemo Recurrent- surgery(pelvic exenteration: removal of all pelvic organs -50% survival), usually but also radiation,
36
Endometrial CA - 2 types
4th most common CA, most common gyn CA but curative Tx available w/ early symptoms and accurate Dx modalities obesity, chronic anovulation, nulliparity, late meno, unopposed estrogen use, HTN, Dm all increased risk ``` 2 etiologies: Type 1(80%) Hx of chronic estrogen exposure unopposed progestin (estrogen dependent neoplasms) atypical hyperplasia-> carcinomas (well differentiated w/ low grade nuclei) more favorable ``` Type 2(20%) - estrogen INdependent- occur in w/in background of atrophic endometrium or polyps. High grade nuclear atypia w/ Serous or clear cell histology; p53 mutation
37
Prognosis of endometrial CA
Depth of myometrial invasion key to staging and prognosis; worse w/ >1/2 thickness of myometrium Direct extension most common; lymphatic system w/ sig penetration; shed transtubally through the fallopian tube; hematogenous spread less frequent to liver/lungs/bone Histionlogic grade key(Grade 1- high dif
38
most common endometrial Ca
endometriod adenocarcinoma (75-80%) - 2/2 proliferation of glandular cells also- mucinous, clear cell, papillary serous, squamous
39
Epidemiology and Risk of endometrial CA
premenopausal - 25%, postmenopausal 75%; Avg age is 61 Unopposed estrogen obesity, nulliparity, late meno, chronic anovulation(PCOS), tamoxifen(SERM- partial agonist/weak estrogen in endometrium), also: DM, HTN, CA of breas(unknown BRCA)t/ovary/colon(Lynch II) and FHx endometrial hyperplasia - risk of transformation depends on type Protective: combo OCPs, progestin contraceptives, high parity, pregnancy, physical activity, smoking
40
Hx and PE of endometrial CA
postmeno bleeding or abnormal vaginal bleeding (menorrhagia, postcoital spots, intermenstrual bleeds); 10% nonbloody d/c; pelvic pain, pelvic mass and weight loss Obesity, acanthosis nigricans, HTN, typically NORMAL pelvic exam , advaced-
41
DDx for endometrial CA
abnormal uterine bleeding-> uterine fibroids, endometrial polyps, adenomyoisis, endometrial hyperplasia, ovarian cysts, thyroid dysfunction post menopause- atrophy, exogenous estrogens, in addition; CA responsible for 20% of postmenopausal bleeding amount of blood does not equal risk of malignancy
42
Dx of endometrial CA
endometrial biopsy (90-98%) sensitive; postmeno a transvaginal US can help - thickness 45 and those at risk regardless of age D and C +/- hysteroscope if EMB can't be done TSH, prolactin level and possibly FSH and estradiol; CBC r/o anemia preop. CA125 often pre op and followed; Pap smear- (endometrial cells in 40+ y/o an EMB should be done); pelvic US
43
Tx for endometrial CA
Need surgical staging w/ path confirmation Stage I and II - total abdominal hysterectomy and bilateral salpingo-oohorectomy, pelvic washings, pelvic and para-aortic lymph node resection and complete resection of visible tumor Stage III and IV - malignancy to or beyond the uterine serosa, need pelvic radiation chemo or high dose progestin for recurrent disease F/u- PE q3m for 3y
44
High risk features for endometrial CA Suggests?
