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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
Leukoplakia
Tumors of Vulva
Benign-Papillary hidradenoma
Condyloma accuminatum
(HPV 6&11)
Venereal Wart,Mucosal Polyp
Syphilitic Condyloma latum
Viral cytopathic effect-Koilocytic
atypia
female genital system
female genital system
Premalignant and malignant
neoplasms –SCC,BCC,melanomas or
adenocarcinomas.
SCC-HPV related
SChyperplasia
Vulvar Intraepithelial Neoplasia
Extramammary Paget Disease
female genital system
female genital system
female genital system
female genital system
female genital system
Paget’s Disease
female genital system
Melanoma
Vagina
VIN and Sq.cell carcinoma
Adenocarcinoma
Embryonal Rhabdomyosarcoma
female genital system
female genital system
Uterine Cervix
 Cervicitis
 Tumors
female genital system
female genital system
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.
female genital system
female genital system
Cervicitis
Leukorrhea
Culture interpretation*
.
If severe >>>differentiation from carcinoma:
colposcopy and biopsy
.
Subsoil for carcinogenesis?
May lead to sterility (fibrosis/ unfavorable medium
for sperm).
female genital system
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.
female genital system
female genital system
female genital system
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.
Cervical Intraepithelial Neoplasia (CIN)
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*.
female genital system
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.
Cervical Intraepithelial Neoplasia (CIN)
and Carcinoma
Cervical Intraepithelial Neoplasia (CIN)
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.
Cervical Intraepithelial Neoplasia (CIN)
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
female genital system
female genital system
female genital system
Cervical Intraepithelial Neoplasia (CIN)
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]
Cervical Intraepithelial Neoplasia (CIN)
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%.
Schilling test
Invasive Carcinoma of the Cervix
80-95%: Squamous cell carcinomas
Multifactorial disease
Preventable
Gross (macroscopic appearance)
Fungating (exophytic)
Ulcerative (endophytic)
Infiltrative
Invasive Carcinoma of the Cervix
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
female genital system
female genital system
female genital system
Invasive Carcinoma of the Cervix
 Squamous cell carcinoma
Well to poorly differentiated
 Adenocarcinomas
 Adenosquamous carcinomas
 Staging
female genital system
female genital system
female genital system
Invasive Carcinoma of the Cervix
 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.
Invasive Carcinoma of the Cervix
 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%
Invasive Carcinoma of the Cervix
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.
Invasive Carcinoma of the Cervix
Management
 LEEP
 Conization
 Hysterectomy
 Pelvic exenteration
 Radiotherapy
FEMALE GENITAL SYSTEM
Endometrium
female genital system
female genital system
female genital system
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
female genital system
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
female genital system
Endometriosis
sites
Ovaries,
ligaments,
rectovaginal areas,
pelvis
scars,
umbilicus,
vagina,vulva&appendix
female genital system
female genital system
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 Hyperplasia
female genital system
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
Endometrial Polyp
female genital system
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
Leiomyoma
female genital system
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
Leiomyosarcoma
Microscopy: Increased cellularity, mitosis,
nuclear atypia, and necrosis.
Recurrence and metastasis are not uncommon
5 year survival rate: 40%
Leiomyosarcoma
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
Endometrial Carcinoma
Hyperestrinism : HRT, estrogen secreting
ovarian tumors, etc.
Background of endometrial hyperplasia
20%: no Hyperestrinism and no hyperplasia:
older patients, poor prognosis
Endometrial Carcinoma
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
female genital system
Endometrial Carcinoma
Adenocarcinomas (Adenocarcinomas with
squamous metaplasia, Adenoacanthoma,
Adenosquamous carcinoma)
Endometrioid
Papillary serous carcinoma
Clear cell adenocarcinoma
female genital system
female genital system
Endometrial Carcinoma
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
Endometrial Carcinoma
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)
FEMALE GENITAL SYSTEM
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
female genital system
female genital system
female genital system
female genital system
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.
