female genital system

Pathology of the Female GenitalTract
DEPT OF PATHOLOGY

LOWER GENITAL TRACT
Vulva, Vagina, Cervix-
Infections and neoplasms
Embroyology and Anatomy

Female Genital Infections-
Candida
Trichomoniasis
Gardnerella – most common
Gonnorrhoea,Chlamydia –female infertility
Mycoplasma –spontaneous abortion
Viruses asHPV- cancer

HSV Type II
-cervix, vagina, vulva
Papules-vescicle-ulcers
Cx and vagina-- Leukorrhea
Latent Infection
Recurrence
To neonates
Diagnosis-serology,microscopy

Trichomonas Vaginalis
flagellated ovoid protozoan
Strawberry Cx
Mycoplasma
Candida species

Pelvic inflammatory disease
Symptoms
Organisms_Gonococcus,
Chlamydia trachomatis, Clostridium
Perfringens
Mode of infection and spread

Gonococcus
-an intracellular diplococcus
Diagnosis-culture,
papsmear
Endometrium spared
Cl .features--A/c Suppurative salpingitis
salpingo-oophoritis
Tubo ovarian abscesses
Pyosalpinx,
Hydrosalpinx

Complications
Peritonitis
Intestinal obstn
Bacteraemia
Infertility

Vulva
Vulvitis
Bartholin Cyst
Vestibular Adenitis

Non-neoplastic lesions
Leukoplakia
Lichen sclerosus-subepithelial fibrosis
Lichen simplex chronicus-acanthosis, and
hyperkeratosis
Squamous Hyperplasia

Vulvar Leukoplakia
Leukoplakia: A descriptive clinical term;
refers to a white plaque or patch on a mucosal
surface
Causes of vulvar leukoplakia:
1.Vitiligo (loss of pigment)
2.Inflammatory dermatosis: p.e. psoriasis
3.Squamous intraepithelial neoplasms of the vulva
(VIN) and invasive carcinoma
4.Paget’s disease

Tumors of Vulva
Benign-Papillary hidradenoma
Condyloma accuminatum
(HPV 6&11)
Venereal Wart,Mucosal Polyp
Syphilitic Condyloma latum
Viral cytopathic effect-Koilocytic
atypia

Premalignant and malignant
neoplasms –SCC,BCC,melanomas or
adenocarcinomas.
SCC-HPV related
SChyperplasia
Vulvar Intraepithelial Neoplasia
Extramammary Paget Disease

Vagina
VIN and Sq.cell carcinoma
Adenocarcinoma
Embryonal Rhabdomyosarcoma

Uterine Cervix
 Cervicitis
 Tumors

Cervicitis
“Erosions” and development of the transformation zone
(T zone). Nabothian cysts.
Infectious and non-infectious cervicitis
Vaginal flora, Chlamydia trachomatis, Ureaplasma
urealyticum, Trichomonas vaginalis, Candida
species, Neisseria gonorrhoeae, Herpes simplex II,
and HPV.

acute nonspecific: postpartum, Staphylococci/Streptococci
Nonspecific (chronic) cervicitis
Gross: reddening, swelling, and granularity around
margins of external cervical os.
Microscopy: Hyperplasia and reactive atypia of
epithelium, no dysplasia, glycogen depletion .
Mononuclear cell infiltrate, nabothian cysts. Viral
inclusions (HSV). Plasma cells in C. trachomatis.

Cervicitis
Leukorrhea
Culture interpretation*
.
If severe >>>differentiation from carcinoma:
colposcopy and biopsy
.
Subsoil for carcinogenesis?
May lead to sterility (fibrosis/ unfavorable medium
for sperm).

Endocervical polyp
 Inflammatory polypoid masses, cm.
 Smooth surface composed of columnar
mucus-secreting cells (endocervical
epithelium) with underlying cystically
dilated glands filled with mucus. Stromal
edema inflammatory mononuclear cells.
 Squamous metaplasia and ulceration.

Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Cervical cancer was the most frequent form of
cancer around the world.
Impact of Papanicolaou screening: Decrease
incidence of invasive tumors and increase
incidence in the detection of precursors
(dysplasias/CINs) lesions.

and Carcinoma
Peak incidence
1. CIN : 30 Y
2. Invasive carcinoma: 45 y
Risk factors
1. Early age at first intercourse
2. Multiple sexual partners
3. A male partner with multiple previous
sexual partners

Cervical Intraepithelial Neoplasia
(CIN) and Carcinoma
Higher incidence in lower socioeconomic
groups
Genital infections
Exposure to oral contraceptives
Rarity among virgins
Multiple pregnancies

Cervical Intraepithelial Neoplasia
(CIN) and Carcinoma
T zone
High grade dysplasia/HPV 16 and 18
Viral isolation and typing do not predict the
course.
Follow up: cytology, colposcopy (acetic acid
test), biopsy*.

HPV: 85-90% of lesions
Serotypes:
1. High risk: 16, 18, 31, and 33.
2. Low risk (associated with condylomas):
6, 11, 42, and 44.
Integration of viral genes into host
genome>>transcription>>translation of
specific proteins that inactivate p53 and
retinoblastoma tumor suppressor genes.
and Carcinoma

and Carcinoma
Viral infection does not mean that a women
will develop cancer.
10-15% HPV: negative
Other carcinogens, genetic factors, host
immunity, cigarette smoking.

and Carcinoma
Importance of early detection, adequate follow up
and management.
Histologic grading of precursor lesions:
1. CIN I: Mild dysplasia
2. CIN II: Moderate dysplasia
3. CIN III : Severe dysplasia/carcinoma in situ

and Carcinoma
Cytologic grading of precursor lesions
1) LOW GRADE SQUAMOUS
INTRAEPITHELIAL LESIONS
[CIN I and Condylomas (koilocytosis)]
2) HIGH GRADE SQUAMOUS
INTRAEPITHELIAL LESIONS
[CIN II, CIN III/CIS]

and Carcinoma
Natural History
Different studies = different populations = different
results
CIN I: 50 to 60% regress, persists 30%, and progress
to CIN III 20%. 1 to 5% become invasive.
CIN III: 33% regress, progression varies from 6 to
74%.

Invasive Carcinoma of the Cervix
80-95%: Squamous cell carcinomas
Multifactorial disease
Preventable
Gross (macroscopic appearance)
Fungating (exophytic)
Ulcerative (endophytic)
Infiltrative

ROUTES OF INVASION
Direct spread-adjacent stroma, vagina,
pelvic wall.
Local and distant spread to lymph nodes
Distant metastasis to lungs , liver ,bone
marrow etc

 Squamous cell carcinoma
Well to poorly differentiated
 Adenocarcinomas
 Adenosquamous carcinomas
 Staging

 CIS: Asymptomatic, Leukorrhea
 Carcinoma: Vaginal bleeding, leukorrhea,
painful coitus, and dysurea
 DX: Colposcopy: acetic acid test, Bx
 Mortality: Related to local extension*:
ureter obstruction or invasion of bladder or
rectum.

 Importance of early diagnosis
 Time….?
 5-year survival rate:
1. Stage 0 (CIS): 100%
2. Stage I: 85% to 90%
3. Stage II: 70 to 75%
4. Stage III: 35%
5. Stage IV: 10%

Stage 0: Carcinoma in situ
Stage I: Tumor confined to the cervix
Stage II: Tumor extends beyond the cervix but not
onto the pelvic side wall
Stage III: Tumor extends to the pelvic side wall or
to the lower one third of vagina, or causes
hydronephrosis, or a nonfunctioning kidney
Stage IV: Tumor extends beyond true pelvis, or
biopsy-proved involvement of bladder or rectal
mucosa.