radiation even if low stage I and II >50% myometrial invasion, papillary or clear cell tumors, grade 3 tumors, large tumor >2cm, spread beyond uterine fundus, lymphovascular involvement
45
Ovarian CA - 3 types
5y survival 25-45%; 2nd most common gyn CA, lack of screening; 1/70 women avg age 61 Surface epithelium -90%; germ cells; ovarian stroma - Spread by: direct exfoliation (peritoneal-> carcinomatous ileum in the bowels), lymphatic, hematogenous (rare) 5-10% mets from primary - kruckenberg tumor
46
kruckenberg tumor
mets to ovarvian CA from GI, breast or endometrium
47
Pathogenesis of ovarian CA
unclear cause, malignant transformation of ovarian tussle after prolonged chronic uninterrupted ovulation(ovulation ruptures epithelium -> repair mech and can lead to somatic gene deletions and mutations) 10-15% familial CA, mutations in BRCA I mainly w/ small proportion of Pts w/ BRCA2; Lynch II syndrome -> breast, ovarian, colon, endometrial
48
Risk factors for ovarian CA
familial ovarian CA syndome, family Hx, personal Hx of breast CA, uninterrupted ovulation (early menarche infertility, nulliparitym delayed childbearing, late onset menopause). Increasing age Protective:OCPs >5y, breastfeeding, multiparty, chronic anovulation, tubal ligation and hysterectomy (less blood flow)
49
PE and Hx of ovarian CA
asymptomaic, vague, nospeccific complaints-> vague lower abdominal pain, abdominal dissension, bloating, early satiety, GI, urinary frequency, pelvic pressure, ascities-> SOB PE: solid fixed irregular pelvic massm ascitis, Ovarian CA METS= mary joseph nodule (umbilicus)
50
Dx eval of ovarian CA tumor markers
Pelvic US - dx of adnexal mass, CT and MRI of pelvis/abdomen can assist (DON"T percents or cyst aspire) METS disease looked for - barium enema and IV pyelography; Serum tumor markers: CA125, AFP, lactate dehydrogenase (LDH), hCG
51
Staging of ovarian CA
surgically staged -TAHBSO (toal abdom hys, bilat salpingo-oophorctomy), Omenectomy, peritoneal washing, pap smear of diaphragm, sampling of pelvic and para aortic lymph nodes
52
Epithelial cell types- ovarian CA
65-70%; age 20+ serous, mucinous, endometroid, clear cell, brenner, undifferentiated
53
Germ Cell types - ovarian CA
15-20%, 0-25+y teratoma, dysgerminoma, endodermal sinus tumor, choriocarcinoma, embryonal carcinoma
54
Sex cord-stromal types - ovarian Ca
5-10%, all ages granulose-theca cell tumor, stroll-leydig cell tumor, fibroma
55
US of Benign vs malignant of malignant mass
Benign: 8cm, solid or cystic, nodular/papillary components, Multilocular thick septations, doppler flow, bilateral, ascities, peritoneal mass, LAD
56
Epithelial tumors epidemiology
low malignant potential -> serous cystadenocarcinoma (bad) seen in 50s accounting for 6%% of all all ovarian tumors and 90% of ovarian CA Serous most common- CA125 elvaated 80% and used to track Tx and recurrence
57
Staging of Ovarian CA
1- limited to ovaries 2- extention to the pelvis 3 - extension to the abdominal cavity 4- distant METS
58
Tx of epithelial tumors
Surgery mainstay -> TAHBSO w/ omentectomy, cytoreduction/debulking Tx after w/ chemo: carboplatin and paclitaxel; optimal debulking-> cisplatin and paclitaxel chemo 5 yr surrvival rate is 20% overall
59
CA 125 elevated in
gyn CA(epithelia, fallopian, endometrial, endocervical), Non gyn CA: pancreatic, lung, brest, colon Benign gyn: ectopic, endometriosis, fibroids, PID Benign Non-gyn: pancreatitis, cirrhosis, peritonitis, recent laparotomy
60
Germ cell pathogenesis and tumor markers
arise from primordial gem and 95% benign. undifferentiated, totipoten cells -> yolk sac, placenta, fetus benign- cystic mature teratoma(dermoid cyst) - mature tissue w/ skin, hair, teeth w/ sebacious materua dysgerminomas(no differentiation, malig)(50%) -LDH - more common in girls (asian/african) immature teratoma (20%) - N/A endodermal sinus (yolk sac) (20%) -AFP and hCG choriocarcinoma(trophoblast) - hCG *grow rapid and limited to 1 ovary and stage 1 @ diagnosis- curable
61
Epidem and Manifestations of Germ cell tumors
20-25% of all ovarian tumors, acute pelvic pain, pressure symptoms of bladder/rectum or pain from torsion/rupture
62
Tx of germ cell tumors
All curable surgery if benign dermoid cysts w/ ovarian cystectomy or oophprectomy - > usually unilateral Childbearing complete -> TAH/BSO all require multiagent chemo after unless dysgerminomas and immature teratomas Radiation post op - dysgerminomas
63
Sex cord stromal tumors pathogenesis
originate the cells surrounding the oocyte(before differentiation into m/f) or from the ovarian stroma low grade malignancies which can occur at any age; Usually unilateral and rarely recur Granulosa theca - low grade malignancies and most common(70%)~ fetal ovaries, coffee-bean nuclei Cell-enaer bodies-> estrogen Sertoli-leydig - rare ~ testes -> testosterone Ovarian fibroma- mature fIbroblasts -> ascities
