BENIGN AND MALIGNANT

TUMOURS OF UTERUS
TOPICS:

1. LEIOMYOMA (UTERINE FIBROID)

2. ADENOMYOSIS
3. ENDOMETRIAL POLYP
4. ENDOMETRIAL HYPERPLASIA
5. ENDOMETRIAL CARCINOMA
6. LEIOMYOSARCOMA
 LEIOMYOMA
(UTERINE FIBROID)
 UTERINE WALL ANATOMY
LAYERS OF UTERINE
WALL
PERIMETRIUM (OUTER • Doubled serous layered
LAYER) membrane, continuous
with abdominal
peritoneum

MYOMETRIUM (INNER • Thick, smooth muscle

LAYER) layer.
• Common site of uterine
fibroid

ENDOMETRIUM (INNER • Made up of glandular

LAYER) cells that make secretion
• 2 types: Deep Stratum
Basalis & Superficial
Stratum Functionalis
UTERINE WALL HISTOLOGY
 INTRODUCTION

• Leiomyoma is a benign tumor that most commonly arise from smooth muscle cells in
myometrium (they can develop in various sites of the body; eg: Ovary, Uterine
ligament& Cervix)

• It is called “Fibroid” because of its firmness (Fibro: Fibrous tissue, oid: Resemblance)

• Estrogen-dependent tumor
Can enlarge during pregnancy in response to hyperestrogenic state

• Most common benign tumor female genital tract, affecting 40% (30%-50%) of
women in a reproductive age
 GROSS APPEARANCE

• Sharply well-demarcated, firm, gray-white

masses with a characteristic white-whorled
appearance on cross section

• Fibroids are paler than the surrounding

myometrium

• There is usually a sharp line of demarcation

between the tumor and the normal uterine
muscle
 HISTOLOGY
• Bundles of spindle smooth muscle cells mimicking the appearance of normal
myometrium (Picture A: Normal Myometrium, Picture B: Leiomyoma/Fibroid
myometrium)

• May also present with foci of fibrosis, calcification and degenerative softening
 CLASSIFICATION OF FIBROIDS

• Fibroids can occur singly, but more often occur as multiple tumors that
are scattered within uterus, ranging from small to large tumors.

• Uterine enlargement is equated to pregnant uterus, however it is

usually irregular in shape

• They are classified according to location in related to uterine wall

 CLASSIFICATION OF FIBROIDS
TYPES (BASED ON POSITION IN UTERINE
WALL)
INTRAMURAL • Most common type of fibroid
• Embedded within myometrium

SUBMUCOSAL • Lie immediately beneath the endometrium

SUBSEROSA • Lie beneath the serosa

PEDUNCULATED • Attach to the normal myometrium by a stalk

PARASITIC • Extend out on attenuated stalks & attached to

surrounding organs from which they may develop
blood supply
 NATURAL HISTORY
• Fibroids can undergo 3 forms of degenerative change, usually in
response to outgrowing their blood vessels:
DEGENERATIVE CHANGES
RED • Hemorrhage & Necrosis iccurs within
the fibroid
• Typically presenting in mid-second
trimester pregnancy with acute pain

HYALINE • Asymptomatic softening &

liquefaction of fibroid

CYSTIC • Asymptomatic central necrosis leaving

cystic spaces at the centre
• Can initiate Calcium deposition that
can lead to calcification
 RISK FACTORS OF FIBROIDS

1. Reproductive age women (30%-50%)

2. Nulliparous
3. Black women (African descent)
4. Obese women
5. Prolonged use of Contraceptive Pills
6. Environmental factors (Alcohol consumption, Sedentary lifestyles, Diet,
Vitamin D Deficiency)

