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OB/GYN > Gyn-Onc > Flashcards

Gyn-Onc Flashcards

1
Q

Preinvasive neoplastic disease of the vulva is divided into two categories

A

squamous
- vulvar intraepithelial neoplasia

nonsquamous intraepithelial neoplasias

  • Paget disease
  • melanoma in situ
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2
Q

Vulvar intraepithelial neoplasia

- definition

A

= cellular atypia contained within the epithelium

Characterized by:

  • loss of epithelial cell maturation,
  • cellular crowding,
  • nuclear hyperchromatosis,
  • abnormal mitosis
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3
Q

How is the lesion of VIN determined?

A

Mild - severe dysplasia based on depth of epithelial involvement

VIN 1 = koilocytic atypia
VIN 2 &3 = Usual VIN vs Differentiated VIN

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4
Q

How many % of pts with VIN will have coexisting invasive carcionma (penetrated BM)

A

20%

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5
Q

Risk factors for VIN

A

HPV 16, 18

  • 80-90% VIN will have DNA fragments from HPV
  • 60% of women w/ VIN will have cervical neoplasia too

Cigarette smoking

Immunodeficiency

Immunosuppression

Most VIN are in premenopausal women (75%)

  • median age = 40 yo
  • incidence decreases as age increases
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6
Q

VIN has 2 distinct forms - what are they?

A

Younger premenopausal women
- more likely to have more aggressive multifocal lesions that rapidly become invasive and are associated with HPV 75% to 100% of the time.

Older postmenopausal women

  • more likely to involve focal lesions that are slow to become invasive
  • not typically associated with HPV
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7
Q

Sx of VIN

A
  • vulvar pruritus or vulvar irritation
  • palpable abnormality,
  • perineal or perianal burning,
  • dysuria

Often, these women would have been examined several times and diagnosed with candidiasis, but experience no relief of symptoms with antifungal treatments or topical steroids.

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8
Q

Any time a pruritic area of the vulva does not respond to topical antifungal creams - what should be done?

A

further evaluation with vulvar biopsy should be undertaken

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9
Q

Tx VIN

A

VIN + no evidence of invasion

  • wide local excision
  • disease free margin of at least 5-10 mm

VIN + multifocal disease

  • simple vulvectomy or skinning vulvectomy
  • use split thickness grafts to replace excised lesions
  • can use laser vaporization to eradicate multifocal lesions
  • younger –> 5-FU topical and imiquod but only 40-50% effective
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10
Q

Follow up for VIN

A

Recurrence 18-55%
- more common w/ multifocal lesions, mod-severe dysplasia, + margins

Colposcopy of entire genital tract q6 months for 2 years
- after 2 years, do this yearly

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11
Q

Paget disease of the vulva - age of presentation

A

50-80 yo

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12
Q

Is extramammary paget disease of the invasive? Does it recurr?

A

NOT invasive usually

Tends to recurr locally

Only 20% of pts w/ pagets NOT of breast will have underlying adenocarcionma
- mets common with this

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13
Q

Dx Paget disease of vulva

A

Lesions consistent w/ chronic inflammatory changes

Usually there’s a long standing pruritus that accompanies velvety red lesions of skin —> eczematous and scar into white plaques

Usually > 60 yo

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14
Q

Tx paget disease of vulva

A

Wide local excision if not invasion

BE CAREFUL! It is fatal if it spreads to lymph nodes

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15
Q

1 vulvar cancer

A

Squamous cell carcionma

Most are on labia majora

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16
Q

Spread of vulvar cancer is via

A

lymphatics –> superficial inguinal lymph nodes

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17
Q

Vulvar carcinoma accounts for what % of GYN cancers?

A

5%

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18
Q

Staging of vulvar carcionma

A

Surgically staged

  • radical local excision + inguino-femoral LN dissection
  • if superficial (< 1 mm) and unilateral disease, can forego unilateral LN dissection
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19
Q

Tx vulvar carcionma

A

For all

  • wide radical local excision
  • LN dissection

+

Stage 1
- ipsilateral lymphadenectomy

Stage 2

  • modified radial vulvectomy
  • resection LN

Stage 3 + 4
- radical vulvectomy

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20
Q

Tx Melanoma of the vulva

.

A

occurs predominantly in postmenopausal Caucasians

It can be treated similarly to SCC, except that lymphadenectomy is rarely performed

Depth of invasion is the key prognostic factor.

Once the melanoma has metastasized, the mortality rate is near 100%

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21
Q

The 5-year survival rate for all patients after surgical treatment of invasive SCC of vulva is approximately

A

75%

The most important prognostic factor is the number of positive inguinal lymph nodes

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22
Q

Vaginal intraepithelial neoplasia (VAIN) is a

A

premalignant lesion similar to that of the vulva and cervix.