Management
 LEEP
 Conization
 Hysterectomy
 Pelvic exenteration
 Radiotherapy

FEMALE GENITAL SYSTEM
Endometrium

Body of the Uterus
Endometritis
Adenomyosis
Endometriosis
Dysfunctional uterine bleeding
Endometrial hyperplasia
Endometrial polyps
Leiomyomas and leiomyosarcomas
Endometrial carcinomas

Endometritis
 Clinical settings:
1. Chronic gonorrheal pelvic disease
2. Tuberculosis
3. Retained Product of conception
4. IUD
5. Spontaneously
 Histology: Irregular disposition and
proliferation of endometrial glands, plasma cells
and lymphocytes in the stroma

Adenomyosis
 Growth of the basal layer of endometrium
(glands and stroma) down into the
myometrium between the muscle bundles
 Thick myometrium: reactive hypertrophy
 Nonfunctional: no bleeding*
 Menorrhagia, dysmenorrhea, and
premenstrual pain

Endometriosis
 Infertility, dysmenorrhea, pelvic pain.
 Foci of endometrial tissue in pelvis
(ovaries, pouch of Douglas, uterine
ligaments, tubes, rectovaginal septum).
 Sometimes in umbilicus, LNs, lungs, skin,
heart, bone.
 Theories of genesis: Regurgitation,
metaplastic, and lymphovascular

Endometriosis
 Functional endometrium: cyclic bleeding
 Complications:Fibrosis,adhesions: pain, sterility
 Gross: red-blue to yellow-brown nodules,
chocolate cysts in ovaries
 Microscopy: Endometrial glands, stroma, and
hemosiderin deposition

Endometriosis
Theories of genesis:
1. Regurgitation: menstrual backflow
through fallopian tubes and subsequent
implantation
2. Metaplastic: metaplasia of coelomic
epithelium
3. Lymphovascular dissemination

Endometriosis
sites
Ovaries,
ligaments,
rectovaginal areas,
pelvis
scars,
umbilicus,
vagina,vulva&appendix

Dysfunctional Uterine Bleeding
abnormal bleeding with no organic lesion
Etiology of uterine bleeding varies with age
:prepuberty
, adolescence,
reproductive age,
perimenopause, and postmenopause.

Dysfunctional Uterine Bleeding
Three functional groups (E/P)
1. Anovulatory cycles-metabolic
disorders, ovarian lesions,sys
diseases,unexplainable
2. Inadequate luteal phase-inadequate
corpus leuteum
3. Contraceptive induced bleeding

Anovulatory Cycles
 Common at both ends of reproductive life
 Hypothalamic-pituitary axis, thyroid, or adrenal
dysfunction
 Functioning ovarian producing lesion,
malnutrition, obesity, stress, debilitating disease
 Persistence of proliferative “growth” until
endometrium collapse, spiral arteries rupture, and
bleeding occurs.

Inadequate Luteal Phase
 Corpus luteum fail to mature normally or regress
prematurely: less progesterone is produced: delay
and inadequate secretory phase
Contraceptive Induced Bleeding
 Imbalance in the ratio Estrogen/Progesterone

Endometrial Hyperplasia
 estrogen>>>>Progesterone: Polycystic
ovaries(Stein-Leventhal syndrome), cortical stromal
hyperplasia, granulosa-theca ovarian tumors
 Simple Hyperplasia
 Complex Hyperplasia without atypia
 Complex Hyperplasia with atypia: 20/25% risk of
carcinoma
 Continuum of changes based on duration and level of
estrogen excess
 Causes irregular uterine bleeding
 Biopsy and follow up

Endometrial Polyps
Uterine bleeding
Gross: Sessile(rarely pedunculated) rounded
lesions: 0.5 to 3 cm
Microscopy: Surface lined by columnar
epithelium, stroma (monoclonal stromal cells with
rearrangement of 6p21) with thick-walled vessels,
and endometrial glands some of which appear
cystically dilated.
Occur at any age, but common around menopause