 Smoking appear to reduce the risk of uterine fibroids

 PATHOPHYSIOLOGY

• Pathophysiology of fibroids remain poorly understood

• However, it is believed that there are some factors

1. Increased in Bcl-2
• Myometrium has receptor for ovarian steroid hormones (Estrogen & Progesterone)
• There is an alteration of apoptosis which control the binding of steroid hormones to the
receptor in myometrium
• In fibroids, the is a factor that inhibits this apoptosis which is Bcl-2
2) Cytogenic Abnormalities
• Occurs in 40% of fibroid
• Translocation within/deletion of chromosome 7, translocation of chromosome 12 &14,
structural aberration of chromosome 6
• Not observed in normal myometrial tissue

3)Mutation in gene encoding Fumarate Hydratase (enzyme of

tricarboxylic acid cycle)
• Predispose women to hereditary syndrome that involved the presence of multiple uterine
fibroid in association with cutaneous leiomyomata & Renal Cell Carcinoma

4)Abnormalities in Uterine Blood Vessels & Angiogenic Growth Factor

• No mature vessels running through uterine fibroids despite the fact that they have a well-
developed blood supply
 CLINICAL FEATURES

1. Menstrual disturbance (Menorrhagia, Dysmenorrhea)

2. Pressure/bulk symptoms (urinary frequency, difficulty in micturition,
incomplete bladder, abdominal distension)
3. Bowel problem (constipation)
4. Pain (acute red degeneration, pedunculated fibroid)
5. Reproductive dysfunction (subfertility, miscarriage, PPH)
 DIAGNOSIS
INVESTIGATIONS
FULL BLOOD COUNT • In women with Heavy Menstrual Bleeding
• Can cause severe anemia
TRANSVAGINAL ULTRASONOGRAPHY • Good for detecting submucous fibroids and small
intramural fibroids
TRANSABDOMINAL ULTRASONOGRAPHY • Good for detecting large intramural & subserosal
fibroids
• Exclude hydronephrosis pressure from fibroids
obstructing the ureters
SALINE-INFUSION SONOGRAM • Good for detecting submucous fibroids
HYSTERESCOPY • Good for detecting submucous fibroids
• Good for planning subsequent hysteroscopic
surgical treatment
MRI • Good for describing morphology & location of
fibroids
• Indicated prior UAE & to monitor treatment
response
 TREATMENT

1. Medical
2. Surgical
3. Radiological
 MEDICAL
PHARMACOLOGICAL
Gonadotrophin-Releasing Hormone antagonist • Downregulation of pituitary receptors that stimulate gonadotrophin release,
followed by gonadotrophin output reduction and consequent reduction in
ovarian steroid production within 2 – 3 weeks of commencing treatment
• Induce menopausal state by shutting down estradiol production
• Usually given as 1 - or 3 - monthly depot injections

Selective Progesterone Receptor Modulator (SPRM) Ulipristal Acetate • For women who cannot tolerated with severe menopausal symptoms from
GnRH therapy

Progesterone Receptor Modulator • Antiprogestins have been shown to lead to the shrinkage of uterine fi
broids, they are not widely used in clinical practice
• When administered to women, they cause amenorrhoea in a vast majority of
cases without causing anovulation

Levonorgestrel - secreting intrauterine system (Mirena IUS ) • Dysfunctional uterine bleeding

• It is well known that the Mirena IUS is associated with irregular bleeding
for 3 – 4 months after insertion in many women
 SURGICAL

TYPES OF SURGERY
MYOMECTOMY • Removal of fibroid only
• Preferred option when preservation of fertility is
required
• Significant risk of uncontrolled life-threatening
bleeding especially when removing multiple
fibroids that might lead to hysterectomy

HYSTERECTOMY • Permanent removal of uterus

• The most common surgical option
• It ensures immediate resolution of menstrual upset
and other fibroid - associated symptoms
 RADIOLOGICAL

• Uterine Artery Embolization (UAE)