Degenerating
Corpus luteum
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
female genital system
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
FOLLICULAR CYST OF OVARY
CORPUS LUTEUM CYST OF OVARY
Corpus luteum of pregnancy can be up to 20 cm.
female genital system
female genital system
female genital system
female genital system
Polycystic Ovarian Disease
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
female genital system
female genital system
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
female genital system
female genital system
female genital system
female genital system
female genital system
Serous Tumor
of Low Malignant potential
Serous Tumor
of Low Malignant Potential
 Papillary Tufting  No evidence of
stromal invasion
female genital system
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
female genital system
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
female genital system
Benign
Mucinous Tumor of Ovary
female genital system
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
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)
female genital system
Mucinous tumor
of low malignant potential
Mucinous Carcinoma
Destructive stromal invasion, resemble
mucin secreting adenocarcinoma of
intestinal tract
female genital system
Mucinous Carcinoma
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
female genital system
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.
female genital system
Brenner Tumor
Over 95% are diagnosed between the ages of
30-70.
Are usually unilateral and benign.
female genital system
Fibroma
 Any age
 Unilateral
 Solid grey
 Most hormonally inactive
 Can produce hydrothorax and ascites
(Meigs Syndrome)
 Rarely malignant
Ovarian Fibroma
female genital system
Thecoma
 Any age
 Unilateral
 Yellow
 Can elaborate estrogen resulting in excess
endogenous estrogen
 Can also elaborate androgen resulting in
hirsutism
female genital system
female genital system
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.
female genital system
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
Granulosa cell tumor
Note presence of Call Exner Bodies
female genital system
Granulosa cell tumor
Diffuse pattern
female genital system
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.
female genital system
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.
female genital system
Mature Teratoma
female genital system
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.
female genital system
Metastases to Ovary
Older women
Usually bilateral
Tumors can be up to 20 cm
Common primary sites include breast,
lung, gastrointestinal tract
Krukenberg Tumor
Other tumors of the ovary
 Embroyonal carcinomas
 Mixed germ cell tumors
 Gonadoblastoma
FEMALE GENITAL SYSTEM
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.
female genital system
female genital system
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
female genital system
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
CHORIOCARCINOMA
Placental Site Trophoblastic
Tumor
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
PLACENTA ACCRETA, PERCRETA TYPE,
WITH UTERINE RUPTURE
female genital system

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female genital system

  • 1. Pathology of the Female GenitalTract DEPT OF PATHOLOGY
  • 2. LOWER GENITAL TRACT Vulva, Vagina, Cervix- Infections and neoplasms Embroyology and Anatomy
  • 3. Female Genital Infections- Candida Trichomoniasis Gardnerella – most common Gonnorrhoea,Chlamydia –female infertility Mycoplasma –spontaneous abortion Viruses asHPV- cancer
  • 4. HSV Type II -cervix, vagina, vulva Papules-vescicle-ulcers Cx and vagina-- Leukorrhea Latent Infection Recurrence To neonates Diagnosis-serology,microscopy
  • 5. Trichomonas Vaginalis flagellated ovoid protozoan Strawberry Cx Mycoplasma Candida species
  • 6. Pelvic inflammatory disease Symptoms Organisms_Gonococcus, Chlamydia trachomatis, Clostridium Perfringens Mode of infection and spread
  • 7. Gonococcus -an intracellular diplococcus Diagnosis-culture, papsmear Endometrium spared Cl .features--A/c Suppurative salpingitis salpingo-oophoritis Tubo ovarian abscesses Pyosalpinx, Hydrosalpinx
  • 10. Non-neoplastic lesions Leukoplakia Lichen sclerosus-subepithelial fibrosis Lichen simplex chronicus-acanthosis, and hyperkeratosis Squamous Hyperplasia
  • 11. 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
  • 13. Tumors of Vulva Benign-Papillary hidradenoma Condyloma accuminatum (HPV 6&11) Venereal Wart,Mucosal Polyp Syphilitic Condyloma latum Viral cytopathic effect-Koilocytic atypia
  • 16. Premalignant and malignant neoplasms –SCC,BCC,melanomas or adenocarcinomas. SCC-HPV related SChyperplasia Vulvar Intraepithelial Neoplasia Extramammary Paget Disease
  • 25. Vagina VIN and Sq.cell carcinoma Adenocarcinoma Embryonal Rhabdomyosarcoma
  • 31. 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.
  • 32. 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.
