GYNAECOLOGY

ONCOLOGY
(Cervix,Uterus and Ovary)
CERVIX
1.INTRODUCTION
• Cervical cancer is the most common gynaecologic cancer in women
worldwide.
• Most o these cancers stem from infection with the human
papillomavirus (HPV)
• disease prognosis differs with tumor stage, and stage is the most
important indicator o long-term survival.
• 57 percent o invasive cervical cancer cases were attributable to HPV
serotype 16
• HPV 16 is more commonly associated with squamous cell carcinoma o
the cervix, whereas HPV 18 is a risk actor or cervical adenocarcinoma
2.
R
I
S
K
PATHOPHYSIOLOGY
 3. GROSS PATHOLOGY
• Pap smear (in invasive CA) shows:
 Tadpole cells
 Fibres & malignant cells
 Haemorrhage
 Necrosis in the background.

• Site of lesion:
Ectocervix (80%)
Endocervix (20%)

a. Naked eye
i. Exophytic – arise from ectocervix & form friable masses almost filling up the upper vagina in
late cases.
ii. Ulcerative – the lesion excavates the cervix & often involves the vaginal fornices.
iii. Infiltrative – found in endocervical growth. They cause expansion of cervix, resulting in barrel-
shaped cervix.
 3. GROSS PATHOLOGY
b. Histopathology Squamous cell carcinoma of the cervix,
keratinizing type. Malignant squamous cells
Squamous cell carcinoma form irregular nests invading the stroma. In the
center of the nest, laminated keratin pearls are
 commonest variety (85-90%) & arise from present. Individual cells have abundant
the ectocervix. eosinophilic keratinized cytoplasm.
(Hematoxylin-eosin stain, red bar: original
 The sources of the squamous epithelium magnification.)
which turn into malignancy are:
 Squamocolumnar junction
 Squamous metaplasia of the columnar
epithelium

 Squamous cell carcinoma is histologically

Squamous cell carcinoma of the cervix, non-
divided into: keratinizing type. Malignant squamous cells
 Large cell keratinising have abundant eosinophilic cytoplasm, distinct
cell borders, and individual cell keratinization.
 Large cell non-keratinising
The irregular, large nuclei contain multiple
 Small cell type nucleoli. (Hematoxylin-eosin stain, red bar:
original magnification.)
*small cell type have poor prognosis compared to
large cell types.
 3. GROSS PATHOLOGY
b. Histopathology
Adenocarcinoma
 (10-15%) develops from the endocervical canal – either from the lining
epithelium or from the glands.

 Currently increased numbers of cervical adenocarcinomas are observed specially

in the younger age group.

 The majority (80%) of them are purely endocervical type.

• The remainders are:

o Endometroid
o Clear cell
o Adenosquamous
o Mixed type
 4. MODE OF SPREAD
Direct extension Lymphatic
The growth spreads directly to the adjacent structures • Primary group involved are:
(vagina & body of uterus): parametrial LN, internal iliac LN,
obturator, external iliac LN, sacral
• Laterally extends to : parametrium, paracervical & paravaginal tissues. (here the tumour LN
cells surround & compress the ureter)
• Secondary group involved:
• Posteriorly spread to : utero-sacral ligament, rectum
common iliac group, inguinal LN,
• Anteriorly involves the : base of the bladder (specially in endocervical growth). paraaortic LN

Sentinel lymph node (SLN) Haematogenous Direct implantation

First nodes that drains Blood-borne metastasis is Of the cancer cell at
a primary tumour: late & often via veins. operation on the vault/
Usually involves lungs, liver domelike structure of the
• (85% cases) there is a or bone. vagina /abdominal/
single sentinel LN. perineal wound. (rare)
FIGO staging
• To determine the prognosis, to formulate line of treatment & to
compare the results of one to the other

• Staging of cervical cancer is based principally on clinical examination

• Perspeculum examination
• Bimanual examination
• Rectal examination
 Confirmation of diagnosis is by biopsy
Ancillary aids for confirmation:
• Cystoscopy
• X-ray chest
• Intravenous pyelography
• Signs • Proctoscopy
• Speculum examination
• Nodular growth or ulcer, lesion bleeds on friction
• Done prior to bimanual examination
• Bimanual examination
• Lesion is indurated, friable and bleed to touch
• Cervix freely mobile
• Rectal examination
• Parametrium absolutely free
• Symptoms
• Irregular or continued vaginal bleeding
• Offensive vaginal discharge
• Pelvic pain
• Leg edema
• Bladder symptoms (urgency, dysuria, hematuria, true incontinence d/t
fistula formation
• Rectal involvement (diarrhea, rectal pain, bleeding per rectum,
rectovaginal fistula)
• Ureteral obstruction d/t progressive growth of tumor laterally later
on becomes pyelonephritis

