Gynaecology cancer awareness

1. GYNAECOLOGY CANCER
AWARENESS

2. World 10 most common cancer in
women (GLOBOCAN 2008)
Breast
Colorectum
Cervix uteri
Lung
stomach
Corpus uteri
Ovary
Liver
Thyroid
Non – Hodgkin
lymphoma

3. Cervical Cancer
Third most common cancer in women.
8.8 % of all female cancer.
Responsible for a total of 275,000 deaths; 58% were
reported from Asia.

4. Uterine Cancer
6th most common women cancer.
More than 90 % of patients with uterine cancer are
more than 50 years old.
Cancer of the uterus has a much more favourable
prognosis than ovarian and cervical cancer with 5 –
year survival rates of around 80 – 90 % in developed
countries and 70 % in developing countries.

5. Ovarian Cancer
Cancer of the ovary is one of the most lethal
gynaecological malignancies due to late presentation,
poor respond to treatment and high recurrent rate.
3.7 % of all women cancer; with 4.2 % of all cancer
deaths in women.

7. Risk factors
Can be considered as sexually transmitted disease.
Early age of sexual activity predisposes to cervical
cancer. Relative risk is 2.5 if the age of the first sexual
exposure is < 18 years old.
Women with hx of HPV infection is also at a higher
risk. Women with multiple sexual partners have a
relative risk of 2.8 if the no. of partners > 4.
Multiparous women are at a higher risk. Women in
lower socio-economic class are at a higher risk.

8. Women who are married to a man with multiple
sexual partners are at a higher risk.
Cigarette smoking has been identified as a significant
risk factor by 2 – 5 folds.
Patients who are immunodeficient are at a higher
risk.
In-utero exposure to DES.
Women with uncircumcised sexual partner may be at
higher risk.

9. Prevention
There are 3 modalities of cervical cancer prevention:
1. Primary prevention:
- prevention of HPV infection either through sexual
abstinence, healthy lifestyle and HPV vaccination.
2. Secondary prevention:
- detection and treatment of precancerous state
through screening.
3. Tertiary prevention:
- detection and treatment of an early stage of cancer.

10. 1. HPV vaccination
HPV is the primary aetiology of cervical cancer.
Following the limitations of secondary prevention:
- 2` prevention does not prevent HPV infection or
pre-invasive lesions of the cervix.
- lesion that has rapid progression rate may not be
detected in time.
- higher chances of missing the lesions in the cervical
canal.
- limited sensitivity and specificity.
- high cost and labour intensive.

11. Oncogenic types of HPV are estimated to cause
almost 100% of cervical cancer.
2 potential benefits of HPV vaccination:
- prevention of HPV-related precancerous and
cancerous lesions.
- prevention of HPV-related benign lesions.

12. Currently 2 types of prophylactic HPV vaccines
available in the market:
- quadrivalent HPV vaccine against HPV 16,18,6,11
- bivalent HPV vaccine against HPV 16 and 18

13. 2. Screening of cervical cancer
Screening of precancerous lesions and invasive
cervical cancer is secondary prevention.
It stops the progression of disease once it has already
started.
Comprehensive analysis of data by International
Agency of Research on Cancer (IARC) showed:
- well organised screening programs were effective in
reducing cervical cancer incidence and mortality.

14. - the greatest reduction in the cervical cancer
incidence was in women aged between 30 and 49
years, for whom the focus of screening was the most
intense.
Target age range of a screening program was a more
important determinant of risk reduction than
frequency of screening, within the defined age range.
Screening interval every 2 – 3 years have been found
to be as effective as annual screening.

15. The protective effect of 5 years screening interval in
the organised screening program was still high
(> 80 %).
Screening every 2 years is approximately 50% more
expensive than screening every 3 years.
Risk of developing invasive cervical cancer is 3 – 10 x
greater in women who have not been screened. Risk
also increases with long duration following the last
normal screening test.

16. Type of screening tests
1. cytology
2. visual inspection
3. HPV testing
4. others

17. 1. Cytological screening
2 types:
1. conventional cytology
2. liquid – based cytology

18. Conventional cytology:
- Pap smear screening program significantly reduced
the incidence and mortality of cervical cancer.
- in UK, since the introduction of the organised pap
smear screening program in 1988, the incidence and
mortality rate of cervical cancer have fallen by more
than 50%.

