CERVIX

A. Non neoplastic disorders

Cervicitis
- Chronic and acute
- Caused by vaginal aerobes and
anaerobes, streptococci, enterococci,
E,Coli ,and staphylococci= non specific
inflammation.
- most commonly involves the
endocervix and SCJ
-some degree of inflammation is found
in virtually all multipara=little clinical
consequence

- specific infections by gonococci

,Chlamydia , mycoplasma and HSV
should be identified for their
relevance to UGTI ,pregnancy
complications or sexual transmission
 Acute cervicitis acute inflammatory
cells, erosion, ulceration and reactive
or reparative epithelial change
Chronic cervicitis extremely
common, may cause (PID,
endometritis, salpingitis,
chorioamnionitis,) mononuclear cell
infiltration, necrosis ,granulation
tissue
Manifest with cervical discharge or
may be asymptomatic
 Endocervical polyp
2-5% of adult women
Usually multigravidas , 30 59 years
Irregular vaginal bleeding (suspicion of
malignancy) / mucoid discharge
Most arise in the endocervical canal
Inflammatory / hyperplastic
Produces postcoital bleeding
 Gross
Usually single , up to 1 cm
Not precancerous
Rarely mimic malignant tumor
protruding in to endocervical canal
Simple curettage or surgical excision
is a cure
 Intraepithelial and invasive
squamous tumors
Squamous intraepithelial lesions(SIL)
Invasive carcinoma usually preceded
by SIL
Which may exist for 20 years before
tumor becomes invasive
SIL cells usualy initially detected by
cytologic examination= Pap smear
 Majority of cases are associated with HPV.
Low risk-types 6, 11
High risk-types 16, 18
Risk factors
Early age of onset of sexual intercourse
Multiple, high-risk partners
High-risk types of HPV in the biopsy
Smoking, oral contraceptive pills (OCPs),
immunodeficiency
 SIL cells have similar histology as
invasive carcinoma cells
Including :
Loss of Maturation & polarity, Mitotic
activity, N/C ratio, pleomorphism,
Hyperchromasia, Coarse chromatin, Large
nucleoli
 SIL usually affects transformation
zone near endocervical epithelium

May end abruptly

May extend up to endocervical canal

 As the squamous epithelium overgrows &
obliterates the surface columnar
papillae, it obstructs crypt openings
with accumulation of mucus in deeper
crypts (glands) to form mucus
(nabotian) cyst
 Low grade SIL(LSIL)
Usually euploid or polyploid
2/3 regress
1/6 progress
Others are unchanged
 High grade SIL(HSIL)
Usually aneuploid
Less regression
1/3 become invasive at 9 years
Associated with HPV 16,18,31,33
Peaks during age 30 39
 Treatement
Conization
Electrodiathermy
Cryosurgery
laser
 Microscopy
Loss of Maturation & polarity
Mitotic activity, N/C ratio
Pleomorphism,
Hyperchromasia,
Large nucleoli
 Three systems of diagnosis
1. cervical intraepithelial neoplasia(CIN)
CIN l, CIN ll , CIN lll

2. Low grade SIL Vs high grade SIL

3. Dysplasia
mild , moderate , severe
CIN l / low grade dysplasia / LSIL

Flat slightly raised

Thickened epithelium
Dysplastic cells in lower 1/3
With koilocytotic atypia in middle or
upper epithelium
Normal / CIN I
CIN ll/Moderatedysplasia/HSIL
Persistant abnormal differentiation
towards prickle and keratinizing layers
With at least focal maturation
= Lower 2/3 involved
CIN I/CIN II
CINlll/severe dysplasia/HSIL
Epithelium totally replaced by atypical
cells in at least part of the lesion
Loss of maturation
koilocytosis
 Progression from CIN I to CIN III is
not inevitable
Reversal to normal is more likely in CIN I.
Requires 10 years to progress from CIN I
to CIN III
Requires 10 years to progress from CIN
III to invasive cancer
Average age for cervical cancer is 45 years old
 Invasive cervical Neoplasms
Squamous cell carcinoma
Adenocarcinoma
Others:
Adenosquamous cell carcinoma
Undifferentiated carcinoma
Clear cell adenocarcinoma
 Invasive squamous cell
carcinoma
# 1 in many countries(including ours)
Incidence decreased in Western
society
Pap smear test to detect premalignant
lesions
Mean age 51 years
 Risk factors
Early age at first intercourse
Multiple sexual partners
Male partener with multiple sexual
parteners
History of HSIL
Immunocompromization of any cause
Oral contraceptives
 Cigarette smoking