Uterine Malignancy
Endometrial- glands
Stroma
Both glands and stroma
Myometrial-

Leiomyoma
Benign smooth muscle tumor
“Fibroids”, “Myomas”
30 to 50% of women during reproductive life.
Estrogen stimulates their growth
Involutes after menopause
Monoclonal, 40% have non-random
chromosomal abnormalities

Leiomyoma
Gross: Well circumscribed, firm, gray, white mass.
Whorled cut surface.
Singly or multiple. Few cm to large masses.
Intramucosal, intramural, and/or subserosal
location. Parasitic leiomyomas
Microscopy: Interlacing bundles of smooth muscle
cells. Foci of ischemic necrosis, fibrosis, cyst
degeneration, hemorrhage, and calcification are not
uncommon.

Leiomyoma
Asymptomatic
If Symptoms: Bleeding (menorrhagia) or “mass
effect”
Progression to sarcomas?

Leiomyosarcoma
usually solitary tumors
Derived from mesenchymal myometrial cells
Gross:
1. Bulky masses infiltrating uterine wall
2. Polypoid lesions projecting into uterine
cavity
3. Discrete tumors(~ leiomyomas)

Leiomyosarcoma
Microscopy: Increased cellularity, mitosis,
nuclear atypia, and necrosis.
Recurrence and metastasis are not uncommon
5 year survival rate: 40%

Endometrial Carcinoma
Most frequent cancer of the female genital tract in
USA
55 to 65 y (uncommon <40y)
Risk factors:
1. Obesity: synthesis of estrogen in fat deposits
2. Diabetes
3. Hypertension
4. Infertility: anovulatory cycles

Hyperestrinism : HRT, estrogen secreting
ovarian tumors, etc.
Background of endometrial hyperplasia
20%: no Hyperestrinism and no hyperplasia:
older patients, poor prognosis

Gross:
Diffuse thickening of uterine wall: Infiltrative
Exophytic form
Filling of the endometrial cavity with a firm
to soft partially necrotic tumor.
Myometrium invasion/ serosa/ LN

Adenocarcinomas (Adenocarcinomas with
squamous metaplasia, Adenoacanthoma,
Adenosquamous carcinoma)
Endometrioid
Papillary serous carcinoma
Clear cell adenocarcinoma

Grade: Degree of cytologic differentiation. GH1,
G2, and G3
Stage: Spread of the tumor
1. I: Confined to corpus
2. II: Extension to cervix
3. III: Extension outside the uterus , but still
confined to pelvis
4. IV: Extension outside the pelvis

Leukorrhea and irregular bleeding in a
postmenopausal patient
Enlargement of uterus and fixation to surrounding
structures
Late metastasizing neoplasm to LN and other organs
5-year survival rate:
1. Stage I: 90%
2. Stage II: 30 to 0%
3. Stage III and IV: less than 20%

Mixed Mullerian Tumors
adenofibroma
adenosarcoma
Carcinosarcoma
with or
withoutdifferentiation(Cartilage,bone&
muscle)

FALLOPIAN TUBES AND OVARY

Fallopian tube
Common affliction is inflammation, pelvic
inflammatory disease
gonorrhea, chlamydia, mycoplasma, streptococci
and staphylococci
fever, lower abdominal pain and pelvic mass
•Tubal pregnancy
•Adenocarcinoma

Ovary
 Normal ovary measures 3-5 x 1.5-3 x 0.6-1.5 cm and
weighs 5-8 grams during reproductive age.

Newborn ovary
Note presence of
numerous
primordial follicles
filling the cortex

Four Primordial
Follicles and two
primary follicles

Mature follicle,
Granular cells,
marked by an arrow,
produce estradiol.
(diameter 4-5mm)
The preovulatory follicle
reaches a diameter of
15-25mm.

Corpus Luteum
The cells produce
progesterone.

Hilar cells of
ovarian medulla,
these cells are
mainly responsible
for androgen
production.