However, VAIN is much less common than either VIN or CIN.

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23
Q

Dx VAIN

A

Usually asymptomatic
- if sx: vaginal d/c or postcoital spotting, abnl pap smear

  • suspicion of vaginal neoplasia should be raised in patients with persistently abnormal Pap smears but no cervical neoplasia detected on colposcopy or cervical biopsy.
  • Pts s/p hysterectomy for a history of high grade CIN should continue to have annual Pap smears to screen for VAIN until three consecutive negative Pap tests have been obtained
  • VAIN can be diagnosed with a thorough colposcopy of the cervix (if present) and upper vagina using both acetic acid and Lugol’s solution
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24
Q

Tx VAIN

A
  • local excision or laser ablation

Intravaginal 5-FU useful for tx pts w/ multifocal lesions and immunosuppression

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25
Q

Most types of vaginal cancer

A

Squamous cell carcinoma
- may appear ulcerated, nodular, or exophytic
- usually involves the posterior wall and upper one-third
of the vagina.

Spread may occur via lymphatic drainage to the inguinal nodes and deep pelvic nodes or via direct extension to the bladder or rectum.

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26
Q

What vaginal cancer was found to be associated w/ in utero exposure of diethylstilbestrol?

A

Clear cell adenocarcionma

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27
Q

The cause of SCC of the vagina is

A

unknown

Similar to vulvar and cervical cancers, vaginal cancers can be associated with HPV infection.
- However, because the vaginal mucosa is not undergoing constant metaplasia like cervical epithelium, the vagina is much less susceptible to the oncogenic effects of the virus

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28
Q

Does vaginal cancer have better 5 years survival than vulvar cancer?

A

NO!

40-55%

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29
Q

Tx vaginal carcinoma

A

Small stage I malignancies of the upper vagina can be treated with surgical excision

all other lesions are treated with internal and external radiation therapy

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30
Q

When does CIN more commonly occur?

A

menarche and after pregnancy

  • During menarche, the production of estrogen stimulates metaplasia in the transformation zone (TZ) of the cervix.
  • These metaplastic cells are more susceptible to oncogenic factors
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31
Q

Risk factors for cervical dysplasia include

A
  • characteristics that predispose to multiple and early
    exposure to HPV (early intercourse, multiple sexual partners, early childbearing, “high-risk” partners, low socioeconomic status, and sexually transmit-ted infections).
  • cigarette smoking
  • Immunodeficiency / Immunosuppression
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32
Q

Screening guidelines for cervical cancer

A

All women should begin cervical cancer screening at age 21 regardless of risk factors, including age of onset of sexual activity.

Onset of sexual intercourse

  • if HIV +, SLE, organ transplants
  • q6 months x2, then annually

Age 21-29
- pap test q3 years

> 30 yo

  • screen with both a Pap test and an HPV test
  • –if both (-) –> q5 yr screening Pap + HPV test
  • if HPV testing NOT available, screen w/ pap smear q3 yr

> 65 yo

  • stop screening if >=3 nl Pap tests in a row, have not had CIN 2/3 or higher in past 20 years
  • if had CIN 2/3, screen for 20 years after; stop then or at 65, whichever is later

Total hysterectomy for benign indications + no hx CIN 2/3 or higher
- can stop pap tests at time of hysterectomy

Total hysterectomy + hx of CIN 2 or 3
- stop Pap smear after 20 yr or age 65, whichever later

If supracervical hysterectomy, need to continue routine Pap test screening appropriate for age

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33
Q

If pt is Negative for intraepithelial lesion and malignancy pap, High-risk HPV positive

What do you do?

A

Repeat both pap and HPV in 1 year

OR

screen for HPV 16 and 18.

If either is positive then immediate colposcopy

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34
Q

ASC-US (Atypical squamous cells of undetermined significance)
+
High-risk HPV negative

What do you do?

A

Continue routine pap smear screening

You always get an HPV status if the pap is abnormal/ASCUS

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35
Q

When do you do colposcopy and cervical biopsies?

A

You do a colpo for all ASCUS that are also HPV + and anything higher

ASC-US + High-risk HPV positive

ASC-H (Atypical squamous cells cannot exclude high-grade squamous intraepithelial lesion)

LSIL (Low-grade squamous intraepithelial lesion)

HSIL (High-grade squamous intraepithelial lesion)

No need to do HPV for anything higher than ASCUS (ASCH, LSIL, HSIL)

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36
Q

When do you do colposcopy + cervical bx + endometrial bx?

A

atypical glandular cells

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37
Q

Pap smear reveals SCC - what do you do?