• Embolize both uterine arteries under radiological guidance

• Small incision made in the groin area under Local

Anaesthesia then cannula placed into femoral artery and
guided to uterine artery

• Embolization particle is injected then blood supply to uterus

reduced that induce infarction & degeneration of fibroids

• Required overnight admission and opiate analgesia for pain

• Complications: Fever, infection, fibroid expulsion and

potential ovarian failure
 IMPOTANCE OF MULTIDISCIPLNARY
APPROACH
• Multidisciplinary approach is important in order to establish ultimate
diagnosis and treatment

• Multidisciplinary approach improves patient and disease outcomes with

reduction in adverse events

• Patient with suspected fibroid-related symptoms need to attend consultation

by both a radiologist and gynecologist
• The available treatment options can be offered for women with
symptomatic uterine fibroids include pharmacological, surgical and
radiological treatment

• Numerous factors including patient preference, desire for future

pregnancy, symptoms, and fibroid number, size, and location are
carefully assessed in deciding treatment options.
 PATIENT SAFETY MEASURE
• The main issue to consider in women who have fibroids, is the general
condition of the patient:
• Assess patient condition not only regarding their fibroid symptoms but also in terms of
their psychological health
• Observe for the most efficient treatment according to the patient’s preferences and
clinical situation.
• Observe for the appropriate investigations according to patient’s condition

• Aim for the good quality of life and patient satisfaction. Therefore, the
number of interventions should be minimized, and if radical treatment is
needed (hysterectomy), it is better to perform it as soon as possible.
• Treatment should be efficient with the maximum efficacy and the minimum
risk and cost. It should also be indicated proportionally according to the
severity of symptoms.

• If a symptomatic medical treatment is effective, we should maintain it

until we need to gradually increase to other option such as surgical or
radiological therapy

• It is not necessary to emphasize that asymptomatic fibroids a treatment

regardless of their size. However, the bigger the size, the more probable it is
that they cause symptomatology. Nevertheless, follow-up is required, and 6
months seems reasonable, extending it to 1 year if there is no growth
detected. 
Reference:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5592915/
2. Robbins Basic Pathology 10th Edition
3. Gynaecology by Ten Teachers 20th Edition
4. Dewhurst’s Textbook of Obstetrics & Gynaecology 8th Edition
5. https://www.youtube.com/watch?v=LYc7yGUYqTY&t=305s
 
Adenomyosis
 Content

 Definition
 Pathophysiology
 Risk factors
 Classification
 Clinical features
 Investigations
 Treatment options

 Definition

Presence of ectopic nests of endometrial glands and stroma within the
myometrium, surrounded by reactive smooth muscle hyperplasia.

Pathophysiology


 Pathophysiology

 Abnormal invagination of the basalis layer of the endometrium into the
adjacent myometrial layer.
 The endometrial-myometrial interface is composed of the basalis
endometria and the subendometrial myometrium (myometrial
junctional zone)
 The absence of any discrete transitional layer permits abnormal
invagination of the basalis endometria directly into the myometrium
when endometrial invasion is provoked
 Pathophysiology

 If the basal layer is only present, the tissue reaction is much less, as it is
unresponsive to hormones
 But, if the functional zone is present which is responsive to hormones, the
tissue reaction surrounding the endometrium is marked
 There is hyperplasia of the myometrium producing diffuse enlargement of
the uterus, sometimes symmetrically but at times, more on the posterior
wall
 Risk Factors

 Middle age - women in their fourth and fifth decades
 Multiparous status
 History of gynecologic surgery
 Women with conditions which are hyperestrogenic such as fibroid,
endometrial hyperplasia, endometrial cancer, endometriosis
Classification

 Clinical Features
 Asymptomatic (50%)

 Menorrhagia
 Dysmenorrhea
 Dyspareunia
 Frequency of urination
 Chronic Pelvic pain
 Postmenstrual spotting
 Subfertility
 Palpable mass per abdomen – enlarged uterus less than 14 weeks of pregnancy
 Uterine feels soft and boggy
 Investigations

