+

The Female Genital Tract

Aileen Ong-Sy, M.D., FPSP
+ ANATOMY
+
Uterus
 Vary in size – depends on the age and parity

 50-80 gms and 8x5x4cm – nulliparous

 in size following pregnancies;  in half the size

after menopause

3 anatomic and functional regions:

 Fundus
 Body
 Cervix
+
+
+
+
+
Mullerian anomalies

Mullerian ducts – embryologic anlage which develops into

fallopian tubes, uterus, cervix and upper 2/3rds

of the vagina

- amenorrhea

- infertility

- recurrent pregnancy loss

- pain
+
+
 Cervix
 ecto/exocervix or
portio vagina (WDSSE);
visible to naked eye
and continuous with the
vaginal vault 
external os
 Endocervix
(SCE;mucin-secreting)
 invaginates forming
endocervical glands
 Squamocolumnar
junction/transformation
zone  SQUAMOUS
METAPLASIA 
susceptible to HPV 
CA
+

 Fundus
 Consistsof
endometrium
surrounded by
myometrium

 LUS

 Fallopian tube
+
Uterine wall
+  Ovaries
 4x2.5x1.5 cm – active
reproductive life
 Divided into cortex
and medulla
 Cortex – closely
packed stromal cells;
Follicle  ovulation
 Graafian Follicle
 Corpus Luteum 
senescence 
Corpus albicans
 Medulla – loose
mesenchymal
tissues, vessels,
nerves
+
INFECTIONS
+
INFECTIONS

 Candida, Gardnerella and Trichomonas – common;

significant discomfort; NO serious sequelae

 N. gonorrhae and C. Trachomatis – infertility

 Ureaplasma urealyticum and Mycoplasma hominis

– preterm deliveries

 Viruses
e.g. HSV and HPV (tumors of cervix, vulva
and vagina)

 Most common ROT: Sexually transmitted

+
Herpes Simplex Virus
 HSV type 2 – cervix, vagina and vulva
 DNA virus
 Clinicalsns and sxs: 3-7 days after sex  red
papules  vesicles  painful coalescent ulcers in
vulvar skin and mucosa; pelvic pain and
tenderness and purulent discharges in cervical or
vaginal lesions; dysuria and urine retention
(urethra)
 Systemic sxs: fever, malaise and tender inguinal
nodes
 Activeinfection – most infectious phase; numerous
viral particles within vesicles and ulcers
+
 Latent
infection – after 1-3 wks; virus migrates to
lumbosacral nerve ganglia

 Transmission
may occur in both active and latent
phase; however, more so in active phase

 Reactivation: immune system, stress, trauma, UV

radiation and hormonal changes

 C/S done in pregnant women

 Dx: clinical
findings; tissue culture from purulent
exudates; PCR and direct immunofluorescent Ab
test

 Tx: no
effective treatment for latent HSV infection;
Acyclovir or Famciclovir may shorten
+
Herpes Simplex type 2
+
Molluscum Contagiosum

 DNA
Poxvirus; infection of the skin and mucous
membranes

 MCV1 - Common in young children (2-12 y.o.);

transmitted through direct contact or shared
articles; trunk, arms and legs

 In
adults – MCV2; sexually transmitted; genitals,
lower abdomen, buttocks and inner thigh

 1-5mm papules; central waxy core –

intracytoplasmic viral inclusions
+
Molluscum Contagiosum
+ Candida albicans  Trichomonas vaginalis
 Flagellated protozoan
 m.c.;part of normal  Sexually transmitted;
flora 4days to 4 weeks
 Disturbance in vaginal  Frothy yellow vaginal
microbial ecosystem discharges
 DM, Abx, Pregnancy,  Dysuria, dyspareunia
Immunocompromised  PE: red and inflamed
CMI cervical mucosa
(strawberry cervix)
+
 Gardnerella
vaginalis  U. urealyticum and
 Gm (-) bacillus M. hominis
 mc cause of bacterial  Vaginitis and
vaginosis cervicitis
 Green-gray,
malodorous (fishy)
discharge
 Clue cells
+
Pelvic Inflammatory Disease
 Ascending infection fr vulva or vagina  spreads
upwards to involve most structures in the female
genital system

 Pelvic
pain, adnexal tenderness, fever and vaginal
discharges

 Gonococcus – mc cause of PID

 Chlamydia – 2nd mc

 Polymicrobial (staph, strep, Cl. Perfringens);

usually after spontaneous or induced abortions;
normal to abnormal deliveries (puerperal
infections)
+
Gonococcal infection
 2-7
days after inoculation; involves usually
endocervical mucosa

 May spread upwards to involve the fallopian tubes

and tubo-ovarian region

 Mx: marked acute inflammation confined to the

superficial mucosa

 Inflammatory exudates – intracellular gm (-)

diplococci

 Def. Dx: Culture or PCR

+

 Acute suppurative salpingitis  tubal mucosa becomes

congested and infiltrated with neutrophils, lymphocytes
and plasma cells  tubal lumen fills with purulent
exudate  leaks out to the fimbriated end  spillage into
ovary  salpingo-oophoritis

 Tubo-ovarian abscess – pus within ovary and tube

 Pyosalpinx – pus within tubal lumen

 Hydrosalpinx – dilated fluid-filled tubal lumen

+

 Acute
Cx: peritonitis, bacteremia  endocarditis,
meningitis, suppurative arthritis

 Chronic sequelae: tubal adhesions and obstruction

 infertility, ectopic pregnancy, intestinal
obstruction

 Tx: early– can be treated with penicillin; later

stage - difficult
+
+

Vulva
+ Bartholin Cyst
 Infection
of Bartholin
gland  abscess

 Bartholinduct cysts –
secondary to obstruction
of the duct by
inflammation

 Liningepithelium –
squamous metaplastic
epithelium

 3-5cm; pain and

discomfort

 Tx: excised
or
marsupialization
+ Non-neoplastic Epithelial Disorders
 Lichen Sclerosus
 White plaques or papules 
may coalesce over time
 Entire vulvar involvement 
parchment-like
 Labia becomes atrophic and
stiffened with constriction of
the vaginal orifice
 Postmenopausal women
 Hx: thinning of epidermis with
disappearance of the rete
pegs, hydropic degeneration
of the basal cells, superficial
hyperkeratosis; dermal
fibrosis/sclerosis; dermal
chronic inflammation
+ Squamous cell
hyperplasia
 Formerly called as
Lichen simplex
chronicus
 Nonspecific condition
resulting from
scratching or rubbing
the skin to relieve
pruritus
 Hx: marked epithelial
thickening; expansion
of the S. granulosum
and significant
hyperkeratosis;
dermal infiltrates is
pronounced
+
Benign Exophytic Lesions
 Condyloma
Acuminatum
 Sexually transmitted
 Verrucous warty growth
 HPV 6 and 11
 Koilocytes
 NOT a precancerous
lesion
+
Squamous Neoplastic Lesions

 Uncommon; 3%; >60 y.o.

