ovarian & endometrial cancer

Made by: Dr. Isha Jaiswal

Moderator: Dr. Madhup Rastogi

Date:12th February, 2014

OVARIAN & ENDOMETRIAL

CANCER

Topics:

OVARIAN & ENDOMETRIAL CANCER

Gynecological Anatomy Blood supply & lymphatic

drainage Epidemiology of ovarian &

endometrial cancer Risk factors Radiological anatomy Clinical presentation Examination

Anatomy : the ovariesDEFINITION: Ovaries are female gonads. The oocytes are formed here.

SIZE: in premenopausal age 4×2.5×1 cm with average wt. of 4-5gm. In menopausal female: ovaries shrink

SITUATION: lies in ovarian fossa in lateral pelvic wall.

POSITION: variable

in nulliparous: nearly vertical so upper & lower pole

in multiparous: nearly horizontal due to pull by gravid uterus so medial & lateral ends

EXTERNAL SURFACE:

before puberty: smooth surface, greyish-pink color

After puberty: uneven surface, grey color

PERITONEAL RELATIONS: covering-mesovarium transmit vessel & nerves to & from ovaries

SUSPENSORY LIGAMENT OF OVARY:infundibulopelvic ligament. Extend from infundibulum of fallopian tube & upper pole of ovary to ext. iliac vessels. Contain ovarian vessel & nerves.

*ligaments

*PERITONEAL FOLDS

Relations: TUBAL POLE: fallopian tube, ovarian fimbria,

suspensory ligaments UTERINE POLE: connected to lat. end of uterus via

ligament of ovary. ANTERIOR BORDER: attached to the broad ligament via

mesovarium POSTERIOR BORDER: free border related to ureter &

fallopian tube. LATERAL SURFACE: obturator nerves &vessels

seperated by peritoneum MEDIAL SURFACE: fallopian tube

ARTERIAL SUPPLY& VENOUS DRAINAGEARTERIAL SUPPLY: ovarian & uterine artery

Ovarian artery: arises from abdominal aorta just below renal artery

enters suspensory ligament

send branches through mesovarium

content of broad ligament

anastomose with uterine artery

VENOUS DRAINAGE: different on both sides

Pampiniform plexus:form single ovarian vein

drain into IVC on rt. Side

drain into left renal vein on left side

NERVE SUPPLY: ovarian plexus derived from renal, aortic & hypogastric plexus, accompanies ovarian artery.

sympathetic : (T10-11)

parasympathetic:(S-2,3,4)

*Ovarian & uterine artery anastomosis

LYMPHATIC DRAINAGE

Lymphatic of ovary communicate with lymphatics of uterus & fallopian tube.

Ascend along the ovarian vessel to drain preaortic & paraaortic nodes

Some lymph nodes also drain into inguinal & iliac gp. of nodes

HISTOLOGYOvaries are derived from embryonic yolk sac cells

Has 2 parts: outer cortex & inner medulla

Cortex covered by mesothelium

Medulla contains stroma & maturing follicles

Follicle give rise to ova germ cells

Stromal cells that produce steroid hormones

Mesothelium forms epithelial covering of follicular cystThese cell types give rise to germ cell tumor, sex

cord stromal tumor & epithelial tm of ovary respectively

EPIDEMIOLOGY OF OVARIAN CANCERS

*UNITED STATES

*2nd m.c genital cancer(1stendometrium)

*Lifetime risk of ovarian cancer is 1 in 72 women

*Incidence increases with age, peaks at seventh to eight decade of life. Median age of diagnosis 63 years

*INDIA*2nd mc genital cancer (1st cervix)

*Lifetime risk of developing ovarian cancer ranges from 1:70 to 1:100

*Incidence of ovarian cancer increases from 35 years of age and reaches a peak between the ages 55-64.years

Ovarian cancer is the 9th most common cancer in women

*Incidence Rates

*Incidence Rates

Ovarian cancer is not as treatable as the other cancers… due to lack of early detection.