Parity

Family history

Associated genital infections

Lack of circumcision in male partner

 HPV
Found in DNA of 90% of cancers
90% of condyloma and premalignant
lesions
High risk HPV types for cervical
carcinoma: 16,18,31,33
Low risk : 6,11,42,44= associated
with condyloma
 Pathogenesis
HPV acts via E6 and E7 genes
Integrated with tumor DNA
E6 binds to p53 causing its proteolytic
degradation
E7 binds to Rb gene displacing
transcription factors normally bound
by Rb gene.
 Other cofactors are important, b/s
- Most with HPV don't get cervical ca
- 10-15% of cervical carcinoma not
associated with HPV

HIV , HTLV- l adversely affect the

prognosis

Associated with rapidly progressive

course
 Clinic
SSx: Vaginal bleeding, Leucorrhea,
pain, dysparuinia, dysuria
Spread:
Direct contiguity
Lymphatic
Hematogenous
Treatments : surgery , radiotherapy
, chemotherapy
 Morphology
Patterns
Fungating (exophytic)
Ulcerating
Infiltrative
Histology
Large cells (keratinizing/Non-
keratinizing)
Small cell carcinoma (poorly
differentiated
 Prognosis
Stage I: 80-90% 5 year SR
Stage II: 75% 5 year SR
Stage III: 35% 5 year SR
Stage IV: 10-15% 5 year SR
Cause of Death:
Urinary obstruction (uremia)
 Adenocarcinoma
15-20% of invasive cervical
carcinomas

Associated with HPV 18 & 16 in 95%

of cases
Endometrium and body of
uterus
 Endometrial dating
The endometrial tissue is made up of glands
and stroma
It is divided into a deeply seated basal layer
and a superficial functional layer
During child-bearing age, the normal
endometrium undergoes a series of sequential
changes in the course of the ovulatory cycle
that prepare it to receive the ovum
 If the ovum is not fertilized, the proliferative
endometrium is cast off by menstruation,
and the cycle repeats itself
A normal endometrial cycle is associated with
changes in both endometrial glands and stroma
this allow the pathologist to diagnose
microscopically the phase of the menstrual cycle.
 The cycle has two phases
Proliferative phase ( before ovulation)
Secretory phase (after ovulation)
Biopsy Must
uterine corpus above the level of the
isthmus
functionalis as basalis layer does not
respond to progesterone
D and C
 Proliferative phase
Length varies from 10-20 days
ideal is 14 days;
in response to estrogen production and
estrogen receptors on epithelium
Early proliferative:- days 4-7
Mid proliferative:- days 8-10
Late proliferative:- days 11-14
 Secretory/luteal phase
Traditionally assumed to be 14 days,
but may vary
Progesterone secretion inhibits
endometrial proliferative activity and
induces secretory activity
Post ovulatory date
 Luteal phase defect
Due to inadequate progesterone
production
Associated with infertility and
spontaneous abortions
Lag of histologic endometrial date of
3+ days from actual post-ovulatory
date
 Pregnancy related changes
Similar changes seen with
-intrauterine pregnancy,
-ectopic pregnancy,
-progesterone therapy
 Arias-Stella reaction
Exaggerated gestational hyperplasia;
endometrial glands are enlarged with
abundant clear or eosinophilic
cytoplasm and
marked nuclear changes:- large,
hyperchromatic, pleomorphic, smudged
 Decidua