 Squamous cell carcinoma – mc
2 groups:
 Basaloid and Warty CA – 30%; assoc with
oncogenic HPV
 Keratinizing SQCA – 70%; NOT assoc with
oncogenic HPV
+
 Basaloid/Warty CA’s
 Results from an in-situ precursor lesion - Classic VIN;
formerly called Bowen disease; similar to CIN III;
nuclear dysplasia, full thickness involvement without
breaching the bm, increase mitoses and loss of
polarity
 Risk factors: young age on 1st intercourse, multiple
partners
 HPV-related – HPV 16; multicentric
 Peak age – 6th decade
***exophytic, papillary architecture and prominent
koilocytic atypia
+

 Keratinizing SQCA
 Etiology: unknown; Long-standing lichen sclerosus or
squamous cell hyperplasia (Chronic irritation) with
TP53 mutation
 Peak age: 8th decade
 Premalignant lesion: Differentiated VIN or VIN simplex
(marked atypia of the basal squamous layer with normal
superficial epithelial maturation
 Gx: nodules in a background of vulvar inflammation
 Sn/Sxs: Non-specific (local discomfort, itchiness or (+)
exudates with secondary bacterial infection)
+

 InvasiveSQCA – initial spread is to inguinal, pelvic,

iliac and periaortic LN

 <2cm lesions: 60-80% 5 yr survival rate

 Largerlesions with LN involvement - <10%

survival rate

 Tx: Vulvectomy and lymphadenectomy

+
Classic VIN
+
Basaloid/Warty Carcinoma
+ VIN simplex KeratinizingSQCA
+

Vagina
+
Developmental Anomalies
 Septate/Double vagina – failure of fusion of the
mullerian ducts  accompanies Double Uterus
(Uterine Didelphys)
 DES exposure

 Gartnerduct cyst
 Common; lateral walls of the vagina derived from
the Wolffian (mesonephric) duct rests
 1-2 cm fluid-filled cysts
+
Premalignant and Malignant
Neoplasms
 Stromal
polyps, Leiomyoma and
Hemangiomas
 VAIN : Vaginal Intraepithelial Neoplasm
 Similar to classic VIN; rare; 1%- primary
 Assoc with oncogenic HPV’s
 mc location: upper posterior portion

 Invasive SQCA
+ Embryonal Rhabdomyosarcoma
 aka Sarcoma botryoides

 mcin infants and children

younger than 5 y.o.

 Consists
of embryonal
rhabdomyoblasts

 Gx: polypoid, grape-like,

bulky masses projecting
out

 Hx: tc
are small with oval
nuclei with small
protusions of cytoplasm
from one end; “tennis
racket” appearance
+

Cervix
+
Inflammations – Acute and Chronic
Cervicitis
 intracellular glycogen vacuoles in squamous cells
 cells shed  glycogen provides a substrate for
endogenous vaginal aerobes and anaerobes (
strep, enterococci, E. coli and Staph)

 Some degree of inflammation is found in all women

 Exceptions: Chlamydia, Gonorrhea, HSV, HPV,

mycoplasma
 spread to upper portion (upper genital tract dse)
 Complications during pregnancy
 Abnormal PAP test result
+
Endocervical Polyp
 Benign exophytic growth
 2-5%

 Irregular vaginal spotting and bleeding

 Arise from endocervical canal
 Varyfrom small sessile to large 5 cm mass
protuding out the cervical os
 Softto mucoid lesions with loose edematous
fibromyxoid stroma and several dilated mucin-
secreting endocervical glands; (+) inflammation
 Surgical excision or simple curettage
+
+
Premalignant and Malignant
Neoplasms
 3rd mc cancer in women

 Previouslyleading cause of death (50 years ago);

rank 13th cause of mortality

 Early
detection by PAP (Papanicolaou) and
colposcopy (visual exam)  potentially curable

 HPV – DNA virus; single most impt factor in

cervical oncogenesis
 15 high oncogenic risk HPV’s identified
 HPV 16 (60%) and HPV 18 (10%) – most impt
 5% - rest of oncogenic HPV
+
 RiskFactors:
 Multiple sexual partners
 A male partner with multiple previous or current
sexual partners
 Young age at 1st intercourse
 Low parity
 Persistent HPV 16 or 18 infection
 Immunosuppression
 Certain HLA subtypes
 Use of oral contraceptives
 Use of nicotine
+
 On average, 50% of HPV
infections are cleared
within 8 mos and 90%,
within 2 years

 Durationof HPV is related

to HPV type

 HPV’sinfect immature
basal cells in areas of
epithelial breaks or
immature metaplastic
squamous cells at the
squamocolumnar junction

 HPV requires damage the

surface epithelium; cervix
– more susceptible
+
HPV
 Act
as a carcinogen – E6 and E7  interfere with
tumor suppressor proteins (TSP) regulating cell
growth and survival

 Infects
the immature epith BUT replicates in
maturing squamous cells (N – arrested in G1 cycle)

 ViralE7 protein
 binds the hypophosphorylated (active) form of RB
 Binds and inhibits p21 and p27 – CDK inhibitors
***enhances cell cycle progression, impairs the
ability of the cells to repair DNA damage
+
HPV
 Viral
E6 protein
 Exacerbates damage of DNA repair
 Binds to TSP p53
 Upregulates telomerase expression

 Physical state of HPV viral DNA is integrated into

host cell genome

 HPV infection alone - NOT sufficient to cause CA

 exposure to co-carcinogens
 Host immune status
+
Cervical Intraepithelial Neoplasia
(Squamous Intraepithelial Lesions)
+

 Two-tiered management: Observation and surgery

 LSIL
– high level of viral replication; BUT does NOT
progress directly to INVASIVE CA; most cases
regress spontaneously

 HSIL– progressive deregulation of the cell cycle 

 cellular proliferation,  or arrest epithelial
maturation
***low rate of viral replication