Ovarian cancer is the 5th most common cancer death for women

*Mortality Rates

Global Trends

DIFFERENCE IN RACE & ETHNICITY:age adjusted annual incidence per 1 lakh women in year 2005-2012

White women:13.4

Hispanic11.3

American : 11.2

Black:9.8

Asian :9.8

DIFFRENCE IN GEOGRAPHY:

Incidence in North America & Europe is 3 to 7 times higher than other parts of asia

*Risk factors• Pelvic contaminants &

toxic agents, e.g. mumps virus

• Diet high in saturated fats, red meat

• Obesity• Cigarette smoking• Talc power

• Early menarche, late menopause

• Nulliparity • Excessive gonadotropin

• Infertility• Estrogen replacement therapy

• Polycystic ovary syndrome, pelvic inflammatory disease

• A positive family history (for breast, uterine, ovarian,colorectal cancer, mainly on behalf of 1st-degree relatives (sister, mother)

• Increasing age

AgeGenetic

predisposition

Environmental factors

Reproductive factors

RISK FACTORS

*Risk Factors

*AGE:

* Ovarian cancer incidence increases with advancing age

*The lifetime risk of ovarian cancer is approximately 1 in 70, the median age at diagnosis is 63 years, and >80% of ovarian cancer occurs after the age of 40 in the United States

< 20 20 - 34

35 - 44

45 - 54

55 - 64

65 - 74

75 - 84

85+0

5

10

15

20

25

30

1.33.6

7.2

18.5

23.720.4

17.2

8.2

0.1 0.72.5

10.7

20.9

24.9 26.2

14

Percentage of Incidence and mortality of specific age groups among all cases

incidencemortality

Age

Perc

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f ag

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ases

AGE

Median age at Diagnosis: 63 Median age at death: 71

GENETICS-Hereditary tumors account for 10 to 15 % of all ovarian cancer.-Family history is the strongest risk factor after increasing age.-The risk of developing ovarian cancer in the general population is 1.4%.-The risk for a woman with one first-degree family member affected by this disease has a lifetime risk of 5% and with two first-degree relatives, the lifetime risk climbs to 25% to 50%

Three distinct syndromes are identified

Hereditary breast-ovarian cancer (HBOC) syndrome: BRCA 1/2

Hereditary Nonpolyposis Colorectal Cancer (HNPCC) syndrome/Lynch syndrome

MMR-DNA mismatch repair genes

*Familial ovarian cancer syndromes

*Each cell has two copies of

BRCA1 and BRCA2

BRCA2BRCA1

*Hereditary Breast and Ovarian CA (HBOC)

*5-10% of all cases of breast and ovarian cancer

*About 70 to 85% of HBOC cases are caused by mutations in either the BRCA1 or BRCA2 gene

*Genetic testing for BRCA1 and BRCA2 gene mutations is available to women with family history

*REPRODUCTIVE FACTORS*Associated With Higher Frequency Of Ovulation

*Increasing age

*Low parity

*Infertility

*Early menarche late menopause

*Exogenous estrogen & HRT

*Increased androgen and gonadotropins

*Chronic inflammation

*Polycystic ovarian syndrome

*endometriosis

*ENVIORMENTAL FACTORS

1) obesity2) Lack of exercise3) Diet – saturated fat increases risk4) high fiber lowers risk5) Red meat6) Talc powder

* Pregnancy: interrupt ovulation cycles, reduce gonadotropin secretion, and increase estrogen and progesterone

*Progesterone: supress epithelial proliferation

*Breastfeeding: linked to incessant ovulation, excess gonadotropin,

*Oral contraceptive pill (OCP): suppress gonadotropin surge ,inhibit ovulation.

*NSAIDS

*Bilateral oophorectomy

*Tubal ligation

*Hysterectomy

*Vitamin D: induce apoptosis, inhibit cell growth down regulate telomerase

*Protective factors

*Etiologic Model

Etiologic Model

Damage to ovarian surface epithelium

malignant transformation

low-grade tumor-slow growth-less responsive to chemo

high-grade carcinoma-rapidly metastatic-chemo-sensitive

inflammation

Hormonal stimulation(follicle-stimulating hormone, luteinizing hormone, polycystic ovarian syndrome

Genetic mutation

Incessant ovulation

Local/peritonealLymphaticTrans

diaphragmatichematogenous

*PATTERN OF SPREAD

Malignant cells exfoliate along peritoneal cavity, follow intraabdominal fluid stream.