 Laboratory Studies – TRO Pregnancy, anemia, thyroid and/or pituitary
dysfunction, sexually transmitted infections.
 Transvaginal Ultrasound and Colour Doppler
• Diffusely enlarged, globular, asymmetric uterus
• Distorted, heterogenous myometrium with increased or decreased areas of
echogenicity
• Presence of myometrial cysts: poorly defined areas with abnormal
echotexture
• Myometrial mass with ill-defined border

 Investigations

 Ultrasonography of Pelvis
• Uterine enlargement with absence of leiomyoma
• Asymmetrical enlargement of anterior or posterior myometrial wall
• Heterogeneous echogenicity – presence of cystic glands amongst smooth
muscle
• Increase vascularity within myometrium
• Echogenic nodules or linear striations radiating out from the endometrium
into the myometrium.

 Investigations

 Magnetic Resonance Imaging
• Low signal intensity JZ < 8 mm excludes the disease
• JZ thickness > 12 mm is suggestive of adenomyosis


 Medical Treatment

 Symptomatic Relief
• NSAID – Mefenamic Acid 500mg TDS
• Tranexamic Acid 1g TDS or QID
 Medical Treatment

 Suppresion of Menstruation
 Surgical Treatment

 Conservative Surgery
• Adenomyomectomy
• Endometrial ablation
• Uterine artery embolization

 Definitive Surgery
• Hysterectomy
 

Endometrial ablation is a procedure that surgically destroys (ablates) the

lining of your uterus (endometrium). The goal of endometrial ablation is
to reduce menstrual flow. In some women, menstrual flow may stop
completely.
Differences between Adenomyosis and Uterine Fibroid


ENDOMETRIAL POLYP

 Content

 Definition
 Pathogenesis
 Risk Factors
 Clinical Features
 Investigations
 Treatment
 Definition

Discrete outgrowths of the endometrium that contain a variable amount of
glandular tissue, stroma and blood vessels.

 Pathogenesis

 A part of the thick endometrium projects into the cavity and ultimately
attains a pedicle.
 Naked eye appearance:
• small polyp size of about 1–2 cm
• looks reddish and feels soft.
 Pathogenesis

 Microscopically:
 The core contains stromal cells, glands and large thick-walled vascular
channels
 The surface is lined by endometrium. The tip may undergo squamous
metaplasia
 The pedicle contains thin fibrous tissue with thin blood vessels.

 Pathogenesis

 Predictors of malignancy are:
(a) Size >10 mm
(b) Postmenopausal status and
(c) Abnormal uterine bleeding
 Risk Factors

 Hormone replacement therapy
 Tamoxifen therapy
 Increased patients age
 Diabetes and Hypertension
 Obesity
 Late menopause
 Clinical Features

 Asymptomatic
 Unscheduled vaginal bleeding or spotting
 Irregular uterine bleeding
 ™Contact bleeding, if the polyp is situated at or outside the cervix
 ™™Excessive offensive vaginal discharge
 Colicky pain in the lower abdomen
 ™Excessive vaginal discharge which may be offensive.
 ™™Sensation of something coming down.
 ™™Infertility or miscarriage in young women.
 Polyp is soft, slippery and small in size
 Reddish in color, usually attached with a slender pedicle.
 Investigations

 Transvaginal ultrasound: to visualize the uterine cavity, abnormal
thickening of the endometrium
 Intrauterine injection of saline: increased diagnostic performance of TVS
 Hysteroscopy
 - distinguish between pedunculated fibroids and malignant polyps
 Pelvic Ultrasound
 

Transvaginal Ultrasound
 Treatment

 Removal of polyp under direct vision or excision with the use of
specially developed hysteroscopic instruments.
• hysteroscopy and resection
• uterine curettage using ring or ovum forceps.
 Hysterectomy
 

Uterine Curettage
 

Hysteroscopy and resection

 Recurrence

 Due to:
• Incomplete removal
• Persistence of cause leading to polyp formation
• Malignancy
 References

 https://emedicine.medscape.com/article/2500101-overview#a3
 https://www.uptodate.com/contents/endometrial-polyps
 Robbins Basic Pathology 10th Edition
 Gynaecology by Ten Teachers 20th Edition
 Dewhurst’s Textbook of Obstetrics & Gynaecology 8th Edition
THANK
 YOU
ENDOMETRIAL HYPERPLASIA
Definition