 LSIL is 10X more common than HSIL

+
Morphology of SIL
 Nuclear atypia
(enlargement,
hyperchromasia, coarse
chromatin granules,
pleomorphism)

 Cytoplasmic ‘Halos’ – E5
protein (localizes to
membranes of ER) 
perinuclear halo

 Koilocytic atypia – nuclear

atypia with perinuclear
halo
+
+
+

 >80% of LSIL and

100% of HSIL – assoc
with high-risk HPV
(more with HPV16)

 Majorityof HSILs arise

from LSILs

 20% HSIL – arise de-

novo
+
Cervical Carcinoma
 45 y.o. – average age

 SQCA – mc subtype

 AdenoCA – 2nd mc; 15%; adenoCA-in-situ

(precursor lesions)

 Raretypes: Adenosquamous CA and

Neuroendocrine CA
 5%; high-risk HPVs
 Shorter progression from in-situ to invasive
 Aggressive; poorer prognosis
+

 Fungating (exophytic) or infiltrative masses

 Types:
 SQCA - Composed of nests and tongues of malignant
squamous epithelium; keratinizing to non-keratinizing;
invade the underlying cervical stroma
 AdenoCA - Proliferation of glandular epithelium
composed of malignant endocervical cells with large,
hyperchromatic nuclei and mucin-depleted cytoplasm
 hyperchromasia
+

 Adenosquamous CA - Intermixed malignant

glandular and squamous epithelium
 Neuroendocrine CA’s - Uniform small round cells
resembling Small cell CA of the lung

 Advanced dse – direct extension (paracervical

tissues, vagina, UB, rectum; LVI – distant mets (liver,
lungs, bone, BM, etc)
+
+
+
Adenosquamous Neuroendocrine
CA tumor
+
Clinical Features
 MicroinvasiveCA’s – may be treated by cervical
cone excision alone
 Invasive CA’s – hysterectomy with LND
 Advanced dse – plus radiation and chemoTX
 Prognosis: 100%
5 yr. SR - Microinvasive CA’s
 <50% - advanced dse

 COD: consequence of tumor invasion rather than

distant mets
 Ureteral obstruction
 PN
 Uremia
+
Cervical CA screening and Prevention
 PAP (Papanicolaou) method
 Circumferential scraping with a spatula or brush –
partic on the transformation zone
 Smeared into slides  fixation and staining

 MolecularMethod – HPV DNA in cervical scrapes

 High sensitivity but low specificity

 Combined method – women over 30 y.o.

 ROT: 1st– 21 y.o. or within 3 yrs after onset of sexual
activity  every 3 yrs thereafter
 After 30 y.o. w/ (-)cytology and (-) HPV DNA – every 5
yrs
 (-) cytology with positive HPV DNA – cytology every
6-12 mos
+ Cytology (PAP) test – (+)
 Colposcopic exam of cervix and vagina is done
 Using a magnifying glass  acetic acid application 
white spots (acetowhite areas) in abnormal epithelium
 Bx
 (+) LSIL – conservative tx; local ablation (cryotherapy)
 (+) HSIL – conization (superficial excision)

 PREVENTION
 Vaccine – recommended for all girls and boys by age
11 to 12 y.o. up to age 26 y.o.
 2 vaccines are FDA-licensed; HPV16 and HPV18; HPV 6
and 11
 Current studies: offer 10 years protection
 Does NOT protect against ALL high-risk HPV types
+
+
+

Body of Uterus
and
Endometrium
+ 2 major components:
 Myometrium
 Composed of tightly
interwoven bundles
of smooth muscle
 Form the walls of the
uterus
 Endometrium
 Lined the internal
cavity of the uterus
 Composed of glands
embedded in a
cellular stroma
 Affectedby endocrine
imbalances, Cx of
pregnancy and
neoplasms
+ Endometrial Histology in the
Menstrual Cycle
 affectedduring the menstrual cycle
 2 layers: Functional and Basal Layer
 Phases: Proliferative, Secretory Phase and Menstrual
Phase

 Menstrual phase superficial portion (Functionalis) is

shed

 Proliferative phase  rapid growth of glands and

stroma arising from the basal layer (preovulation)
 Glands are straight to tubular lined by PSCC
 Mitotic figures are numerous
 NO evidence of secretion and vacuolation
+
 Secretory phase  post ovulation
 Presence of vacuoles ( subnuclear to supranuclear )
 Tortuous to serrated glands “saw-toothed”
 Early secretory phase
 Subnuclear vacuoles
 Late secretory phase – progesterone
 Supranuclear vacuoles
 Prominent spiral arterioles and edema (days 21 to
22)
 Stromal cell hypertrophy with edema (predecidual
change) – days 24-28
 Dissolution of Corpus luteum and drop in
progesterone levels  stromal breakdown
+
+ Papanicolaou smears
+
+
+
Dysfunctional Uterine Bleeding
(DUB)

 mc cause: hormonal imbalance

 Othercauses with structural abn:
 Chronic endometritis
 Endometrial polyps
 Submucosal leiomyoma
 Endometrial neoplasms
+ Anovulatory Cycle
 Most frequent cause of DUB

 Failure to ovulate

 mc – hormonal imbalance; common in menarche and

in perimenopausal pd

 Less
common causes:
 Endocrine d.o. – thyroid, adrenal or pituitary d.o.
 Ovarian lesions – ovarian tumor or polycystic ovaries
 General metabolic disturbances – obesity,
malnutrition or other chronic systemic diseases

 Excessive
endometrial stimulation by estrogen with
unopposed by progesterone
+
Inflammatory Disorders
Acute Endometritis
 Uncommon; bacterial infections arising after
delivery or miscarriage

 Retained POC – usual predisposing factor

 Gp A hemolytic strep, staph and other bacteria
 Inflammation usually limited to stroma
 Tx: Removal of retained POC by curettage and
Abx Tx
+
Chronic Endometritis
 Associated with the ffg. d.o.:
 PID
 Retained POC, postpartum or post-abortion
 Intrauterine contraceptive devices
 TB – miliary TB or TB salpingitis

 15% - cause is unknown

 Abn bleeding, pain, discharge and infertility
 Chlamydia – can cause acute or chr dse

