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97 Cards in this Set

  • Front
  • Back
preeclampsia in 26th week, what's the tx?
Labetolol
What's more safe/effective: male or female sterilization
female
fibroids present as
bleeding

and little less often: pain
emergency contraceptives
oral hormones, prohibit LH surge and ovulation, change endometrium, change tubal motility, do not disrupt pregnancy, 72h
pseudostratification of endometrial cells
complex endometrial hyperplasia
hCG is made by
Syncytiotrophoblast
corpus luteum makes
progesterone
26yo, hirsutism, G0, infertility, acne,
pelvic ultrasound shows:
multiple bilateral cysts

PCOS
is endometrioid adenocarcinoma dependent on estrogen for growth and proliferation?
yes
is endmoetrial hyperplasia dependent on estrogen for growth and proliferation?
yes
are leiomata dependent on estrogen for growth and proliferation?
yes
is papillary serous endometrial carcinoma dependent on estrogen for growth and proliferation?
no

this is an endometrial CA, but it's not as common and not necessarily dependent on estrogen; not the classical presentation - thin older lady
is endometriosis dependent on estrogen for growth and proliferation?
yes
contraindications to using corticosteroids prenatally include
chorioamnionitis (helps fetal lung maturity, helps decrease incidence of necrotizing enterocolitis, prevent interventricular hemorrhages)

not contraindications: maternal asthma, 26wk gestation, pre-eclampsia, premature rupture of membranes
most effective, most convienient method of contraception
IUD
split of wins causing : conjoined twins

what was the date?
post 13 days
mono-amniotic twins
when did the split occur?
8-13days
3rd trimester bleeding can be due to
abruptio placentae - massive bleeding
placentae previa - painless bleeding
vasa previa (obstetric complication defined as "fetal vessels crossing or running in close proximity to the inner cervical os")
placenta accreta - painful bleeding
majority of chomosomal abnormalities occur in early conception due to
no disjunction in maternal meiosis I
indications for early delivery in pre-eclampsia
rising liver enzymes
falling platelet count
anuria

HELLP (hemolysis, elevated liver enzymes, low platelets)


worsening peripheral edema - is not indicative for early delivery
gestational DM is a risk for
developing DM later in life (30-50% chance)
fetal macrosomia
neonatal hypoglycemia
non-coiled umbilical artery is associated
single umbilical artery
endometriosis

causes pain when?
powder-burn implants

most likely causing pain in: luteal phase
benign cystic teratomas in ovaries

incidence?
unilateral?/bilateral?
malignant?
are not rare - 29% of all ovarian neoplasms

are bilateral in 10-15%

can contain fully developed teeth

risk of malignancy is very low in

women of reproductive age

managed by surgical excision
most common origin of breast CA
TDLU
terminal duct lobular unit

the epithelial cells - that's where the milk is made; here most CA arise

if circumscribed by myoepithelial cells is CIS
where in the breast do we see the sarcomas of the breast
Stroma:
Dense fibroconnective tissue – sarcomas of the breast
cancer close to the nipple in the ducts
DIS
papillary CA

most of the lesions here are benign
TDLU in post-menopausal woman
atrophy - no more lobules

looks like a male breast
categories of benign breast disease
Nonproliferative disease -Inflammatory conditions
-Fibrocystic changes

Proliferative (Premalignant)
-May mimic cancer clinically
inflammatory conditions
Acute mastitis – usually during lactation, bacterial infection, erythema and swelling can mimic inflammatory breast cancer

Duct ectasia – dilatation of ducts, inspissated secretions, inflammation of lobules
Fibrocystic changes
Lumpy, sometimes tender breasts
Very common – 60% of women, usually premenopausal
Composed of cysts (fluid filled sacs, tender), fibrosis, adenosis
Mass effect, tiny microcalcifications on mammogram, need biopsy to distinguish from cancer
Proliferative Lesions Without Atypia
Usual ductal hyperplasia – very common, several cell layers with mixed cell population, ER+; look ugly but are benign

Sclerosing adenosis – proliferation of glands within a fibrotic stroma, microcalcifications

Intraductal papilloma – growth inside duct, can cause nipple discharge; tree in the duct, if there are many many - they might get malignant

Fibroadenoma – most common benign growth in younger pt, not precancerous, can go away; but they can become bad - Phylloides tumor
Proliferative Lesions with Atypia
Premalignant
Miniature version of carcinoma in situ
Homogeneous cell population (clonal)
Cytologic atypia