Stromal change
Bland nuclei, minimal atypia, abundant
cytoplasm
 Endometritis
Rare in reproductives
No time of establishment
Acute endometritis
Post abortion, Post partal, IUD
Mixed bacterial
Edema, exudate, ulcer
Inflmmatory infiltrates: Stroma &
Mucosa (gland abscess)
 Chronic endometritis
Follow acute endometritis
Primary chronic: Tuberculosis
Thickened endometrium
Lymphoplasmacytic infiltrates,
fibrosis, vascular proliferation
Presence of plasma cell is diagnostic
Manifestation: Normal/Abnormal
cycle, infertility, pain & discharge
 Tuberculous endometritis
Always secondary to Tb salpingitis
Infertility
Premenopausal
Granulomas, not with usuall
caseation
Postmenopausal
Caseous granulomas, Shaggy thick
endometrium, caseous content
 Adenomyosis
Endometrial tissue well below deep in
the myometrium
Gross Features:
Uterine enlargement
Myometrial thickening with many
small cysts
Histologic features:
Unencapsulated endometrial stroma
and glands
Hemosiderin and chronic
inflammation
 Adenomyosis Manifestation
Menorrhagia
Colicky dysmenorrhea
Dyspareunia
Pelvic pain
Assymptomatic in menopause
Rarely cause rupture during pregnancy
 Endometriosis
Endometrial tissue outside the uterus
20-30 yrs , up to 10% of all women
affected
Consists of functional layers of
endometrium that go through menstrual
changes
Causes pain,
infertility (1/3 of women )
 Sites
- It occurs in the following sites, in
descending order of frequency
1. Ovaries
2. Uterine ligaments
3. Rectovaginal septum
4. Pelvic peritoneum
5. Laparatomy scars
6. rarely in umbilicus, vagina
 Three potential explanation exists
regarding the origin of these lesions
The regurgitation/implantation theory
The metaplastic theory
The vascular or lymphatic pathway
 AUB
Abnormal uterine bleeding is the
occurrence of excessive bleeding during
or between menstrual periods
Causes can be organic or functional
 Dysfunctional uterine bleeding
(DUB)
Abnormal uterine bleeding due to functional
disturbance
Known causes
endometriosis,
submucous myoma,
endometrial polyp (5-15%),
cancer (5-15% of postmenopausal bleeding),
precocious puberty,
anovulatory cycle,
pregnancy complication, etc.
 Endometrial polyp
Grossly pedunculated mass
composed of cystically dilated glands
with fibrous stroma and thick walled
blood vessels
Asymptomatic or associated with
bleeding
 Endometrial hyperplasia
Proliferation of glands of irregular
size and shape with an increase in the
gland to stroma ratio
Usually in perimenopausal women
Usual predecessor to endometrial
carcinoma
 Causes
prolonged estrogenic stimulation with
reduced progestational activity
E.g. anovulatory cycles, estrogen
producing tumors, exogenous estrogen
adminstration
- A key factor in development of
endometrial hyperplasia & related
carcinoma is inactivation of the PTEN
tumor suppressor gene
- In the absence of PTEN endometrial cells
become more sensitive to stimulation by
estrogens
 Morphology
Gross : polypoid endometrium

Mic: gland to stroma ratio should be

> 50%
 CLASSIFICATIONS OF
ENDOMETRIAL HYPERPLASIA
> Hyperplasia with no atypia
-Simple
-Complex
> Atypical hyperplasia
-Simple
-Complex
 Endometrial carcinoma
Age: 50-60 years,
>80% post menopausal
Pathogenesis:
long unopposed estrogen, evolving
from endometrial hyperplasia
Spontaneous (atrophic endometrium)
Associate factors: nulliparous,
obesity, estrogen therapy, ovarian
tumors, DM, hypertension, infertility
 In terms of potential pathogenesis, two
general groups of endometrial cancer can
identified
The first group develops on a background of
prolonged estrogen stimulation & endometrial
hyperplasia
These tumors tend to be well differentiated,
mimicking normal endometrium (endometrioid)
The second group is less commonly associated
with endometrial hyperplasia & occur at
relatively older age
Tumors in this group are poorly differentiated & resemble
serous ovarian carcinoma
 Morphology
Enlarged uterus
Diffuse nodular or polypoid thickening
Bulky friable necrotic filling
endometrium
Histology:
Well differentiated adenocarcinoma
Solid, cribriform, papillary
Endometroid and serous
Adenosquamous carcinoma
Adeoncarcinoma muscle
invasion
 Manifestation
Irregular vaginal bleeding
Excessive leukorrhea
Diagnosis needs Histology of
curettage
 Spread & Prognosis
Early confined to endometrium
Extension to myometrium,
parametrium & pelvis
Along tube to ovary andbroad ligament
Lymphatic: paraaortic,
Hematogenous: Vagina,liver,lung,bone
Prognosis:
Degree of differentiation, 5year =
66%
Staging
 Carcinosarcomas
Endometrial adenocarcinoma with
stromal differentiation which is
malignant(muscle,cartilage,bone)
Malignant mixed Mullerian
tumor(MMMT)
Postmenopausal women
Bleeding
Previous radiation therapy
 Gross: more fleshy , bulky, polypoid
Mic: adeno carcinoma with malignant
stromal component
Sarcomatous element can be extra
uterine = adipose , cartilage, bone,
skeletal muscle
Metastasize as adeno carcinoma.
Highly malignant tumor , 5 year
survival rate of 25 30%
 Tumors of myometrium
Leiomyoma
aka fibroid
Present in 25% of women during
reproductive years
More common in blacks than whites
usually multiple in blacks
In 77% at autopsy
84% of tumors are multicentric
 Clinically apparent lesions are more
common in nulliparous, postmenopausal
women
May interfere with pregnancy or block
ureters if large
Estrogen responsive
Enlarge during pregnancy
 Gross
sharply circumscribed, round, firm,
gray-white, whorled cut surface
usually within myometrium (intramural)
may be submucosal or subserosal
may be multiple
Mic : whorled (fascicular) pattern of
smooth muscle bundles
separated by well vascularized
connective tissue

