DISEASES OF THE

VULVA
 VULVA: NON-NEOPLASTIC
EPITHELIAL DISORDERS

There are two forms of NNED:

lichen sclerosus
lichen simplex chronicus.

Both may coexist in different areas in the same

patient, and both may appear macroscopically as
depigmented white lesions, referred to as
leukoplakia.
Condylomas and Low-Grade Vulvar Intraepithelial
Neoplasia (VIN I)

The more common may be papillary and sometime flat.

They occur anywhere on the anogenital surface,
sometimes singly but more often in multiple sites.
The histologic appearance: perinuclear cytoplasmic
vacuolization with nuclear angular pleomorphism-
koilocytosis.
Cause: HPV infection. there is a strong association
with at least two types of HPV (HPV 6 and HPV 11),
closely related to the virus that causes common warts.
Not precancerous but may coexist with foci of
intraepithelial neoplasia in the vulva and cervix.
 Carcinoma of the Vulva

Carcinoma of the vulva represents about 3% of

all genital tract cancers in women
occurring mostly in women older than age 60
years.
Approximately 90% of carcinomas are
squamous cell carcinomas; the remainder are
adenocarcinomas, melanomas, or basal cell
carcinomas
 Carcinoma of the Vulva

2) The other subgroup of vulvar carcinoma occurs

in older women.
It is not associated with HPV but is often
preceded by years of non-neoplastic epithelial
changes, principally lichen sclerosus and, rarely,
lichen simplex chronicus.
 TUMORS OF THE CERVIX

Cervical carcinoma, despite dramatic

improvements in early diagnosis and treatment,
continues to be one of the major causes of
cancer-related deaths in women, particularly in
the developing world.
 Cervical Intraepithelial Neoplasia and Squamous
Cell Carcinoma
Cervical carcinoma was once the most frequent form of
cancer in women around the world. but the widespread
use of Papanicolaou (cytologic) screening of women
has dramatically lowered the incidence of invasive
tumors and by contrast, the incidence of precursor
cervical intraepithelial neoplasia (CIN) has increased
Most invasive cervical squamous cell carcinomas arise
from precursor epithelial changes referred to as CIN.
However, not all cases of CIN progress to invasive
cancer, and indeed many persist without change or even
regress.
 CERVICAL INTRAEPITHELIAL NEOPLASIA
(CIN), SQUAMOUS INTRAEPITHELIAL LESION
(SIL)
However, in cytologic smears the precancerous lesions are separated into only
two groups:

The low-grade lesions correspond to CIN I or flat condylomas (described later

The high-grade lesions to CIN II or III.

CIN I the likelihood of:

regression is 50% to 60%;
persistence, 30%;
progression to CIN III, 20%.
Only 1% to 5% become invasive.

CIN III, the likelihood of regression is only 33% and of progression 6% to

74% (in various studies).
CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN),
SQUAMOUS INTRAEPITHELIAL LESION (SIL)

Epidemiology and Pathogenesis.

The peak age incidence of CIN is about 30 years, whereas that of invasive carcinoma is
about 45 years.
precancerous changes take many years, to evolve into overt carcinomas.
Prominent risk factors for the development of CIN and invasive carcinoma
are as follows:
Major risk factors
HPV infection
Early age at first intercourse
Multiple sexual partners
A male partner with multiple previous sexual partners
Minor risk factors
lower socioeconomic groups
cigarette smoking
exogenous or endogenous immunodeficiency including HIV infection
Rarity among virgins, and association with multiple pregnancies.
 CERVICAL INTRAEPITHELIAL NEOPLASIA
(CIN), SQUAMOUS INTRAEPITHELIAL LESION
(SIL)
Epidemiology and Pathogenesis.
HPV can be detected in 85% to 90% of precancerous
lesions and invasive neoplasms, and more specifically,
certain high-risk types, including 16, 18, 31, 33, 35, 39,
45, 52, 56, 58, and 59.
By contrast, condylomas, which are benign lesions, are
associated with infection by low-risk types (i.e., 6, 11,
42, and 44)
In low-risk types , the viral DNA does not integrate
into the host genome, remaining in the free episomal
form.
 CERVICAL INTRAEPITHELIAL NEOPLASIA
(CIN), SQUAMOUS INTRAEPITHELIAL LESION
(SIL)
CIN II (moderate dysplasia)
The dysplasia is more severe, affecting most layers (2/3) of the
epithelium.
It is associated with some variation in cell and nuclear size and with
normal-looking mitoses above the basal layer.
The superficial layer of cells is still well differentiated, but in some cases it
shows the koilocytotic changes described.

CIN III, (severe dysplasia & carcinoma in situ)

affect virtually all layers of the epithelium.