Favored by intestinal peristalsis.

Pass up the peracolic gutters, along the intestinal mesentery to the right hemi diaphragm.

Metastatic deposits are frequently seen in post. cul-de-sac ,paracolic gutters, diaphragmatic surface, liver capsule, intestinal surface & omentum.

Metastasis may also be found in uterus & opposite ovary .

Dense tumor caking can cause infiltration into abdominal organs creating mass effect on omentum,ureter,bowel,liver,pancreas, spleen, adrenals.

INTRAPERITONEAL SPREAD :most common means of

spread.

*LYMPHATIC SPREAD: 2nd most common mode of spread

The lymphatic converge on hilus and follow the ovarian blood vessels in infundibular ligament to drain to the para-aortic nodes @ level of renal hilum

may drain along the broad ligament to the external iliac nodes in the pelvis.

Less frequently, the spread can occur to the inguinal nodes via the round ligament.

involvement of

pelvic nodes in 80%,

para-aortic nodes in 78%,

inguinal nodes in 40%,

mediastinal nodes in 50%,

supraclavicular nodes in 48%

TRANS DIAPHRAGMATIC SPREAD: occur to pleural cavity & m.c finding in stage IV ds: PLEURAL EFFUSION

HEMATOGENOUS SPREAD:inferquent at time of presentation/Only 2 to 3% pt with parenchymal liver or lung disease

Brain metastasis rare.However more than 50% recurrence occur both within & outside peritoneal cavity at time of treatment failure

*Most common location of mets. in metastatic ds.

*Peritoneum 85%

*Omentum 70%

*Liver 35%

*Pleura 33%

*Lung 25%

*Bone 15%

insidious growth and is asymptomatic in the early stage

most women do not present for diagnosis until symptoms arise from disease progression to stage III or IV disease

Often have vague symptoms that are not very severe

75 – 85 % of cases are advanced at the time of diagnosis

CLINICAL MANIFESTATIONS

Ovarian cancer patients may have vague symptoms.

bloating and increased abdominal girth

Pelvic pressure, cramps abdominal pain, back pain

Loss of appetite dyspepsia , nausea ,early satiety

Pain during intercourse, menstrual irregularities.

Unexplained changes in bowel habits, including diarrhea or constipation

Changes in bladder habits, including frequency, urgency, incontinence

Symptoms of ovarian cancer

Physical Examination

Characteristics Benign Malignant

Mobility Mobile Fixed

Consistency Cystic Solid or Firm

Bilateral/Unilateral

Unilateral Bilateral

Cul-de-sac Smooth Nodular

INCLUDESAbdomen examinationPelvic examinationLymph node examination

In order to accurately localize the findings on physical examination Abdomen can be divided in nine quadrants.

*abdominal examination positioning

*Exam Order

InspectionPalpationPercussionAuscultation

41

Examine the patient in good light and warm surroundings.Patient should be lying on supine position with the head resting on one pillow & lower limbs flexed in order to relax the muscles of the abdominal wall.

*ABDOMINAL EXAMINATION

INSPECTIONContour & symmetrySkin: signs of imflammationShape: flat, distended or scaphoid

MOVEMENTS:RESPIRATORY

PERISTALTIC: obstruction-gastric,

-small intestine

-large intestine

PULSATILE:aneurysm

swelling infront of abdominal aorta

*visible swelling?