 Hx: (+) plasma cells in the stroma

 Tx: Abx if EA is known
+ Endometriosis and Adenomyosis
ENDOMETRIOSIS
 Presence of “ectopic” endometrial tissue at a site outside
the uterus
 Contains mostly both endometrial glands and stroma
 May occur in the ff sites (in descending order):
 Ovaries
 Uterine ligaments
 Rectovaginal septum
 Cul de sac
 Pelvic peritoneum
 Small and large bowel, appendix
 Mucosa of the cervix, vagina, and FT
 Laparotomy scars
+ Cause infertility, dysmenorrhea, pelvic pain
 Mainly in 6-10% of reproductive women (3th-4th decade)

 Pathogenesis:
 Regurgitation Theory – implants at ectopic sites via
retrograde flow of menstruation; common in FT 
peritoneal cavity
 Benign Metastases Theory – “spread” to distant sites
(bone, lungs and liver) via lymphatics and bv
 Metaplastic Theory – endometrium arises directly fr
coelomic epithelium (mesothelium of pelvis and
abdomen) from mullerian ducts during embryonic
devt; Mesonephric remnants
 Extrauterine stem/Progenitor cell Theory – stem
cells fr the bm  endometrial tissue
+
 Regurgitation Theory – in vast majority of cases

 Molecular analyses:
 Release of proinflammtory and other factors e.g.
PGE2, IL-1β, TNFα, IL6 or 8, NGF, VEGF, MCP-1,
MMP’s and TIMP’s
  estrogen production by endometriotic stromal
cells due to high levels of enzyme aromatase
(absent in normal endometrial stroma);
 an association between endometriosis and
ovarian CA (endometrioid and clear cell type);
genes PTEN and ARIDIA
+
+
 Endometriotic lesions – bleed secondary to both
extrinsic cystic (ovarian) and intrinsic hormonal
stimulation

 Red-blueto yellow-brown appearance on either

mucosal or serosal surfaces

 Ovary – cystic; aka Chocolate cysts

 Aggressive forms can invade adjacent tissues causing

fibrosis and adhesions

 Hx: (+)
endometrial glands and stroma; hemosiderin-
laden macrophages; sometimes, one or the other is seen

 AtypicalEndometriosis – precursor to endometriosis-

related CA
+
+

 Clinical Features: (secondary to intrapelvic

bleeding and periuterine adhesions)
 Severe dysmenorrhea
 Dyspareunia
 Pelvic pain
 Pain on defecation – rectal wall
involvement
 Dysuria – bladder serosal involvement
 Menstrual irregularities
 Infertility – 30-40% of women
+ ADENOMYOSIS
 defined as the (+) of endometrial tissue within the
uterine wall (myometrium)
 Signify a downgrowth of endometrial tissue in
between smooth muscle fascicles of the
myometrium
 Mx: (+) irregular nests of endometrial stroma, w/
or w/out glands; separated fr the basal layer by 2-
3mm
 Sxs: Menometrorrhagia (irreg and heavy menses)
 Colicky dysmenorrhea
 Dyspareunia
 Pelvic pain

 Can co-exists with endometriosis

+
+
Endometrial Polyps
 Exophytic
masses of variable size projecting into
the endometrial cavity

 May be single or multiple; usually sessile; 0.5 to 3

cm; occasionally pedunculated

 May be asymptomatic or abnormal bleeding

 Cytogenetic
studies:
 Chromosomal arrangements

 Tamoxifen

 Functional, Hyperplastic and Atrophic polyp

+
+
Endometrial Hyperplasia
 Imptcause of abn bleeding; frequent precursor to
the mc type of Endometrial CA

 proliferation of endometrial glds relative to the

stroma  gland-to-stroma ratio

 Molecularstudies: EH and CA share specific

acquired genetic alterations in genes linked to
oncogenesis

 Prolonged estrogenic stimulation – secondary to

anovulation, estrogen production from
endogenous or exogenous sources
+
 Associated conditions include:
 Obesity (peripheral conversion of androgens to
estrogens)
 Menopause
 Polycystic ovarian syndrome
 Functioning Granulosa cell tumors of the ovary
 Excessive ovarian cortical function (Cortical
stromal hyperplasia)
 Prolonged admin of estrogenic substances
(Estrogen Replacement Tx)
***same influences to be of pathogenic significance
in some endometrial carcinomas
+

 Molecular Basis:
 Inactivation of PTEN TSG (negative regulator of
phosphotidylinositol 3-kinase (P13K)/AKT
growth-regulatory pathway)  OVERACTIVE
P13K/AKT pathway
 PTEN – 20% of EH; 30-80% of CA’s

 WHO Classification:
a. Non-atypical Hyperplasia
b. Atypical Hyperplasia (aka Endometrial
intraepithelial neoplasia)
+
 Non-atypical
Hyperplasia
  gland-to-stroma ratio
 Glands show variation
insize and shape
 Few are cystically
dilated
 Crowded glandular
structures, however,
retention of stroma
 Rare (1-3%)  CA
 Withholding estrogen
 cystic atrophy
+
 Atypical Hyperplasia
 Complex pattern of
proliferating glands w/
nuclear atypia
 Back-to-back glands
 Cells are rounded with
loss of perpendicular
orientation to bm
 Nuclei have vesicular
chromatin and
conspicuous nucleoli
 May overlap a well-diff
adenoCA
 23 -48% - may have CA
when hysterectomy is
done
+
Malignant tumors of the Endometrium
 mc invasive cancer of the female genital tract; 7%
+
Type I Endometrial CA
 mc type; 80%; resemble more proliferative endometrial
glds

 Called as ENDOMETRIOID CARCINOMA

 May arise in the setting of EH

 Associated with obesity, diabetes, HPN, infertility and

unopposed estrogen stimulation

 mc mutation: signaling through the P13K/AKT pathway

 TP53 mutation is found in 50% of poorly-diff CA’s; (-) in

well-diff or late events involved in tumor progression
+  Morphology:
 Polypoid or diffuse
 Composed of glandular growth patterns
 3 grades:
1. Well-differentiated AdenoCA
 composed almost entirely of well-formed
glands
2. Moderately-differentiated AdenoCA
 well-formed glds admixed with 50% or less
solid sheets of cells
3. Poorly-differentiated AdenoCA
 >50% solid growth pattern
 20% - may contain squamous elements
(Endometrioid CA with squamous differentiation)
+
+ Type II (Serous) Carcinoma
 gen
10 yrs older than women with type I; 15% of
endometrial CA’s

 Usually arise in the setting of endometrial atrophy

 Usually poorly-diff (grade 3) tumors

 mc subtype: Serous carcinoma

 Lesscommon subtype: Clear cell CA and MMMT

(Malignant Mixed Mullerian Tumor)