 Secondary changes are detectable in

approximately 65% of cases
hyaline degeneration (63%)
mucoid or myxomatous degeneration
(19%)
calcification (8%)
cystic changes (4%)
There is no relation between
symptomatology and the presence of
these changes
 Red degeneration (present in 3% of
the cases) can result in abdominal
pain, vomiting, and fever
This change is characterized by
extensive coagulative necrosis and is
often associated with pregnancy or
the use of contraceptive drugs
leiomyoma has undergone massive red degeneration
Leiomyoma with edematous (hydropic) changes
 Leiomyosarcoma
Uncommon
Myometrium/ endometrial stroma
smooth muscle differentiation
Bulky , fleshy masses invading wall
Polypoid masses projecting in lumen
Mic: well differentiated to anaplastic
tumors
Diseases of Fallopian Tubes
 Salpingitis
Hematogenous and ascending
Acute salpingitis
- Bacterial infection common;mixed
- may cause infertility
Causes:
- sexual transmission most common ( N.
gonorrheae, Chlamydia, Mycoplasma)
post instrumentation,
post-IUD,
post-pregnancy or abortion
 Gross:
pyosalpinx (pus),
hematosalpinx;
tubo-ovarian abscess common
Mic:
marked neutrophilic infiltrate,
congestion and edema;
mucosal ulceration;
reactive epithelial changes
 Chronic salpingitis
Gross: enlarged distorted tube
adherent to ovary;
may be associated with hydrosalpinx
or pyosalpinx that transforms to a
tubo-ovarian cyst
 Micro
blunted, shortened, fibrotic plicae
contain chronic inflammatory cells;
fused plicae may produce a pseudo
glandular pattern (chronic follicular
salpingitis) that resembles malignancy
 Tuberculous salpingitis
Usually bilateral;
hematogenous spread
Associated with young infertile
patients with endometrial involvement,
 Micro:
caseating granulomas within mucosa
extreme adenomatous proliferation
may resemble carcinoma
chronic inflammation and fibrosis in
muscularis
 Tubal Ectopic pregnancy
Chronic salpingitis = destroys the
lining folds and traps the ovum
Congenital abnormalities
Functional tubal disturbances,
Endometriosis,
Small tumor
Often a history of infertility
 Gross:
distension of ampullary segment of
tube with thin or ruptured wall,
dusky red serosa and
Hematosalpinx
Mic:
intraluminal chorionic villi
extravillous trophoblast (may be
degenerated);
variable fetal parts;
 Endometriosis
Nodules in wall or serosa of tube;
May focally replace tubal mucosa
Muscularis is usually not involved
Endometriosis is usually present
elsewhere in the pelvis
 May represent extension of
endometrium from uterine cornu (10%
of women have extension to isthmus)
Associated with intratubal polyps,
causing infertility or ectopic
pregnancy
Also occurs in 20-50% of tubes after
ligation
 Paratubal cysts
Common incidental findings
Called hydatids of Morgani if large
and near fimbriae or broad ligament
Gross: attached to fimbriated end of
tube by a pedicle, thin walled, clear
content
Micro: usually tubal-type lining, may
have plicae
 Tumors
Adenomatoid tumor
-Most common benign tumor of
fallopian tube,
-benign mesothelioma
 Carcinoma
Rare, 0.3 to 1.0% of genital tract
malignancies
Mean age 57 years, rarely teenagers
usually incorrect preoperative
diagnosis
 Symptoms
vaginal bleeding or discharge (2/3),
pain,
adnexal mass
endometrial smear positive in 10%
 Gross
enlarged tube,
with solid or papillary tumor filling the
lumen;
tumors occasionally are primary in the
fimbriae;
80-97% unilateral;
hemorrhage, necrosis and cysts
common
 Micro
invasive papillary adenocarcinoma;
may resemble ovarian serous
adenocarcinoma
with complex papillary architecture
 Diseases of the Ovary
Inflammatory
Usually associated with F. tube
Tuboovarian abscess
Rarely, autoimmune oopharitis
Non-neoplastic masses
Simple / functional cysts
Neoplastic Diseases
 Non-neoplastic diseases
Simple cysts: simulate neoplasms, may
be associated with endocrine manifs.
Follicular cysts
Luteal cyst