Atypical ductal hyperplasia ADH (they have high risk of going to CA)

Atypical lobular hyperplasia ALH
(no E-cadherin - so looks like they hate each other; also they have high risk of going to CA)


ALH -> 4x higher chance to go to invasive BC (if it's already lobular insitu, the risk to become malignant is 8-10x higher)
also, if it's ALH, but they have a + family Hx - the risk is also 8.4x
what drives the changes from nl to proliferative?
Estrogen, Progesterone, other growth factors
10% of breast CA are hereditary:
Mutant gene defective in DNA repair
Passed from parents to offspring
Early onset breast cancer (25-50 years)
Multiple family members affected
BRAC-1 and BRAC-2 account for half

early onset (vs the later onset of sporadic cancer <50yo)
Carcinoma in situ in breast
Lobular carcinoma in situ (LCIS) - less common (NO E-CADHERIN)

Ductal carcinoma in situ (DCIS) – more common (will not kill the pt, but eventually they'll become malignant; they're on a continuum between non-comedo- comedo-high grade)

1970, 3% of all new cases
2005, 30% of cases due to screening
Invasive Breast CA types?
Invasive: cells invade outside duct basement membrane into stroma and potentially into blood vessels (systemic spread)

Requires surgery and systemic therapy
Extremely heterogeneous behavior from patient to patient (indolent/aggressive) based on gene signature

Paradigm for targeted therapy
ER+: Tamoxifen, other endocrine therapies
Her-2+: Trastuzumab

Typically subset by histologic differentiation (degree of microscopic atypia)

TYPES:

Infiltrating “ductal” carcinoma, no special type (NOS); most common;
2/3 in post-menopausal
LN - (75%)
ER + (78%)
PR + (50% )
HER + (25%)

Infiltrating carcinoma: tubular, mucinous, medullary, lobular classic (these have much better prognosis)
10-15% of all cancers
Rarely metastasize, excellent prognosis
Tubular, mucinous-low grade, ER+
Medullary-high grade, ER- but still good prognosis
who is the silent killer of women?
ovarian CA,
we don't have markers, we don't have goo tx
ovarian tumors

rate
Ovarian tumors are common in women.
- 2/3 occur during the reproductive age
- 80% benign:
60% < 40years

- 20% malignant and borderline: 90% >40 years
what's in the ovarian stroma?
epithelium?
Ovarian stroma
- Spindled shaped stromal cells
- Lipid-droplets
- Luteinized stromal cells
- Leydig cells

B. Surface epithelium (like mesothelium of the peritoneum)
- Similar to the adjacent peritoneum
- Ciliated cuboidal to columnar
classification of ovarian tumors
Surface epithelial-stromal tumors
Sex cord-stromal tumors
Germ cell tumors
Secondary tumors
presentation of ovarian tumors
Mild early symptoms/asymptomatic - “silent killer”
Abdominal distention, ascites, pain
Urinary/Gastrointestinal tract symptoms
Abnormal vaginal bleeding associated with functioning tumors
Estrogenic/androgenic symptoms

< 5 cm malignant in 5% of the cases
5-10 cm malignant in 12% of the cases
> 10 cm malignant in 60% of the cases
Bilateral tumors are malignant twice as often as unilateral tumors
ovarian tumor risk:
Incessant ovulation Inc risk 1.5 - 3.2 (Nulliparity)
Oral contraceptive Dec risk 0.4- 0.7

Family history - 10% BRAC-1, 2 mutations (altered DNA repair)
Surface Epithelial Stromal Tumors
2/3 of all ovarian tumors, 90% of all ovarian cancers

Classification:
Cell type:
Serous, Mucinous, Endometroid, Clear, Transitional (looks like urothelium), Squamous

Exophytic/intracystic

Cell proliferation, nuclear atypia or invasion:
Benign 70%
Borderline No invasion 10%
Carcinoma Invasion 20%
Serous Tumors
30% of all ovarian tumors; look like mesothelium (peritoneal)
Most are benign or borderline, 25% are malignant
Cystic neoplasms, mostly uniloculated, lined by ciliated cuboidal
Cells - Marker WT-1
They can be bilateral
Psammoma bodies common finding
Mucinous tumors
25% of all ovarian neoplasms
Most are benign or borderline, 15% are malignant
Cystic neoplasms, mostly multiloculated, lined by tall columnar
Cells with apical mucin - mucinous
Less frequently bilateral
Endometrioid Tumors
2- 4 % of all ovarian neoplasms
Almost 1/2 are associated with ipsilateral ovarian or pelvic endometriosis
- Most are carcinomas
- 30% of the cases are associated with endometrial adenocarcinoma probably related to same risk factors
- Tubular glands similar to endometrial tissue
Sex Cord-Stromal Tumors
Most common functioning ovarian tumors with endocrine manifestations