 TP53 mutation – 90% of Serous CA

 Poorprognosis: propensity to exfoliate , travel through

FT  implant on peritoneal surfaces; often spread
outside the uterus at the time of Dx
+
 Morphology:
 Large bulky tumors; deeply invasive to
myometrium
 Precursor lesion: Serous endometrial
intraepithelial CA
 Papillary or glandular pattern
 High-grade nuclei (Marked cytologic atypia)
 High N:C ratio
 Atypical MF
 Marked hyperchromasia
 Prominent nucleoli

 Grade 3 - irrespective of histologic pattern

+
+
 Uncommon in women younger than 40 y.o; NO current
available screening test
 Postmenopausal vaginal bleeding with excessive
leukorrhea
 Uterine enlargement – usually not present in early
stages
 Prognosisdepends on the clinical stage at Dx as well
as the Hx grade and subtype
 Tx: surgery alone or combine with irradiation – 90% 5
yr SR in stage I (grade1-2) in Endometrioid CA
 Serous CA – 18-27% 5 yr SR; more common in women
of African-American descent; 80% recurrence rate;
Surgery with chemoTx
+ MMMT
 aka Carcinosarcomas
 Endometrial adenoCA with a malignant mesenchymal
component
 Stromalmalignancy:
 Homologous – leiomyosarcoma
 Heterologous – chondroSA, RhabdoSA, OsteoSA

 Molecular
studies: similar to the prev-mentioned
Endometrial CA’s (PTEN, TP53)
 Mx: Bulky and polypoid; protude through the cervical os
 Postmenopausal women; bleeding
 Heterologous cpt has worse Px than homologous
 Overall poor Px: 25-30% 5 yr SR
+
Homologous Heterologous
+
+
Tumors of Endometrial Stroma

 Uncommon; <5%

 ADENOSARCOMAS
 Large broad-based endometrial polypoid
growths  may prolapse through the cervical os
 Malignant-appearing stroma with benign but
abnormally shaped endometrial glands
 4th-5th decade
 Low-grade malignancy
 Estrogen-receptive  responds to oophorectomy
+
 STROMAL TUMORS

2 categories:
 Benign stromal nodules
 Endometrial stromal sarcomas (ESS)

 ESS - aberrant chromosomal translocations 

fusion gene (JAZF1)
 Relapse rates relatively common
 Px: poor; 50% 5 yr SR with Low-grade ESS; lower
in High-grade ESS
+
Adenosarcoma ESS
+ Tumors of the Myometrium
 Leiomyoma
 prev called as Fibroids; mc tumor in women
 Benign sm tumor; can occur anywhere in the uterus
 3 common type: Subserous (beneath serosa),
Submucosal (beneath endometrium); Intramural (within
the myometrium)
 Gx: May be single or multiple; well-circumscribed; gray-
w; nodules to masses
 Mx: Whorled pattern of sm bundles
 40% - cytogenetic abn
 Rearrangement of chr 12q14
 MED12 gene mutation
+
 Asxmatic, abn
bleeding, urinary
frequency
 frequency of
spontaneous abortion,
fetal malpresentation,
uterine inertia (failure
to contract with
sufficient force),
postpartum HgE
 Rare malignant
transformation
+  Leiomyosarcoma
 Uncommon
 Arise fr myometrium or endometrial stromal
precursor cells, rather than leiomyomas
 Cytogenetics: more complex; deletions; also have
MED12 mutations
 Gx: 1. bulky, fleshy masses invading the uterine wall
2. polypoid masses that project into the uterine
lumen
 Mx: well to highly anaplastic; criteria for malignancy
– nuclear atypia, mitotic index, zonal necrosis
 Mitotic index - >10/10hpf; high grade nuclear
atypia (>5/10hpf is enough)
***Mitotically-active benign leiomyoma – in young
or pregnant women
+
 Peakage incidence:
40-60 y.o.

 Hematogenous spread
– lungs, bone, brain

 Dissemination
througout the
peritoneal cavity

 40% 5 yr SR

 Anaplastic
lesions –
10-15% 5 yr SR
+

Fallopian Tubes
+
Inflammations

 Suppurative Salpingitis
 Any pyogenic org; more than one org may be
involved
 Gonococcus – 60% of cases
 Chlamydia

 Tuberculous Salpingitis
 Rarein western countries
 Common in countries where TB is prevalent
 Can cause infertility
+ Tumors and Cysts

 Endometriosis
 mc primary lesions

 Paratubal Cyst
 0.1-2cm translucent cysts filled with clear serous fluid

 Hydatids of Morgagni
 Larger cysts located usually at the fimbriated end
 Arise from mullerian ducts; no clinical significance

 Adenomatoid tumors
 Subserosal location; small nodules with benign glands
+

 Ectopic pregnancy
 Mc in ampulla

 AdenoCA
 Rare; usually metastatic; aggressive
course
 poor Px; abN discharge, bleeding or abN
PAP smear
+

Ovaries
+

 mc lesions: functional, benign cyts and tumors

 Neoplasticdisorders – gp accdg to origin

 Mullerian epithelium
 Germ cells
 Sex-cord stromal cells

 Primary inflammations - uncommon

+
Nonneoplastic and Functional Cysts
 Follicle Cysts
1. Cystic follicles
 very common; originate from an unruptured
graafian follicle or ruptured follicles but
immediately sealed
 Usually multiple; up to 2cm; filled with clear
serous fluid
 Gray glistening membrane

2. Follicle cysts
 >2cm; may cause pelvic pain
 Granulosa-thecal cell lining; assoc with
estrogen
+

 Luteal Cysts
 aka corpora lutea; present in the normal ovaries
of women of reproductive age
 Lined by a rim of bright yellow containing
luteinized granulosa cells
 Occasionally rupture  peritoneal reaction
+
+ Polycystic Ovaries and Stromal
Hyperthecosis
POLYCYSTIC OVARIAN SYNDROME (PCOS)
 is a complex endocrine d.o. charac by:
 Hyperandrogenism
 Menstrual abN
 Polycystic ovaries
 Chronic anovulation
 Decreased fertility

 Formerly called Stein Leventhal syndrome

 Affects 6-10% of reproductive age women

+
 Assoc with obesity, type 2 DM and premature AS

 Etiology: NOT completely understood

 Marked dysregulation of enzymes involved in

androgen biosynthesis and excessive androgen
production (central feature of this d.o.)