Polycystic ovary

Endometriosis
 Follicular cysts
Cystic changes in unr uptured Graffian
follicles
Common in reproductive years
May be related to abnormal releases of
FSH/LH
Usually asymp, may form adnexal mass =
pedicle may twist = hemorrhagic
infarction
 Multiple small cysts (polycystic)
Unilocular contain serous fluid
Lining: Flattened granulosa cells
Estrogen excess = Hyperplasia
(Endometrial & breast) , precocious
puberty
Usually regress with in 2 months
 Corpus Luteum Cyst
Corpus luteum-Un raptured or sealed
Reproductive years: end of menstrual
cycle or pregnancy
Contains hemorrhagic fluid lined by
luteinized cells (yellow lining)
Rupture = Bleeding = Mild oophoritis &
organization
DDx: Endometriosis
 Polycystic ovarian disease
Stein-Leventhal syndrom
Unknown cause associate with abn.
Hormone regulation (Enzyme defect =
excess androgen)
LH to FSH ratio 2:1 or 3:1
3-6% reproductive age
Clinical triad: Infertility,
Obesity(40%), hirsutism(50%)
Oligomenorrhea, persistent an ovulation
 Morphology:
Large ovaries , multiple sub cortical
cysts
Thickened ovarian capsule
Thecal hyperplasia & Luteunization
Numerous follicular cysts

Associated with endometrial

hyperplasia and well differentiated
adenocarcinoma
hirsutism (excess hair)
 Ovary in a patient with SteinLeventhal
syndrome
Numerous follicular cysts beneath the ovarian
surface and the absence of corpusl

 Endometriosis
Presence of endometrial glands and
stroma out side uterus
Common site: Ovaries, Uterine
ligamant, Rectovaginal septum, Pelvic
peritoneum, Laparatomy scar.
Rare sites: Umblicus, Vagina, Vulva &
Appendix
 Theories of Endometriosis
Theories of endometriosis
Regurgitation theory
Metaplastic theory
Vascular or Lymphatic dissemination
theory
Other theories: Genetic, Hormonal
and Immunologic factors
 Morphology
Multiple hemorrhagic cysts (chocolate
cysts)
Distorted structures by organization
Fibrous adhesion or obliteration
Histology: Finding two of these three
Finding endometrial glands
Finding Endometrial stroma
Finding hemosiderin
 Ovarian endometriosis
"chocolate cyst"
 ovarian endometriosis
repeated hemorrhage and accumulation
of hemosiderin-laden macrophages
 Manifestation
10% of women
Infertility
Dysmenorrhea
Menstrual irrregularities
Pelvic pain
Dyspareunia
Painful defication
 Ovarian Neoplasms
80 % benign (ages 20 45 )
90% of malignancies are carcinomas
- 80 % have spread beyond the
ovary at diagnosis
- 40 65 years
Risk factors for carcinoma
- Nulliparity,familyhistory,gonadal
dysgenesis
- BRCA 1 or BRCA 2 mutation
- P53 mutations
 Classification
Based on most probable tissue of
origin
Surface epithelial(coelomicepith):65%
Germ cell: 15%
Sex cord stromal : 10%
Metastasis : 5 %
Surface epithelial classifi.based
On cell type: serous, mucinous
,endometroid , brenner, clear cell
On Pattern : cystic , solid , surface
On Amount of fibrous stroma
eg. Serous cystadenofibroma
On Behaviour:benign,borderline,malig.
Risk of malignancy rises with increase
in grossly solid areas
Prognosis depends on grade and stage
of the tumor.
 Surface epithelial subtypes
Tissue that tumor most
Type of differentiation
closely resemble

Serous Fallopian tube epitheli.