Classification: Derived from the ovarian stroma, that originates from the sex cords of the embryonic gonad:
- Sertoli and Leydig
- Masculinizing effect
- Granulosa and theca
- Feminizing effect
Granulosa Cell Tumors
1-2% of all ovarian tumors
Most common estrogenic ovarian tumor
Symptoms: abnormal uterine bleeding
Rarely androgenic
Unilateral

90% benign
Call-Exner bodies,
inhibin +
10yr survival 85%
Sertoli-Leydig Cell Tumors (Androblastoma)
0.5% of all ovarian tumors
Peak occurrence during reproductive years
Unilateral
Androgenic virilization in 30-50%
Histology: reminiscent of fetal testis
Mostly benign
Germ Cell Tumors
20 % of all ovarian tumors
Capable of developing complex and highly
differentiated tissues
Classification:
Benign (95%) teratomas
Malignant 5%
Teratomas ovarian
Tissues derived from two or three embryonic layers in any combination

Most common ovarian neoplasm
Young females
Can have malignant transformation in post-menopausal women
Tissues found are mature: Sometimes in organoid arrangement

Ectodermal:
Skin and adnexa, glia, cerebrum, cerebellum, choroid plexus and retina
Endodermal:
Respiratory, gastrointestinal, thyroid
Mesodermal:
Muscle, adipose tissue, bone, teeth, cartilage
Malignant germ cell tumors
Girls and young women

Dysgerminoma – (seminoma) marker PLAP
[Monotonous cell population of round cells
Excellent prognosis: Stage I 95%,
Radiosensitive and chemosensitive tumor]

Yolk sac tumor – marker AFP
[Histological hallmark: Papillary projections surrounded by embryonic epithelial cells, Schiller-Duval bodies
- Survival: Stage I 80%, advanced stage 40% ]


Choriocarcinoma – marker β HCG
[Highly malignant; Advanced stage at presentation
Rare
Young patients, before puberty
Most are associated with other
tumors
Poor prognosis;
chemotherapy resistant ]
secondary tumors of ovaries
Metastatic tumors involve the ovaries more often than any other site
Occur in 30% of women dying of cancer,
maybe the initial manifestation

GI tract - the signet cell from stomach (krukenberg)

cervical, breast....
Abnormal Uterine Bleeding

causes by Age Groups
Adolescence:
Anovulatory cycle

Reproductive age:
Complications pregnancy – abortion, ectopic pregnancy, Organic lesions – leios, polyps, hyperplasia, cancer
Anovulatory cycle
DUB

Perimenopausal:
Anovulatory cycle
Organic – cancer, hyperplasia, polyps

Postmenopausal:
#1 Endometrial Atrophy
#2Organic – cancer, hyperplasia, polyps
biochemical changes are according to the main goals of:
1) proliferative
2) secretive
3) menstrual breakdown
1) growth
2) maturation
3) apoptosis
Functional Disorders of Endometrium (No organic lesion) DUB

1) low estrogen
2) high estrogen
3) low progesterone
1) low estrogen
-no follicle development
-amenorrhea, oligomenorrhea, infertility

2) high estrogen
-anovulatory cycle (most common cause)
-metrorrhagia

3) low progesterone
-defective corpus luteum, intermenstrual bleeding, irregular cycles
-infertility
3 versions of DUB
heavy uterine bleeding
prolonged uterine bleeding
intermenstrual bleeding
AUB Non-proliferative/ Non malignant

causes
a) Inflammation PID – chronic endometritis
b) IUD
c) Retained POC
AUB Proliferative Causes – Benign
1) Polyp:
- Single or multiple
- May cause bleeding
Adenocarcinoma
- Clonal
> in patients on
Tamoxifen
Contain glands and
stroma


2) Leiomyoma:
- ”Fibroids”
- Common 40y → 40%
- Hormonal influence
- Pain, intermenstrual bleeding
- Examination to exclude malignancy
-decrease after menopause (they're responsive to E )
-the large one's on the outside, cause the pain, but the submucosal ones cause the abnormal bleeding
-made of smooth muscle