Ultimately, patient may be cachectic, anemic with edema legs

UREMIA develops
Complications
• Hemorrhage
• Frequent attacks of ureteric pain d/t pyelitis, pyelonephritis and
hydronephrosis
• Pyometra
• Vesicovaginal fistula
• Rectovaginal fistula
• Death uremia, massive hemorrhage, sepsis, cachexia, metastases
Treatment for Ca cervix :-
• Age
• Need to preserve fertility
• Size of lesion
• Stage
• General condition
Uterine Carcinoma
• Introduction  

-is cancer that form in tissue Risk factor

lining of the uterus
-7th post commonest cancer
among women
 
-Overweight
-Nulliparity
-Late menopause
-Diabetes Mellitus
-Hypertension
-Unapposed estrogen replacement
therapy in post menopausal women
increases the risk by 7 fold
Pathology
Premalignant condition is endometrial Hyperplasia

Type of hyperplasia progressing to cancer Percentage

Simple(Cystic without atypic) 1

Complex ( Adenomatous without atypic) 3

Simple ( Cystic with Atypia) 8

Complex ( Adenomatous without atypic) 29

Histology
1) Endometroid Adenocarcinoma
-most common type 80%

2)Serous Carcinoma
-10% of all cases
- Common in elderly women

3) Others
-Clear cell carcinoma 4%
Endometrial cancer Figo staging Prognosis
5 years survival with Figo staging

Stage 5 years Survival

1 75%

2 58%

5 years survival with Figo staging

3 30%

4 10%
Clinical Presentation
• Predominantly occur in postmenopausal women and classically will
present with postmenopausal bleed
- Bleeding usually slight and intermittent at first
- Later bleeding will become heavy and continuous
- Vaginal discharge will present later will become offensive
- Sense of discomfort in pelvis later will become PAIN as a late
symtoms which indicate extensive of disease.
1)History
Presenting symptoms. • Menstrual history. • Parity. • Comorbidities. •
Drug history (COCP, HRT, tamoxifen, antihypertensives, oral
hypoglycaemic
2)Examination
• Rule out other causes of bleeding (vulval, vaginal, and cervical
pathology) with vulval, vaginal, and speculum examination.
• Bimanual examination: uterine size, mobility, adnexal masses.
3) Haematological investigations
• FBC, U&E, LFTs.
Imaging investigations
• TVUSS: <4mm endometrial thickness, very low risk of endometrial
pathology in post menopausal women, no requirement of
endometrial sampling

• CTTAP- Staging of disease

• MRI pelvis: Can be used to determine local extent of tumor and

present of involvement of pelvic LN. Not routinely done
• Endometrial biopsy

-Perform endometrial sampling if ET ≥4mm or persistent bleeding in

woman with ET <4mm( case consider formal hysteroscopy)
1) Blind outpatient sample( Pipelle, Vabra)
2) Hyteroscopy: Under LA or GA
• Endometrial cancer: treatment
1) Treatment Surgery TAH and BSO and pelvic washings:
this can be performed. Increasingly, laparoscopic hysterectomy is gaining popularity and is
approved by NICE.
2)Pelvic lyphadenectomy
Role) in low-grade early disease is controversi. Two RCTs (and Cochrane systematic review)
suggest no survival advantage in early disease .
3)Adjuvant radiotherapy
Adjuvant radiotherapy limited to vault brachytherapy, if intermediate risk (see below), EBRT ±
vault brachytherapy boost for high risk (G3, stage Ib) or locally advanced disease. Role of
adjuvant chemotherapy in addition to ERBT in high risk disease being examined in clinical trial
(PORTEC 3).
4)Hormonal
High dose progesterone used for advanced and recurrent disease. • Largely aiming for palliation
of symptoms (bleeding)—no survival advantage demonstrated.
5)Palliative radiotherapy •
EBRT given at lower dose and in few fractions to control local symptoms (e.g. bleeding)
Ovarian cancer
Epidemiology
● 1 in 70 will develop ovarian cancer
● Mean age of presentation is 64 years old
● More prevalent in higher socioeconomic group
● Variation in ethnicity (white women have the highest prevalent at
approximately 14/100000, Asian women at 10/100000)
● Ovarian cancer is rare in younger women (<3% in women less than 35
years old)
Classification of ovarian cancer
Origin Overall frequency Types
Epithelial ovarian tumors 65-70% Serous
Endometrioid
Clear cell
Mucinous