19. - Pap smear is highly specific in detecting invasive
cervical cancer and HGSIL, but less specific in low
grade lesions.
- pap smear is not very sensitive. Low sensitivity was
attributed to poor sample collection, incorrect slide
preparation and lab interpretation errors.
To reduce the false negative, sample from the
endocervix has to be taken. Cytobrush can obtain
more cell than Ayre’s spatula and cotton tip
applicator.

20. Liquid – based cytology:
- introduced to increase the sensitivity and specificity
of cervical screening.
- more positive results with LBC.
- large reduction in unsatisfactory smear in LBC
group.
- per test cost of LBC is higher.

21. 2. Visual inspection
Direct visualisation of the cervix after application of
either acetic acid 3-5% or Lugol’s iodine.
A result is obtained immediately and treatment can
be performed at the same time.

22. 3. HPV testing
HPV DNA is identified in almost all 99.7% verified
cases of cervical cancer worldwide.
4 potential roles of HPV testing:
1. triage of women with equivocal cytology
2. following up of patient after treatment of CIN
3. HPV testing in “see and treat” approach
4. HPV testing as primary screening test

23. 4. Others
Optoelectronic device - for optical and electrical
assessment of the cervix to detect any abnormal
epithelium.
New technologies:
- HPV genotyping
- HPV mRNA
- HPV viral load
- HPV integration

24. Presentation
Asymptomatic at an early stage.
Abnormal vaginal bleeding = speculum exam.
Most common - post coital bleeding.
Passing out blood stained mucus.
Pelvic pain.
Copious foul smelling PV d/c.
Constitutional symptoms.

25. Pelvic pain, urinary problems and constitutional
symptoms – strong indication of advance stage
disease.
Pyometra – if the d/s has obstructed the uterine
outflow tract. Presents with pelvic pain, purulent
vaginal d/c and fever.
Invasion posteriorly may cause tenesmus and PR
bleeding.

26. late stage – SOB, bone pain, severe headache,
neurological problems, LOA and LOW.
Lymphatic obstruction may result in lower limb
lymphoedema.
Venous outflow obstruction can lead to DVT.

28. Type of endometrial cancer
Broadly classified into 2 main categories:
Type I endometrial cancer:
- is related to exposure to unopposed endogenous or
exogenous oestrogen.
- frequently arise on a background of atypical
hyperplasia.
- have an association with obesity, nulliparity, insulin
resistance and hyperoestrogenism.
- usually well differentiated and have a better
prognosis.

29. Type II:
- has no association with predisposing factors.
- example – uterine papillary serous, clear cell
carcinoma.
- patients tend to be elderly and thin.
- have a poorer prognosis.
80% of endometrial cancer are type I.

30. Risk factors
Prolonged exposure to oestrogen.
High level of endogenous oestrogen is often seen in
obese women, patients with PCOS and oestrogen
producing tumour.
50% of patients has BMI > 25 kg/m2.
In premenopausal women, obesity causes insulin
resistance, ovarian androgen excess, anovulation and
chronic unopposed oestrogen.

31. DM and HPT – risk factors independent of their
association with obesity.
The use of COCP for 1 year decreased the risk of
endometrial cancers by more than 40%.
Women on combined HRT have also been found to
have lower risk.
About 5% of endometrial cancer is hereditary, a/w a
hereditary non-polyposis colon cancer syndrome
(HNPCC).

32. Smoking is said to reduce the risk.
Pregnancy has a natural protective effect because of
high production of progesterone by placenta.

33. Risk factors for Type I
endometrial cancer
Obesity:
- >30 lb ideal BW 3x
- >50 lb ideal BW
10x
Nulliparous 2-3x
Late menopause 2.5x
Heavy PMB 4x
DM 2.8x
HPT
1.5x
Unopposed exog. E
untx complex atypical
hyperplasia – 29% will
develop adenoCa
Tamoxifen 6.4-7.5x

34. Endometrial hyperplasia: progressing to
Ca
- simple hyperplasia (no atypia) 1%
- complex (adenomatous, no atypia) 3%
- atypical simple (cystic w atypia)
8%
- atypical complex (adenomatous w atypia)
29%

35. Prevention
Can be prevented by treating the precursor lesions
either by hormonal or surgical treatment.
Adding a progestogen for at least 10 - 12 days per cycle
in HRT.
Women with amenorrhoea or oligomenorrhoea
(including women with PCOS) should be treated with
cyclical progestogen, to avoid prolonged exposure of
the endometrium to a high level of oestrogen.
Withdrawal bleeding of 3 monthly is sufficient to
prevent endometrial pathology.

