r

f Neoplasm ) f

Functional Cysts Symmetrical ) ( Asymmetrical j

lalways benign)

Other Gynaecological

Abdominal pregnancy

Pelvic adhesions {causing

peritoneal inclusion cysts)

Pelvic adhesions

{ resulting in fluid entrapment)

Nodule of deeply

infiltrating endometriosis

Corpusluteum cyst

Follicular cyst

Theca lutein cyst

Hemorrhagic cyst

PCOS

Tubo-ovarian abscess

Luteoma of pregnancy

Pregnancy

Hematometra

'

pyometra

Endometrial cancer

Adenomyosis

Leiomyoma

Leiomyosarcoma

Benign

Dermoid cyst

Imost common)

Endometrioma

Malignant

Epithelial cell

Imost common in >40 yr)

Germ cell

(most common in <20 yr)

Sex-cord stromal

tumours and metastases

Gastrointestinal

Appendiceal abscess

Diverticular abscess

Drverticulosis, diverticulitis

Carcinoma of rectunt'colon Ectopic pregnancy

Hydrosalpinx/Pyosalpimo

Paratuba l/paraovarian

cyst ( benign)

Tubo-ovarian absess

Malignancy

Genitourinary

Distended bladder

Pelvic kidney

Carcinoma of bladder

Imperforated hymen

(causing hematocolpos)

Lymphoma

Figure 21. Differential diagnosis of pelvic mass

Uterus

Incidence of Malignant Gynaecological

Lesions in North America

endometrium > ovary > cervix > vulva >

vagina > fallopian tube

ENDOMETRIAL CARCINOMA

Epidemiology

• most common gynaecological malignancy in North America (40%); 4th most common cancer in

women

• 2-3% of women develop endometrial carcinoma daring lifetime

• mean age is 60 yr

• majority are diagnosed in early stage due to detection ofsymptoms

• 85-90% 5 yrsurvival for stage 1 disease

• 70-80% 5 yr survival for all stages

Risk Factors for Endometrial Cancer

COLD NUT

Ca ncer (ovarian, breast, colon)

Obesity

Late menopause

Diabetes mellitus

Nulliparity

Unopposed estrogen: PCOS.

anovulation. HRT

Tamoxifen (chronic use)

(Genetic syndromes:Hereditary

Nonpolyposis Colorectal Cancer

(HNPCC) - Lynch II syndrome,Cowden

syndrome)

Table 21. Features of Type I and Type II Endometrial Cancer

Type I Type II

Description Estrogen-related|i.e.eicess/ unopposed

estrogen ):

Endometrioid

Includes well- differentiated (grade1and 2)

endometrioid adenocarcinoma

80% of cases

PCOS

Diabetes mellitus

Unbalanced HRT (balanced HRT is protective)

Nulliparity or history of infertility related to

anovulation

late menopause|

»55 yr).early menarche

Estrogen-producing ovarian tumoars|e.g.

granulosa cell tumours)

HNPCC'/lynch llsyndrome

Tamoxifen

Prior pelvic radiation

Postmenopausal bleeding

AUB in premenopausal women (menorrhagia.

intermenstrual bleeding)

Non-estrogen related:

Non-endometrioid

Includesserous,clear cell,grade 4

endometrioid and undifferentiated

carcinomas,carcinosarcoma

20% of cases, poorer prognosis

Parous women

More likely in Black women

Associated with pS3 mutation. HER2

overeipression

Risk Factors(Increasing age and family

history are risk factorsfor both types)

Postmenopausal bleeding *endometrial

cancer until proven otherwise (95%

present with vaginal bleeding)

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An endometrial thickness of 5 mm

or more is considered abnormal in a

postmenopausal woman with vaginal

bleeding and a thickness of more than

11 mm is considered abnormal in a

postmenopausal woman without vaginal

bleeding

Clinical Features AUB

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'HNPCC = Hereditary non-polyposis colorectal cancer

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Screening

• no known benefit for mass screening

• annual endometrial sampling starting at age 30-35 only for women at high-risk (HNPCC/Lynch II

syndrome)

• routine pelvic ultrasound should not be used asscreening test (high false positive rates)

Prognostic Factors

• FIGO stage (most important factor)

• Age

• Grade

• Histologic subtype

• Depth of myometrial invasion

• Presence of LVSI

Investigations

• endometrial sampling in all suspected patients (office endometrial biopsy most commonly)