 Endometrial hyperplasia (EH) is a pre-cancerous, non-physiological, non-invasive

proliferation of the endometrium.
 results in increased volume of endometrial tissue with alterations of glandular
architecture (shape and size).
 Precursor of endometrial cancer which is the most common gynecological
malignancy ; at least 3 times higher than endometrial cancer.
What causes endometrial
hyperplasia (EH)?
How does the endometrium normally changes throughout
the menstrual cycle ?
Pathogenesis
 Hyperplasia usually develops in the presence of continuous ESTROGEN
stimulation unopposed by PROGESTERONE.

PROGESTERONE
maintains and control
this growth.
u t er ine lin ing.
an g es in the
o l t h e ch
Contr
ESTROGEN builds
up the uterine
lining.
Risk factor
 Nulliparity, infertility
 Obesity / high BMI (BMI>35)
 Anovulation - polycystic ovary syndrome, perimenopause
 Early menarche / menopause
 Pre-existing disease – DM, HTN
 Hormone therapy- estrogen replacement therapy, prolonged exogenous
estrogen exposure, tamoxifen
Clinical features
 Abnormal uterine bleeding
 Heavy menstrual bleeding (menorrhagia)
 Inter-menstrual bleeding ( metrorrhagia )
 Post-menopause uterine bleeding

 Vaginal discharge
 Lower abdominal pain
Classification

Classification (WHO) 1994 Progression of cancer

Simple hyperplasia without atypia 1%

Complex hyperplasia without atypia 3%

Simple hyperplasia with atypia 8%

Complex hyperplasia with atypia 29 %

Classification (WHO 2014 revised classification)
There are two types of endometrial hyperplasia:
 Hyperplasia without atypia.
 In this type, the lining of the womb is thicker, as more cells have been produced. The
cells are all normal, however, and are very unlikely to ever change to cancer. Over
time, the overgrowth of cells may stop on its own, or may need treatment to do so.
 Atypical hyperplasia.
 In this type, the cells are not normal (they are said to be atypical). This type of
hyperplasia is more likely to become cancerous over time if not treated.
 Investigations

 Transvaginal ultrasound – to assess thickness of the endometrium.

 Endometrial biopsy
 Hysteroscopy – if hyperplasia is diagnosed by biopsy, one should consider
dilation and curretage and hysteroscopy to more definitely rule out atypia or
cancer prior to conservative medical management
Management
Endometrial hyperplasia without atypia
Initial management
Counselling
Progression to endometrial Ca <5% over 20 years
Majority of cases regress spontaneously during f/up (74%-81% in 2 cohort studies)
Identify and address reversible risk factor
HRT usage
Obesity

Observation with f/up endometrial biopsies

Inform patient higher regression rate with progestogens as compared to observation alone
Progestogens treatment
Failed to regress following observation
Symptomatic with AUB
Endometrial hyperplasia without atypia
1st line medical treatment

LNG-IUS (Mirena) – higher disease regression rate, fewer side effects.

Continuous oral progestogen – if declined Mirena Duration of treatment and f/up

LNG-IUS/ oraly progestogen – minimum of 6/12

LNG-IUS is encouraged to retained up to 5 years if no fertility concern

Endometrial surveillance – minimum 6 monthly, at least 2 consecutive 6 monthly negative biopsies prior discharge

