DIFFERENT PATHOLOGIES

OF THE UTERUS
 UTERUS WITH PE
SUBSEROUS AND INT
DIAGNOSTIC METHODS
CLINICAL EXAMINATION

- ABDOMINAL PALPATION
- BIMANUAL
EXAMINATION
IMAGING STUDIES
-ULTRASONOGRAPHY
-COMPUTERIZED TOMOGRAPHY
-MAGNETIC RESONANCE
IMAGING
Ultrasound image of uterus with
submucous fibroid
 HYSTEROSCOPY
DIRECTLY VISUALIZING THE
ENDOMETRIAL CAVITY AND
SUBMUCOUS FOBROIDS
 TREATMENT

THE ONLY EFFECTIVE

METHOD OF TREATMENT
IS OPERATION
Laparoscopic view of a uterus
with a pedunculated posterior myoma
 FIBROID UTERUS
AN ENLARGED UTERUS AFTER SURGICAL
REMOVAL
Uterine leiomyomas (fibroids)
are benign, hormone-sensitive uterine neoplasms.

These tumors are classified as either

•
submucosal (beneath the endometrium),
•
intramural (within the muscular uterine wall of the uterus),
•
subserosal (beneath the peritoneum).

Symptoms depend on the location, size, and number of myomas, and include *menstrual
abnormalities (menorrhagia), heavy menstruation
*features of mass effects (e.g., back/abdominal/pelvic pain or bladder and bowel
dysfunction)
infertility.

• Physical examination and sonohysterography are used to establish the diagnosis.

•
Treatment for symptomatic patients includes surgery ( myomectomy or hysterectomy) as
well as interventional (uterine artery embolization) and/or medical therapy (
GnRH agonists)
 Laparosco
of pelvis showing
TREATMENT

• Hormonal – progestagens
• Endometrial electroresection
• Hysterectomy
The majority of patients
with uterine myomas
do not require surgical
treamtent.
Surgery is necessary if:
• Heavy bleeding occures that causes anemia
or significant life-style and hygiene
problems
• There is rapid growth of the tumor
(malignancy?!)
• There are pain and pressure- related
symptoms
• Leiomyomas are large
• There are infertility problems
 The choice of treatment depends
on:
• Localization of tumors

• Size and numbers of fibroids

• Patient’s wish ( desire for future pregnancies)

TRADITONAL SURGERY
TECHIQUES
• Hysterectomy ( with or without adnexa)
• Myomectomy with histologic typing!!!
during operation

• August Martin
• Ludwig Rydygier
• William Alexander
ENDOSCOPIC TECHIQUES

• Hysteroscopy

• Electroresection

• Laparoscopy
 PHARMACOLOGIC
THERAPIES- inhibition of
estrogen secretion
• Analogues of GnRH
• Antagonist of GnRH
• Drugs which block E and P receptors
• Interferon
ENDOMETRIAL CANCER
ENDOMETRIAL CANCER

• The 5th most common malignant neoplasm

in women in Poland about 11-12%
•

• The 14 th cause of death

•

• The most common in women over 60 years

of age
ETIOPATHOGENESIS

• Unopposed by progesterone- oestrogen

predominates ( especially oestrone)
„oestrogen-dependent noeplasm”

• Family inheritance adenomatous –

endometrial, breast, ovary and digestive
tract – cancer ( Lynch syndrome)
 ENDOGENOUS SOURCES OF
EXCESS ESTROGEN
• OBESITY!!!!
Overweight 4 - 8,5 kg risk 2x

Overweight 8,5 – 20 kg risk 3x

Owerweight >20 kg risk 10x

 Atypical hyperplasia is
considered particularly
important as a precursor lesion
to endometrial carcinoma and
is so-colled „carcinoma in situ”
of the endometrium
DIAGNOSIS

The diagnosis of
endometrial hyperplasia
can be made by taking a
sample of endometrium for
histologic examination.
The most common indication
for endometrial sampling is
abnormal bleeding.
Dilation and curettage (D&C)
can also be used for
diagnostic sampling of the
endometrium
 EXOGENOUS SOURCES OF
ESTROGEN
• Incorrect HRT for menopause
• Long-term use of SEQUENTIAL
contraceptives
• Long-term hormonotherapy of
gonadal dysgenesis
Factors increasing risk

• Increasing age
• Long-term exposure to unopposed
oestrogens
• High concentrations of oestrogens
postmenopausally
• Early pubescence
Factors increasing risk

• Years of menstruation- late

menopause
• Nulliparity
• Hormonally active ovarian tumors
• PCOS
• Hystory of braest cancer
OTHER RISK FACTORS
• Long-term use of tamoxifen
• Persistent liver matabolic disorders
• Hormone-replacement therapy with less
than 12-14 days of progestagens
• First-degree relative with endometrial
cancer
• Metabolic syndrome (diabetes, arterial
hypertension, obesity)
Factors decreasing
• Grand multiparity (pragnancy with intense
placantal production of progestagens
protectsagainst endometrila cancer)
• Oral-contraceptive use (conceptive pills
containing oestrogens and progestagens lower the
endometrial-cancer risk)
• Physical activity
• Diet of some phyto-oestrogens (diet rich in soy)
• Smoking
CLINICAL SYMPTOMS
•
ABNORMAL UTERINE
BLEEDING !!!
Abdominal pain
Loss of body weight
Anaemia
The probability of endometrial cancer in women
presenting with postmenopausal bleeding is
5-10%, but chances increase with age and risk
factors
 Special consideration should be
given to the patient who presents
with postmenopausal bleeding
=
bleeding that occurs after 6
months of amennorhea in a
patient who has been diagnosed
as menopausal.
 DIAGNOSIS
Is established on the basis of
HISTOLOGICAL examination
of material taken during uterine
curettage or biopsy by
hysteroscopy
ADDITIONAL TESTS