• hvsteroscopv considered in patients with persistent uterine bleeding with benign sampling or

inadequate sampling

• additional tumour markers, CT, MRI only in specific casessuch as high-grade tumours,suspected

extrauterine spread Complications of Therapy

Table 22. FIGO Staging of Endometrial Cancer (2009) Surgical Complications

• Surgical site infection

• Lymphedema

• VTE

• Urinary retention

. UTI

• Pelvic lymphocyst

• Leg weakness

• Vaginal dryness

Stage Description Stage Description

Confined to corpusuteri including endocervical ItIC

glandular involvement

Less than 50% myometrial invasion

More than 50% myomelrialinvasion

Invades cervical stroma,but does not extend beyond IV

uterus

Involves serosa,adnexa,vagina,or parametrium IYA

Invasion ofserosaiadnexae

Metastasis lo pelvic t para-aorbc INs

IIIC1 Positive pelvic LN

Positive para-aortic LN ± positive pelvic LNs

Invades bladder!bowel mucosa tdistant metastases (note:

omental disease is stage IV)

Invades bladder!bowel mucosa

Distant metastases,including intra-abdominal and

intraperitoneal metastases,!inguinal LNs

IA

IS IIIC2

II

Radiation Complications

• Radiation fibrosis

• Cystitis

• Proctitis

• Long term increase in other types of

malignancy

III

II1A IY3

1113 Vagaal!parametrial involvement

FIGO: International Federation ot Gynaecology andObstetrics

Treatment

• surgical: total hysterectomy + BSO

• pelvic washings ± pelvic and para-aortic node dissection ± omentectomy in more advanced cases

goals: treatment,staging, determining need for adjuvant treatment

• adjuvant therapy: includes radiation and chemotherapy, depends on clinical and histological features

• hormone therapy: can be used in fertility-sparing treatments (e.g. progesterone 1UD or oral

progestins)

Uterine Sarcoma -Presentation

Bleeding, abdominal distention,pelvic

pressure

UTERINE SARCOMA

• rare; 3-9% of all uterine malignancies

• arise from stromal components (endometrial stroma, mesenchymal, or myometrial tissues)

• behave more aggressively and are associated with worse prognosis than endometrial carcinoma; 5 vr

survival is 35%

• vaginal bleeding is most common presenting symptom

CA-125 is indicated for monitoring

response to treatment

Table 23. Summary of Uterine Sarcoma Subtypes and Features

Type Epidemiology Features Diagnosis Treatment

PURE TYPE

1.Leiomyosarcoma Most common type of uterine

sarcoma

Average age of presentation

is 55 yr,but may present in

premenopausal women

Often coexists with benign

leiomyomata (fibroids)

Histologic distinction from leiomyoma:

1Increasedmitotc count (»10 mitoses/10 highpouter fields)

2,Tumour necrosis

3.Cellular atypia

Rapidly enlarging fibroids In a premenopausal

woman

Enlarging fibroids in a postmenopausal woman

Abnormal uterine bleeding

Good prognosis

Often postoperabvely after uterus

removed for presumed fibroids

Stage using FIGO 2009staging for

leiomyosarcomas andESS

Hysterectomy!BSO usually

No routine pelvic lymphadenectomy

Chemotherapy is used in cases oimetastatic

disease

Radiation therapy does not improve local

control or survival

Poor outcomes overall,even for early stage

disease

HysterectomyiBSO (remove ovaries as

ovarian hormones may stimulate growth)

No routinepelvic lymphadenectomy

Adjuvant therapy based on stage and

histologic features (hormones and/or

radiation)

Hormonal therapy (progestins) may be used

for metastatic disease

Treatment primarily surgical

Radiation and/or chemotherapy for

advanced diseased or unresectabledisease

2.Endometrial Stromal

Sarcoma (ESS)

Oragnosed by histology ol

endometrial biopsy or DSC

Stage usrng FIGO 2009 staging for

leiomyosarcomas and ESS

Usually presents In

perimenopausal or

postmenopausal women with

abnormal uterinebleeding

3.Undifferentiated

Sarcoma

Rare;less common than

leiomyosarcoma and ESS

Severe nuclear pleomorphism.high mitotic Often found incidentally

activity,tumour cellnecrosis,and lackolsmooth postoperatvetyforabnormal

muscle or endometrial stromal differentiation bleeding

Poor prognosis

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MIXEDTYPE

Ibe rarest of the uterine sarcoma Present with abnormal vaginal bleeding

Mixed tumour of low malignancy Polypoidmass inuterine cavity

potential

Mixture of benignepithelium with treatment is surgical with hysterectomy

malignant low-grade sarcoma A BSO

Often foundincidentally at time of

hysterectomy (or PMB

Stage using FIGO 2009 staging lor

adenosarcoma

d.Adenosarcoma

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I Gynaecology Toronto Notes 2023