Germ cell tumors 15-20% Dysgerminoma

Endodermal sinus (yolk sac)
Teratoma
Choriocarcinoma

Sex cord stromal tumors 5-10% Granulosa cell

Sertoli–Leydig
Gynandroblastoma
Epithelial ovarian tumors Germ cell tumors Sex cord stromal tumors
● Most common in postmenopausal ● Usually affects younger women ● Usually present in 4th and 5th
women ● Originate from undifferentiated decades
● Median age for ovarian primordial germ cells of gonad ● Originate from stroma of gonad
adenocarcinoma is 60-65 years old ● Rapidly growing
● Histology may demonstrate
‘borderline’ malignancy, whereby
malignant histological features are
present but invasion is not
Risk factors
Decreased risk of ovarian cancer Increased risk of ovarian cancer

Multiparity Nulliparity
Combined oral contraceptive pill Intrauterine device
Tubal ligation Endometriosis
Salpingectomy Smoking
Obesity

Early menarche
Late menopause
Presentation
Often have non specific, vague symptoms
Common symptoms include:
● Increased abdominal girth
● Bloating
● Persistent pelvic/abdominal pain
● Early satiety
● Change in bowel habit
● Urinary symptoms
● Irregular bleeding
● Weight loss
Signs of ovarian cancer
Woman with pelvic mass and ascites, diagnosis is ovarian cancer until
proven otherwise
In advanced disease, examination of upper abdomen may reveal a central
mass (omental caking)
Investigations
Biochemistry: Imaging:

Full blood count Ultrasound

Urea and electrolyte CT scan

Liver function test MRI

Tumor markers
Risk of malignancy index (RMI)
RMI is calculated using ultrasound scan score (U), menopausal status (M) and
serum CA125 level
Feature Score
Ultrasound features 0 = ultrasound score of 0 points
● Multilocular cysts 1 = ultrasound score of 1 point
● Solid areas 3 = ultrasound score of 2-5 points
● Metastases
● Ascites
● Bilateral lesions

Menopausal status 1 = premenopausal

3= postmenopausal
FIGO staging of ovarian cancer
Management
Stages of ovarian cancer Recommended management

Early ovarian cancer

Low risk (Stages 1A and 1B, grade 1) TAHBSO

High risk (Stages 1A and 1B, grade 2 and 3; stages 1C, IIA, IIB and TAHBSO
IIC, no residual) Adjuvant therapy with combination carboplatin and paclitaxel
chemotherapy

Advanced ovarian cancer

Stage III with optimal residual disease Maximal surgical cytoreduction

Combination chemotherapy with systemic carboplatin and
paclitaxel or systemic paclitaxel plus intraperitoneal cisplatin and
paclitaxel

Stage IV or suboptimal disease, or both Maximal surgical cytoreduction

Combination chemotherapy with carboplatin and paclitaxel
Follow up and prognosis
● Monitor using levels of CA125
● CT scan aids detection of residual disease
● Interval debulking may be beneficial if all could not be removed at first
surgery
● Chemotherapy prolongs short term survival and improves quality of life
● Poor prognostic indicators are advanced stage, poorly differentiated
tumours, clear cell tumours and slow or poor response to chemotherapy.
● Death is commonly from bowel obstruction or perforation.
Ovarian cancer survival by stage at diagnosis

FIGO stage 5 year survival rate (%)

1 80-90

2 65-70
3 30-50

4 15
Palliative care
Aim to improve quality of life for patient and her family
Addressing symptoms like pain, nausea, vomiting, PV bleeding, and bowel
obstructions
Meeting patient’s social, psychological and spiritual needs

The terminal stage should be managed sensitively with time for the patient
and relatives in a quiet environment. Good symptom control with anxiolytics
and analgesics without overly sedating can allow valuable time with the
family.