A

Colposcopy , HPV screen, and cervical biopsies, potential cold-knife conization (CKC)

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38
Q

When do you not test for high risk HPV?

A

no high-risk HPV testing is recommended for ASC-H, LSIL, and HSIL, because nearly all of these lesions will be positive for high-risk HPV types

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39
Q

Changes that can be seen on colposcope stained with acetic acid on cervix

A

Acetowhite epithelium
Mosaicism
Punctation
Atypical vessels

Bx all these lesions and send to path

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40
Q

% regress spontaneously in CIN I - III

A

CIN 1 = 60

CIN 2 = 40

CIN 3 = 30

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41
Q

Management of

CIN
CIN II
CIN III

A

CIN I

  • repeat Pap q6 months for 1 year OR
  • High risk HPV screen in 1 yr…..if persistent x 2 year, offter LEEP procedure (loop electrosurgical excision procedure)
  • if all paps WNL, can return to pap test appropriate for age

CIN II

  • LEEP OR
  • repeat pap + colpo q6months for 2 years for young women

CIN III
- LEEP

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42
Q

Surgical excision options for cervical dysplasia based on characteristics of lesion or patient

  • when use:
  • LEEP?
  • laser conization?
  • Cold knife conization?
A

LEEP
- if confined to ectocervix

Laser conization

  • large lesion
  • upper vagina involved

LEEP (2 stage) or CKC
- endocervix involved

excisional procedure, such as cold knife biopsy or LEEP, is not warranted without a tissue diagnosis of dysplasia

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43
Q

Types of cervical cancer

A

Squamous cell (80%)

Adenocarcionma (20%) - usually DES exposure if clear cell

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44
Q

How much does routine pap smear + HPV typing decrease risk of cervical cancer?

A

90%

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45
Q

High Risk HPV serotypes

A

16
18
31
45

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46
Q

Sx of cervical cancer

A

1 sx = postcoital bleeding

Early disease = asymptomatic

Mass on bimanual
Abnl vaginal bleeding

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47
Q

Dx cervical cancer

A

Tissue bx s/p abnormal pap or lesion found

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48
Q

Cervical cancer staging

A

ONLY GYN cancer that is CLINICALLY staged
- cannot use MRI or CT to stage

Stage w/ :

  • exam under anesthesia
  • CXR
  • cystoscopy
  • proctopscopy
  • IVP
  • barium enema

Stage I
- confined to cervix

Stage II
- beyond cervix but not to pelvic side walls or lower 1/3 of vagina

Stage III
- extend to pelvic sidewalls or lower 1/3 vagina

Stage IV
- extension beyond pelvis, invasion into local structures (eg bladder, rectum) or distant mets

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49
Q

Tx cervical cancer

A

Stage 0 + 1

  • simple hysterectomy
  • cold knife cone if want to maintain fertility
  • 5yr survival = 85-90%

Stage II

  • radial hysterectomy or radiation
  • 5yr survival = 60-75%

Stage IIb - IV

  • Chemoradiation (cisplatin + radiation)
  • 5yr survival as low as 15%
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50
Q

Tx recurrence cervical cancer

A

If only surgery 1st round –> radiation to tx

If already radiated –> surgery + pelvic exenteration (remove all pelvic organs)

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51
Q

Classification of Ovarian neoplasms

A

By cell type

Epithelial

  • Serous (#1) cystadenoma / cystadenocarcionma
  • Mucinous (#2) cystadenoma / cystadenocarcionma
  • Endometriod (M) - assoc w/ endometriosis
  • Brenner

Germ cell

  • Teratoma
  • Dysgerminoma (M)
  • Embryonal carcionma
  • –Endodermal sinus (yolk sac) - extraembryonic tissues
  • –Choriocarcionma (M) - trophoblastic (placental) tissues
  • –Immature teratoma - embryonic (fetal) tissues

Stromal cell

  • Granulosa theca (M)
  • Sertoli-Leydig (M)
  • Lipid cell fibroma
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52
Q

Malignant epithelial serous tumors (serous cystadenocarcionma)

A

1 malignant epithelial cell tumors

Can arise from benign serous cysadenoma

Psammoma bodies

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53
Q

Malignant mucinous epithelial tumor (mucinous cyadenocarcionma)

A

2 malignant epithelial cell tumor

Lower rate of bilaterality
Associated w/ pseudomyxomatous peritonei = widespread peritoneal extension with thick, mucinous ascites

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54
Q

Meigs syndrome

A

Ascites

R pleural effusion

Benign ovarian fibroma (stromal neoplasm)

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55
Q

Genes increasing risk of ovarian cancer

Risk factors of ovarian cancer

A

BRCA 1
HNPCC

Risk factors:

  • long periods of uninterrupted ovulation (early menarche, infertility, nulliparity, delayed childbearing, lateonset
    menopause)
  • older age
  • use of talcum powder on the perineum
  • obesity (BMI > 30).
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56
Q

1 ovarian cancers in women < 20 yo

A

Germ cell tumors

Blacks and asians more common than caucasians

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57
Q

When is CA-125 useful in ovarian cancer?