Table 24. FIGO Staging of Uterine Sarcoma (2009)

Stage Description Stage Description

Ovaries are like GEMS

Germcell

Epithelial

Metastatic

Sex cord stromal

Tumour limited to uterus

<5cm

>5cm

Tumour extends beyond uterus

To the pelvis,adnexal involvement

To extra - uterine pelvic tissue

Tumour invades abdominal tissues

One site

I III

IA MIA

IB NIB More than one site

Metastasis to pelvic and/or para aortic lymph nodes

Distant spread

Tumour invades bladder and/or rectum

Distant metastasis

II IIIC

IIA IV

MB IVA Most(70%) epithelial ovarian cancers

IVB present at stage III disease

Ovary

Ovarian Tumour Markers

Epithelial cell:

• CA 125 (serous and endometrioid)

Sex-cord stromal cell:

• Granulosa cell:inhibin

• Sertoli-Leydig: androgens

Germ cell:

• Dysgerminoma:LDH

. Yolk sac: AFP

• Choriocarcinoma:p-hCG

• Immature teratoma:none

• Embryonal cell: AFP *

(5-hCG

BENIGN OVARIAN TUMOURS

• sec Table 25

• many are asymptomatic

• usually enlarge slowly, if at all

• may rupture or undergo torsion, causing pain

pain associated with torsion of an adnexal mass usually originates in the iliac fossa and radiates

to the flank

• peritoneal irritation may result from an infarcted tumour (rare)

MALIGNANT OVARIAN TUMOURS

• see Table 25

Epidemiology

• lifetime risk 1.4%

• majority of ovarian cancer cases are detected in women >50 yr

• causes more deaths in North America than all other gvnaecologic malignancies combined

• 4th leading cause of cancer death in women

• 85% epithelial; 15% non-epithelial

• 10 -15% of epithelial ovarian cancers are related to hereditary predisposition

Diagnosis of ovarian tumours requires

surgical pathology

Any adnexal mass in postmenopausal

women should be considered malignant

Risk Factors (for epithelial ovarian cancers) until proven otherwise

• early menarche and/or late menopause

• personal history of hreast, colon, or endometrial cancer

• family history of breast, colon, endometrial, or ovarian cancer

• advanced age

• BUGA mutation (serous) and Lynch syndrome ( non-serous, non-mucinous)

• use of fertility drugs (limited evidence)

Protective Factors (for epithelial ovarian cancers)

• OCR:likelv due to ovulation suppression (significant reduction in risk even after 1 vr of use, 50% alter

5 yr)

• pregnancy/breastfeeding

Prophylactic Measures

• prophylactic BSO in high-risk women (i.e. BRCA mutation carriers)

• prophylactic salpingectomy in high-risk women (i.e. BRCA mutation carriers who do not want

oophorectomy yet)

Screening

• no effective method

• routine CA-125 or U/S not recommended

Omental Cake:a term for ascites plus a

fixed upper abdominal and pelvic mass;

almost always signifies ovarian cancer

Screening forOvarian Cancer Updated Evidence

Deport and Systematic Review forthe US

fteventive Services Task Force

JAMA 2018:319(6):595 606

Purpose: losystematically review evidence on

benefits and harms ol ovarian cancer screening

among average-risk, asymptomatic women.

Methods Systematic review of RCtsof ovarian

cancer screening in average-risk women that

reported mortality or qualrty-of -lrfe outcomes.

Interventions included liansvaginallFSard/ni

CA-125 lesbng.Comparators were usual care or no

screening.

Results:Fcortrials(n ^ 293587)»rere ircl.ded.No

trialfound a significant difference in ovarian cancer

mortality with screening. In two braIs.screening

led to surgery lor suspected ovarian cancer In 11s

ol women without canter and lor transvagad tl/S

with or without CA-125 screen mg m 3V with major

complications occurring wr 3% to 15V olsurgeries.

Evidence ol psychological harms wasfou- jIn cases of

repeat follow -up sea ns and tests.

Conclusions:Ovarian cancer mortality did not

significantly differ between screened women and

those with no screening or in usual care.