Luteinized stromal
cells
Stromal luteinization
(stromal hyperthecosis)
are associated with
androgenic or estrogenic
manifestation.

Normal Cycle of Endometrium
 Proliferative phase: Active growth of
glands, stroma and vessels influenced by
estradiol production by granular cells in the
follicles ( follicular phase).
 Secretory phase: reflects the effect of the
combined production of progesterone and
estradiol by luteinized granulosa and theca
cells of the corpus luteum (luteal phase).

PAROVARIAN/PARATUBAL (MESONEPHRIC)
CYST
Common lesions, vary in size, often bilateral
Large cysts may become palpable, undergo
torsion with/without infarction, and cause pelvic
pain
They are benign
mesonephric cysts: lined by cuboidal cells;
usually arise in ovarian hilum
paramesonephric cysts: lined by columnar
tubal - type epithelium; adjacent to fallopian
tube

FOLLICLE AND LUTEAL CYSTS OF OVARIES
Functional Cysts
Very common
Originate in unruptured Graffian follicles or in
follicles which have ruptured and resealed
Often multiple, they are located immediately
subjacent to the serosa
Lined by granulosa cells or by luteal cells
Usually small (1 - 1.5 cm), filled with clear fluid
Occasionally larger, up to 5cm, and may then be
palpable
Occasionally rupture, causing pain and
intraperitoneal bleeding

CORPUS LUTEUM CYST OF OVARY
Corpus luteum of pregnancy can be up to 20 cm.

Ovarian Neoplasms
Clinical Presentation
Despite their considerable pathologic
diversity, the clinical presentation of
ovarian neoplasms is similar:
Usually asymptomatic until large enough
to cause pressure symptoms (pain, GI
complaints, urinary frequency)
30% are discovered incidentally during
routine GYN exams

Ovarian Neoplasms
Clinical Presentation
large masses may cause increased
abdominal girth
Occasionally, the masses undergo torsion
severe abdominal pain and acute
abdomen
Fibromas and malignant epithelial tumors
can cause ascites
mucinous tumors can cause
pseudomyxoma peritonei
tumors may cause endocrinopathies

Surface Coelomic Ovarian
Neoplasm
SEROUS TUMORS
MUCINOUS TUMORS
ENDOMETRIOID TUMORS - Most are
malignant; adenocarcinoma of
endometrium present in 15-30% of
cases
BRENNER TUMORS- Most are benign

Surface Coelomic Ovarian
Neoplasm
Most surface tumors present with
nonspecifically low abdominal pain
and/or abdominal mass
Malignant tumors grow through
capsule and widely seed the
peritoneal cavity with tumor
nodules and ascites; also distant
metastases

Surface Epithelial Tumors
They are derived from coelomic
epithelium.
They can be strictly epithelial, e.g.
serous, mucinous or endometroid.
They can also have a distinct stromal
component, cystadenofibroma or
Brenner tumor.
They are traditionally divided into
benign, low malignant potential or
malignant.

Serous Tumors
60% Benign, 15% borderline (LMP),
and 25% malignant.
Size ranges from 5-40cm.
Unilocular or multilocular containing
clear serous fluid.
Benign forms show smooth glistening
surface.
The surface of the malignant forms
appears multinodular.

Serous Tumors of the
Ovary
Single most common group of ovarian
tumors
benign and borderline: ages 20 - 50
years
malignant: ages 40 - 60+ years
Usually at least partially if not entirely
cystic:
“cystadenomas;
cystadenocarcinomas”

Serous Tumors of the Ovary
Behavior depends on degree of
differentiation and distribution
May occur on the ovarian surface,
occasionally arises from peritoneal
surface

Serous Tumor
of Low Malignant potential

Serous Tumor
of Low Malignant Potential
 Papillary Tufting  No evidence of
stromal invasion