64
Call-Exner bodies
granulosa cells w/ grooved "coffee bean" nuclei and cells arranges in small clusters around a central cavity
65
Meigs syndrome
triad of ovarian tumor (fibroma), ascities and R hydrothorax
66
Epidemiology and Clinical manifestations of Sex cord- stromal cells
Ages 40 and 70 w/ avg age 50 Dx; Sertoli-leydig at 40y/o Granulosa cell tumors -> estrogen w/ endometrial hyperplasia and 5% have concurrent endometrial CA Granulosa-theca -> estradiol and inhibin A/B-> feminization, precocious puberty, menstrual irregularities, secondary amenorrhea, post meno bleeding; endometrial hyperplasia and need to sample Sertoli leydig -> androgens (testosterone, androstenedione) w/ virilizing effects w/ breast atrophy, hirsutism, deep voice, acne, clitoromegaly, receding hair
67
Tx of sex cord-stromal tumors
low grade lesions, unilateral and do not recur -> unilateral salpingo-oophorectomy if childbearing complete get hysterectomy and bilateral NO chemo or radiation 5yr survival 70%-90%, slow growing and late recurrence at 15-20y for granulosa
68
Fallopian tube cancer
RARE- progression of tumors similar to ovarian w/ periotoneal spread and ascites Usually adenocarcinoma arising from mucosa, often result of metastasis from primary tumors Caucasion w/ risks of BRCA1/2, nullparity and infertility See: asymptomatic;Latzkostriad-profuse watery d/c, pelvic pain, and pelvic mass Dx: CA125, US Staged surgercially w/ chemo (carboplatin and paclitaxel f/u)
69
Gestational trophoblastic disease def and 4 types
abnormal proliferation of trophoblastic (placental) tissue); maternal tumor results from abnormal fetal tissue; make hCG; sensitive to CHEMO and still fertile molar-80%; persistent/invasive-10-15%; choriocarcinoma - 2-5%; placental site trophoblastic tumors (rare)
70
Hydratidiform moles stats and risks
complete(90%) or partial(10%) - 80% of GTD complete- no fetus; partial - abnormal fetus 1/1000 oregnancies w/ global rates higher in asians Risk: extreme age and Hx of GTD; null parity; diets low in beta-carotene, folic acid and animal fat; smoking, infertility SAB, blood group A, OCP
71
Complete molar pregnancy
90% vs incomplete; 2/2 fertilization of empty egg and 1 normal sperm that replicates; (paternal derived) -> chromosome pattern of 46, XX trophoblastic proliferation, diffuse swelling of chorionic villi and hydropc degeneration -? grape like vesicles filling uterus in absence of fetus villi syncytiotrophoblasts ->hCG >100,000 w/ large theca lutean cyst (~LH) and hyperthyroidism (~TSH); hyperemesis gravidarum and preeclampsia before 20 wks; higher malignent potential -15%
72
Hx and PE of complete mole
irreugular or heavy bleeding **(2/2 tumor separation from decidua), High hCG-> nausea/vomitting, irritability, dizziness, photophobia, (preeclampsia), nervousness, anorexia, tremors (hyperthyroidism) HTN, tachycardia, tachypnea, absence of fetal heart sounds, uterine size > GA, grape like molar clusters in vagina or cervical os e/ blood, bilateral large theca lutein cysts)
73
DDX and eval of complete mole
serum hCG >100,000, pelvic US w/ no fetus or amniotic fluid, "snowstorm" pattern due to chorionic villi, bilateral theca lutein cysts(15%) definitive is intrauterine tisse DDx: mtpl gestations, erythroblastosis fetalis, intrauterine infection, uterine fibroids, threatened abortion, ectopic, normal intrauterine pregnancy
74
Tx and F/u for complete mole
immediate removal of uterine contents w/ D and C. IV oxytocin after, +/- RhoGAM. maybe hysterectomy get baseline CBC, coag, hCG, renal, thyroid and liver tests prior, RH status antihypertensives(beta blockers) symptomatically. serial hCG, 48 hrs post evac + weekly q3w, normal at 14w; subsequent pregnancy have early US and hCG levels
75
PArtial molar pregnancy -
formed w. normal ovum and 2 sperm simultaneous -> tripled karyotype (69, XXY) focal hydropic villi and trophblastic hyperplasia w/ cytotrophoblast(not making hCG)-> normal/slight elv hCG levels presence of a fetus on histo w/ amniotic fluid and HR. mtpl anomalies, syndactyl and hydrocephalis and growth restricted, SAB late 1st/early 2nd tri; LOW malign potential
76
Hx and PE of partial molar pregnancy
delayed menses and pregnancy diagnosis, NORMAL/slight elv hCG-> less severe symptoms 90% w. vaginal bleeding from miscarriage or ab bleeding 1st tri; diagnosed later Typically normal exam, may have coexistent fetus w/ HR. IUGR and size
77
Diagnosis and Ddx of partial molar pregnancy
Heg will be normal/slight elv. pelvic US may show fetus w/ HR , congenital malformations and IUGR. Amniotic fluid is REDUCED. -- -intrauterine tissue may contain anechoic spaces juxtaposed against chorionic villi to look like swiss cheese; need path exam
78
Tx and f/u of incomplete molar pregnancy
D and C.