*Engorged veins? Location:central/sides

Direction of flow

*Umblicus: inverted/everted

TANYOL’S SIGN displacement-

-upwards:pelvic lump

-downwards:ascitis

*Scars

*Pigmentation

*ABDOMINAL DISTENSION* Localised: malignancy, hepatomegaly, splenomegaly

*Generalized:* Fat (obesity):inverted umblicus

*fluid (ascites): dullness

* flatus (obstruction): tympanic

*faeces (constipation),visible peristalsis

* fetus (pregnancy: central dullnes

*Full urinary bladder: duul & painfull hypogastrium

Prominent veins (caput medusae) in portal hypertension blood flows trough portocaval anastomoses

1. Ensure that your hands are warm

2. Stand on the patient’s right side

3. Help to position the patient

4. Ask him to relax & breathe deeply

5. Palpation should be done with flat of hand using flexor surface of finger


PALPATION

Ask whether the patient feels any pain before you start. Leave the painful area for last

Begin with superficial examination

Move in a systematic manner through the nine regions of the abdomen in the direction of the painful area

Repeat palpation deeply.

ABDOMINAL EXAMINATION

PALPATION

*Abdominal palpation light palpationDeep palpation

Characteristics

Benign Malignant

Mobility Mobile Fixed

Consistency

Cystic Solid or Firm

Bilateral/Unilateral

Unilateral

Bilateral

Cul-de-sac

Smooth Nodular

pelvic mass :benign/malignant

Evaluation of a pelvic mass will be influenced by patient's age,clinical presentationimaging features. most adnexal masses require moderate size for palpation.

Ovarian mass is more likely to be: a malignant in the pediatric, peri-, and postmenopausal age groupsbenign during the reproductive years.


PALPATION: findings*Tenderness point: discomfort and resistance to palpation

*Involuntary guarding: reflex contraction of the abdominal muscles

*Rebound tenderness: patient feels pain when the hand is released

*Tenderness + rigidity: perforated viscus

*Palpable mass (enlarged organ, faeces, tumour)

*Pain with coughing: Peritoneal inflammation

*Also called as rebound tenderness

*Pain upon removal of pressure rather than application of pressure to the abdomen

*Peritonitis and/ or appendicitis

ABDOMINAL EXAMINATION

BLUMBERG’S SIGN

Liver Palpation

Align your hand parallel to the Rt. costal margin, begin in the Rt. Iliac fossa and ask the patient to breath in & out through the mouth.

With each expiration, the hand is moved by 1 or 2 cm closer to the Rt. costal margin.

During inspiration, the hand

is kept still waiting for liver edge to strike it.

PALPATION OF THE LIVER

Spleen Palpation

One-hand technique: start from Rt. iliac fossa toward Lt. costal margin and ask the patient to breath in & out through the mouth. With each expiration, the hand is moved by 1 or 2 cm closer to the Lt. costal margin.

Two-hand technique: Lt. hand is placed posterolaterally over Lt. lower ribs and Rt. hand is placed below umbilicus toward Lt. costal margin.

If spleen is not palpable, roll the

patient to Rt. Side and palpate again.


PALPATION OF THE SPLEEN

FLUID THRILL: ascitis/large ovarian cyst

Place the palm of your left hand against the left side of the abdomen

Flick a finger against the right side of the abdomen

Ask the patient to put the edge of a hand on the midline of the abdomen: to cut off any transmitted wave

If a ripple is felt upon flicking we call it a fluid thrill = ascites

May be positive in cyst

Min fluid 2 litres

*SHIFTING DULLNESS: for small amount of fluid

*Pt. lies flat

*Percussion started fro midline & continued to either flank untill the note becomes dull.

*Finger is kept at that point

*Pt. asked to turn opposite side

*Wait for minute

*Area again percussed.

*Surest sign of free fluid

*Min 500ml

Palpation in Ascites

Dipping Maneuver:

To palpate for organomegaly with ascites.

Both hands are placed

flat on abdomen and fingers are flexed at MCPs rapidly to displace the underlying fluid.

*Difference between ascites & ovarian cyst on percussion

ascitis Ovarian cyst

Resonant anteriorly & Dull ness in flanks

Fluid thrill positive Shifting dullness

positive

Dullness anteriorly & resonant in flanks

Fluid thrill positive Shifting dullness

negative

* Percussion

Notes ElicitedTympanic

Predominant due to gas in GI tractDull

Organs, fluid and feces

Clinical inferenceDistension of abdomen

Fluid vs. AirOutline Organs

Liver, spleen, and gastric An enlarged spleen expands anteriorly, downward, and

medially, often replacing the tympany of the stomach and colon with the dullness of a solid organ

58

Liver Span

Upper liver border is defined by percussing down at Rt. 2nd IC space in MCL, until dullness is encountered.