A

Postmenopausal women with pelvic mass can predict higher likelihood of malignant neoplasm w/ CA 125
- but nl CA 125 doesn’t r/o cancer

Not as useful in premenopausal becausse many benign conditions (PID, uterine leiomyomata, etc) can cause increased CA 125

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58
Q

Tumor markers for germ cell tumors

A

hCG - choriocarcionmas
AFP - endodermal sinus
LDH - dysgerminomas

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59
Q

Dysgerminomas

A

Germ cell malignant tumor of ovary

Unilateral
#1 germ cell tumor in pts w/ gonadal  dysgenesis

Radio + chemosensitive

Spread via lymphatics

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60
Q

What is esp important in ovarian tumors such as granulosa tumor?

A

Endometrial sampling

These tumors can secrete estrogen –> endometrial hyperplasia –> carcionma

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61
Q

What do the stromal cell malignant ovarian cancers secrete?

A

Graunlosa –> estrogen

Sertoli Leydig –> testosterone

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62
Q

Krukenberg tumor

A

Ovarian tumor that is metastatic from other sites like the GI and breast

Usually signet ring cell type
Bilateral

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63
Q

How does ovarian cancer usually spread

A

Direct exfoliation of malignant cells from ovaries

Usually follow path of peritoneal fluid

Lymphatic spread can occur
Heme is for more rare and distant mets to lungs and brain

64
Q

Protective factors for ovarian cancer

A 
Oral contraceptives > 5 yrs
Breastfeeding
Multiparity
Chronic anovulation
Tubal ligation
Hysterectomy
65
Q

1 diagnostic tool for investigating adenexal mass

A

Pelvic US

DO NOT do paracentesis and cyst aspiration because malignant cells can spread via direct exfoliation

66
Q

Tx epithelial tumors

A

Surgery

  • TAHBSO
  • omentectomy
  • cytoreduction
  • debulking
  • paraaortic LN sampling

Chemo combo
- Carboplatin + paclitaxel

CA 125 and CT to evaluate success of treatment

Tumor stage is most important for survival rate

67
Q

Most common type of germ cell tumor

A

Benign cystic mature teratoma

68
Q

Epithelial vs germ cell tumors

A

Germ cell tumors

  • grow rapidly
  • usually unilateral
  • in young women, esp the malignant ones
  • usually at stage 1 at diagnosis
  • better prognosis

Epithelial cell tumors

  • tend to be in 6th decade
  • bilateral
69
Q

Tx germ cell tumors

A

Surgery
- unilateral salpingo-oophorectomy

Chemo
- bleomycin + etoposide + cisplatin

70
Q

carl exner bodies

A

In granulosa cell tumors

Have groove coffee-bean nuclei in cells arranged in small clusters around central cavity

PATHOGNOMONIC for granulosa cell

71
Q

Tx stromal tumors

A

Surgery
- unilateral salpingo-oophorectomy

NO chemo or radiation

72
Q

Fallopian tube cancers are mostly…

A

adenocarcionmas

Bilateral in 10% usually 2/2 mets

73
Q

Latzko’s triad

A

Profuse watery d/c

Pelvic pain

Pelvic mass

In fallopian tube cancer, pathognomonic

74
Q

Hydrops tubae profluens

A

Pathognomonic for fallopian tube cancer

Spontaneous or pressure induced d/c or water or blood tinged vaginal d/c resulting in shrinkage of adenexal mass

75
Q

Tx fallopian tube cancer

A

Same as epithelial ovarian cancer

Surgery

  • TAHBSO
  • omentectomy
  • cytoreduction
  • debulking
  • paraaortic LN sampling

Chemo combo
- Carboplatin + paclitaxel

76
Q

Types of endometrial cancer (2)

A

Type I = estrogen dependent neoplasm

  • most common = 80%
  • occurs in women with a history of chronic estrogen exposure unopposed by progestin
  • usually well differentiated, more favorable prognosis

Type II = estrogen independent neoplasm

  • less common = 20%
  • usually occur within background of atrophic endometrium or polyps
  • high grade
  • many assoc w/ p53 suppression
77
Q

Spread of endometrial carcionma

A

4 primary routes of spread.

#1 common
- direct extension of the tumor downward to the cervix or outward through the myometrium and serosa.