79
Malignant gestational trophoblastic disease
molar (complete and incomplete) typically benign but 20% transform potenital for local invasion (3 types) persistent invasive (75%); Choriocarcinoma (25%) and PSTT(rare) malignancy occurs months to years after mole (25% after normal pregnancy, 25% after miscarriage/ectopic). can be metastatic v nonmetastaic (1-uterus, 2 to pelvis vagina, 3 -lung, 4 distant), good or poor prognosis
80
Tx of malignant gestational trophoblastic disease
chemo- NO surgery except is high risk of=r PSTT serum hCG monitotes
81
persistent invasive moles
follow D and C of molar pregnancy. characterized by penetration of large, swollen (hydropic) villi and trophoblasts into the myometrium, sometime through -> rupture, hemoperitoneum and anemia. Rarely mets and can spontaneous regress 1 in 15000 pregnancies
82
Hx and PE of persistent invasive mole
plateauing or rising hCG after treatment for molar pregnancy asymptomatic but can have abnormal uterine bleeding exam similar to molar pregnancy- high hCG, large uterine size and prominent theca lutein cyst
83
Dx and Tx of persistent intrauterine mole
hCG levels and pelvic US key US-> 1+ intrauterine masses w. possible myometrium invasion; doppler shows high vascular flow Tx- single agent chemo: methotrexate or actinomycin D. If mets: low risk -> single agent, high risk -> multi agent F/u with hCG and reliable contraception
84
Choriocarcinoma pathogen and epidemiology
malignant necrotizing tumor- arise wks to yrs after any pregnancy; pure epithelial tumor ->histo: sheets of anaplastic cytotrophoblasts and syncytiotrophoblasts in absence of chorionic villi Spreads hematogenously and often METs 1/20,000-40000, > Asian/african
85
PE and Hx of choriocarcinoma
late post partum bleeding (after 6-8 wks) but also can have irregular uterine bleeding often present METS-> lungs (cough, dypsnea, resp distress), CNS (HA, dizzy, blackout,) hepatic, urologic, GU, Vaginal PE-? uterine enlargement and masses
86
Dx and DDx fo choriocarcinoma
measure hCG and assess for METS w/ CBC, coag, renal and hepatic function tests pelvic US-> uterine masss w/ hemorrhave and nectosis. High vascular -> + doppler. CXR or CR of abdomen/chest or MRI (brain?) DDx: great imitator-> dx delayed due to context outside of pregnancy(wks to yrs)
87
Tx and f/u of choriocarcinoma
Tx w/ single agent chemo, poor prognosis gets multi agent chema F/u w/ hCG and reliable contraception
88
Placental site trophoblastic tumors
Rare and arise from placental implantation site. intermediate cytotrophoblasts from placental site infiltrate myometrium -> vessels Histo see absence of villi and prolif of intermediate trophoblasts and production of hPL (human placental lactogen) See irregular vag bleeding and maybe enlarged uterus LOW chronic hCG w/o syncutiotophoblast. highr hPL. pelvic US to see mass Tx: NOT as sensitve to chemo but rarely mets beyond uterus -> hystorectomy