3)Endometrial Hyperplasia
Simple (more related to high E):
Without atypia – cancer risk: 1%
With atypia - rare

Complex (already has genetic changes closer to malignancy)
Without atypia – cancer risk: 3%
With atypia – cancer risk: 25 -40%
Endometrial Adenocarcinoma
Post menopausal women 80%
Risks – High estrogenic states:
HRT
Tamoxifen
Ovarian Neoplasm
Obesity
Reproductive factors


types:
Endometriod - most common
- early stage
- good prognosis

Papillary serous - less common
- aggressive
- older patients
leiomysarcoma of uterus
leiomysarcoma - rare
- cellular
- necrosis
- ↑mitoses

bad spindle, fish-flesh like
Carcinosarcoma of uterus
Carcinosarcoma
worst of all
- malignant glands
- malignant stroma
- 2-5% of uterine malignancies
- postmenopausal
- poor prognosis

homologous
heterologous (chondrosarcoma, osteosarcoma)

seen in older pt
Molar Pregnancy Hydatidiform Mole
Complete
Origin – Fertilization of empty ovum
Diploid – No maternal DNA
More Common in Asian Women (Indonesia 10/1000 deliveries

Clinical Symptoms:
Excessive Uterine Size for Gestational Age
Pre-eclampsia
Hyperemesis


Lab:
Increased β-HCG


Appearance and Histology:
Enlarged villi (Up to 2 cm), grape-like clusters
Microscopically: Large villi with central cisterns and circumferential proliferation of trophoblasts
Androgenic diploid, p57 immunostain neg.
No fetal tissue
After evacuation, levels of β-HCG decrease
Chemotherapy may be needed
2% may progress to choriocarcinoma


Partial mole/incomplete mole:
Origin: Union of oocyte with either a diploid spermatozoid or with two spermatozoids
Triploid – DNA Analysis – p57 immunostain+
Incidence is similar as complete mole


Appearance and Histology:
Large and small villi
Less formation of central cisterns
Less trophoblastic proliferation
A fetus with multiple congenital malformations may be seen
Rarely progress to choriocarcinoma


Choriocarcinoma:
Malignant tumor of admixed proliferating trophoblasts
No villi
1 in 24,000 pregnancies in USA, 1 in 2,500 in Ibadan, Nigeria
Uniquely sensitive to chemotherapy, cure rate of >95%
Lab: Markedly elevated increased β-HCG
Normal pregnancies after treatment
choriocarcinoma of ovary vs choriocarcinoma of uterus
choriocarcinoma ovary: chemoresistant

choriocarcinoma uterus - from a molar pregnancy : uniquely sensitive to chemo
uterine cancer types
Adenocarcinoma (90% of all uterine malignancies)
-Endometrioid (garden variety adenocarcinoma)
-Adenosquamous
-Mucinous
-Papillary serous (bad actor)
-Clear cell (bad actor)
-Rare subtypes – primary squamous

Sarcomas (3-5% of all uterine malignancies)
-Leiomyosarcoma
-Endometrial stromal sarcoma
Mixed homologous müllerian sarcoma (if malignant mesodermal elements are normally present in the uterus)
-Mixed heterologous müllerian sarcoma

Extension from cervical or ovarian cancers
endmetrial adenocarcinoma
incidence
highest incidence, best survival

endometrial > ovarian > cervical

Ovarian (worst) > cervical > endometrial (best)
endometrial CA types
Type I (90%)
Estrogen Related
Younger and heavier patients e.g. PCO
Low grade
Perimenopausal
Exogenous estrogen

Type II (10%)
Aggressive
Unrelated to estrogen stimulation
Occurs in older & thinner women
Potential genetic basis
Lynch syndrome
Familial trend
[breast CA, uterine CA, colon CA]
endometrial CA risks
Peak incidence in late 50s-early 60s

Associated with prolonged and uninterrupted exposure to estrogenic stimulation (endogenous or iatrogenic)

Other risk factors: obesity, previous irradiation, early menarche, late menopause, hypertension, diabetes

On a stage for stage basis the survival is slightly worse in african-american women than
Caucasian women.