2) Lymphatic –> pelvic and paraaortic LN
3) Exfoliated cells may also be shed transtubally through the fallopian tubes to the ovaries, parietal peritoneum, and omentum.
4) Hematogenous spread occurs less frequently, but can result in metastasis to the liver, lungs, and/or bone.

#1 place to mets = lungs
- that's why do CXR always
78
Q

1 type endometrial cancer

A

endometrioid adenocarcinoma (75% to 80%).

79
Q

Most important prognostic factor for endometrial carcinoma

A

Histologic grade

Grade 3 = More than 50% of the tumor shows a solid growth pattern = poorly differentiated

80
Q

Risk factors endometrial cancer

A 
unopposed estrogen exposure, 
obesity (higher conversion to estrogen 2/2 happening in fat cells, many are anovulatory)******* - most impactful
nulliparity, 
late menopause, 
chronic anovulation,
tamoxifen use

diabetes mellitus;
hypertension;
cancer of the breast, ovary, or colon;
family history of endometrial cancer

81
Q

How long after you stop OCPs are they still protective for endometrial cancer?

A

15 years!

82
Q

Protective factors for endometrial cancer

A 
OCPs
high parity
pregnancy
exercise / skinny
SMOKING! (don't encourage though - increases hepatic metabolism of estrogen)
83
Q

Endometrial thickness of what is indicative of low risk for malignancy?

A

=< 4 mm
- These women do not require endometrial bx unless their bleeding is persistent/recurrent or they are at high risk for malignancy.

Persistent abnormal bleeding, even in the setting of normal imaging warrants a tissue diagnosis for
women ≥ 45 and those at risk for malignancy regardless of age

84
Q

Initial workup for woman with abnormal vaginal bleeding includes…

A

office endometrial biopsy (EMB) has an accuracy of 90% to 98%

TSH
Prolactin
FSH
Estradiol

CA-125 - Very high CA-125 levels are suggestive of spread beyond the uterus.

up-to-date Pap smear

Pelvic US

D&C for further eval

85
Q

Tx endometrial cancer

A

TAH-BSO,
pelvic and para-aortic LN sampling

Radiation if higher stage

Treatment options for recurrent disease are radiotherapy
(if not previously radiated), chemotherapy, or highdose
progestin therapy

CXR to look for lung mets

86
Q

Most cases of endometrial ca recur within

A

3 years of tx

87
Q

1 reason for abnormal vaginal bleeding

A

endometrial atrophy

88
Q

Gestational trophoblastic disease

  • what is it
  • major classifications
A

abnormal proliferation of trophoblastic (placental) tissue.

molar pregnancies (80%),
persistent/invasive moles (10% to 15%),
choriocarcinoma (2% to 5%),
very rare placental site trophoblastic tumors (PSTTs).

89
Q

Risk factors for GTD

A

< 20 yo
> 35 yo (high risk)

Previous GTD
Nulliparity

Diet low in beta-carotene, folic acid, and animal
fat

blood group A,
OCP use

90
Q

Pathogenesis of COMPLETE mole

A
  • fertilization of an enucleate ovum or empty egg, one whose nucleus is missing or nonfunctional, by one normal sperm which then
  • OR rarely - fertilization of an empty egg by two normal sperm.

Usually 46XX

Placenta
- noninvasive trophoblastic proliferation associated
with diffuse swelling of the chorionic villi = hydropig degeneration is grape like!

HCG

  • abnormal proliferation of the syncytiotrophoblasts that produce hCG –> causes extremely high hCG
  • can cause hyperemesis gravidarum
  • alpha subunit of hCG is like LH, FSH, TSH —–> can cause:
  • —theca lutein cysts
  • —hyperthydoidism

Fetus
- none

91
Q

Complete vs partial mole - which one has higher malignant potential?

A

Although most molar pregnancies are benign, complete

moles have a higher malignant potential than do partial moles

92
Q

most common presenting symptom of molar pregnancy

A
  • irregular or heavy vaginal bleeding during early pregnancy
    (97%).
  • 2/2 separation of the tumor from the underlying decidua, resulting in disruption of the maternal vessels.
93
Q

Dx complete molar pregnancy

A
  • High hCG —-> higher hCG means bigger tumor
  • Confirm w/ US —> no fetus or amniotic fluid seen, will see snowstrom pattern 2/2 swelling chorionic villi
  • definitive = path exam after take out
94
Q

Tx complete molar pregnancy

A

D&C

IV oxytocin s/p D&C to minimize blood loss

Even though no fetal tissue is present, Rh Ig should be given to all Rh-negative women.