 Insulin
resistance and altered adipose tissue
metabolism  diabetes and obesity

 Hx: Numerous cystic follicles or follicle cysts that

enlarge the ovaries (only in 20-30% of women)
  estrone levels   risk for EH and CA
+
+
STROMAL HYPERTHECOSIS
 aka cortical stromal hyperplasia
 d.o. of ovarian stroma in postmenopausal women
 May overlap with PCOS in younger women
 Gx: uniform enlargement of the ovary (up to
7cm); white to tan; usually bilateral
 Mx: hypercellular stroma and luteinization of the
stromal cells forming discrete nests of cells with
vacuolated cytoplasm
 Clinical features: similar to PCOS but virilization
more striking
+
Ovarian Tumors
 80% are benign; bet 20-45 y.o.; borderline tumors
at slightly older age
 Malignant tumor in older women (45-65 y.o.)
 3% of all cancers in females; 5th mc COD; spread at
the time of Dx
 WHO classification
 Surface epithelium/FT epithelium and
endometriosis
 Germ cells – fr yolk sac; pluripotent
 Stromal cells, sex cords
+
+
+
Epithelial Tumors
 Most arise from Mullerian epithelium
 Classification - based on differentiation and extent
of proliferation of the epithelium
3 major histologic types: Serous, Mucinous and
Endometrioid tumors
 epithelial proliferation are benign, borderline,
malignant
 Benign – cystic areas - cystadenomas
 Cyst and fibrous areas – cystadenofibromas
 Predominantly fibrous – adenofibromas
+

 Borderline and malignant tumors with

cystic cpt – cystadenofibromas
2 different types with regards to
clinicopathologic and molecular studies:
 Type 1 – low-grade tumors; in assoc with
borderline tumors or endometriosis
 Type II – high-grade tumors; high-grade
serous CA’s
+
SEROUS TUMORS
 mc malignant ovarian tumors of the ovary
 30% of all ovarian tumors: 70% (benign or borderline)
and 30% (malignant)
 Benign and Borderline Tumors – unknown etiology
 Malignant– incompletely understood: nulliparity, family
history and heritable mutations; BRCA1 and BRCA2
mutations
 Serous ovarian carcinomas
 Low-grade (WD) CA – may arise from borderline
tumors
 High-grade (Mod to poorly diff) CA – may arise from
in-situ lesions if FT fimbriae or fr serous inclusion cysts
+
 Mutations:
 Low-grade tumors – KRAS, BRAF, ERBB2, TP53
 High-grade – TP53; (-)KRAS or BRAF
 Gene amplification of PIK3CA
 Deletion of RB gene
 BRCA1/2

 Gx: Multicystic lesions; Intracystic or outside ovary

 Benign – smooth glistening cyst wall
 Borderline – (+) papillary projections
 Malignant – papillary outgrowths or polypoid
projections; larger solid areas with fixation or
nodularities to the capsule
+
 Mx:
 Benign – SCE with cilia
 Borderline - complexity of the stromal
papillae;epithelial stratification and mild nuclear
atypia; NO stromal invasion
 LG and HG CA’s – complexity of growth pattern,
infiltrative involvement; stromal involvement;
nuclear stypia, (+) atypical MF; multinucleation
 Psammoma bodies – concentric Ca++ -
characteristic of serous tumors but not indicative
of malignancy only
 LG to HG serous tumors – involves peritoneal
surface and omentum  ascites
+
+
+

 Bilaterality
is common:
 20% in benign
 30% in Borderline
 66% in malignant

 Px:
 100% 5 yr SR – borderline; confined within ovary
 70% 5 yr SR – malignant; confined within ovary
 90% - borderline with peritoneal involvement
 25% - malignant with peritoneal involvement
+
MUCINOUS TUMORS
 20-25% of all ovarian neoplasms

 Middle adult life (rare b4 puberty and postmenopause)

 Classification:
 Benign
 Borderline
 Malignant – 3% of all ovarian tumors

 Mutationof KRAS proto-oncogene

 58% in benign
 75-86% in Borderline
 85% - malignant
+
 Gx:
 Surface of ovary rarely involved
 Bilaterality – uncommon; 5%
 Larger cystic masses, >25kg; usually multiloculated
filled with sticky, gelatinous fluid rich in
glycoCHONs
 Mx:
 Benign – lined by tall columnar cells with apical
mucin that lacks cilia (endocervical type or
Intestinal type)
 Borderline – epithelial stratification, tufting and/or
papillary intraglandular growth
 Malignant – confluent glandular growth (expansile);
marked epithelial atypia
+
+
ENDOMETRIOID OVARIAN TUMORS
 10-15% of all ovarian CA’s

 (+)
tubular glds; may arise in the setting of
endometriosis; 15-20% may coexist with
endometriosis

 Similar
genetic alterations with endometrial CA,
endometrioid type

 Gx:
 Solid and cystic areas of growth
 Bilaterality is common – 40%

 Mx: Glandular patterns resembling endometrial origin

+
+
CLEAR CELL CARCINOMA
 Extremely
rare; composed of large epithelial cells with
abundanr clear cytoplasm

 Stage3; 90% 5 yr SR rate for tumors confined within

ovary; very poor outcome if spread has occured
+
TRANSITIONAL CELL TUMORS
 Usually benign
BRENNER TUMOR
 May be solid or cystic; unilateral (90%)
 Small (<1cm) to massive tumors (20-30cm)
 Fibrousstroma is sharply demarcated nests of
epithelial cells resembling the epithelium of the
urinary tract
 Mostare benign; small cases: borderline and
malignant
+
+ SUMMARY of ovarian epithelial tumors:
 Sn/Sx: lower abdml pain and abdml enlargement
 GI complaints
 Urinary frequency
 Dysuria
 Pelvic pressure
 For MALIGNANT: progressive weakness, weight loss,
cachexia; ascites (seeding into peritoneal cavity);
tumor exfoliation and seeding is common
 Regional nodes usually involved
 Distant mets: lungs, liver, GIT
***most women with ovarian CA present with high stage
dse
***NO specific specific tumor marker; CA-125 (use more
for dse recurrence/progression)
+
Germ Cell Tumors