Seek referral if AUB recurs after completion of treatment – relapse

Higher risks of relapse (eg: BMI >35, treatment wirh oral progestogen) – 2 consecutive negative biopsies then long

term f/up with annual endometrial biopsy

Endometrial hyperplasia without atypia
Surgical management
 NOT as first line treatment
 Indicated in women who not wanting to preserve fertility
 Postmenopausal – TAHBSO
 Premonopausal – TAH/TLH + Bilateral salphingectomy (recommended) +/-
ovarian conservation
 Endometrial ablation – not recommended (persistent endometrial destruction,
endometrial adhesion preclude future endometrial surveillance
Atypical endometrial hyperplasia
Initial management
 Total hysterectomy (suprecervical hysterectomy should not be perform)
 Laparoscopic approach is preferable
 No benefit from intra-op frozen section analysis of endometrium or routine
lymphadenectomy
 Post menopausal – TAH + BSO
 Premenopausal – TAH + bilateral salphingesctmy +/- ovarian conservation
 Endometrial ablation – not recommended
Management for those who WISH TO PRESERVE FERTILITY/NOT
SUITABLE FOR SURGERY

 Counsel about the risks, complications and progression.

 Pretreatment investigations
 Histology, imaging and tumor marker results
 First line treatment (LNG-IUS)
 Second best alternative (oral progestogens)
 Once fertility is no longer required
 hysterectomy - in view of the high risk of disease relapse
Follow up on women NOT undergoing hysterectomy
 Review every 3 monthly with endometrial surveillance until 2 consecutive
negative biopsies
 Asymptomatic women + evidence of histological disease regression and
minimum of 2 consecutive negative endometrial biopsies
 Long term follow up with biopsy 6-12 monthly until hysterectomy done
 If fertility therapy failed to induce regression of the disease by 12 months,
strongly recommended for hysterectomy
Management of women wishing to conceive

 Disease regression should be achieved on at least one endometrial sample

before women attempt to conceive.
 Referral to a fertility specialist to discuss the options for attempting
conception, further assessment and appropriate treatment.
 Regression of endometrial hyperplasia should be achieved prior to assisted
conception.
UTERINE SARCOMA
Uterine Sarcoma
 Uterine sarcoma refers to soft tissue tumors of the uterus and the tumors are of
mesenchymal origin.
 The tumors are very rare.
 Uterine sarcomas comprise less than 1% of gynecologic malignancies and 3-
7% of all uterine malignancies
Classification (WHO 2014)
 The following tumors arise primarily from three distinct tissues:
 Leiomyosarcomas arising from myometrial muscle
 Sarcomas arising in the endometrial stroma
 Undifferentiated uterine sarcoma

 Rare uterine mesenchymal sarcoma subtypes include :

 Adenosarcomas
 Perivascular epithelioid cell tumor (PEComas)
 Rhabdomyosarcoma
FIGO staging of Uterine sarcoma
(ULMS & ESS)
FIGO staging of Uterine sarcoma
(Adenosarcoma)
Leiomyosarcoma

 40-60% uterine sarcoma : Most common.

 Smooth muscle origin
 Associated with tamoxifen therapy
 Stage 1 and II 5 yr survival:40-70%
 Overall 5 yr survival: 15-25 %
Leiomyosarcoma
Risk factors

 Prior pelvic radiation

 Long term Tamoxifen use
 Genetic and Immunologic abnormalities
 Increasing age

 Exact cause of Uterine leiomyosarcoma is unknown.

Clinical features
 Abnormal vaginal bleeding
 Pelvic pain
 Feeling of fullness in the abdomen
 Frequent urination
 Abnormal vaginal discharge – offensive, watery with expulsion of fleshy necrotic
mass.

 A Fibroid increasing in size in a postmenopausal woman should be investigated as a

