Gyn-Onc Flashcards
Preinvasive neoplastic disease of the vulva is divided into two categories
squamous
- vulvar intraepithelial neoplasia
nonsquamous intraepithelial neoplasias
- Paget disease
- melanoma in situ
Vulvar intraepithelial neoplasia
- definition
= cellular atypia contained within the epithelium
Characterized by:
- loss of epithelial cell maturation,
- cellular crowding,
- nuclear hyperchromatosis,
- abnormal mitosis
How is the lesion of VIN determined?
Mild - severe dysplasia based on depth of epithelial involvement
VIN 1 = koilocytic atypia
VIN 2 &3 = Usual VIN vs Differentiated VIN
How many % of pts with VIN will have coexisting invasive carcionma (penetrated BM)
20%
Risk factors for VIN
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
VIN has 2 distinct forms - what are they?
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
Sx of VIN
- 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.
Any time a pruritic area of the vulva does not respond to topical antifungal creams - what should be done?
further evaluation with vulvar biopsy should be undertaken
Tx VIN
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
Follow up for VIN
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
Paget disease of the vulva - age of presentation
50-80 yo
Is extramammary paget disease of the invasive? Does it recurr?
NOT invasive usually
Tends to recurr locally
Only 20% of pts w/ pagets NOT of breast will have underlying adenocarcionma
- mets common with this
Dx Paget disease of vulva
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
Tx paget disease of vulva
Wide local excision if not invasion
BE CAREFUL! It is fatal if it spreads to lymph nodes
1 vulvar cancer
Squamous cell carcionma
Most are on labia majora
Spread of vulvar cancer is via
lymphatics –> superficial inguinal lymph nodes
Vulvar carcinoma accounts for what % of GYN cancers?
5%
Staging of vulvar carcionma
Surgically staged
- radical local excision + inguino-femoral LN dissection
- if superficial (< 1 mm) and unilateral disease, can forego unilateral LN dissection
Tx vulvar carcionma
For all
- wide radical local excision
- LN dissection
+
Stage 1
- ipsilateral lymphadenectomy
Stage 2
- modified radial vulvectomy
- resection LN
Stage 3 + 4
- radical vulvectomy
Tx Melanoma of the vulva
.
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%
The 5-year survival rate for all patients after surgical treatment of invasive SCC of vulva is approximately
75%
The most important prognostic factor is the number of positive inguinal lymph nodes
Vaginal intraepithelial neoplasia (VAIN) is a
premalignant lesion similar to that of the vulva and cervix.
However, VAIN is much less common than either VIN or CIN.
Dx VAIN
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
Tx VAIN
- local excision or laser ablation
Intravaginal 5-FU useful for tx pts w/ multifocal lesions and immunosuppression
Most types of vaginal cancer
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.
What vaginal cancer was found to be associated w/ in utero exposure of diethylstilbestrol?
Clear cell adenocarcionma
The cause of SCC of the vagina is
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
Does vaginal cancer have better 5 years survival than vulvar cancer?
NO!
40-55%
Tx vaginal carcinoma
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
When does CIN more commonly occur?
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
Risk factors for cervical dysplasia include
- 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
Screening guidelines for cervical cancer
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
If pt is Negative for intraepithelial lesion and malignancy pap, High-risk HPV positive
What do you do?
Repeat both pap and HPV in 1 year
OR
screen for HPV 16 and 18.
If either is positive then immediate colposcopy
ASC-US (Atypical squamous cells of undetermined significance)
+
High-risk HPV negative
What do you do?
Continue routine pap smear screening
You always get an HPV status if the pap is abnormal/ASCUS
When do you do colposcopy and cervical biopsies?
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)
When do you do colposcopy + cervical bx + endometrial bx?
atypical glandular cells
Pap smear reveals SCC - what do you do?
Colposcopy , HPV screen, and cervical biopsies, potential cold-knife conization (CKC)
When do you not test for high risk HPV?
