Transcript PREMALIGNANT LESIONS OF THE FEMALE GENITAL ORGANS

PREMALIGNANT LESIONS
OF THE FEMALE GENITAL ORGANS.
Mounir M F Elhao,Professor of Ob & Gyn.
Ain Shams University,Cairo Egypt
Vulva disorders ranging from
vulvadynia to vulvar dystrophy to
premalignant vulvar dysplasias.
Premalignant lesions of the vulva.
Vulvar dystrophy is another very poorly understood disorder
Atrophic type:in which the mucous membrane of the vulva
(vaginal introitus) changes its appearance. It can either be
thin, pale white, and loses all of its elasticity with atrophy of
the labia, especially the labia minora, with fusion of the labia
minora over the clitoris. The mucous membrane then tears
with any attempted stretching, such as intercourse, and
itches incessantly.
Hypertrophic type is similar except the epithelium is
thickened and contains white plaques. Again, it causes
itching, tears easily, but does not give the atrophy as the
atrophic type does. The hypertrophic kind can have a
premalignant tendency
Vulvar dysplasia
(Means a premalignant lesion of the
vulva.)
Mild referred to as VIN-I,
Moderate referred to as VIN-IIS
Severe referred to as VIN-III, or in situ
carcinoma.
( If left alone, the majority will eventually
develop into invasive carcinoma. )
TTT OF VIN:
Each can be resected locally by simply
removing skin-deep tissue. The
cosmetic and therapeutic results are
outstanding.
The vagina(Va IN )
Can also have premalignant lesions
similar to that described on the vulva,
which can be treated in a similar
manner.
lichen planus
A rare but severe symptom-producing
problem of the vagina. Here the
vaginal mucosa completely sloughs
leaving bare areas with no epithelium
and the vagina is severely scarred.
This can also be treated with steroid
creams.
PREMALIGNANT LESIONS of the •
vagina.
Vaginal neoplasia is more common in
patients who have previously been
treated for cervical or vulvar
neoplasia.
The vaginal apex, in the fornices or
about the vestibule and lower vagina
.
PML of the
Endometrium.
Endometrial hyperplasias
.
Simple hyperplasia - Increased number of
glands but regular glandular architecture
Complex hyperplasia - Crowded irregular
glands
Simple hyperplasia with atypia - Simple
hyperplasia with presence of cytologic
atypia (prominent nucleoli and nuclear
pleomorphism)
Complex hyperplasia with atypia - Complex
hyperplasia with cytologic atypia
CGH and Adenomatous
Hyperplasia.
Endometrial Hyperplasia:
Continuous estrogen stimulation that is unopposed by
progesterone. This could be due to endogenous estrogen or
exogenous estrogenic sources.
Endogenous estrogen may be caused by chronic anovulation
associated with polycystic ovary syndrome (PCOS) or
perimenopause.
Obesity also contributes to unopposed estrogen exposure due
to chronic high levels of estradiol that result from
aromatization of androgens in adipose tissue and conversion
of androstenedione to estrone.
Endometrial hyperplasia and cancer can also result from
estradiol-secreting ovarian tumors such as granulosa cell
tumors.
Exogenous estrogen without
progesterone
Has been associated with increased
endometrial hyperplasia and
adenocarcinoma (Lethaby, 2004).
The Postmenopausal Estrogen/Progestin
Interventions (PEPI) trial found that
unopposed estrogen exposure increased
the risk of complex hyperplasia by 22.7%
and atypical hyperplasia by 11.8% over 3
years of use compared with a less than 1%
increase in placebo controls (PEPI, 1996).
TTT of ENDOMETRIAL HYPERPLASIA.
Treatment depends on patient
symptoms such as
1. Degree of bleeding,
2. Presence of cytologic atypia,
3. Patient's surgical risks, and
4. wish for future childbearing
TTT
. Progestins can effectively treat endometrial
hyperplasia and they can serve as prevention of
recurrence in those with continued risk factors.
Hyperplasia without atypia responds well to
progestins. More than 98% of women with
hyperplasia treated with cyclic progestins saw
regression of the disease in 3-6 months (Gambrell,
1995).
The PEPI trial showed a 94% normalization of
complex or atypical hyperplasia in 45 women
treated with progestins (PEPI, 1996). Multiple
regiments of progestin therapy have been found
effective in reversing hyperplasia.
If hyperplasia with atypia is found on
dilation and curettage (D&C) or
endometrial biopsy,
Definitive treatment with
hysterectomy is recommended due
to the high rate of concurrent
endometrial cancer.
Pap tests can detect precancerous
and cancerous conditions
by collecting cells from the surface of the
cervix. Sometimes these cells appear
abnormal, or atypical, when looked at
under a microscope, but they are not
completely cancerous. These are called
premalignant or precancerous cells, which
means they might turn into cancer if not
found and treated early enough. These
precancerous lesions are commonly called
cervical intraepithelial neoplasia (CIN).
