pre malignant disorders of the uterine corpus

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PREMALIGNAN T A MALIGNANT DISORD ERS OF THE UTERINE CORPUS

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Page 1: Pre Malignant Disorders Of the Uterine Corpus

PREMALIGNANT A

ND

MALIGNANT

DISORDERS OF THE

UTERINE CORPUS

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EMBRYOLOGY OF UTERUS:

The paramesonephric duct develop into main genital ducts of the female.Three parts can be recognized in each duct 1.cranial 2.horizental and caudal vert ical part that fuses with its partner from the opposite side to form uterine canal.The fold ,which extend from the sides of the fused part fom the broad l igament of the uterus.The fused paramesonephric ducts give rise to the corpus and cervix of uterus.They are sorrounded by a layer of mesenchyme that forms the muscular coat of uterus the Myometrium and its peritonail covering, the perimetrium.

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ANOTOMY OF UTERUS

Uterus is the child bearing organ in females,situated in the in the pelvis between bladder and rectum.The direction can either be anteversion or anteflexion.Uterus is divided into body and cervix.Body is divided into fundus,anterior ar vesical surface,posterior or intestinal surface and lateral border.Various supports of the uterus includes peritonail and f ibromuscular l igaments.Arterial supply is mainly from uterine artries and partly from ovarian artr ies.Lmphatic dranaige fol lows the track as upper lymphatics from the fundus and upper part of the body into aort ic and superficial inguinal. lower to external i laic.middle to E. i l iac.

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Most common malignant diseases affecting the uterus is endometrial carcinoma, which arises from the l ining of the uterus. However, sarcoma also arise from the stroma of the endometrium or from the myometrium.

Epidemiology :

• The median age of presentation is just over 60 years of age, however it can occur in their 20s, but the vast majority of cases occur in women over 45 years of age. with less than 5 % diagnosed under 40 years of age .

Highest incidence is in white north americans.

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Aetiology : The exact cause is unknown, however r isk factors in

postmenapausal and premenapausal women include the following :

1 – Obesity. 2 – Impaired carbohydrate tolerance. 3 – Null iparity. 4 – Late menopause. 5 – Unopposed oestrogen therapy. 6 – Functioning ovarian tumors.

7 – Previous pelvic irradiation. 8 – Sequential oral contraceptives with dimethisterone 9 – Family history of carcinoma of breast, ovary or

colon. 10 – Polycystic ovary disease. 11 – Tamoxif in therapy which has weak oestrogen

effects on the endometrium

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* Many of the factors are related to an increase in oestrogen levels.

* In post – menopausal period, the majority of circulating oestrogen is derived from aromatization of peripheral androgens. This conversion take place principally in adipose t issue. Also post – menopausal women with diabetes have increased oestrogen levels.

* Null iparity and late menopause are both associated with increased risk of endometrial cancers, which may be explained by the prolonged oestrogenic effect on the endometrium.

* Women who use oral contraceptive or progesterone have up to a 50 % reduction in the incidence of endometrial cancer and protection lasts for many years after the discontinuation of these treatments. Cigarette smoking has also been associated with the reduced risk of endometrial cancer.

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Screening for endometrial cancer :

Screening stratagies includes

1.Endometrial sampling

2.Vaginal or cervical cytology

3.Progesterone challenge test

4.ultrasonography;Measurement of endometrial thickness.

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Classif ication :

A Endometrial hyperplasia :

Glandular hyperplasia of the endometrium are benign conditions that may produce symptoms clinical ly indist inguishable from early endometrial carcinoma. Some of hyperplasias, even though reversible, are considered premalignant lesions. Divided into:

1/ Hyperplasia without atypia

which is subdivided into either simple ( cystic ) hyperplasia and complex ( adenomatous ) hyperplasia.

2/ Hyperplasia with atypia, these hyperplasia are generally considered premalignant.

3/ Carcinoma insitu

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B Endometrial carcinoma : Characterized by obvious hyperplasia and anaplasia of

glandular element, with invasion of underlying stroma, myometrium or vascular spaces.

* Endometrial cancer can spread by 4 possible routs :1 – Direct extension. 2 – Lymphatic metastasis.3 – peritoneal implants after transtubal spread.4 – haematogenous spread.

* Pathologist recognized 3 major histological types of endometrial carcinoma:

1 – Adenocarcinoma. Mucinous type 2 – Adenocarcinoma with squamous differentiation.3 – Adenosquamous carcinoma.

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CARCINOMA OF THE ENDOMETRIUM 10

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Al l 3 types have identical presenting symptoms and signs, patterns of spread, and general cl inical behavior.

* Papil lary serous and clear cell carcinoma of the endometrium are other unusual histological subtypes that carry a poor prognosis even when apparently confined to the superficial myometrium.

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Clinical presentation : 1 – About 75 – 80 % of women with endometrial

carcinoma wil l present with postmenopausal bleeding. Sometimes bloody stain postmenopausal vaginal discharge may be associated with endometrial carcinoma.