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
Changes that can be seen on colposcope stained with acetic acid on cervix
Acetowhite epithelium
Mosaicism
Punctation
Atypical vessels
Bx all these lesions and send to path
% regress spontaneously in CIN I - III
CIN 1 = 60
CIN 2 = 40
CIN 3 = 30
Management of
CIN
CIN II
CIN III
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
Surgical excision options for cervical dysplasia based on characteristics of lesion or patient
- when use:
- LEEP?
- laser conization?
- Cold knife conization?
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
Types of cervical cancer
Squamous cell (80%)
Adenocarcionma (20%) - usually DES exposure if clear cell
How much does routine pap smear + HPV typing decrease risk of cervical cancer?
90%
High Risk HPV serotypes
16
18
31
45
Sx of cervical cancer
1 sx = postcoital bleeding
Early disease = asymptomatic
Mass on bimanual
Abnl vaginal bleeding
Dx cervical cancer
Tissue bx s/p abnormal pap or lesion found
Cervical cancer staging
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
Tx cervical cancer
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%
Tx recurrence cervical cancer
If only surgery 1st round –> radiation to tx
If already radiated –> surgery + pelvic exenteration (remove all pelvic organs)
Classification of Ovarian neoplasms
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
Malignant epithelial serous tumors (serous cystadenocarcionma)
1 malignant epithelial cell tumors
Can arise from benign serous cysadenoma
Psammoma bodies
Malignant mucinous epithelial tumor (mucinous cyadenocarcionma)
2 malignant epithelial cell tumor
Lower rate of bilaterality
Associated w/ pseudomyxomatous peritonei = widespread peritoneal extension with thick, mucinous ascites
Meigs syndrome
Ascites
R pleural effusion
Benign ovarian fibroma (stromal neoplasm)
Genes increasing risk of ovarian cancer
Risk factors of ovarian cancer
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).
1 ovarian cancers in women < 20 yo
Germ cell tumors
Blacks and asians more common than caucasians
When is CA-125 useful in ovarian cancer?
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
Tumor markers for germ cell tumors
hCG - choriocarcionmas
AFP - endodermal sinus
LDH - dysgerminomas
Dysgerminomas
Germ cell malignant tumor of ovary
Unilateral #1 germ cell tumor in pts w/ gonadal dysgenesis
Radio + chemosensitive
Spread via lymphatics
What is esp important in ovarian tumors such as granulosa tumor?
Endometrial sampling
These tumors can secrete estrogen –> endometrial hyperplasia –> carcionma
What do the stromal cell malignant ovarian cancers secrete?
Graunlosa –> estrogen
Sertoli Leydig –> testosterone
Krukenberg tumor
Ovarian tumor that is metastatic from other sites like the GI and breast
Usually signet ring cell type
Bilateral
How does ovarian cancer usually spread
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
Protective factors for ovarian cancer
Oral contraceptives > 5 yrs Breastfeeding Multiparity Chronic anovulation Tubal ligation Hysterectomy
1 diagnostic tool for investigating adenexal mass
Pelvic US
DO NOT do paracentesis and cyst aspiration because malignant cells can spread via direct exfoliation
Tx epithelial tumors
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
Most common type of germ cell tumor
Benign cystic mature teratoma
Epithelial vs germ cell tumors
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
Tx germ cell tumors
Surgery
- unilateral salpingo-oophorectomy
Chemo
- bleomycin + etoposide + cisplatin
carl exner bodies
In granulosa cell tumors
Have groove coffee-bean nuclei in cells arranged in small clusters around central cavity
PATHOGNOMONIC for granulosa cell
Tx stromal tumors
Surgery
- unilateral salpingo-oophorectomy
NO chemo or radiation
Fallopian tube cancers are mostly…
adenocarcionmas
Bilateral in 10% usually 2/2 mets
Latzko’s triad
Profuse watery d/c
Pelvic pain
Pelvic mass
In fallopian tube cancer, pathognomonic
Hydrops tubae profluens
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
Tx fallopian tube cancer
Same as epithelial ovarian cancer
Surgery
- TAHBSO
- omentectomy
- cytoreduction
- debulking
- paraaortic LN sampling
Chemo combo
- Carboplatin + paclitaxel
Types of endometrial cancer (2)
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
Spread of endometrial carcionma
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
1 type endometrial cancer
endometrioid adenocarcinoma (75% to 80%).