• Ultrasonography
• Chest X-ray
• Cystoscopy
• Recto- or colonoscopy
 SPREADING OF
ENDOMETRIAL CANCER
• Continues infiltration of the uterine wall and
cervix, later extending to the periuterine tissues,
vagina, uterine bladder and the rectum
• It spreads by lymphatic vessels to the pelvic
lymph nodes, paraaortic l.n., that groin
mediastineum and supraclavicular l.n.; the adnexal
struktures-fallopian tubes and ovaries- may be
involved by this pathway
• It spreads by blood vessels to the lungs and liver
(rarely to the bowel, bones, skin and kidneys)
FIGO CLINICAL STAGING OF
ENDOMETRIAL
CARCINOMA I - IV
STAGE I – carcinoma is
confined to the CORPUS
• Ia – tumor limited to endometrium

• Ib – invasion to less than ½ of the

myometrium

• Ic – invasion to more than ½ of the

myometrium
 STAGE II –carcinoma involves
the CERVIX

• IIa – endocervical glandular

involvement only
•

• IIb – cervical stromal invasion

 STAGE III – carcinoma extends
OUTSIDE THE UTERUS but not
• outside
IIIa – tumor the true
invasing pelvis
serosa, adnexa, or
both; and/or positive peritoneal cytology

• IIIb – vaginal metastases

• IIIc – metastases to pelvic and/or paraaortic

lymph nodes
STAGE IV – carcinoma extends
OUTSIDE THE PELVIS
• IVa – tumor invades bladder, bowel
mucosa or both

• IV b – distant metastases including

intraabdominal and/or inguinal lymph node
About 80% of all endometrial
carcionomas are of the endometrioid
typeOther adenocarcinomas:
mucinous, serous, clear-cell , mixed,
squamous-cell, undifferentiated
Most endometrioid carcinomas are
well to moderately differentiated and
arise on background of endometrial
hyperplasia. These tumours, also
known as type-1 (low-grade)
endometrial cancer:- favourable
prognosisassociated with lond-
Type-2 (high-grade) endometriial
carcinomas:
•
About 10% of endometrial cancers
•
Women with such tumors are at high risk of
relapse and metastatis disease
•
These tumours are not oestrogen driven
•
Most of them are associated with endometrial
atrophy
•
Surgery is commonly followed by adjuvant
therapy
•
The hystological type is either poorly
differentiated endometrioid or non-endometrioid
 The most important prognostic
factor is histologic grade
• G1 – well differentiated adenocarcinoma
(<5% of solid infiltration)
• G2 – moderately differentiated
adenocarcinoma (6 – 50% of solid infiltration)
• G3 – cancer mostly solid or completely
undifferentiated (>50% of solid infiltration)
Histological grading applies only to
endometrioid carcinomas, serous and
clear-cell carcinomas are classed as
high grade by definition
PROGNOSIS 5-years survival

• Stage I G1 95%
•

• Stage II G1 <60%
•

• Stage III G3 15%

TREATMENT

• SURGICAL TREATMENT

• RADIATION THERAPY

• HORMONOTHERAPY

• CHEMOTHERAPY
 SELECTON OF METHOD
DEPENDS OF:
• Clinical stage of malignancy
•

• Histologic differentiation of malignancy

•

• Patient’s health status

 As a surcically staged
disease, primary surgical
treatment
is the cornerstone of
management.
 Adjunctive therapy after
hysterectomy which may
include external beam radiation,
has been shown to significantly
reduce the risk of pelvic and
vaginal recurrence.
 The first line of treatment for
recurrent disease is hormonal and
includes various progestin
preparations given in high doses.

Chemotherapy with drugs

including doxorubicin and cisplatin
produce occasionaly short-term
results but not long-term remision.
 STAGE I, II

• COMBINATED THERAPY
-hysterectomy with the adnexa, vaginal margin
and pelvic l.n.
-radiation therapy- external beam radiation
therapy and intracavitary th.
-radiation therapy ( for patients with underlying
medical diseases who cannot undergo surgery)
STAGE III

• Radiation therapy which is completed with

hormono- or chemo-hormonotherapy
•

• Patients with metastases to the ovaries –

combined treatment
STAGE IV

• Hormonotherapy
•

• Hormono-chemotherapy
•

• Symptomatic treatment
FOLLOW - UP
• Control examinations every 3 months for
the first 3 years, than 2 times a year
• After radiation therapy- the first 3 control
examinations every 6 weeks + D&C+
hysteroscopy
• Patients are at higher risk than normal
population for developing the breast,
ovarian and bowel cancer
Thanks for attention