 15-20% of all ovarian tumors

TERATOMAS
3 categories: Mature (Benign), Immature
(Malignant) and Monodermal or highly
specialized
A. Mature (Benign) Teratomas
 Most are cystic; aka Dermoid Cysts
 Almost always lined by skin structures
 In young women of active reproductive years
+
 Gx:
 Bilateral in 10-15% of cases; unilocular cysts
containing hair and sebaceous material
 Common to find tooth structures and areas of Ca++
 Mx:
 Thin walled lined by epidermis (SSE) with hair
follicles, sebaceous glds, and other skin adnexal
elements
 Structures originating fr other germ cell layers:
cartilage, bone, thyroid and neural tissue
 1% undergo malignant transformation (mc: SQCA,
others are thyroid CA and melanoma)
+
+

B. Monodermal or Specialized Teratoma

 Rare gp of tumors
 mc: Struma ovarii and Carcinoid; usua unilateral
 Struma ovarii – composed entirely of mature
throid tissue; may be fxnal  hyperthyroidism
 Ovarian carcinoid – may arise from intestinal
tiss; may be fxnal (esp >7cm)  produce 5-
hydroxytryptamine; metastatic intestinal
carcinoid usually bilateral
+
+
C. Immature Malignant Teratomas
 rare tumors; (+) embryonal or immature fetal
tissue
 Found in prepubertal adolescents and young
women; mean age: 18 y.o.
 Gx: Bulky tumors; still see components of the
mature counterpart
 Mx: (+) immature neuroepithelium, cartilage,
bone, muscle and other elements
 Grow rapidly; penetrate capsule  local or distant
spread
 Good prognosis
+
+
DYSGERMINOMA
 2%of ovarian CA’s; 50% of malignant germ cell
tumors

 Female counterpart of testicular seminoma

 May occur in childhood; 75% - 20-30 y.o.

 NO endocrine fxn

 expresses OCT3, OCT4 and NANOG (transcription

factors); KIT gene mutations
+  Gx: 80-90% - unilateral tumors; size range: barely
visible nodules to masses filling virtually entire
abdomen
 Solid yellow-white to gray pink surface
 Often soft and fleshy appearance

 Mx: composed of large vesicular cells with clear

cytoplasm and centrally placed nuclei
 t.c. grow in sheets and cords separated by scant
fibrous stroma (infiltrated by mature lymphocytes)

 All are malignant tumors; only 1/3rd is aggressive

 96% cure rate when limited to ovary; highly responsive

to chemoTX  even for tumors extending beyond
ovary; overall survival is high (80%)
+
+
YOLK SAC TUMOR
 aka Endodermal Sinus tumor
 2nd mc malignant tumor of germ cell origin
 Derived fr malignant germ cells differentiating along
the extraembryonic yolk sac lineage
 Elaborate α-fetoprotein
 Charac feature: glomerulus-like structure composed
of a central bv enveloped by tc within a space also
lined by tumor cells
 Intracellular and extracellular hyaline droplets are
seen; stained (+) for α-fetoprotein by peroxidase
 Mostly in children and young women; abdml pain
and rapidly growing pelvic mass; unilateral
 Tx: surgery + chemoTx  80% SR
+
+
CHORIOCARCINOMA
 Similar to yolk sac tumor; extraembryonic
differentiation of malignant germ cells
 Usually in assoc with other germ cell tumors; pure
chorioCA is extremely rare
 Aggressive; hematogenous spread  lungs, liver,
bone and other sites (at the time of Dx)
 Secrete  levels of βHCG
 Unresponsive to chemoTx  fatal

OTHER GERM CELL TUMORS

 Embryonal CA – highly malignant
 Polyembryoma –embryoid bodies
 Mixed Germ cell tumors
+
ChorioCA Embryonal CA
+
Sex Cord-Stromal Tumors

 Derived fr ovarian stroma (derived fr the sex cords

of the embryonic gonads)

 Undiff
gonads  males (Sertoli and Leydig) and
females (Granulosa and Theca)

 Secreteestrogen (granulosa and theca)

feminizing

 Secrete
androgens (sertoli and leydig) 
masculinizing
+
GRANULOSA CELL TUMOR
 Composed of cells resembling granulosa cells of a
developing ovarian follicle
 Divided into: Juvenile and adult GCT (based on Px’s
age)
 5% of all ovarian tumors; 95% - adult type granulosa
cell tumor (postmenopausal women)
 Gx: usually unilateral; size vary from small to large,
solid and cystic encapsulated masses
 Yellow hue – hormonally-active; due to intracellular
lipids
 Mx: small cuboidal cells growing in anastomosing
cord, sheets and strands
 Small, distinctive gland-like structures filled with
acidophilic material (Call-Exner bodies)
+
2 clinical importance:
 May elaborate large amts of estrogen
 May behave like low-grade malignancy

 In prepubertal age – precocious sexual devt

 In
adult women – proliferative breast dses, EH,
endometrial CA

 Occasionally, GCT secrete androgens  musculinizing

the Px

 All
GCT are potentially malignant; indolent course;
recurrences are not uncommon; 10 yr SR – 85%

 tissueand serum inhibin, product of granulosa cells;

used as biomarker
+
 Assoc with FOXL2 gene mutation – 97% of cases
+
FIBROMAS, THECOMAS and FIBROTHECOMAS
 Fibromas – arise fr fibroblast; hormonally inactive
 Usually unilateral (90%)
 Gx: Solid, round or slightly lobulated, encapsulated,
hard, gray to white masses
 Mx: well-diff fibroblasts and scant interspersed
collagenous stroma

 Thecomas – composed of plump spindle cells with

lipid droplets; pure thecomas – rare; hormonally active
 Fibrothecomas – mixture of both
+
 Clinsnx/sxs:
 Pelvic mass, occasionally with pain
 Ascites – 40% (esp with tumors >6cm)
 Hydrothorax – R side
*** Meigs syndrome: ascites, hydrothorax and
ovarian tumor

SERTOLI-LEYDIG TUMORS
 Fxnal; masculinization or defeminization
 Peak age: 20-30 y.o.
 Mutations of DICER1
 Gx: same as GCT
 Mx: sertoli or leydig cells interspersed with stroma
+
+
METASTATIC TUMORS
 mcis from mullerian origins, ft, contralateral ovary,
pelvic peritoneum

 mc extramullerian tumors: breast and GOT

 Rare
case: Pseudomyxoma peritonei – from
appendiceal tumors

 Krukenberg tumor – metastatic from gastric

adenoCA; bilateral involvement; charac by mucin-
secreting, signet-ring cancer cells
+
Pseudomyxoma Krukenberg tumor
peritonei
+