The cervix:
Squamous Intraepithelial Lesion (SIL) is
the abnormal growth of squamous cells on
the surface of the cervix.
Tools.
Most common premalignant
disorders
vulva, vagina, and cervix.
The cervix is obviously the most
common due to the fact that it is
reflected in abnormal Pap smears.
There are also ovarian neoplasms that
are premalignant
Conservative approach to abnormal
Pap smears, especially in young
women who have not fulfilled their
reproductive desires. This includes
colposcopy for identifying and
diagnosing the origin of the abnormal
Pap smears as well as outpatient
management.
Based on location of the lesion,
the severity of the pathological abnormalities,
and the potential for childbearing.
Each patient is individualized as to
whether their proper management
would be close follow-up,laser,
cryotherapy or LEEP procedures in
the office or cold knife conizations
under anesthesia
Abnormal vessels
The surface of the cervix is made
up of two different types of cells,
squamous epithelial cells (the lining
cells of the outer part of the cervix, or
ectocervix) and
columnar epithelial cells (the lining
cells of the inner part of the cervix, or
endocervix).
Early detection and treatment
of precancerous cells can prevent them
from becoming cancerous.
Otherwise, the abnormal cells can
become cancer and spread to other
parts of the body.
LG- SIL
SIL-HG &
Carcinoma.
Adenocarcinoma in situ.
These lesions have also been called squamous
intraepithelial lesions (SIL) and there are two types:
Low-grade SIL - In this type of SIL, the changes are thought to
be just starting. The changes can be in the size, shape, or
number of cells that are on the surface of the cervix. In these
low-grade lesions, the cells have only a few abnormal
characteristics, but are still somewhat similar to the normal
cells. Other common names for this low-grade SIL are mild
dysplasia or cervical intraepithelial neoplasia type I (CIN 1).
High-grade SIL - In this type of SIL, the cells look very abnormal
under the microscope. However, these cells are still only on
the surface of the cervix. They are not invading the deepest
parts of the cervix yet. These lesions are also called
moderate or severe dysplasia, CIN II or III or carcinoma in
situ (CIS).
The next step, in many cases, is a colposcopy
( an exam with an instrument that visually magnifies
the cervix)
Removal of any areas likely to be precancerous or
cancerous. Sometimes, the physician and patient
may decide to repeat the Pap test later and
proceed to colposcopy only if the second test
shows more abnormal cells that might need
removal.
Borderline ovarian tumors
Are a subset of epithelial ovarian
tumors that have a very favorable
prognosis. The accepted initial
treatment is surgical removal of the
tumor and biopsies.
Frequency: One woman in 55 (1.8%)
develops some form of ovarian
cancer in her lifetime. Approximately
90% of these cancers are tumors of
epithelial origin. If benign lesions are
included, epithelial tumors account for
60% of all ovarian tumors.
Borderline tumors comprise
approximately
15% of all epithelial ovarian tumors.
The mean age of occurrence is
approximately 10 years younger than that
of women with frankly malignant ovarian
cancer.
Factors reportedly linked with borderline
tumors include oral contraceptive use,
menarche, age at first pregnancy, age at
first delivery, menstrual history, smoking,
and family history of ovarian cancer,
although none of these has been shown to
be statistically significant.
Borderline ovarian cancer is staged
according to the FIGO classification of
ovarian cancer.
Many clinicians group stages II-IV together
for prognostic consideration.
Another common component of staging is
the description of the type of implants, as
these have significant prognostic value. As
opposed to its true malignant counterpart,
epithelial ovarian carcinoma, borderline
ovarian cancers are often found at early
stages.
Border line ovarian tumors.
Etiology: The etiology of this disease remains
unclear because of the small number of cases and
the lack of randomized controlled studies.
Pathophysiology: The 2 major histologic tumor
subtypes are serous and mucinous, with serous
being more common. Other much less common
tumors include clear cell and endometrioid.
Serous tumors are presumed to originate from the
germinal epithelium. Mucinous tumors do not have
a clearly defined origin.
Many authorities consider borderline tumors to
occupy an intermediate position between their
benign and frankly malignant counterparts.
BOT
Clinical: These tumors, as with other ovarian
tumors, are difficult to detect clinically until they
are advanced in size or stage. In one study, the
most common presenting symptoms were
abdominal pain, increasing girth or abdominal
distension, and abdominal mass. Approximately
23% of patients were asymptomatic.
When a complex ovarian mass is discovered,
surgery is often, if not always, indicated.
Preoperatively, borderline tumors are often
presumed to be either benign or malignant ovarian
masses; regardless, surgery is required to
determine the type of mass.