36. Suggestions of a protective effect of high phyto-oestrogen
consumption among post menopausal
women.
The use of IUCD and tubal ligation have also been
associated with a lower risk.
Weight reduction and physical activities to achieve
ideal body weight, can reverse the effect of prolonged
exposure to a high level of oestrogen.

37. Pregnancy is a physiological protection, due to a high
level of of progesterone produced b the placenta.
The use of COCP for 1 year decreased the risk by >
40%. Also known to reduce the incidence of ovarian
cancer.

38. There is no effective screening method for
endometrial cancer.
For available methods - accuracy in asymtomatic
population is limited.
In women presenting with PMB, TVS showing ET of
5mm or less and negative endometrial sampling, have
nearly 100% negative predictive value.

39. Presentation
Majority of patients with endometrial cancer are
postmenopausal women.
Most common presenting Sx is PMB.
Abnormal PV d/c.
abnormal PV bleeding in 80% (including PMB and
irregular menses in premenopausal women).
Pressure Sx due to uterine enlargement.
Sx indicating extrauterine spread.

40. Ovarian cancer

41. Epithelial cancer is infrequent below 40 years old.
Peak rate is at 70 - 74 years age group with the
incidence of 57/100,000 population.
Ovarian cancer at the older age group carries a poorer
prognosis.

42. Risk factors
1. Reproductive factors:
Parous women have 30 - 60% less risk compared to
nulliparous.
The birth of the first child reduces the risk by 45%.
Every further pregnancy reduces the risk by 15%.
Breast feeding reduces the risk.
Tubal ligation is also associated with lower risk.
Ovulation induction agent increases the risk by 2-3 x,
if taken for > 12 ovulatory cycles.

43. OCP reduces the risk by 30 - 60 %.
History of breast cancer increases the risk.
Early menache and late menopause are risk factors.
Slightly increased risk with HRT.

44. 2. Genetic factors:
Lifetime risk in general population is 1.6%.
Increased to 4% in women with a first degree relative
affected.
Increased to 7% when 2 first degree relatives are
affected.
5-10% of all epithelial ovarian ca results from
hereditary predisposition.

45. The frequency of BRCA 1 mutation is about 1 in 800.
62% of patients with epithelial ovarian cancer have a
mutation of p53.

46. 3. Environmental factors:
Incidence highest in industrialised countries except
Japan.
Incidence lowest in under developed and developing
countries.
High intake of meat and animal fat diet increases the
risk.
Low fat diet may reduce the risk in postmenopausal
women.
Obesity has been attributed to risk of ovarian cancer.

47. Prevention
OCP (chemoprevention) has the highest protective
effect against ovarian cancer.
Taking OCP for at least 5 years reduces the relative
risk of by 50%.
Tubal ligation and hysterectomy reduces the risk.
Prophylactic oopherectomy is often performed
together with hysterectomy for benign conditions.

48. Prophylactic oopherectomy to women with BRCA1
and BRCA2 mutations after the age of 30 - 35 years,
reduces the risk by 80%.
For women with BRCA1 and BRCA2, recommended to
do TVS and CA125 levels every 6 - 12 months, in
women age 25 - 35 years old.
Genetic testing for BRCA1 and BRCA2.

49. Screening
There is no effective screening method.

50. Presentation
75 - 85% of patients already has peritoneal spread at
the time of the diagnosis.
Most common presentation:
- abdominal discomfort
- abdominal pain and distension
- GIT symptoms e.g. nausea, dyspepsia, constipation.

51. Diagnosis of early stage cancer is usually made by
abdominal and pelvic examination.
In premenopausal women, functional cyst is rarely >
8cm, and will resolve after 2-3 months without
treatment.
Adnexal mass in pre-menarchal and post menopausal
women has a higher likely hood of being malignant.