Gynecology

1. MALIGNANT TUMORS OF THE
UTERUS
Mujinya juliusBMS/7711/163/DU
SUPERVISOR. DR,Bwaga
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2. OUTLINE
• ENDOMETRIAL HYPERPLASIA
• ENDOMETRIAL CARCINOMA
• UTERINE SARCOMA
• Definitions
• Classification
• Risk factors
• Clinical features
• Staging
• Management
• Follow-up
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3. ENDOMETRIAL HYPERPLASIA
• Definition
– overgrowth of the endometrium, due to increase in
gland proliferation
• Diffuse
• Focal- endometrial polyp
• Histological Classification
– Simple or
– complex
• Based on the degree of glandular crowding or complexity of
cells with or without atypia Based on cytological features,
especially cellular atypia.
• Atypia (Dysplasia): loss of polarity, with increased nucleus-
to-cytoplasm ratio and prominent nucleoli, and irregularly
condensed chromatin.
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4. Architectural description
TYPE ARCHITECTURE
SIMPLE
-Increased glandular to stromal ratio
-Cystic glandular dilatation
-Some glandular budding and
infolding
COMPLEX
-glandular crowding with less intervening
stroma
-glands show significant infolding and
budding
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5. Risk factors
• Unopposed estrogen action on the
endometrium
– Obesity, DM, HTN
– Anovulation(PCOS)
– Tamoxifen use
– Hormonal Replacement Therapy-HRT(Estrogen)
– Infertility/low parity
– Early menarche/late menopause
– Estrogen-secreting tumors, such as granulosa cell
tumors of ovary.
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6. Risk factors
– Family history
• Lynch syndrome---HNPCC
PROTECTIVE FACTORS
– Combined Oral contraceptives appear to be
protective by 50%
– Smoking is protective
– Multiparity
– Normal weight
– Menopause <49yrs
– Progestin therapy
– Age >65yrs
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7. Clinical presentation
• There are no specific clinical presentations for
premalignant endometrial hyperplasia but,
the constant feature is premenopausal
abnormal uterine bleeding.
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8. • World Health
Organization
Classification of
Endometrial Hyperplasia
• Types
• Simple hyperplasia
• Complex hyperplasia
• Simple atypical
hyperplasia
• Complex atypical
hyperplasia
World Health Organization
Classification of
Endometrial Hyperplasia
Types Progressing to Cancer(%)
Simple typical hyperplasia 1
Complex typical hyperplasia 3
Simple atypical hyperplasia 8
Complex atypical hyperplasia 29
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9. Diagnosis
• Trans vaginal ultrasonography: To measure
the endometrial thickness
– Endometrial thickness >5mm in post menopausal
women
– Endometrial thickness >12mm in any phase of the
menstrual cycle
• Uterine curettage for Endometrial biopsy and
histology.
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10. Management options
OPTIONS
• Medical
– Progestin: MPA,
DMPA, Mirena
– COC
• Surgical
– Fractional D&C
– Endometrial ablation
– TAH+BSO
ENDOMETRIAL ABLATION
• Layers to ablate
– Endometrium
• Functionalis and the basalis
– 3mm of the myometrium
• Useful in
– Patients unfit for hysterectomy
with atypia
• Contraindications
– Active pelvic infection
– Malignancy
– Previous uterine surgery
• C/S, Myomectomy, perforations
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11. Management
Type Premenopausal/desire
for fertility
Post menopausal/no
desire for fertility
Comments
Hyperplasia
without atypia
Simple or
Complex
--Hormonal therapy MPA 10-20mg, day 10-25,
for 3months
--D&C,
Progestin are effective
without atypia
If normal, continue for 1 year then COCs or
Mirena (levenogestrol releasing IUD)
If abnormal
--increase MPA dose
Repeat D&C, if
normal, progestin till
menopause
--Consider surgery
If abnormal, consider -
--TAH+BSO,
--Endometrial ablation
Hyperplasia
with atypia
Simple or
Complex
Strongly recommend surgery
Increased risk
of recurrence
And
development
of cancer
High dose progestin
Repeat D&C after 3
months, if persistent
,do surgery, if normal
induce ovulation with
clomiphene, FSH
TAH+BSO,
If unfit for surgery,
progestin and follow-
up D&C in 3 months
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12. ENDOMETRIAL CARCINOMA
Incidence:
• Fourth most common cancer in women
• Most common gynecologic cancer in the Western
World
• Generally a disease of postmenopausal women
– ¼ may occur premenopausal,
– about 5% occur in women under the age of 40
• Commonly in association with Lynch syndrome, anovulation,
obesity
• Peak age at diagnosis is between 50 - 65 years
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13. Types (Bohkman): Type I &II
Feature Type I Type II
Age <40 >40
Estrogen dependent Yes No
Endometrial
hyperplasia
Commonly follows
endometrial hyperplasia
No
Histology Adenocarcinoma Clear cell, papillary
serous carcinoma.