Mucinous Endo cervical / GI

Endometroid Proliferative endom.

Clear cell Gestational endom.

Transitional cell / Urothelium

brenner
 Surface epithelial behavior
Behavior Pathologic features
Benign Simple,nonstratified
epithelium with out atypia
Borderline Epithelial proliferation
with stratification ,
tufting, mitotic activity,
nuclear atypia. No
stromal invasion

Carcinoma Stromal invasion &

cytologic atypia
 Ovarian neoplasms
Most malignant tumors are surface
epithelial
Bilateral carcinomas: serous(65%),
metastatic (>50%), endometroid(40%)
Lower abdominal pain ,abdominal mass,
increased pressure on adjacent organs
Elevated CA 125 in 80% of serous &
endometroid carcinomas
 Ovarian tumor in children
60% germ cell tumors

10-25% sex cord stromal tumors

15-20% surface epithelial tumors,

usually benign
 Serous tumors
25% of all ovarian tumors
60% benign, 15% borderline, 25%
malignant
Ciliated columinar cells , filled with
clear serous fluid
Carcinomas frequently have psammoma
bodies
 Serous cyst adenoma
Benign; 25 % bilateral

Gross: smooth or papillae on outer

surface or protruding in to cavity

Mic: single layer of ciliated columonar

cells : no atypia ,no architectural
complexity , no invasion.
Serous cystadenoma
 Serous cystadenoma
Papillary projection
 Serous borderline tumor
Bilateral 1/3 of cases
Papillary stratification , detached
papillae
No stromal invasion
Peritoneal implants seen in 1/3 of
patients
5 year survival =100% if confined to
ovaries ; 90% with peritoneal implants
 Serous cyst adenocarcinoma
Gross: solid , hemorrhagic , necrotic

Mic : nuclear atypia & stratification ,

frequent mitosis , stromal invasion

5 year survival 70% if confined to

ovary , 25% with peritoneal
involvement
 Mucinious tumors
15% ovarian neoplasms

80% benign, 10%borderline,10% ca

Compared to serous neoplasms: have

more cysts, larger size, unilateral

Filled with sticky ,gelatinous fluid rich

in glycogen
 Mucinious cystadenoma
5 % bilateral

Mic: tall columnar non ciliated cells,

abundant intracellular mucin

Usually endocervical type ; intestinal /

mixed
 Mucinious borderline tumor
10% bilateral

Mic: resemble villous or tubular

adenomas of intestine , non invasive

Either endocervical or intestinal type

Mucinious cyst adenocarcioma
Gross: unilateral , >10cm ,smooth
capsule , cystic and solid areas

Stromal invasion
 Pseudomyxoma peritoneii
jelly belly

Mucinious Ascites with bland to low

grade adenomatous epithelium
intimately associated with pools of
extracellular mucin and fibrosis

Usually all cases have appendiceal not

ovarian origin.
 Other surface tumors
Endometrioid tumor
Usually malignant; Coexist with
edometrial ca & endometriosis
Brenner tumors
Nested Transitional epithelial type
with surrounding fibroblastic
proliferation = more solid
Rarely malignant
Clear cell carcinoma
 Clinical Course
Most assymptomatic and present late
Benign easily resectable
Malignant: Poor % yr SR
Progressive weaknes, cachexia, wt.
loss. Ascites and peritoneal seeding
Regional L. nodes metastasis
Metastasis to liver, lung & GIT
Treatment needs follow up of CA-125
 Germ cell tumors
20% of ovarian tumors