Hysterectomy if no longer want children
- eliminates risk of local invasion; but does not prevent mets of disease

95
Q

F/u with Complete molar pregnancy

A

Excellent cure rate

Serial hCG titers

  • 48 hrs after D&C
  • weekly until (-) x 3 consecutive weeks
  • then monthly for 6 months

Plateau or rise in hCG during monitoring or hCG > 6mo later = persistent/invasive dz

DEFINITELY prevent preggers during f/u period

96
Q

Pathogenesis of partial mole

A
  • normal ovum is fertilized by two sperm simultaneously
  • 69,XXY

Placenta

  • focal hydropic villi
  • trophoblastic hyperplasia mainlyof CYTOtrophoblast

hCG

  • cytotrophoblasts don’t make hCG
  • hCG usually nl or only slightly higher

Fetus
- yes! amniotic fluid, HR may be there too

97
Q

Dx partial mole

Tx partial moles

F/u partial mole

A

Dx = pathologic examination of the intrauterine tissue once the uterus is evacuated

Tx = D&C

F/u

  • serial hCG
  • less time for partial mole to normalize hCG
98
Q

Are complete and partial moles benign or malignant?

A

Benign!

Have potential to transform to malignant choriocarcionma, invasive mole, or PSTT!

99
Q

Tx malignant GTD

A

Chemo!

  • MTX
  • atinomycin-D

NO surgery because it is super chemo sensitive

100
Q

Invasive moles are characterized by

A

the penetration of large, swollen (hydropic) villi and trophoblasts into the myometrium.

101
Q

Dx malignant GTD

A

Pelvic US

hCG

102
Q

Choriocarcinoma pathogenesis/characteristics

A
  • malignant necrotizing tumor that can arise weeks to years after any type of pregnancy.
  • dont have to have molar pregnancy to get
  • is pure epithelial tumor

Histo:
- sheets of anaplastic cytotrophoblasts and syncytiotrophoblasts in the absence of chorionic villi.

Hematogenous spread

103
Q

Presentation of choriocarcionma

Tx?

A

Often vaginal bleeding

Often present with mets

Need to do full body mets workup

Tx - chemo

104
Q

Placental site trophoblastic tumor characteristics/pathogenesis

A
  • arise from the placental implantation site
  • cytotrophoblasts from the placental site infiltrate the myometrium and then invade the blood vessels.

Histo:

  • NO villi and the proliferation of intermediate trophoblasts
  • excessive production of human placental lactogen
105
Q

Dx PSTT

A
  • NOT hCG b/c no prolif of syncytiotrophoblasts
  • hPL may be used as a diagnostic tool.
  • pelvic US
106
Q

Tx PSTT

A

NOT chemosensitive

But rare mets beyond uterus

Tx = hysterectomy
Multiagent chemotherapy is given 1 week after surgery to prevent recurrent disease.

107
Q

When malignant GTD is encountered after a nonmolar pregnancy, the diagnosis is almost always

A

choriocarcinoma and rarely placental site trophoblastic tumor.

108
Q

Pstt- Stage III is defined as

A

pulmonary metastasis with or without uterine, vaginal, or pelvic tumor metastasis

109
Q

Bx choriocarcinoma?

A

NO!

Because metastatic choriocarcinoma is quite vascular, suspicious lesions should never be biopsied.
–Tissue diagnosis is the standard in establishing a diagnosis of almost all malignancies, with the exception of choriocarcinoma.

Only a positive Beta-hCG in a reproductive-aged woman who has a history of a recent pregnancy (term, miscarriage, termination, mole) is necessary to establish the diagnosis.

110
Q

The risk of having a molar pregnancy is increased in women with

A

two or more miscarriages.

111
Q

Major blood supply to breast

A

Internal mammary

Lateral thoracic A

112
Q

Nerves of breast at risk of injury during surgical dissection

A

Intercostobrachial N - sensation to upper medial arm

Long thoracic N - serratus anterior - winged scapula

Thoracodorsal N - lat dorsi

Lateral pectoral N - pec major and minor

113
Q

What does estrogen and progesterone do to the breast?

Prolactin? Oxytosin?

A

Estrogen - ductal development + fat deposition

Progesterone - lobular-alveolar (stromal) development that makes lactation possible

Prolactin - milk production

Oxytocin - milk letdown

114
Q

When to start mammos?

A

Age 40

115
Q

Med to tx mastalgia

A

Danazol (only one approved!)

116
Q

Most concerning type of nipple discharge

A

Spontaneous
Bloody
Serosanguineous

Unilateral
Persistent
From single duct
Assoc w/ mass

117
Q

What nipple discharge is usually benign?