Gestational and
Placental Disorders
+  Impt cause of IU or perinatal death, congenital
malformations, IUGR, maternal death
+
+
Disorders of Early Pregnancy
 Spontaneous Abortion
 “miscarriage”; pregnancy loss before 20 wks of
gestation
 Most occure at 12 weeks
 Most cases: unknown cause
 Fetal chromosomal anomalies – aneuploidy and
translocations; 50%
 Maternal endocrine factors – poorly controlled DM
 Physical defects of the uterus – leiomyomas
 Systemic d.o. affecting maternal vasculature – HPN
 Infections - toxoplasma
+

 Ectopic Pregnancy
 Implantation of the fetus other than normal
intrauterine location
 m.c.: FT in 90% of cases; others: ovary (trapping of the
fertilized ovum within the follicle), abdml cavity
(fertilized ovum fails to enter or drops out of the
fimbriated end of FT), intrauterine portion of the FT
(cornual pregnancy)
 Most impt predisposing condition: PID; other cause of
peritubal scarring and adhesions: AP, Endometriosis,
prev surgery; use of IU contraceptive device
+
 m.c. cause of
hematosalpinx (bld-
filled FT)  growth of
gestational sac 
rupture  massive
intraperitoneal he
 Medical emergency;
onset of moderate to
severe abdml pain
and vaginal bleeding
 Hemorrhagic shock
+
Disorders of Late Pregnancy
 3rdtrimester; related to the complex anatomy of the
maturing placenta
 Twin placentas – arteriovenous shunts 
preferential blood flow to one twin at the expense of
the other
 Abnormalities of placental implantation
 Placenta previa – placenta implants at the LUS or
cervix
 Placenta accreta – partial or complete absence of
decidua; chorionic villi adheres directly to the
myometrium  failure of placental separation at
birth
+
+
+
 Placental Infections
 2 pathways:
1. ascending infection through the birth canal
- mc; almost always bacterial; may cause
PROM and preterm delivery
- amniotic fluid is cloudy with purulent
exudate; (+) neutrophils in C-A membrane
2. hematogenous (transplacental) infection
- classic cpts of the TORCH gp
(toxoplasmosis, rubella, CMV, HSV)
- chronic inflammation in C-A membrane
+
 Preeclampsia and eclampsia
 Systemic syndrome charac by widespread
maternal endothelial dysfunction that presents
during pregnancy with HPN, edema and
proteinuria
 3-5% in last trimester; mc in primigravida
 Starts after 34 wks of gestation
 Mx:
 Infarcts
 Exaggerated ischemic changes in cv (syncytial
knots)
 Retroplacental hematoma
 abN placental vessels – thrombi, fibrinoid
necrosis
+
Gestational Trophoblastic Disease
Hydatidiform Mole
 Cystic swelling of the cv
 Variable trophoblastic proliferation
 Usually dx during early pregnancy (average 9 wks)
by sonogram
 Can occur at any age BUT common during the 2 ends
of reproductive life (teenagers and between 40-50
y.o.)
 2 types:
 Complete Mole
 Fertilization of an egg that has lost its female
chromosome  genetic material is paternally
derived
+
 90% have a karyotype 46XX
 Embryo dies very early in devt
 2.5% risk of subsequent chorioCA and 15% to
invasive mole
 Partial Mole
 Fertilization of an egg with 2 sperm
 Karyotype is triploid (69XXY)
 Fetal tissues are (+)
 NOT assoc with chorioCA

 Gx: delicate, friablemass of thin walled,

translucent, cystic, grapelike structures consisting
of edematous (hydropic) villi
+

 Complete Mole – involve most villous structures;

cv are enlarged with scalloped shape with
central cavitation (cisterns)
 Extensive trophoblastic proliferation involving
the entire circumference of the villi

 Partial
Mole – only a fraction of the villi are
enlarged and edematous
 Trophoblastic hyperplasia is focal
+
+
 ClinicalFeatures:
 Most women present with spontaneous
miscarriage or undergo D&C due to sonogram
findings
 HCG – markedly increase
 Most moles are successfully removed by D&C
 Pxs subsequently monitored for 6 mos to a yr to
ensure HCG levels decrease to non-pregnant
levels
 Continuous  of HCG  indicative of a
persistent or invasive mole
+
Invasive Mole
 Mole that penetrates or even perforates the uterine
wall
 Invasion of the myometrium by hydropic cv with
proliferation of both cyto and syncytiotrophoblasts
 Locally destructive tumor; may invade parametrial
tissue and bv
 cv may embolize to distant sites e.g. lung and brain
(BUT do not grow as true metastases); regress
spontaneously
 Sn/Sxs: vaginal bleeding
 Irregular uterine enlargement
 Persistent elevated serum HCG
 Responsive to chemoTx; however, uterine rupture
may necessitate hysterectomy
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Choriocarcinoma
 Malignant neoplasm of trophoblastic cells derived
from a previous normal or abnormal pregnancy e.g.
extrauterine ectopic pregnancy
 Rapidly invasive and metastasize widely
 Responds well to chemoTx
 Uncommon; 50% may arise fr complete H mole,
25% from previous abortions, 22% ffg normal
pregnancies, remainder in ectopic pregnancy
 Gx: soft and fleshy, yellow-white tumor with large
pale areas of necrosis and extensive he
 Mx: proliferation ofcyto and syncytiotrophoblasts
within the myometrial wall, bv, serosa; (-) for cv
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 Clinical features:
 Irregular vaginal spotting of bloody, brown fluid
 High propensity for hematogenous spread
 HCG: variable; maybe be high like in H mole;
necrotic tumors may have low HCG
 Metastases: 50% - lungs, 30-40% - vagina, brain,
liver, bone and kidney
 Tx: depends on stage; usually involves surgery +
chemoTx
 Responsive to chemoTx  100% remission with
high rate of cures
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Placental Site Trophoblastic Tumor (PSTT)
 <2%; neoplastic proliferations of extravillous
trophoblasts k.a. Intermediate trophoblasts
(polygonal mononuclear cells with abundant
cytoplasm
 Produce human placental lactogen
 Presents with a uterine mass, abN uterine bleeding
or amenorrhea with moderately elevated HCG
 Mx: malignant trophoblastic cells infiltrating
endomyometrium
 May follow normal pregnancy (50%), spontaneous
abortion or H mole
 Localized dse – excellent Px; Disseminated dse –
very poor
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