Resemble germ cell tumors in testis

Usually children and young adults

Usually benign cystic teratomas

8 % are mixed
Classification of germ cell tumor

o Dysgerminoma- No differentiation
o Embryonal carcinoma- Poorly
differentiated
o Extraembryonic tissue- Endodermal
sinus tumor (yolk sac)
o Trophoblast- Choriocarcinoma
o Embryonic tissue- Teratoma
 Mature cystic teratoma
Dermoid cyst
Predominantly ectodermal
differentiation( skin , brain)
Young women
15 % bilateral
1% undergo malignant transformation
usually squamous cell carcinoma
 Mature cystic teratoma
Tangles of hairs & sebum
Mature cystic teratoma
 Immature malignant
teratoma
Solid component tissues resemble that
of the fetus or embryo
Prepubertal adolescents and young
women
Most cases recur in 2 years
Monodermal or Specialized teratomas
- These are rare group of tumors
- Struma ovarii & carcinoid are most common
- Struma ovarii is composed entirely of mature
thyroid tissue
- It can rarely be cause of hyperthyroidism
- Ovarian carcinoid, which presumably arises
from intestinal epithelium in a teratoma, can
be functioning producing 5-
hydroxytryptamine & carcinoid syndrome
 Sex cord stromal tumors
5% of ovarian neoplasms
Granulosa Theca cell tumor
Thecoma fibroma
Sertoli leyding cell tumor
Meigs syndrom : ovarian fibromas ,
right sided hydrothorax,ascites
After tumor excision hydrothorax and
ascites disappear.
 Granulosa Theca cell tumors
- These ovarian neoplasm are composed of
varying proportions of granulosa & theca
cell differentiation.
- These neoplasms account for about 5%
of all ovarian tumors
- Two thirds occur in postmenopausal
women
 Morphology
- They vary form microscopic foci to
large solid & cystic encapsulated masses
- Microscopically, cords, strands & sheets
of cuboidal to polygonal cells are seen.
Occasionally, small distinctive , gland
like structures filled with eosinophlic
material resembling immature follicles
(call-exner bodies) are seen
- These tumors potentially can elaborate
large amounts of estrogen.
- Functionally active tumors in young girls
can produce precocious sexual
development in young girls.
- In adults , they may be associated with
endometrial hyperplasia, cystic disease
of the breast & endometrial carcinoma
 Ovarian metastasis
Usually uterus , f.tube , etc
Breast,stomach,biliarytree,panceras
Krukenbergs tumor bilateral
metastasis composed of mucin
producing signet ring cancer cells ,
most often of gastric origin.
Krukenberg tumors of ovary.
Krukenberg tumors of ovary.
Pathology of pregnancy
 Disorders of early pregnancy
Spontaneous abortion
10-15% of clinically recognized pregn.
22% of pregn. detected via hCG levels
Maternal factors : developmental, cervical
incompetence, inadequate implantation, leiomyomas,
infection
Fetal factors: fetal genetic abnormalities >50%
chromosomal abnormalities
Dx: villi, trophoblasts, fetal parts
 Spontaneous abortion
villi, trophoblasts, fetal parts
 Ectopic pregnancy
Implantation of fetus in any site
other than a normal uterine location
1 per 150 pregnancy
Fallopian tube (90%), ovary, abdominal
cavity, cornua of uterus
Risk factors: 35-50% have PID or
peritubal adhesions (appendicitis,
endometriosis, surgery, leiomyomas);
50% have normal tubes
 In all sites the fertilized ovum
undergoes its usual development =>
placenta, amniotic sac, fetus,
implantation site decidual changes
Hematosalpinx, tubal rupture (6wks)
=> shock
Regression or tubal abortion less
common
Tubal pregnancy
Tubal pregnancy
Tubal pregnancy
 Tubal pregnancy
Chorionic villi tubal mucosa
The decidua
 Disorders of late pregnancy
Abnormalities in placental shape,
structure, & implantation, retro
placental hemorrhage (abruptio
placentae)
Umbilical cord knots
Infection
Rupture of fetal vessels
Utero placental insufficiency
 Term Placenta
Fetal surface
 Term placenta
Maternal surface
Chorionic villi
 Disorders of late pregnancy
lack of normal separation of placenta at
delivery
The classification of placental invasion into
myometrium

Type Invasion of chorionic villi

Accreta Superficially into myometrium

Increta Deep into myometrium

Percreta Through the myometrium

Placenta accreta
Placenta accreta
 Placenta infection
Villitis, chorioamnionitis (fetal
membrane), funisitis (umbilical cord)