A

Bilateral
Nonbloody
Multiductal secretion

118
Q

1 reason for bloody nipple discharge

A

Intraductal papilloma

119
Q

Galactorrhea is associated with

A

Pregnancy
Pituitary adenomas
Hypothyroidism
Stress

Meds:
OCPs
AntiHTN
Antipsychotics

120
Q

Serous discharge of nipple ddx

A

Nl menses
OCPs
Fibrocystic change
Early pregnancy

121
Q

Yellow discharge ddx

A

Fibrocystic change

Galactocele

122
Q

Green sticky discharge ddx

A

Duct ectasia

123
Q

Purulent discharge ddx

A

Superficial or central breast abscess

124
Q

What should you do after you find bloody discharge of nipple?

A

Guaiac

Cytologic eval

125
Q

Preferred imaging for breast mass eval

A

> 30 yo - mammo

< 30 yo - US

126
Q

Mass on palpation + mass on mammo or US…what next?

A

Tissue sample!

< 30 yo

  • FNA
  • Excisional bx if FNA doesn’t have fluid or tissue or if cytology or histo is nondiagnosed

> 30 yo
- core needle bx

127
Q

Pain breast mass
Multiple
Usually bilateral

Changes w/ menstruation

A

Fibrocystic change

128
Q

What is fibrocystic change due to?

Associated cancer risk?

Ages?

A

Due to exaggerated stromal response to hormones and growth factors

No associated cancer risk

30-40 yo

129
Q

Tx fibrocystic change

A

No caffeine

Support bra

Primrose oil
Vit E
Vit B6
Danazol
Progestins
Bromocriptine
Tamoxifen
130
Q

Usually solitary, but can be multiple breast masses

Well circumscribed
Mobile
Firm lesions
Rubbery
NON-tender

Bilateral 25% of time

Can change lesion during menstrual cycle

A

Fibroadenoma

131
Q

Fibroadenomas

  • age
  • tx
A

15-35 yo

Most common benign tumors of breast

Tx:

  • Usually watch clinically if no fhx breast cancer
  • FNA for cytology
  • if confirmed on bx + asymptomatic —> watch
132
Q

Large bulky mobile mass
Painless
Well circumscribed

Rapid growth

A

Cystosarcoma phyllodes

133
Q

Cystosarcoma phyllodes

  • what is it
  • concerning for malignancy?
  • dx
  • tx
A

Rare variant of fibroadenoma
- epithelial + stromal prolifereation

Is concerning for malignancy

Dx - core needle bx

Tx - wide local excision + 1cm margin
- simple mastectomy for large lesions not able to widely excise

134
Q

Bloody nipple discharge

Solitary lesion

Benign

A

Intraductal papilloma

135
Q

Intraductal papilloma

  • traits
  • dx
  • tx
A 
Involves epithelial lining of lactiferous duts
# cause of bloody nipple discharge

Dx
- cytology of d/c

Tx

  • excision of involved ducts
  • usually not malignant transformation possible
136
Q

Usually post-menopause

Nipple d/c (multicolored, sticky)

Noncyclic breast pain

Nipple retraction

A

Mammary duct ectasia (plasma cell mastitis)

137
Q

Mammary duct ectasia (plasma cell mastitis)

  • traits
  • dx
  • tx
A

Subactue inflammation + fibrosis of ductal system —-> dilated mammary ducts

Dx

  • mammo
  • excision bx

Tx

  • usually improve w/o tx
  • abx if infected
  • excision of inflammed area
138
Q

Breast cancer risk factor

A

Older age

Personal hx breast cancer
Fhx breast cancer

Exposure to ionizing radiation of chest

Younger age menarche
Nulliparity
Later date of 1st live birth
Later age at menopause
----cumulative lifetime estrogen exposure

Use of hormonal replacement therapy > 5yrs

DOES NOT INCREASE WITH:

  • OCP
  • caffeine
  • breast implants
  • hair dyes
  • electric blankets
139
Q

Preventative factors for breast cancer

A

Early preggers

Prolonged lactation

Exercise

Abstinence from EtOH

Low fat diet

Tamoxifen

140
Q

LCIS

  • traits
  • epi
  • dx
  • tx
A

Prolif of malignant epithelial cells
Contained within breast lobules - no invasion of stroma

Multicentric
Bilateral (90%)
Pre-malignant

Epi - ~ 40 yo, premenopausal

Dx

  • incidentally on bx for another findings
  • NOT palpable
  • NOT seen on mammo

Tx

  • observation
  • ppx chemoprevention (SERMs)
  • b/l mastectomy
141
Q

DCIS

  • traits
  • epi
  • dx
  • tx
A

Prolif of malignant epithelial cells in mammary ducts w/o spread to breast stroma
More common than LCIS
More progressive to invasive carcionma than LCIS