  • 35. Cervicitis Leukorrhea Culture interpretation* . If severe >>>differentiation from carcinoma: colposcopy and biopsy . Subsoil for carcinogenesis? May lead to sterility (fibrosis/ unfavorable medium for sperm).
  • 37. 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.
  • 41. 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.
  • 42. Cervical Intraepithelial Neoplasia (CIN) 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
  • 43. Cervical Intraepithelial Neoplasia (CIN) and Carcinoma Higher incidence in lower socioeconomic groups Genital infections Exposure to oral contraceptives Rarity among virgins Multiple pregnancies
  • 44. 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*.
  • 46. 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. Cervical Intraepithelial Neoplasia (CIN) and Carcinoma
  • 47. Cervical Intraepithelial Neoplasia (CIN) 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.
  • 48. Cervical Intraepithelial Neoplasia (CIN) 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
  • 52. Cervical Intraepithelial Neoplasia (CIN) 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]
  • 53. Cervical Intraepithelial Neoplasia (CIN) 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%.
  • 55. Invasive Carcinoma of the Cervix 80-95%: Squamous cell carcinomas Multifactorial disease Preventable Gross (macroscopic appearance) Fungating (exophytic) Ulcerative (endophytic) Infiltrative
  • 56. Invasive Carcinoma of the Cervix 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
  • 60. Invasive Carcinoma of the Cervix  Squamous cell carcinoma Well to poorly differentiated  Adenocarcinomas  Adenosquamous carcinomas  Staging
  • 64. Invasive Carcinoma of the Cervix  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.
  • 65. Invasive Carcinoma of the Cervix  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%
  • 66. Invasive Carcinoma of the Cervix 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.
  • 67. Invasive Carcinoma of the Cervix Management  LEEP  Conization  Hysterectomy  Pelvic exenteration  Radiotherapy
  • 72. Body of the Uterus Endometritis Adenomyosis Endometriosis Dysfunctional uterine bleeding Endometrial hyperplasia Endometrial polyps Leiomyomas and leiomyosarcomas Endometrial carcinomas
  • 73. 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
  • 74. 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
  • 76. 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
  • 77. 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
  • 78. Endometriosis Theories of genesis: 1. Regurgitation: menstrual backflow through fallopian tubes and subsequent implantation 2. Metaplastic: metaplasia of coelomic epithelium 3. Lymphovascular dissemination
  • 83. Dysfunctional Uterine Bleeding abnormal bleeding with no organic lesion Etiology of uterine bleeding varies with age :prepuberty , adolescence, reproductive age, perimenopause, and postmenopause.
  • 84. 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
  • 85. 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.
  • 86. 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
  • 87. 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
  • 90. 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
  • 93. Uterine Malignancy Endometrial- glands Stroma Both glands and stroma Myometrial-
  • 94. 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
  • 95. 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.
  • 99. Leiomyoma Asymptomatic If Symptoms: Bleeding (menorrhagia) or “mass effect” Progression to sarcomas?
  • 100. 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)
  • 102. Leiomyosarcoma Microscopy: Increased cellularity, mitosis, nuclear atypia, and necrosis. Recurrence and metastasis are not uncommon 5 year survival rate: 40%
  • 104. 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
  • 105. Endometrial Carcinoma Hyperestrinism : HRT, estrogen secreting ovarian tumors, etc. Background of endometrial hyperplasia 20%: no Hyperestrinism and no hyperplasia: older patients, poor prognosis
  • 106. Endometrial Carcinoma 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
  • 108. Endometrial Carcinoma Adenocarcinomas (Adenocarcinomas with squamous metaplasia, Adenoacanthoma, Adenosquamous carcinoma) Endometrioid Papillary serous carcinoma Clear cell adenocarcinoma
  • 111. Endometrial Carcinoma 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
  • 112. Endometrial Carcinoma 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%
  • 113. Mixed Mullerian Tumors adenofibroma adenosarcoma Carcinosarcoma with or withoutdifferentiation(Cartilage,bone& muscle)
  • 115. 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
  • 120. Ovary  Normal ovary measures 3-5 x 1.5-3 x 0.6-1.5 cm and weighs 5-8 grams during reproductive age.