Lower liver border is defined by percussing up at Rt. Iliac fossa in MCL, until dullness is encountered.

Measure the distance

between the two dull areas.

Normal liver span is 10+/-2.

*Place the diaphragm of the stethoscope to the right of the umbilicus

*Bowel sounds (borborygmi) are caused by peristaltic movements

*Occur every 5-10 sec.

*Absence of b.s.: paralytic ileus or peritonitis

*Bruits over aorta and renal a. could be a sign of an aneurysm and stenosis


AUSCULTATION

*Part 2:

anatomy of endometrium & endometrial carcinoma

*ANATOMY OF ENDOMETRIUM

Endometrium The uterine cavity is lined by endometrium, made up

of columnar cells forming tubular glands.The normal endometrium is hormone responsive

tissue.Estrogenic stimulation produces cellular growth

&glandular proliferation which is cyclically balances by maturational effect of progesterone.

The blood supply, nerve supply & lymphatic drainage of endometrium is same as whole uterus

*ARTERIAL SUPPLY OF UTERUS

Chiefly by uterine arteries

Partly by ovarian arteries

INTERNAL ILLIAC VEINS

UTERINEVEINOUS PLEXUS

VAGINAL VEINOUS PLEXUS

OVARIAN VEINOUS PLEXUS

*VENOUS DRAINAGE OF UTERUS

*Supplied by both parasympathetic and parasympathetic nerves through inferior hypogastric and ovarian plexus

*Sympathetic nerves from T12 and l1 segment of spinal cord

*Parasympathetic nerves from S2 S3 S4.

INNERVATION OF UTERUS

Lymphatic drainage of the uterus

* ENDOMETRIAL CARCINOMA

Endometrial cancer usually begins in the lining of the uterus (endometrium). It is sometimes called uterine cancer.

Vast majority are adenocarcinomas – commonly detected during perimenopause

Endometrial Cancer – Uterine Cancer

DEVELOPED COUNTRIES CA ENDOMETRIUM

DEVELOPING COUNTRIES CA CERVIX

*MOST COMMON CANCER OF GENITAL TRACT

*Uterine cancer is one of the most common malignancy of female genital tract in west, accounting for 20-25% of all genital cancer in developed countries

*In developing countries the incidence is 5-7% of all genital cancer.

*The incidence is increasing worldwide in recent years because of longer survival of women ,decline in cervical cancer & role of enviormental factors

*EPIDEMOLOGY

endometrial cancer is the 4th most common cancer in women

endometrial cancer is the 8th leading cause of cancer death for women

Endometrial hyperplasia

Complex hyperplasia without atypia

Complex hyperplasia with atypia

Simple hyperplasia

ENDOMETRIAL CARCINOMA

How endometrial hyperplasia is associated with endometrial cancer

WHO Classification of Endometrial Hyperplasia

Simple Hyperplasia Without Cytologic Atypia Increased number of glands relative to stroma

Crowded, clustered glands

Complex Hyperplasia Without Cytologic Atypia Back-to-back glands (crowded glands with little or no

intervening stroma)

Hyperplasia With Cytologic Atypia Variation of size and shape of nuclei

Nuclear enlargement Loss of polarity

Coarse chromatin clumping Prominent nucleoli Hyperchromatism

endometrial hyperplasia progression to endometrial cancer

Simple hyperplasia– 1% progress to endometrial cancer

Complex hyperplasia– 3%Complex hyperplasia with atypia—28%

30-40% of endometrial cancers are found in a background of atypical hyperplasia. Overall, these tend to be lower grade tumors.

EPIDEMIOLOGIC DIFFENCES:

TYPE I:Estrogen-related endometrial cancer (Type I) tends to be a lower grade histologically, adenocarcinoma.