likely case of Uterine sarcoma.
Investigation
Diagnostic Challenges
 Most commonly used imaging (Ultrasound, MRI) can not differentiate between
uterine sarcoma and uterine fibroid
 MRI is better but it’s neither sensitive nor specific. It’s also too expensive to
be used for screening
 No tumor markers available for detecting uterine sarcoma.
 Histopathology gives the definitive diagnosis but it is done postoperatively.
Management
 Early stage disease : Total hysterectomy with bilateral salpingo-oophorectomy (TAH
+ BSO)
 Follow surgery by reviewing operative findings, histology reports, endocrine status
and other results to aid in staging and determine need for any other therapy.
 Followed by external pelvic radiation
 Chemotherapy
 Patients should be examined routinely after surgery (high risk of recurrence).
Prognosis
 generally poorer than that with endometrial cancer of similar stage; survival is
generally poor when the cancer has spread beyond the uterus.
 In one study, 5-year survival rates were
 Stage I: 51%
 Stage II: 13%
 Stage III: 10%
 Stage IV: 3%
 Most commonly, the cancer recurs locally, in the abdomen, or the lungs.
References
 Gynecology by Ten Teachers
 J Gynecol Oncol. 2016 Jan;27(1):e8.
 https://www.msdmanuals.com/professional/gynecology-and-obstetrics/
gynecologic-tumors/uterine-sarcomas
 https://www.curesarcoma.org/patient-resources/sarcoma-subtypes/uterine-
leiomyosarcoma/
ENDOMETRIAL CARCINOMA
 OUTLINE
Introduction
Pathophysiology(classification )
Risk factors
Clinical features
Relevant investigation
Staging
Management
Prognosis
Prevention
 INTRODUCTION
• Endometrial carcinoma is the cancer of endometrium,which is the
lining of uterus.

• Endometrial cancer is the most common gynaecological malignancy

affecting UK women with an age related incidence of 95 per
100,000 women.

• Lifetime risk developing endometrial cancer is approximately 1 in

46. 25% of endometrial cancer occurs before the menopause.
 PATHOPHYSIOLOGY
• Endometrial carcinoma is usually arises from glandular
component of endometrium and stromal tumor are
exceedingly rare

• Endometrial carcinoma usually preceded by endometrial

hyperplasia.

• Endometrial carcinoma commonly classified into two types.

 CLASSIFICATION
Type 1 Type II
Endometrioid adenocarcinomas that are High grade serous and clear cell
estrogen driven and arise from a histological subtypes and arise from an
background of endometrial hyperplasia. atrophic endometrium.
 RISK FACTORS - TYPE 1
FACTORS THAT INCREASE ENDOMETRIAL CANCER FACTORS THAT PROTECT AGAINST ENDOMETRIAL
RISK CANCER
Obesity Hysterectomy

Diabetes Combined oral contraceptive pill

Nulliparity Progestin-based contraceptives, including injectable

Late menopause >52 yrs Intrauterine device, including Cu-IUD and LNG-IUS

Unopposed estrogen therapy Pregnancy

Tamoxifen therapy Smoking

Family history of colorectal and endometrial cancer

 CLINICAL FEATURES
AT EARLY STAGE:

ONSET OF POST MENOPAUSAL BLEEDING.

MOST COMMON SYMPTOM IN PREMENOPAUSAL WOMEN. - (HEAVY,IRREGULAR,OR INTERMENSTRUAL
BLEEDING)

AT ADVANCED STAGE :
ABDOMINAL PAIN ,URINARY DYSFUNCTION,BOWEL DISTURBANCES, RESPIRATORY SYMPTOMS

SIGNS
BLEEDING FROM CERVICAL OS ON SPECULUM EXAMINATION.
BULKY UTERUS ON BIMANUAL PELVIC EXAMINATION
 DIAGNOSIS & INVESTIGATION
TRANSVAGINAL ULTRASONOGRAPHIC SCANNING (TVUSS)

• A QUICK AND ACCURATE ASSESSMENT OF ENDOMETRIAL THICKNESS

• ENDOMETRIUM MEASURES LESS THAN 4MM, CANCER IS VERY UNLIKELY
• ANY MEASUREMENT GREATER THAN THAT NEEDED FURTHER INVESTIGATION

HYSTEROSCOPY

• A THIN CAMERA IS PASSED INTO UTERINE CAVITY, ALLOWING VISUALIZATION OF ENDOMETRIUM AND DIRECTED
BIOPSY OF ANY ABNORMAL AREAS.
• HISTOLOGY REPORT DESCRIBES TYPE& GRADE OF TUMOUR
• COMPLEX HYPERPLASIA WITH ATYPIA IS A PREMALIGNANT CONDITION, COEXISTS WITH LOW GRADE
ENDOMETRIOID TUMORS OF ENDOMETRIUM
• RISK OF PROGRESSION IS 25-50%
 STAGING
• The extent of disease (stage) is determined by magnetic
resonance imaging(MRI) scan. FIGO staging uses this
information.