Routes: Ascending (most common &

bacteria) => premature rupture of
membranes or hematogenous
Acute chorioamnionitis
Funisitis
 Toxemia of pregnancy
Preeclampsia
symptom complex characterized by
hypertension, proteinuria, & edema
6% of pregnant women
last trimester & usually first
pregnancies
When preeclamptic patients develop
convulsion => eclampsia => DIC
 Gestational trophoblastic
disease ( GTD)

Hydatidiform mole (partial or

complete)
Invasive mole
Choriocarcinoma
Placental site throphoblastic tumor
 Hydatidiform mole
Abnormal placenta with marked cystic
swelling of chorionic villi caused by
central edema of stroma, abnormal
blood vessels, variable trophoblastic
hyperplasia
High serum hCG
Complete or partial
1 per 100 or 1,000 pregnancies
 Risk factors
Prior mole, first pregnancy, born in
southeast Asia, maternal age <19 or
40+, diet deficient in Vitamin A
precursors
 Complete mole
Abnormal gametogenesis and fertilization
90% 46, XX ; 10% 46XY/XX karyotype
that is paternally derived
Usually no fetus
Usually presents at 15 weeks gestational
age with excess uterine enlargement; may
pass molar vesicles or have vaginal bleeding
due to spontaneous abortion
Preeclampsia often occurs in first
trimester; also hyperemesis gravidarum
10-17% progress to invasive moles
2% to choriocarcinoma
1% will have another molar pregnancy
 Complete mole
Uterus
 Gross: Complete mole
Placenta has grape-like appearance,
villi fill uterus, exhibit hydropic
degeneration, no embryo present
Complete hydatidiform mole
Complete hydatidiform mole
 Mic: complete mole
Diffuse trophoblastic proliferation &
edema of all villi

Central cistern formation

Villi usually avascular

Complete mole
Complete hydatidiform mole
 Partial mole
20% of all moles; triploid (69,XXY)
Contain extra set of paternal
chromosomes, either from second
sperm or one diploid sperm (diandric)
Embryo is usually present, although
often abnormal
Usually small for date uterus; hCG not
markedly elevated as in complete mole
4-12% develop persistent gestational
trophoblastic disease; very low risk of
choriocarcinoma
 Gross: Partial mole
Some of the villi are edematous
Micro: mixture of edematous villi and
relatively normal villi; circumferential
mild trophoblastic hyperplasia, villi
have vessels with nucleated RBCs if
fetal development present
Partial hydatidiform mole
Partial hydatidiform mole
Partial hydatidiform mole
Partial hydatidiform mole
 Feature Complete mole Partial mole

Karyotype 46XX (46XY) Triploidy

Villous edema All villi Some villi

Throphoblast Diffuse Focal;slight

proliferation

Atypia Often present Absent

Serum HCG Elevated Less elevated

Choriocarcinoma 2% Rare
 Invasive mole
Mole that penetrates uterine wall
Associated with high serum hCG after
evacuation of a mole
Occurs in 10-16% of all complete
moles
Invade parametrial tissue, broad
ligament and blood vessels; may
perforate uterus
Gross: irregular hemorrhagic lesion
penetrating into myometrium
Micro: mole, usually complete, with
villi that penetrates myometrium
Invasive mole
Invasive mole
 Choriocarcinoma
Most aggressive form of gestational
trophoblastic disease
Secondary to a prior pregnancy
(normal or abnormal)
1 per 40 moles (usually complete)
50% arise from prior moles, 25%
from prior abortions, 22% from
normal pregnancies
Clinical: bloody, brown, foul-smelling
discharge
Rapidly invasive and metastasizing;
may present with metastases but have
small or necrotic primary tumor
 Metastases commonly to lungs (50%),
vagina, brain, liver, kidney => risk of
hemorrhage
Treatment: chemotherapy associated
with 100% survival if restricted to
uterus vs. 83% survival for all
metastatic gestational trophoblastic
disease
Monitor via serum hCG and chest X-
rays
Gross: soft, fleshy, yellow-white,
necrotic, hemorrhagic
Micro: mixture of cytotrophoblast and
syncytiotrophoblast ; no villi
Uterine choriocarcinoma
Choriocarcinoma
Choriocarcinoma