TYPEII:Endometrial cancers unrelated to hormones (Type II)tend to be a higher grade and stage eg. Papillary serous or clear cell tumors.

55-65 yrs

oestrogen dependant

previous h/o exposure to unopposed oestrogen.

obesity/hypertension/diabetes

‘well differenciated’ & mimics proliferative endometrial glands.

ER/PR +

excellent prognosis

*Type 1endometrial cancer Type 2 65 – 75 yrs

oestrogen independent

unrelated to hormone exposure

usually arises in an atrophic endometrium

usually undifferenciated & aggressive.deep muscle invasion

ER/PR -

bad prognosis

RISK FACTORS

NULLIPARITYPCOSEARLY

MENARCHELATE

MENOPAUSE

OBESITYDIABETES

HYPERTENSION

LYNCH 2 /

HNPCC

TAMOXIFEN

HRT

Risk factors for endometrial cancerThese risk factors are only helpful in identifying women at risk for type I disease.

Risk Factor Approximate Risk Ratios

Obesity 1.8–2.4

Nulliparity 2.0–3.0

Diabetes mellitus 2.8

Granulosa-theca cell tumors

5.0

Exogenous estrogen therapy

3.0–8.0

Late menopause (>age 52)

2.4

OBESITY -- particularly BMI=more than 30 obesity reduces level of serum hormone binding protein

free estrogen circulates in body

peripheral fat : conversion of epiandrostenedione to oestrone

TYPE 2 DIABETES – insulin resistance:insulin induces LH to cause thecal hyperplasia

MENSTURTION-early menstruation (periods starting before age 12) & late menopause (after age 52)

NULLIPARITY

OVARIAN DISEASES: pcod, fibroid, granulosa cell tumor

Liver chirhosis: dec SHBG

Risk Factors

ESTROGEN-ONLY REPLACEMENT THERAPY (ERT)

oestrogen used alone increases riskoestrogen + progestins decreases risk.

TAMOXIFEN:SERMpotent antagonist in breast – RX OF CA BREAST

partial agonist in uterus-long term use- cause endometrial proliferation,carcinoma

Even though tamoxifen is associated with endometrial cancer, the benefits in treating women with breast ca. outweigh the risks…but

women need a yearly gyne examwomen should monitor themselves for abnormal vaginal bleeding, discharge, etc

screening such as pelvic U.S. is NOT recommended (too many false positives)

Limit tamoxifen use to 5 yearsif there is atypical endometrial hyperplasia, treat and reassess tamoxifen (ie. Consider hysterectomy)

*Tamoxifen :What’s ACOG have to say about tamoxifen?...

FAMILY HISTORY – possible genetic link.

genetic predisposition seen in 10%,

5% of these have lynch syndrome :Hereditary nonpolyposis colorectal cancer (HNPCC).

AD: mutation in DNA repair gene-MSH2,MLH1,MSH6early age of presentationSCREENING after 35 years by

yearly colonoscopy, tvusg & endometrial biopsy

* Family history of breast & ovarian cancer:Unclear if there’s a risk with BRCA 1 and 2

89

Spread of endometrial cancer*Local

*Tubal

*Lymphatic

*Hematogenous

90Carcinoma of the Endometrium

LOCAL SPREADSlow invasion of the myometrium is the commonest spread. It may produce considerable uterine enlargement; or spread may involve the vaginal vault.

91

From the upper part of uterus, it reaches paraaortic nodes.

From middle & lower portion of uterus ,it reaches pelvic nodes

via round ligament to superficial inguinal nodes

*LYMPHATIC SPREAD

92

*TUBAL SPREADMalignant cells can pass along the tube This may account for isolated ovarian metastasis

HEMATOGENOUS SPREAD*This pathway might account for the occasional appearance of a low vaginal metastasis;

*Liver & lung metstasis

*CLINICAL PRESENTATION

Type of patient:

Nullipara or low parity Middle or upper social

classOverweight and obese

patientsEarly menarche and

late menopauseHormone therapy

Age groups:

m.c age of presentation is 55-70 years

75% after menopause.20-25%

perimenopausal.Only 5% before age of

45

m.C symptom: post menopausal bleedingDischarge per vaginum:Abnormal pap smearDifficult or painful urinationUrinary or rectal bleedIn later stages of the disease, women may feel pelvic pain and experience unexplained weight loss