• Patient with high grade tumours undergo a computated

tomography (CT ) scan of chest,abdomen and pelvis to rule
out metastases.
International Federation of Gynecology and Obstetrics
(FIGO)
STAGE I Confined to uterine body

STAGE IA Less than 50% invasion

STAGEIB More than 50% invasion

STAGE II Tumour invading cervix

STAGE III Local and / or regional spread of tumor

STAGE IIIA Invades serosa of uterus

STAGE IIIB Invades vagina and /or parametrium

STAGE IIIC Metastases to pelvic and/or para-aortic nodes

STAGE IV Tumour invades bladder ±bowel±distant metastases

 MANAGEMENT
Surgery
• Main primary intervention in endometrial cancer.
• Radiotherapy is alternative, but surgery has better survival rate.
• Removal of uterus and ovaries (total hystrectomy and bilateral salpingo-
oophorectomy)
• open laparotomy or laparoscopic approach
• Vaginally could be performed, when ovaries are removed and some
peritoneal washing obtained.
 MANAGEMENT
Lymphadenectomy
• Risk of lymphatic spread in endometrial cancer is influenced by
tumour grade , type and depth of invasion into uterine wall.
 Fertility-sparing surgery
• Fertility-sparing surgery was defined as a procedure that
preserved the uterus and at least part of one ovary with the
goal of fertility preservation.

• Women at reproductive age delaying having children, need to

consider this treatment.

• Counsel the patient about the present condition.

• Start with various progestagenic agents with careful evaluation
of response by curettage at 6 weeks,3 months and 6 months.
• response poor : immediate surgery
• response well: pregnancy hysterectomy after a
successful pregnancy
Radiotherapy
• can be used as primary or adjuvant
• Primary : when disease spread renders surgery impossible or
in appropriate.
• Adjuvant : uses of brachytherapy with external beam pelvic
radiotherapy may be beneficial in those with high grade
disease.
Chemotherapy
• When distant metastases present, systemic treatment
required.
• For endometrial cancer, chemotherapeutic agents or
hormonal therapies are used.
 (cisplatin &doxorubin- commonest cytotoxics)
 (medroxyprogesterons most hormonal therapy)
• Reduces local pelvic recurrences with combination of
chemotherapy and radiotherapy.
 RELAPSED ENDOMETRIAL CARCINOMA
• The main issues to decide best therapy for patients with
relapsed endometrial carcinoma:
– previous exposure to non-surgical intervention
– site of disease relapse (localised or multiple sites)
– Patient’s physical condition

Commonest site of relapses :

Vaginal vault
 PROGNOSIS
• Endometrial carcinoma is a disease with a reasonably good
prognosis
• Primary intervention is mainly surgical and advance in surgical
techniques reduces the surgically associated morbidity.
 PREVENTION
• Prevention is inevitably the ultimate goal and can be partially
achieved through educational health policies for reducing
incidence of obesity.
• Screening is another tool that may either detect premalignant
or downstage the disease at presentation and will improve
survival rates.
 REFERENCES
• DEWHURST’S TEXTBOOK OF O&G 8TH EDITION
• GYNAECOLOGY BY TEN TEACHERS 20TH EDITION
• https://teachmeobgyn.com/gynaecology/uterine/endometrial-
cancer/

• https://www.msdmanuals.com//professional/Gynecology-and-
Obstetrics/Gynecologic-Tumors/Endometrial-Cancer
THANK YOU