AA women tend to present with later stage disease; almost always this is a failure to detect disease earlier because of either lack of access to healthcare system or delays in getting through our system
endometrial hyperplasia
“overgrowth” of endometrium secondary to prolonged unopposed estrogen
May be generalized or focal
Seen in adolescents through menopause
Progression to carcinoma is possible, esp. with atypical histology
Presents with abnormal uterine bleeding, typically following amenorrheic intervals
If detected and properly treated should never progress to cancer
obesity
endometrial hyperplasia is associated with (other risks)
Anovulatory cycles in teens
Granulosa cell tumors of the ovary
Polycystic ovary syndrome
Adrenal cortical hyperplasia
Iatrogenic unopposed estrogen (women with a uterus should not, as a rule, ever receive estrogen therapy alone without progesterone)
Paradoxically, use of some anti-estrogens such as Tamoxifen
management of endometrial hyperplasia
with or without atyppia
we can treat and cure this medically

progestin
endometrial carcinoma presentation
Abnormal bleeding (>90%)
Abnormal cells detected on Pap – not so common as you would think
Screening asymptomatic low risk patients is not cost effective.
HNPCC
Hereditary nonpolyposis colorectal cancer (HNPCC) [Lynch syndrome] is a colon cancer, characterised by a risk of other cancers of the endometrium, ovary, stomach, small intestine, hepatobiliary tract, upper urinary tract, brain, and skin. The increased risk for these cancers is due to inherited mutations that impair DNA mismatch repair.


Endometrial cancer is most common malignancy: 40-60% lifetime risk, then colon cancer, then ovarian cancer
Endometrial carcinoma Diagnosis
Endometrial biopsy (office procedure)
Dilation & curettage (D&C)
Hysteroscopy with directed biopsy
The latter two are done in the OR
Transvaginal sonography can be suggestive but rarely diagnostic


Opportunity to diagnose early
Rare cases in young women desiring fertility preservation can be managed with aggressive progesterone therapy provided a narrow set of strict criteria are met
Most everyone else will be treated primarily with surgery
Radiation therapy as primary treatment reserved for patients who are too high-risk to undergo surgery
Endometrial carcinoma Surgical staging
Abdominal exploration
Total hysterectomy
Bilateral salpingo-oophorectomy
Peritoneal cytology
Pelvic and para-aortic node sampling
Directed biopsies as needed
Omentum, diaphragm, bowel surface, liver
NOTE: the trend in the past five years has been to perform this surgery laparoscopically, with or without the Robot


Stage 1 - uterus only
stage 2 - uterus + cervix
stage 3 - uterine serosa, adnexa, vagina, pelvic/aortic mets
stage 4 - bladder, bowel, inguinal node, distant mets



We can get some valuable information in the operating room about the risk factors the individual patient has for spread, and can make a “tailored” staging decision.
Ideally, all patients should be surgically staged, but staging is not without potential complications so we are flexible
We also have some idea pre-op about who has to be staged – e.g. high grade on biopsy, visible cervical lesion biopsy proven, elevated CA-125


Properly staged patients may be able to avoid post-operative pelvic (or other) radiation therapy
Most patients with rarer subtypes (papillary serous, clear cell) are treated like ovarian cancers even if stage I because they tend to behave that way
Endometrial Cancer: Pre-op Evaluation
CA125
Chest X-ray
Mammogram
Colon Evaluation.
Transvaginal Ultrasound
Others as indicated. Like physical exam. And, maybe even talk to the patient and take a real history
Endometrial Cancer: Poor Prognostic Factors
Increasing age (over 65)
Stage (> IB)
Vascular invasion
Grade
Histologic Subtypes (Clear-cell, Serous, Adenosquamous)
Aneuploidy
Altered oncogene/tumor suppressor gene expression
Very elevated serum CA-125 in absence of surgical evidence of spread.

(This creates a problem for us because we have to counsel the patient as well as decide on possible therapy, and it’s not clear what the best therapy should be in the absence of a “site”. )



Some patients with early cancers require less surgical staging because they have a much lower risk of having metastases - endometroid...
Endometrial Cancer: Adjuvant Therapy
Brachytherapy
External beam radiotherapy
Hormonal therapy
Cytotoxic chemotherapy
Combination therapy – chemo and hormonal
Endometrial Cancer: Recurrence
responds less to chemo than ovarian

80% of recurrences happen first 3 years
Most will be symptomatic
Rare to cure distant recurrences
50% vaginal recurrences cured
Endometrial Cancer: Who Needs an Endometrial Biopsy?
Postmenopausal bleeding
Postmenopausal women with endometrial cells on Pap
Perimenopausal intermenstrual bleeding
Abnormal bleeding with history of anovulation
Thickened endometrial stripe via sonography*