Clinical Features

• most women with epithelial ovarian cancer present with advanced stage disease (i.e.stage I 11C high

grade serous histology)

• symptoms:

• abdominal symptoms ( nausea, bloating, pain, dyspepsia,anorexia, early satiety)

• symptoms of mass effect

increased abdominal girth (from ascites or tumour itself)

urinary urgency and frequency

• constipation

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GYI5 Gynaecology Toronto Notes 2023

Treatment

• debulking surgery including totalhysterectomy,BSO,omentectomy,removal ofall visible disease

• many epithelial ovarian cancers (i.e. serous ovarian carcinoma) are chemosensitive: treat with

platinum-based chemotherapy t taxol

• neo-adjuvant chemotherapy (if needed) to shrink down tumours prior to debulking

• adjuvant chemotherapy to treat microscopic disease

Low Malignant Potential (also called "Borderline") Tumours

• a subcategory of epithelial ovarian cancer (

-

15% of all epithelial ovarian tumours)

• approximately one-third of tumours are identified in women <40 yr

• pregnancy and breastfeeding are protective factors

• tumour cells with histologically malignant characteristics arise from the ovarian surface, but do not

invade ovarian stroma

• able to metastasize, but uncommon

• treated primarily with surgery (BSO/omental biopsy ± hysterectomy)

chemotherapy haslimited benefit:can be treated with hormonal manipulation (letrozole)

young patients can be treated with fertility-sparing options such as cystectomy or unilateral

salpingo-oophorectomy

• generally slow growing, excellent prognosis

• 5 yr survival >99%

recurrences tend to occur late, may be associated with low-grade serous carcinoma

Malignant Ovaiian Tumour Prognosis

5 Yr Survival

Stage I 75 95%

StageII

Stage III

Stage IV

60-75%

23-41%

11%

Table 25. Ovarian Tumours

Type Description Presentation Ultrasound/Cytology Treatment

FUNCTIONAL TUMOURS (ollbcnign)

Follicular Cyst 4-8 cm mass,unilocular,lined

with granulosa cells

Symptomatic or suspicious masses warrant surgical

ciploration

Otherwise il

- 6 cm,wail 6 wk then ro-exaininc as cyst

usually regresses with nest cycle

OCP (ovarian suppression): will prevent development ol

new cysts

Treatment usually laparoscopic (cystectomy vs.

oophorectomy,based on fertility choice)

Same as for follicular cysts

Follicle tails torupture during ovulation Usually asymptomatic

May rupture,bleed,tort,

infarct,causing pain t signs ol

peritoneal irritation

Corpus luteum Cyst Corpus luteum fails to regress after 14 d,

becoming cystic or hemorrhagic

Larger (10-15 cm) and firmer

than follicular cysts

More likely to cause pain than

follicular cyst

May delay onset of next period

Associated with molar

pregnancy,ovulation induction

with domiphene

Theca-Lutein Cyst Due to atretic follicles stimulated by

abnormalP-hCG levels

Conservative

Cyst willregress asp-hCG levels fall

See Endometriosis. GY11

See Polycystic OvarianSyndrome. GY24

Endometrioma

Polycystic Ovaries

BENIGN GERM CEttTUMOURS

Benign CysticTcratoma

(dermoid)

Single most common ovarian germ cell

neoplasm

Elements of all 3 cell lines;contains

dermal appendages (sweat and

sebaceous glands,hair follicles, teeth)

May rupture,twist, infarct

20% bilateral

20% occur outside of

reproductive yr

Smooth- walled,mobile,

unilocular

U/S may show calcification

which Is pathognomonic

Treatment usually laparoscopic cystectomy:may recur

MALIGNANTGERMCEU TUMOURS

General Information Rapidly growing. 2 3% of all ovarian

cancers

Produces tOH

Suigicalresection (often conservative unilateral salpingo

oophorectomy t nodes) s chemotherapy

When diagnosed at stage IA,no adjuvant treatment is

indicated

If diagnosed at advanced slage.vciy responsive lo

chemotherapy,therefoie complete resection isnot

necessaiylor cure

When diagnosed at stage IA Grade 1,no adjuvant

tieatment is indicated

When diagnosed at Grade 2-3.either adjuvant

chemotherapy or surgical staging is indicated

If diagnosed at advanced stage,very responsive to

chemotherapy,therefore complete resection isnot

necessary for cure

High grade tumour can be treated withadjuvant

chemotherapy or monitor AFP levels

High grade tumour usually treated with adjuvant

chemotherapy

Usually children and young

women1*30 yr|

Dysgcrminoma 10-15%bilateral

Immature Teratoma No tumour marker identified Almost always unilateral

Yolk Sac Tumour Produces AFP Abdominal pain and pelvic mass

Ovarian Choriocarcinoma Produces 0-hCG Precocious puberty and irregular

vaginal bleeding

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