Most important prognostic factor for endometrial carcinoma
Histologic grade
Grade 3 = More than 50% of the tumor shows a solid growth pattern = poorly differentiated
Risk factors endometrial cancer
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
How long after you stop OCPs are they still protective for endometrial cancer?
15 years!
Protective factors for endometrial cancer
OCPs high parity pregnancy exercise / skinny SMOKING! (don't encourage though - increases hepatic metabolism of estrogen)
Endometrial thickness of what is indicative of low risk for malignancy?
=< 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
Initial workup for woman with abnormal vaginal bleeding includes…
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
Tx endometrial cancer
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
Most cases of endometrial ca recur within
3 years of tx
1 reason for abnormal vaginal bleeding
endometrial atrophy
Gestational trophoblastic disease
- what is it
- major classifications
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).
Risk factors for GTD
< 20 yo
> 35 yo (high risk)
Previous GTD
Nulliparity
Diet low in beta-carotene, folic acid, and animal
fat
blood group A,
OCP use
Pathogenesis of COMPLETE mole
- 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
Complete vs partial mole - which one has higher malignant potential?
Although most molar pregnancies are benign, complete
moles have a higher malignant potential than do partial moles
most common presenting symptom of molar pregnancy
- 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.
Dx complete molar pregnancy
- 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
Tx complete molar pregnancy
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
F/u with Complete molar pregnancy
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
Pathogenesis of partial mole
- 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
Dx partial mole
Tx partial moles
F/u partial mole
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
Are complete and partial moles benign or malignant?
Benign!
Have potential to transform to malignant choriocarcionma, invasive mole, or PSTT!
Tx malignant GTD
Chemo!
- MTX
- atinomycin-D
NO surgery because it is super chemo sensitive
Invasive moles are characterized by
the penetration of large, swollen (hydropic) villi and trophoblasts into the myometrium.
Dx malignant GTD
Pelvic US
hCG
Choriocarcinoma pathogenesis/characteristics
- 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
Presentation of choriocarcionma
Tx?
Often vaginal bleeding
Often present with mets
Need to do full body mets workup
Tx - chemo
Placental site trophoblastic tumor characteristics/pathogenesis
- 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
Dx PSTT
- NOT hCG b/c no prolif of syncytiotrophoblasts
- hPL may be used as a diagnostic tool.
- pelvic US
Tx PSTT
NOT chemosensitive
But rare mets beyond uterus
Tx = hysterectomy
Multiagent chemotherapy is given 1 week after surgery to prevent recurrent disease.
When malignant GTD is encountered after a nonmolar pregnancy, the diagnosis is almost always
choriocarcinoma and rarely placental site trophoblastic tumor.
Pstt- Stage III is defined as
pulmonary metastasis with or without uterine, vaginal, or pelvic tumor metastasis
Bx choriocarcinoma?
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.
The risk of having a molar pregnancy is increased in women with
two or more miscarriages.
Major blood supply to breast
Internal mammary
Lateral thoracic A
Nerves of breast at risk of injury during surgical dissection
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
What does estrogen and progesterone do to the breast?
Prolactin? Oxytosin?
Estrogen - ductal development + fat deposition
Progesterone - lobular-alveolar (stromal) development that makes lactation possible
Prolactin - milk production
Oxytocin - milk letdown
When to start mammos?
Age 40
Med to tx mastalgia
Danazol (only one approved!)
Most concerning type of nipple discharge
Spontaneous
Bloody
Serosanguineous
Unilateral
Persistent
From single duct
Assoc w/ mass
What nipple discharge is usually benign?