Borderline Vs. Malignant
Serous Tumors
Both may penetrate (or arise from) the ovarian
surface, shedding cells which implant on
peritoneal surfaces and produce ascites
Only malignant serous tumors invade the ovarian
stroma and metastasize to lymph nodes or other
sites
If confined to ovary, survival at 5 years:
Borderline - 100% ;
Malignant - 70%

Serous Cystadenocarcinoma
of Ovary
These tumor show stromal invasion
Cause elevated CA125 in serum

Serous Cystadenocarcinoma
Involving both Ovaries

Mucinous tumors
Benign tumors usually occur between 3rd.
And 5th. Decade of life
Most common tumor seen during pregnancy
most often associated with acute abdomen due
to torsion

Mucinous Tumors of Ovary
10% BENIGN - only 5% bilateral
10% BORDERLINE
10% MALIGNANT - only 20% BILATERAL
Note that Mucinous tumors are much less likely to
be bilateral and to be malignant than serous
tumors!
Often larger and more likely multiloculated than
Serous tumors; lack psammoma bodies
have endocervix-like or intestine-like lining cells

Mucinous tumors
Benign
Low malignant potential
Malignant

Mucinous Tumors of the Ovary
5% of cases are complicated by
pseudomyxoma peritonei:
peritoneal cavity becomes filled with
gelatinous mucinous fluid (similar to cyst
contents), which mats together the
abdominal viscera.
Rx is surgical, and repeated operations
are sometimes required

Benign
Mucinous Tumor of Ovary

Mucinous tumor of low malignant
potential
10-15% of all mucinous tumors
6-8% of intestinal subtype are bilateral, Vs.
40% of endocervical type
100% long term survival in patients with
stage I mucinous tumor of LMP ( no
malignant potential)

Mucinous tumor
of low malignant potential

Mucinous Carcinoma
Destructive stromal invasion, resemble
mucin secreting adenocarcinoma of
intestinal tract

Endometroid tumors
Benign, unilateral masses, occurring in
older patient>57 Y/O
Endometroid tumor of low malignant
potential, rare, defining criteria are not
well established
Endometroid carcinoma, second most
common of ovarian epithelial
malignancy

Endometroid adenocarcinoma
Occur in 5th. and 6th. Decade
About 15-25% are associated with similar
lesion in the endometrium
Can arise from endometriotic cyst, usually in
younger women
Synchronous or metachronous endometroid
adenocarcinoma of cervix has been reported
Primary extraovarian site has been reported

Clear cell tumor
Benign, rare
Low malignant potential, rare
Malignant
can arise from areas of endometriosis, have
been seen in association with endometroid
adenocarcinoma, both in ovary and
endometrium. They can also be associated
with hypercalcemia

Clear cell carcinoma
These tumors have the highest association
with pelvic endometriosis and Para
endocrine hypercalcemia.

Brenner Tumor
Over 95% are diagnosed between the ages of
30-70.
Are usually unilateral and benign.

Fibroma
 Any age
 Unilateral
 Solid grey
 Most hormonally inactive
 Can produce hydrothorax and ascites
(Meigs Syndrome)
 Rarely malignant

Thecoma
 Any age
 Unilateral
 Yellow
 Can elaborate estrogen resulting in excess
endogenous estrogen
 Can also elaborate androgen resulting in
hirsutism

Sertoli Leydig Cell Tumor
 All ages
 Unilateral, usually small
 Gray to yellow brown
 Composed of tubuli or cords and plump
pink leydig cells
 Most are androgenic
 Small percentage are malignant

Leydig Cell Tumor
These tumors are usually
yellow in color, high
lipid content.
Uniform cell population,
presence of crystals
of Reinke are
diagnostic.