  • 121. Newborn ovary Note presence of numerous primordial follicles filling the cortex
  • 122. Four Primordial Follicles and two primary follicles
  • 123. Mature follicle, Granular cells, marked by an arrow, produce estradiol. (diameter 4-5mm) The preovulatory follicle reaches a diameter of 15-25mm.
  • 124. Corpus Luteum The cells produce progesterone.
  • 126. Hilar cells of ovarian medulla, these cells are mainly responsible for androgen production.
  • 127. Luteinized stromal cells Stromal luteinization (stromal hyperthecosis) are associated with androgenic or estrogenic manifestation.
  • 128. 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).
  • 129. 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
  • 131. 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
  • 133. CORPUS LUTEUM CYST OF OVARY Corpus luteum of pregnancy can be up to 20 cm.
  • 139. 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
  • 140. 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
  • 143. 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
  • 144. 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
  • 145. 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.
  • 146. 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.
  • 147. 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”
  • 148. Serous Tumors of the Ovary Behavior depends on degree of differentiation and distribution May occur on the ovarian surface, occasionally arises from peritoneal surface
  • 154. Serous Tumor of Low Malignant potential
  • 155. Serous Tumor of Low Malignant Potential  Papillary Tufting  No evidence of stromal invasion
  • 157. 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%
  • 158. Serous Cystadenocarcinoma of Ovary These tumor show stromal invasion Cause elevated CA125 in serum
  • 161. 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
  • 162. 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
  • 163. Mucinous tumors Benign Low malignant potential Malignant
  • 164. 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
  • 168. 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)
  • 169. 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)
  • 171. Mucinous tumor of low malignant potential
  • 172. Mucinous Carcinoma Destructive stromal invasion, resemble mucin secreting adenocarcinoma of intestinal tract
  • 175. 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
  • 177. 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
  • 178. 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
  • 179. Clear cell carcinoma These tumors have the highest association with pelvic endometriosis and Para endocrine hypercalcemia.
  • 181. Brenner Tumor Over 95% are diagnosed between the ages of 30-70. Are usually unilateral and benign.
  • 183. Fibroma  Any age  Unilateral  Solid grey  Most hormonally inactive  Can produce hydrothorax and ascites (Meigs Syndrome)  Rarely malignant
  • 186. Thecoma  Any age  Unilateral  Yellow  Can elaborate estrogen resulting in excess endogenous estrogen  Can also elaborate androgen resulting in hirsutism
  • 189. 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
  • 190. Leydig Cell Tumor These tumors are usually yellow in color, high lipid content. Uniform cell population, presence of crystals of Reinke are diagnostic.
  • 192. 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
  • 193. Granulosa cell tumor Note presence of Call Exner Bodies
  • 197. Germ Cell Tumors  Dysgerminoma can occurs with gonadal dysgenesis  Mature teratoma (dermoid cyst)  Immature teratoma  Choriocarcinoma  Endodermal sinus tumor (yolk sac tumor)
  • 198. 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
  • 199. Dysgerminoma Are occasionally encountered in phenotypic females with gonadal dysgenesis.
  • 201. 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
  • 202. 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.
  • 206. Immature Teratoma Usually cause large solid or partially cystic masses. Show immature neural elements consisting of neuroepithelial tubules
  • 207. Specialized Teratoma Struma ovarii can cause hyperthyroidism.
  • 208. 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.
  • 209. Endodermal Sinus tumor Serum AFP (alfa fetoprotein) is elevated in almost all patients. commonly show Shiller Duval Bodies.
  • 211. Metastases to Ovary Older women Usually bilateral Tumors can be up to 20 cm Common primary sites include breast, lung, gastrointestinal tract
  • 213. Other tumors of the ovary  Embroyonal carcinomas  Mixed germ cell tumors  Gonadoblastoma
  • 215. 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.
  • 216. 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.
  • 219. 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.
  • 220. 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
  • 222. 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.
  • 223. MOLAR PREGNANCY Curettage produced this specimen, which consisted of 300 cc of bloody tissue.
  • 224. 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
  • 225. 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
  • 226. 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
  • 227. 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.
  • 228. 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.
  • 229. 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
  • 230. 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.
  • 231. 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.
  • 236. 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
  • 238. PLACENTA ACCRETA, PERCRETA TYPE, WITH UTERINE RUPTURE