Older than age 40 with anovulatory bleeding
Younger than age 40 with Abnormal uterine bleeding PLUS risk factors (e.g., PCOS, obesity)
Atypical endometrial cells or atypical glandular cells on Pap at any stage of menstrual cycle
Any endometrial cells on Pap during secretory phase of menstrual cycle – never heard of this one
uterine sarcomas
All of the information we discussed was about the 90% of uterine cancers. What about the other 10%?
Presentations the same
Surgery the same
Survival NOT the same
Post-operative therapy, if required, generally less effective
For uterine sarcomas it is critical that the disease be surgically confined to the uterus.
Even when it is, up to 50% of patients will recur
risk of ovarian mass being cancer increases with...
Large size
Bilaterality
Solid vs. cystic
Radiologic appearance:
Complex, papillary,density,  pulsatility of blood flow
Age of pt. outside reproductive span (Age of patient
Premenarchal: risk of malignancy 5x
Postmenopausal: risk of malignancy 10×)
Ascites
Elevated serum tumor markers
Adnexal masses Indications for surgery
Cyst > 5 cm (persistent)
Solid
Papillary appearance on sonography
Initial size > 10 cm
Ascites
Age of patient outside reproductive range
Torsion or rupture suspected
ovarian endometriosis is the most common cause of ...
pelvic pain and infertility in women in the US
Benign ovarian masses Functional (Follicular) cysts
Most common cystic mass in reproductive-age women
Rarely >6 cm
Spontaneously resolve
May rupture or undergo torsion
Prevention: hormonal contraception
Corpus luteum cysts
Usually <5 cm
May hemorrhage or undergo torsion
Self-resolving
Cystic teratoma (Dermoid cyst)
Cysts associated with endometriosis
Can fill with blood and become “chocolate cyst"
Ovarian fibroma (Thecoma)
Solid
More common in older women
Spindle cells and fibrous bands
Ovarian Cancer

numbers/incidence
90% are epithelial in origin
1 in 56 women will develop ovarian cancer
4th most common fatal cancer in U.S.
27,000 new cases annually; 16,000 deaths annually in US
High mortality in advanced stage disease (when it is most commonly diagnosed)
Ovarian Cancer Risk factors
Family history
BRCA1 or BRCA2 mutation
Nulligravid
??Use of fertility (ovulation inducing) drugs
Abdominal distension

Ascites (amount does not corrlate
With size of CA)

Bowel obstruction

Vague abdomnial/GI
Ovarian cancer Clinical features
Ovarian cancer Presenting symptoms
Abdominal pain
Abdominal swelling/increased abdominal girth
Vomiting
Altered bowel habits
urinary frequency or retention



clinical:
Abdominal distension

Ascites (amount does not corrlate
With size of CA)

Bowel obstruction

Vague abdomnial/GI
Growth pattern of ovarian cancer
Main mode of spread is by implantation on peritoneal surfaces
Lymphatic spread also important
Omentum usually involved
Ovarian Cancer Management
Surgery: for staging and “debulking”
Second-look after initial treatment
Chemotherapy
Adjunctive or salvage
Radiation
Limited role
Screening for ovarian cancer
Physical exam
Fact: Most ovarian cancer not detected before Stage III or IV
Imaging
Fact: No imaging technique can definitively diagnose or rule out ovarian malignancy
Serologic testing
Fact: No serum marker with sufficiently high sensitivity or specificity, especially in early stage cancer, even for serum markers such as CA-125; it’s good for monitoring – but the big limiting factor is that the lvl is normal for 25%

In women under age 50, elevated CA-125 is associated with malignancy
less than 25% of the time


increased with:
Acute PID Active hepatitis Pericarditis
Adenomyosis Acute pancreatitis Pneumonia
Benign ovarian neoplasm Chronic liver disease Polyarteritis nodosa
Endometriosis Cirrhosis Surgery
Functional ovarian cyst Colitis Renal disease
Meig’s syndrome Congestive heart failure Systemic lupus
Menstruation Diabetes erythematosus
Ovarian hyperstimulation Diverticulitis
Uterine fibroids Mesothelioma
Nonmalignant ascites
Protective factors against ovarian cancer
Pregnancies
Current or former use of OCPs
Tubal ligation
Breast feeding
Prophylactic oophorectomy: not 100%