2 – In premenopausal period, most women with endometrial carcinoma present with intermenstrual bleeding. Although 1/3 may present with heavy periods only.

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3 - Postmenopausal discharge from pyometra carries a 50 % risk of associated malignancy.

4 – Pain may occur with pyometra or metastatic spread . Pain is due to nerve compression on pelvic side wall .

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Diagnosis :

Tradit ionally, post menopausal bleeding was investigated by a dilatation and curettage.

Endometrial sampling;

1.Fractional curettage : di latation and fractional curettage is the definit ive procedure for diagnosis of endometrial carcinoma. It should be performed with the patient under anesthesia and by f irst curett ing the endocervical canal fol lowed by di latation of the canal and circumferential curettage of the endometrial cavity.

At curretage care must be observed to avoid perafort ion of uterus, part icularly in patients with pyometra.

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More recently diagnosis has shifted to outpatient sett ing with :

a – Pap smear.

b–Ultrasound determination of endometrial thickness, also any ovarian pathology may be detected.

In post menopausal woman 5 mm is the cutoff for a normal unilateral endometrial str ip. Color f low imaging may increase specificity.

c–Out-patient endometrial sampling using instruments such as a pipelle Sampler and Sharman currete.

d – Out – patient hysteroscopy.

e- tumour marker ;ca 125 levels

Radiological investigations:

X-ray and MRI may be indicated to see the extent of disease.

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CARCINOMA OF THE ENDOMETRIUM 16

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CARCINOMA OF THE ENDOMETRIUM 17

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Staging : The FIGO classif ication and staging of endometrial

carcinoma are ( i t is surgical staging ) : Stage I : The carcinoma is confined to the corpus. Ia : Tumor l imited to the endometrium. Ib : Invasion to less than ½ of the myometrium. Ic : Invasion more than ½ of the myometrium. Stage I I : The carcinoma has involved the corpus and

the cervix but has not extended outside the uterus.

I Ia : Endocervical glandular involvement only. I Ib : Cervical stromal invasion. Stage I I I : The carcinoma has extended outside the

uterus but not outside the true pelvis. Stage IV : The carcinoma has extended outside the

true pelvis or has obviously involved the mucosa of the bladder or rectum.

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CARCINOMA OF THE ENDOMETRIUM 19

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CARCINOMA OF THE ENDOMETRIUM 20

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CARCINOMA OF THE ENDOMETRIUM 21

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* Surgical stage I tumor account for 75 % of all endometrial carcinoma which explain the relative good overall prognosis.

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Prognosis :

Prognosis of the disease is related to stage, which now include grade of disease, myometrial invation and LN involvement. Other factors such as age and body morphology are also important.other factors that are important from prognosis point of view are 1.tumour size 2.degree of differentiation 3.lymph node involvoment 4.capil lary l ike space involvoment 5.peritonil cytology 6.ploidy status 7.steriod receptor status 8.ca 125 levels.

It is believed that the presence of malignant squamous component ( adeno squamous carcinoma ) is thought to be associated with a poorer outcome.

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Stage 5 year survival

I 85%

II 68%

III 42%

IV 22%

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CARCINOMA OF THE ENDOMETRIUM 24

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Differential diagnosis : Cl inically the differential diagnosis of endometrial

carcinoma include al l the causes of abnormal uterine bleeding.

* In premeopausal patient the fol lowing should be excluded :

1 – Complication of early pregnancy. 2 – Liomyoma. 3 – Endometrial hyperplasia and polyps. 4 – Cervical polyps. 5 – Various genital or metastatic cancers. * In the postmenopausal age group, the fol lowing

should be considered : 1 – Atrophic vaginit is. 2 – Exogenous oestrogen ( HRT ) 3 – Endometrial hyperplasia and polyps. 4 – Various genital neoplasma.

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Treatment :

Stage I : - The treatment of choice is total abdominal hysterectomy and bilateral salpingoopherectomy.

- Radiotherapy is also necessary i f invasion of the myometrium has occurred to more than the inner half of the myometrium.

Stage I I : - I f patient is surgical ly f i t , do radical hysterectomy and bilateral lymphadenectomy with para-aort ic node sampling should be performed.

- If patient unfit surgical ly then radiotherapy may be used.

Stage I I I : If node suggest spread of disease then surgery with adjuvant radiotherapy.

Stage I I I & IV : Radiotherapy,chemothrapy,debulking surgury and hormanal therapy.

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Treatments

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Radiotherapy is performed and then occasionally

residual disease may be involved by surgical intervention.

Progesterone :

Some believe that progesterone may be helpful in preventing recurrence after treatment of early stage disease.

Fol low up;

the objective of post treatment fol low up of endometrial carcinoma are to detect the recurrence and compications of primary treatment and to manage tomour related problems.

Compications of therapy;

includes haematuria from radiation cystit is,diarrhoea,melena from radiation col it is,small bowel obstruction for i leit is, lymph edema of legs and vaginal stenosis.

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ANY QUERIES;

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THANK YOU

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