Myometrial invasion Minimal Deep
Differentiation Well differentiated Poor differentiation
Prognosis Good Poor
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14. Risk factors
1. Estrogenic stimulation-HRT,
2. Late Menopause,
3. Early menarche,
4. PCOS
5. Age- Peak age is 60 ,75% of all Ca endometrium
occur in post menopausal women & 10% of
postmenopausal PV bleeding is Ca endometrium.
6. Nulliparity
7. Family history- its the most commonly inherited
gynecologic cancer( HNPCC)
8. Endometrial hyperplasia
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15. Risk factors
7. Corpus cancer syndrome:
Obesity, HTN, Diabetes.
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16. Diagnosis is linked to clinical history of;
–Patients with Lynch syndrome(HNPCC)
–Post menopausal vaginal bleeding
–Perimenopausal women with abnormal
bleeding In the setting of anovulation,
endometrial hyperplasia, obesity
–Post menopausal women on exogenous
estrogen without progestin
–Post menopausal women with pyometra
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17. Diagnosis
• Screening
– No acceptable screening methods exists
• Patients to suspect and screen for Ca
endometrium…sensitization
– Pap smear showing
• endometrial cells in post menopausal
women
• atypical endometrial cells in non pregnant
women
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18. Diagnostic approach
Endometrial histology is the mode of diagnosis
• Endometrial biopsy
–First line diagnostic procedure
–approaches the accuracy of a formal D&C
(>90%)
–If normal, no other investigation is
necessary, follow up
–If abnormal, treat
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19. • Fractional D&C
–If postmenopausal bleeding is persistent
–or recurrent
–or other high-risk factors exist
• Hysteroscopy
• Trans vaginal ultrasound
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20. Investigations When diagnosis is made
to r/o metastasis
– Repeat thorough pelvic and abdominal exam
– Chest X-ray, MRI/ CT Scan
– barium enema examination or a colonoscopy
– Cystoscopy
– CBC, RFT, LFT
– CA 125 levels ( tumor marker)
• successfully predicts either deep myometrial
invasion or distant metastasis.
• may be useful in follow up
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21. CLASSIFICATION
• Histologically (Microscopic)
– Adeno-carcinoma
• Most common >75%
– Mucinous carcinoma,
– Serous carcinoma, 5-10%
• Highly aggressive, type II
• May have psamoma bodies
–Clear cell carcinoma
–Squamous carcinoma
–Mixed carcinoma
–undifferentiated carcinoma
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22. Macroscopically
Can be;
1. Localized
2. Diffuse
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23. Patterns of spread
• Direct invasion
– Myometrium, serosa
– Lower segment tumors, cervix
– Fundal tumor, tubes & ovaries
• Lymphatic spread
– Haphazard, not sequential
• Hematogenous spread
• Intraperitoneal exfoliation
– Retrograde transtubal transportation
– Serosal perforation
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24. TUMOR STAGING & GRADING
• Surgical staging-most recommended, FIGO 1988
• The clinical staging, FIGO 1971 is reserved for inoperable
cases
Histological
diagnosis
Operable disease!
--Surgical staging-
recommended,
FIGO 1988
Inoperable disease!