Granulosa cell tumor
Any age, two different type, adult form and
juvenile form
Unilateral
Most elaborate large amount of estrogen
5-25% are malignant, adult form only
Composed of mixture of cuboidal Granulosa
cells in cords, sheets, or strands with
spindled or plump lipid laden theca cells

Note presence of Call Exner Bodies

Diffuse pattern

Germ Cell Tumors
 Dysgerminoma can occurs with gonadal
dysgenesis
 Mature teratoma (dermoid cyst)
 Immature teratoma
 Choriocarcinoma
 Endodermal sinus tumor (yolk sac tumor)

Dysgerminoma
 Peak incidence: 2nd
and 3rd
decade.
 80-90% unilateral
 Gross: Solid small or large gray mass
 Micro: Sheets and cords of large cleared
cells separated by scant fibrous strands.
Stroma contains lymphocytes.
 Prognosis: malignant, but only 1/3
aggressive and spread; all radiosensitive
with 80% cure

Dysgerminoma
Are occasionally encountered in phenotypic
females with gonadal dysgenesis.

Teratoma of the Ovary
BENIGN (MATURE) CYSTIC TERATOMA
Histologically mature
IMMATURE MALIGNANT TERATOMA
Average age 18 years
Most are predominantly solid
Foci of immaturity, usually of neuroepithelial type
Aggressive, metastasize widely
SPECIALIZED TERATOMAS
Struma ovarii: mature thyroid tissue; may cause
hyperthyroidism
Carcinoid: may cause carcinoid syndrome

Mature (benign) Cystic Teratoma
(“DERMOID CYST”)
 Unilocular cyst, bilateral in 10% of cases
 Lined by epidermis with all adnexal structures
 bone, cartilage, thyroid, and other organoid
formations including tooth anlage, bronchi, gut,
brain, eye, etc. often present
 Rarely exceed 10 cm diameter
 Young women (late teens, 20’s); present most often
as asymptomatic ovarian masses on PE or X-ray
 10-15% undergo torsion, present as acute abdomen
 Karyotype of benign cystic teratoma always 46,XX
 Malignant transformation in 1%, squamous cell ca.

Immature Teratoma
Usually cause large solid
or partially cystic
masses.
Show immature neural
elements consisting of
neuroepithelial tubules

Specialized Teratoma
Struma ovarii can cause hyperthyroidism.

Endodermal Sinus Tumor
Yolk Sac Tumor
 Predominantly in young patients
 Large partially cystic ovarian mass
 Aggressive behavior, survival rate for
stage I tumors are 70-90% and 30-
50% for higher stage tumors.

Endodermal Sinus tumor
Serum AFP (alfa fetoprotein) is elevated in
almost all patients.
commonly show Shiller Duval Bodies.

Metastases to Ovary
Older women
Usually bilateral
Tumors can be up to 20 cm
Common primary sites include breast,
lung, gastrointestinal tract

Other tumors of the ovary
 Embroyonal carcinomas
 Mixed germ cell tumors
 Gonadoblastoma

PLACENTA

Gestational Trophoblastic Disease
 Hydatidiform mole, complete and partial
 Invasive mole
 Choriocarcinoma
 Persistent trophoblastic Disease”
All elaborate human chorionic gonadotropin
HCG, which can be detected in the blood
and the urine.

Hydatidiform Mole
Is a voluminous mass of swollen , sometimes
cystically dilated, chorionic villi,
appearing grossly as grape like structures.
The swollen villi are covered by varying
amount of banal to highly atypical
chorionic epithelium.

Complete Hydatidiform mole
 All of the chorionic villi are abnormal
 Chorionic epithelial cells are diploid, 46 XX or
uncommonly 46XY.
 An empty egg is fertilized by two spermatozoa.
 Incidence is 1-1.5/ 2000 pregnancies in US, higher
incidence in Asian countries.
 More common before age of 20 and after age of
40.

Complete hydatidiform mole
 The condition is usually discovered in 4th month
of gestation.
 Ultrasound studies show a diagnostic pattern
which resembles snowflakes. Fetal heart tone is
usually absent.
 The uterine cavity is filled with a delicate friable
mass of thin-walled translucent cystic structures.
 Striking proliferation of cytotrophoblasts and
syncytiotrophoblasts present.
 Markedly elevated serum HCG
 2% progress to choriocarcinoma

Partial hydatidiform mole
 Is developed as the result of fertilization of
a normal egg by two spermatozoa.
 Is always triploid (69XXY).
 Villous edema is only seen in some villi.
 Trophoblastic proliferation is focal.
 Serum HCG level is less elevated.
 Rarely progresses to choriocarcinoma.