Bilateral
Nonbloody
Multiductal secretion
1 reason for bloody nipple discharge
Intraductal papilloma
Galactorrhea is associated with
Pregnancy
Pituitary adenomas
Hypothyroidism
Stress
Meds:
OCPs
AntiHTN
Antipsychotics
Serous discharge of nipple ddx
Nl menses
OCPs
Fibrocystic change
Early pregnancy
Yellow discharge ddx
Fibrocystic change
Galactocele
Green sticky discharge ddx
Duct ectasia
Purulent discharge ddx
Superficial or central breast abscess
What should you do after you find bloody discharge of nipple?
Guaiac
Cytologic eval
Preferred imaging for breast mass eval
> 30 yo - mammo
< 30 yo - US
Mass on palpation + mass on mammo or US…what next?
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
Pain breast mass
Multiple
Usually bilateral
Changes w/ menstruation
Fibrocystic change
What is fibrocystic change due to?
Associated cancer risk?
Ages?
Due to exaggerated stromal response to hormones and growth factors
No associated cancer risk
30-40 yo
Tx fibrocystic change
No caffeine
Support bra
Primrose oil Vit E Vit B6 Danazol Progestins Bromocriptine Tamoxifen
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
Fibroadenoma
Fibroadenomas
- age
- tx
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
Large bulky mobile mass
Painless
Well circumscribed
Rapid growth
Cystosarcoma phyllodes
Cystosarcoma phyllodes
- what is it
- concerning for malignancy?
- dx
- tx
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
Bloody nipple discharge
Solitary lesion
Benign
Intraductal papilloma
Intraductal papilloma
- traits
- dx
- tx
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
Usually post-menopause
Nipple d/c (multicolored, sticky)
Noncyclic breast pain
Nipple retraction
Mammary duct ectasia (plasma cell mastitis)
Mammary duct ectasia (plasma cell mastitis)
- traits
- dx
- tx
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
Breast cancer risk factor
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
Preventative factors for breast cancer
Early preggers
Prolonged lactation
Exercise
Abstinence from EtOH
Low fat diet
Tamoxifen
LCIS
- traits
- epi
- dx
- tx
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
DCIS
- traits
- epi
- dx
- tx
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
Paget disease of the nipple
Usually occur w/ DCIS or invasive carcionma
Malignant cells enter epidermis of nipple –> eczematous changes of nipple
Inflammatory breast carcinoma
Very aggressive
Dermal lymphatic invasion
Sx
- erythema
- edema
- warmth
- peau d orange
Tx invasive breast cancer
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
Tx recurrent or metastatic breast cancer
ER -
- doxorubicin + vincristine + cyclophsphamide
ER+
- hormonal therapy better than chemo
- Premenopause:
- –oophorectomy
- –GnRH antagonists
- –tamoxifen
- Postmenopause:
- –tamoxifen
- –aromatase inhibitor
F/u breast cancer treatment
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
When can you get pregnant after breast cancer treatment?
Anytime!
Will recommend wait 2-3 years to defer to period where recurrence is less likely
Finding of mass in Bartholin’s gland in postmenopausal woman. What are you thinking?
Suspicious for malignancy!
- usually adenocarcionma
Need excision/bx
Type of leiomyoma most likely to cause infertility
Submucosal myomas
Tx symptomatic uterine fibroids
GnRH agonists (suppresses estrogen)
Hysterectomy
patients present with menstrual abnormalities, what can you do?
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.
Maximal response to GnRH agonist for fibroids is usually reached by
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.
Why not screen pap < 21 yo?
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
Indications for cold knife conization (CKC) include
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
Postmenopausal women, initial workup of adnexal mass should include
Transvaginal US
CA-125 level
If US simple cyst and CA 125 not elevated, masses < 10cm can be followed conservatively
Premenopausal women + endometrial hyperplasia - how do you manage?
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