Cervical cytology and cervical examinations (colposcopy) remain

the mainstays of cervical cancer prevention.
INVASIVE CARCINOMA OF THE
CERVIX

75% to 90% are squamous cell carcinoma,

peak incidence at about 45 years, some 10 to 15
years after detection of their precursors.
 INVASIVE CARCINOMA OF THE
CERVIX
MORPHOLOGY

GROSS:
Develop in the region of the transformation zone
Range from microscopic foci to grossly conspicuous tumors
May be invisible or exophytic.
Tumors encircling the cervix and penetrating into the underlying
stroma produce a "barrel cervix," which can be identified by direct
palpation.
Extension into the parametrial soft tissues, pelvic lymph nodes, bladder
or rectum.
Distant metastases, including para-aortic nodal involvement
staged from 1 to 4 depending on clinical spread
Here is a normal cervix with a smooth, glistening mucosal
surface. There is a small rim of vaginal cuff from this
hysterectomy specimen. The cervical os is small and round,
typical for a nulliparous woman. The os will have a fish-
mouth shape after one or more pregnancies.
This is the gross appearance of a cervical squamous cell
carcinoma that is still limited to the cervix (stage I). The
tumor is a fungating red to tan to yellow mass.
Here is another cervical squamous cell carcinoma. Note the
IUD string protruding from the cervix. This implies that
someone could have done a Pap smear when it was inserted.
There is a natural history of progression of dysplasia to
carcinoma, so don't leave dysplasias alone.
This is a larger cervical squamous cell carcinoma which
spread to the vagina. A total abdominal hysterectomy with
bilateral salpingo-oopherectomy (TAH-BSO) was performed.
This is a pelvic exenteration done for
stage IV cervical carcinoma. At the
left, dark vulvar skin leads to vagina
and to cervix in the center, where an
irregular tan tumor mass is seen
infiltrating upward to the bladder. A
slit-like endometrial cavity is
surrounded by myometrium at the
mid-right. The rectum and sigmoid
colon are at the bottom extending to
the right.
 INVASIVE CARCINOMA OF THE
CERVIX
MICROSCOPIC:
The most common cervical carcinomas are:
squamous cell carcinomas (75%), followed by
adenocarcinomas and adenosquamous carcinomas (20%)
small cell neuroendocrine carcinomas (less than 5%).
With the exception of neuroendocrine tumors, which
are uniformly aggressive in their behavior, cervical
carcinomas are graded from 1 to 3 based on cellular
differentiation.
This is why you do Pap smears--to prevent invasive squamous
cell carcinomas from occurring. With Pap smears, pre-
neoplastic and neoplastic cervical lesions can be detected
when small and treated. Nests of squamous cell carcinoma
have invaded underlying stroma at the center and left.
 Diseases of Uterine Corpus
Endometrial hyperplasia
Endometrial Polyp
Endometrial carcinoma
Endometritis
Endometriosis and adenomyosis
Dysfunctional uterine bleeding
Leiomyoma and leiomyosarcoma.
 Endometrial Carcinoma
Pathogenesis

Two general groups of endometrial cancer can be identified.

The first and the most common develops on a background

of prolonged estrogen stimulation and endometrial
hyperplasia. (Type 1 endometrial carcinoma).

Both hyperplasia and cancer, are closely related.

Type 1 endometrial carcinoma is associated with a more

favorable prognosis.
 Endometrial Carcinoma
Pathogenesis

Endometrial carcinomas that are associated with hyperplasia

and the mentioned risk factors tend to be well differentiated
and mimic normal endometrial glands (endometrioid) in
histologic appearance.

Type 2 endometrial carcinoma is seen in a subset of patients

with no risk factors that lead to hyperestrinism, no
preexisting hyperplasia, and acquires the disease at an older
average age.

In type 2 group, tumors are generally more poorly

differentiated, and have worse outcome.
 Chronic Endometritis

It is chronic inflammation of endometrium.

Causes:
Seen in the following setting:
In patients with chronic PID
In postpartal or postabortal endometrial cavities, usually due to
retained gestational tissue
In patients with intrauterine contraceptive devices
In patients with tuberculosis.
Clinically some women with chronic endometritis
complain of abnormal bleeding, pain, discharge, and
infertility
Chronic Endometritis

Histologically, it is
characterized by
presence of chronic
inflammatory cells
primarily plasma
cells.
Theories of Endometriosis Origin
Endometriosis
Gross

Endometriosis of the
ovary
The ovaries may become
markedly distorted by
large cystic spaces (3 to
5 cm in diameter) filled
with brown blood debris
to form so-called chocolate
cysts
 Follicular and Luteal Cyst
(Functional cyst)

Very common.
Originate on the ovarian cortex in unruptured
graafian follicles (follicular cyst) or follicles that
ruptured and resealed immediately (Luteal cyst).
Usually small, 1- 1.8 cm. filled with clear fluid.
Occasionally rupture causing pain & intraperitoneal
bleeding.
Lined by granulosa or luteal cells.
 Serous Tumor

These are the most common ovarian tumors.

They are usually cystic filled with clear serous fluid.
Together the benign, borderline, and malignant types
account for about 30% of all ovarian tumors.
About 75% are benign or of borderline malignancy, and 25%
are malignant.
Serous cystadenocarcinomas account for approximately 40%
of all cancers of the ovary and are the most common
malignant ovarian tumors.
Benign and borderline tumors are most common between
the ages of 20 and 50 years.
Cystadenocarcinomas occur later in life on average.
Serous Tumor
Gross
Serous Tumor
Gross