MOLAR PREGNANCY
Curettage produced
this specimen,
which consisted of
300 cc of bloody
tissue.

GESTATIONAL TROPHOBLASTIC DISEASE:
HYDATIDIFORM MOLE, COMPLETE TYPE
Swollen, avascular
villi covered by
chorionic
epithelium
(trophoblast) of
varying atypia
Gross appearance is
that of a
voluminous mass
of grape like
structures

GESTATIONAL TROPHOBLASTIC DISEASE:
COMPLETE VERSUS PARTIAL HYDATIDIFORM MOLE
FEATURE COMPLETE PARTIAL
Karyotype 46, XX (rare XY) 69, XXY
Villous edema all villi some villi
Trophoblast Pro- diffuse; circum- partial
liferation ferential
Atypia often absent
serum HCG elevated less elevated
HCG in tissue ++++ +
Behavior 2% get chorio- rare chorio-
carcinoma carcinoma

GESTATIONAL TROPHOBLASTIC
DISEASE:
PARTIAL HYDATIDIFORM MOLE
 A fetus or fetal parts may also be
present
 Some villi are normal
 Almost always triploid
 Normal egg + two spermatozoa 69,XXY
 Rarely becomes malignant

Invasive Hydatidiform Mole
 An invasive mole retains hydropic villi, which
penetrate the uterine wall.
 Can cause uterine rupture and can be life
threatening.
 Hydropic villi may embolize to distant organs,
but this tumor does not have metastatic potential.
 Cure is possible by hysterectomy or
chemotherapy.

Choriocarcinoma
 Is very aggressive malignant tumor arises
either from gestational chorionic
epithelium or less frequently, from
totipotential cells within gonads or
elsewhere.
 Incidence is 1/ 30,000 pregnancies in US.
 More common in Asian and African
countries.

Choriocarcinoma
Incidence
 In US 1/30,000 pregnancies
 50% follow complete molar pregnancy, 25%
following abortion, remainder following normal
pregnancy
 In Asia and Africa can be as high as
1/2,000 pregnancies

Choriocarcinoma
 Most cases are discovered by the appearance of a
bloody, brownish discharge, accompanied by a
rising titer of HCG, particularly the beta subunit.
 Usually appear as very hemorrhagic, necrotic
masses within the uterus.
 The tumor is entirely composed of
cytotrophoblasts and syncytiotrophoblasts.
 Widespread dissemination via blood, lung (50%),
vagina (30-40%), brain, liver and kidney.

Choriocarcinoma
 Chemotherapy results in almost 100% cure or
remission in all patients except some who have
high risk metastatic trophoblastic disease.
 Many of the cured patients have subsequent
normal pregnancies.
 By contrast, non-gestational choriocarcinoma are
much more resistant to therapy.
 Drug of choice is methotrexate.

GESTATIONAL TROPHOBLASTIC
DISEASE:
CHORIOCARCINOMA

Placental Site Trophoblastic
Tumor

PLACENTA ACCRETA
 DEFINITION: Partial or complete absence of the decidua,
with adherence of the placental villi directly to the
myometrium:
placenta increta - extends part way thru myometrium
placenta percreta - extends thru entire wall of uterus
 CLINICAL IMPORTANCE:
1. 60% of cases associated with placenta previa, in
which implantation is in lower uterine segment or cervix
ante partum bleeding; many cases occur in C-section scars
2. Postpartum bleeding, often life threatening, due to
failure of placental separation

PLACENTA ACCRETA, PERCRETA TYPE,
WITH UTERINE RUPTURE

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