Abdominal distension

Symptoms of endometrial cancer

Examination:physical examination of the patient with endometrial carcinoma is frequently entirely normal.it should include:abdominal examination(might be difficult due to

obesity.)Pelvic examination:Examination of lymph nodes

*PELVIC EXAMINATIONThere are four steps:

External Genital Exam SpeculumExamination:Per vaginum examinationThe Bimanual ExamThe Rectovaginal Exam

*Correct Examining Position of the Patient

*The Lithotomy Position/or Semi-Sitting Lithotomy Position

*Lying in supine position

*Thighs flexed and abducted

*Feet resting in stirrups

*Buttocks extended slightly beyond edge of exam table

*Head supported with a pillow

*Male examiners should always be attended by female assistants

EXAMINATION OF EXTERNAL GENITILLIA

*Separate the labia and inspect Labia minora

Clitoris

Urethral orifice

Vaginal orifice

Note the following: Discharge Inflammation Edema Ulceration Lesions

Pelvic Examination: Inspection contd

*Assess the support of the vaginal outlet:

*With the labia separated by middle and index finger

*Ask patient to strain down

*Note any bulging of the vaginal walls (cystocele and rectocele).

*Inspect the anus at this time, note presence of lesions and hemorrhoids

*The Speculum Exam

*Performed prior to the bi-manual exam.

*Always inserted with the speculum blades warmed with warm water and closed

*Hold speculum in right hand

*Place two fingers to separate labia

*Insert closed speculum obliquely into vagina at a 45 degree angle rotating 50 degrees counterclockwise

*Maintaining downward pressure, open blades slowly after full insertion and position the speculum so that the cervix can be visualized

*When the cervix is in full view, the blades are locked in the open position

*Inspection of the Cervix

*Position—is it anteverted, deviated, etc*The position of the cervix gives clues to the position

of uterus

*Color—should be flesh-colored, but ranges from pink to dark brown (blue or pale??)

*Surface characteristics—cysts, erythema

*Discharge

*Size and shape of os

*Any mass or lesion

*blood clots

inspection of vaginal walls

INSERT THE SPECULUM:

inspect the vaginal side-walls for any ulcers, discoloration, discharge or growths.

WITHDRAW SPECULUM

inspecting the anterior and posterior walls of the vagina, again looking for any ulcers, discoloration, discharge or growths.

*PER VAGINUM EXAMINATION

*Palpate the vaginal walls as you insert your fingers for tenderness, cysts, nodules, masses or growths

*Identify the cervix, noting the following:

*Position--anterior or posterior

*Shape-

*Consistency--firm or soft

*Mobility--move from side to side 1-2 cm in each direction

*Tenderness

*growth

The vaginal fingers now placed into the posterior fornix of the vagina and its shape is assessed (normally concave away from the fingers, but may be convex towards the fingers if there is a mass in the Pouch of Douglas).

Assessing the Pouch of Douglas (recto-uterine pouch):

* BIMANUAL DIGITAL EXAMINATION

The vaginal fingers are now moved into one of the lateral fornices with the abdominal hand moving to the corresponding iliac fossa.

Assess for any adnexal masses

on both sides - size, shape, tenderness, etc.

Move the cervix to assess for PID/Endometriosis.