B/l rare

Epi - ~50 yo

Dx

  • screening mammo = clustered microcalcification
  • neeld loc bx
  • excision bx

Tx

  • surgical excision of all microcalcifications w/ wide margins
  • simple mastectomy if large
  • radiation therapy - but no impact on survival, just dec risk local recurrence
142
Q

Paget disease of the nipple

A

Usually occur w/ DCIS or invasive carcionma

Malignant cells enter epidermis of nipple –> eczematous changes of nipple

143
Q

Inflammatory breast carcinoma

A

Very aggressive

Dermal lymphatic invasion

Sx

  • erythema
  • edema
  • warmth
  • peau d orange
144
Q

Tx invasive breast cancer

A 
Surgery:
- Lumpectomy with radiation
OR
- Modified radical mastectomy
- sentinel LN bx ---> axillary LN dissection if nodes positive

Radiation

  • need for all conservative surgery
  • need for modified radical mastectomy if high risk for recurrence (+ nodes, large tumor, + resection margins

Receptor status

  • tx based on receptors
  • SERM for ER+ or PR+
  • Fulvestrant - new ER antagonist with no agonist effects
  • aromatase inhibitors (anstrozole, exemstane, letrozole)
  • Trastuzumab for Her2/neu +

Chemo

  • use for + LN status
  • use for - LN status but at higher risk (inc tumor size, high grade tumor)
  • Cyclophosphamide + MTX + 5-FU
145
Q

Tx recurrent or metastatic breast cancer

A

ER -
- doxorubicin + vincristine + cyclophsphamide

ER+

  • hormonal therapy better than chemo
  • Premenopause:
  • –oophorectomy
  • –GnRH antagonists
  • –tamoxifen
  • Postmenopause:
  • –tamoxifen
  • –aromatase inhibitor
146
Q

F/u breast cancer treatment

A

PE q3-6 mo for 3 years, then q6-12 mo for 4-5 years, then annually

F/u mammo after 6 mo if breast conserving surgery
- yearly mammo on remaining breast if had mastectomy

Endometrial bx if on tamoxifen + abnormal uterine breathing

147
Q

When can you get pregnant after breast cancer treatment?

A

Anytime!

Will recommend wait 2-3 years to defer to period where recurrence is less likely

148
Q

Finding of mass in Bartholin’s gland in postmenopausal woman. What are you thinking?

A

Suspicious for malignancy!
- usually adenocarcionma

Need excision/bx

149
Q

Type of leiomyoma most likely to cause infertility

A

Submucosal myomas

150
Q

Tx symptomatic uterine fibroids

A

GnRH agonists (suppresses estrogen)

Hysterectomy

151
Q

patients present with menstrual abnormalities, what can you do?

A

the endometrial cavity may be sampled to rule out endometrial hyperplasia or cancer.

This is most important in patients in their late reproductive years or postmenopausal years.

If the patient’s bleeding is not heavy enough to cause iron deficiency anemia, reassurance and observation may be all that are necessary.

152
Q

Maximal response to GnRH agonist for fibroids is usually reached by

A

3 months

After cessation of treatment, menses return in four to ten weeks, and myoma and uterine size return to pretreatment levels in three to four months.

153
Q

Why not screen pap < 21 yo?

A

HPV causes carcinogenesis in the transformation zone of the cervix, where the process of squamous metaplasia replaces columnar with squamous epithelium.

Squamous metaplasia is active in the cervix during adolescence and early adulthood.

Human papillomavirus infections are commonly acquired by young women shortly after the initiation of vaginal intercourse, but, in most, they are cleared by the immune system within one to two years without producing neoplastic changes

154
Q

Indications for cold knife conization (CKC) include

A

positive endocervical curettage,

HSIL lesion too large for LEEP,

patient not tolerant of examination in office,

lesion extending into the endocervical canal beyond vision,

to rule out invasive cancer (classify the depth of invasion if biopsy shows invasion).

Indications for LEEP are similar to CKC

155
Q

Postmenopausal women, initial workup of adnexal mass should include

A

Transvaginal US

CA-125 level

If US simple cyst and CA 125 not elevated, masses < 10cm can be followed conservatively

156
Q

Premenopausal women + endometrial hyperplasia - how do you manage?

A

Simple or complex hyperplasia WITHOUT atypica on endometrial bx

  • use cyclic progestins, regardless if pt is done with babies or not
  • repeat bx 3-6 mo later
  • hysterectomy is not warranted in any case
  • risk of cancer is also low, even complex hyperplasia

Complex hyperplasia WITH atypia

  • cancer risk high
  • if done with babies, hysterectomy is ok
  • if want more babies, cyclic progestins w/ repeat bx 3-6 mo

OB/GYN (7 decks)

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