Clinical staging,
FIGO1971
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25. TUMOR GRADING
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26. SURGICAL STAGING- Operable disease
STAGE GRADE DESCRIPTION
IA G1, or
2,or 3
Tumor limited to endometrium
IB Invasion to <50% of the myometrium
IC Invasion to >50% of the myometrium
IIA Endocervical glandular involvement only
IIB Cervical stromal invasion
IIIA Tumor invades serosa or adnexa, or positive peritoneal cytologic
findings
IIIB Vaginal metastasis
IIIC Metastasis to pelvis, paraaortic lymph nodes, or both
IVA Tumor invasion of bladder or bowel mucosa
IVB Distant metastasis including intra-abdominal or inguinal lymph
nodes
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27. Clinical staging FIGO 1971
used in technically- inoperable cases
STAGE DESCRIPTION
Stage 0 CIS
Stage I Stage I is graded as
Grade 1 or
Grade 2 or
Grade 3
Carcinoma confined to the uterus
Stage I A The length of the uterine cavity is =<8cm
Stage IB The length of the uterine cavity is >8cm
Stage II Disease extends to cervix, BUT not outside the
uterus
Stage III Disease extends beyond the uterus but not
outside the true pelvis
Stage IV A Tumor extends outside the true pelvis or
involves the rectal and/or bladder mucosa
Stage IVB Spread to distant organs
GRADES
Grade 1 Highly differentiated adenomatous carcinoma
Grade 2 Differentiated adenomatous carcinoma with partially solid areas
Grade 3 Predominantly solid or entirely undifferentiated carcinoma
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28. Management
• The primary management is surgery:
–TAH+BSO
–Radical hysterectomy with bilateral
salpingo-oophorectomy and LND may be
considered for stage II
• uterus should be sent immediately for histological
evaluation
• Following surgery and review of the final pathology
report, classify the patients into risk groups
• Post operative treatment depend on the risk for
recurrence
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29. Chemotherapy
• Cisplatin (P), Paclitaxel (T) Adriamycin
(A)
–TAP
• Radiotherapy
– Primary therapy: in poor surgical candidates
– Adjuvant therapy: stage> IC>G3
• Hormonal therapy
– Palliation in poor surgical candidates
– Progestin: DPMA
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30. Post treatment Surveillance
• most recurrences will occur within 3 years
• Follow up patients
– Every 3 months for 2 years, then 6 monthly for 5
years
• Physical exam
• Vaginal cytology
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31. Prognosis
• Prognostic Factors
– Stage of disease
– Histologic differentiation
– Histologic type
– Depth of myometrial invasion
– Lymph node metastasis
– Other Extrauterine metastasis
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32. Prognosis
Stage 5 year Survival %
IA 91
IB 88
IC 81
IIA 77
IIB 67
IIIA 69
IIIB 41
IIIC 32
IVA 20
IVB 5
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33. UTERINE SARCOMAS
• Malignant tumors of the uterine corpus
• broadly divided into three main types:
• Carcinomas,
• Sarcomas
• Carcinosarcomas
• They are rare, <5% of uterine malignancies but
aggressive, grow & metastasize quickly with
poor prognosis.
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34. • Sarcomas are carcinomas that start in the
muscles and supporting tissues of the uterus.
E.g. muscles,fat,bones and fibrous tissue.
• Carcinomas are ca.s that start in epithelial
cells and cover most organs. E.g. cervical CA,
endometrial ca.s.
• Carcinosarcomas
• start in uterus ,have both features of sarcomas
and carcinomas. Are also known as mixed
mesoderm tumors or mixed mullerian tumors.
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35. Types of carcinosarcomas
• Uterine leiomyosarcomas- the most common
type. Can grow and multiply very fast.
• Endometrial stromal sarcoma- start in the
connective tissue ( stroma) of the lining of the
uterus (endometrium).-my be low grade or
high grade-hard to treat.
• Un differentiated sarcomas-cancers start in
endometrium /myometrium,grow quickly and
tend to have poor outlook.
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36. • Adenosarcomas –have normal gland cells that
are mixed with ca cells of the stroma
(supportive connective tissues).
Note; signs of uterine sarcomas
Un usual p v bleeding
Bleeding after menopose
Mass in the vagina
Increased micturition.
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37. • ,,,,,EVERYTHING IS POSSIBLE,,,,
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38. REFERENCES
• WILLIAMS GYNECOLOGY
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