*Combined PR and PV Examination

*It is done with one finger inserted per vaginally and the second finger of same hand in the per rectally

*Aim of the examination is to evaluate the extension of disease up to lateral pelvic wall

*Both the fingers are moved towards lateral pelvic wall

*If tumor extends to pelvic wall the 2 fingers do not converge

RADIOLOGICAL ANATOMY

*CT ANATOMY OF FEMALE PELVIS

*RADIOLOGICAL ANATOMY

*

#1 = Uterus#2 = Bladder#3 = Urethra#4 = Vagina#5 = Psoas#6 = Iliacus#7 = Obturator Internus

*MRI:FEMALE PELVIS

Female Pelvis

*#1 - Bladder #2 - Coccyx/Sacrum#3 - Gluteus Maximus#4 - Gluteus Minimus#5 - Iliacus#6 – Ilium BONE#7 - Levator Ani#8 - Psoas Muscle#9 - Rectum#10 - Rectus Abdominis#12 - Uterus

*OVARIES

ENDOMETRIUM

Colon

Right ovary

Uterus

Broad ligament

RADIOLOGICAL ANTOMY OF LYMPH NODE

Para-aortic lymph nodes

Nodes around the abdominal aorta

1: DESCENDING AORTA

4: INFE RIOR VENACAVA

Nodes around the abdominal aort

4 – inferior vena cava

26 – bifurcation of the abdominal aorta at L4

*L4 VERTEBRA

*Common Iliac Lymph nodeCOMMON ILIAC NODES

1 – right common iliac vein2 – right common iliac artery3 – left common iliac vein4 – left common iliac artery5 – psoas muscle

* L5 VERTEBRA

* Internal ,External iliac Lymphnode

10 – left external iliac artery11 – right external iliac vein12 – right internal iliac vein13 – right external iliac artery14 – right internal iliac artery17 – left external iliac vein18 – left internal iliac19 – iliopsoas muscle

*OBTURATOR NODES

10 – left external iliac artery 11 – right external iliac vein 13 – right external iliac artery 17 – left external iliac vein 19 – iliopsoas muscle20 – piriformis muscle

Inguinal L.N

19 – iliopsoas muscle21 – internal obturator muscle22 – sartorius muscle23 – right femoral vein24 – right femoral artery25 – left femoral vein26 – left femoral artery

*Pre sacral Lymph node

15 – Iliac musCle 16 – confluence of the left ext and internal iliac vein5 – psoas muscle8 – confluence of the right externaland internal iliac veins9 – left internal iliac artery10 – left external iliac artery11 – right external iliac vein12 – right internal iliac vein13 – right external iliac artery14 – right internal iliac artery17 – left external iliac vein18 – left internal iliac

OVARIAN CANCER

A 44-year-old woman with stage ovarian cancer. Axial CT scan of the pelvis shows bilateral complex cystic/solid ovarian masses (o). contiguity to the uterus (u)

OVARIAN CARCINOMA

Ovarian adenocarcinoma involving both ovaries (o) and uterus (u) with ascites (a). CT scan of the pelvis (A) shows bilateral ovarian masses with ascites and uterine involvement on the left

*OVARIAN ADENOCARCINOMA WITH URETERAL INVASION AND OMENTAL CAKE.*show a large,pelvic mass (m).

*A thick inhomogeneous soft tissue is seen under anterior abdominal wall consistent with omental involvement (o)

*.Note the dilated left ureter (long arrow) in A and the pinching of the ureter by the pelvic mass (curved arrow) in B.

*Tumor extension to the pelvic sidewall is seen in B(arrowheads)

*OVARIAN CANCER*B: Lower abdominal CT

scan shows a necrotic paracaval mass (n) consistent with lymphadenopathy.

*C: CT scan of the pelvis shows an enlarged right external iliac lymph node (arrow) measuring 1.5 cm in diameter with some necrotic changes seen in its center. *a-aorta

*v-inferior vena cava.)

Ovarian adenocarcinoma involving both ovaries with ascites

Big mass!! 33.5 cm. Compressing other abdominal organs.

*Ovarian carcinoma

ENDOMETRIAL CANCER

*A 61-year-old woman with endometrial cancer.

*Note enlargement of the uterus (u)central area of hypodensity

*and the surrounding ascites (a)

ENDOMETRIAL CANCER

*Massive para-aortic metastases from endometrial carcinoma with bony invasion.

*A. CT scan of the midabdomen shows massively enlarged para-aortic lymph nodes (n) encircling the aorta (a) and displacing it anteriorly. Note the destructive changes in the vertebral body (arrow

*ENDOMETRIAL CANCER

*thankyou

ovarian & endometrial cancer

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