PPT

1. Made by: Dr. Isha Jaiswal
Moderator: Dr. Madhup Rastogi
Date:12th February, 2014

2.  Gynecological Anatomy
 Blood supply & lymphatic
drainage
 Epidemiology of ovarian &
endometrial cancer
 Risk factors
 Radiological anatomy
 Clinical presentation
 Examination

3. DEFINITION: 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

4. 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.

5. *ligaments

6. *PERITONEAL FOLDS

7.  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

9. ARTERIAL 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)

10. *

11. 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

12. Ovaries 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 cyst
These cell types give rise to germ cell tumor, sex cord
stromal tumor & epithelial tm of ovary respectively

14. *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

15. Ovarian cancer is the 9th most common cancer in women

16. *
*

17. 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

18. *

19. 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

20. *
•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
Age Genetic
predisposition
Environmental
factors
Reproductive
factors
RISK FACTORS

21. *
*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

22. 1.3
3.6
7.2
18.5
23.7
20.4
17.2
8.2
0.1 0.7
2.5
10.7
20.9
24.9
26.2
14
0
5
10
15
20
25
30
< 20 20 -
34
35 -
44
45 -
54
55 -
64
65 -
74
75 -
84
85+
Percentageofagegroupsamongall
cases
Age
Percentage of Incidence and mortality of specific
age groups among all cases
incidence
mortality
 Median age at Diagnosis: 63
 Median age at death: 71

23. GENETICS

24. Hereditary breast-ovarian cancer (HBOC)
syndrome: BRCA 1/2
Hereditary Nonpolyposis Colorectal Cancer
(HNPCC) syndrome/Lynch syndrome
MMR-DNA mismatch repair genes
*

25. *
BRCA2
BRCA1

26. *
*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

27. *
*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

28. *
1) obesity
2) Lack of exercise
3) Diet – saturated fat increases risk
4) high fiber lowers risk
5) Red meat
6) Talc powder

29. * 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
*

30. *

31. 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

32. 



*

33. 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.

34. *
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%

35. 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

36. *
*Peritoneum 85%
*Omentum 70%
*Liver 35%
*Pleura 33%
*Lung 25%
*Bone 15%

37. 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

38. 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

39. Characteristics Benign Malignant
Mobility Mobile Fixed
Consistency Cystic Solid or Firm
Bilateral/Unilateral Unilateral Bilateral
Cul-de-sac Smooth Nodular
INCLUDES
Abdomen examination
Pelvic examination
Lymph node examination

40. In order to accurately
localize the findings on
physical examination
Abdomen can be
divided in nine
quadrants.
*abdominal examination
positioning

41. *
Inspection
Palpation
Percussion
Auscultation
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.

42. *ABDOMINAL EXAMINATION
INSPECTION
Contour & symmetry
Skin: signs of imflammation
Shape: flat, distended or scaphoid
MOVEMENTS:
RESPIRATORY
PERISTALTIC: obstruction-gastric,
-small intestine
-large intestine
PULSATILE:
aneurysm
swelling infront of abdominal aorta

43. *visible swelling?
*Engorged veins? Location:central/sides
Direction of flow
*Umblicus: inverted/everted
TANYOL’S SIGN displacement-
-upwards:pelvic lump
-downwards:ascitis
*Scars
*Pigmentation

44. *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

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

46. 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
*ABDOMINAL EXAMINATION
PALPATION

47.  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

48. *Abdominal palpation
light palpation Deep palpation

49. Characteris
tics
Benign Malignant
Mobility Mobile Fixed
Consistency Cystic Solid or Firm
Bilateral/Un
ilateral
Unilateral Bilateral
Cul-de-sac Smooth Nodular
Evaluation of a pelvic mass will be
influenced by
patient's age,
clinical presentation
imaging 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 groups
benign during the reproductive
years.

50. *ABDOMINAL EXAMINATION
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

51. *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

52. 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

53. 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.
*ABDOMINAL EXAMINATION
PALPATION OF THE SPLEEN

54. 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

55. *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

56. 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.

57. *
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

58. *
Notes Elicited
Tympanic
Predominant due to gas in GI tract
Dull
Organs, fluid and feces
Clinical inference
Distension of abdomen
Fluid vs. Air
Outline 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

59. 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.

60. *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
*ABDOMINAL EXAMINATION
AUSCULTATION

62. *Part 2:
anatomy of endometrium & endometrial
carcinoma

63. *ANATOMY OF ENDOMETRIUM

64. 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

65. *
Chiefly by
uterine arteries
Partly by
ovarian arteries

66. INTERNAL
ILLIAC VEINS
UTERINE
VEINOUS PLEXUS
VAGINAL
VEINOUS PLEXUS
OVARIAN
VEINOUS PLEXUS
*

67. *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

68. Lymphatic drainage of the uterus

69. * ENDOMETRIAL CARCINOMA

70. 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

71. DEVELOPED COUNTRIES CA ENDOMETRIUM
DEVELOPING COUNTRIES CA CERVIX
* MOST COMMON CANCER OF GENITAL
TRACT

72. *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
*

74. endometrial cancer is the 4th most common cancer in women

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

76. Endometrial hyperplasia

77. Complex
hyperplasia
without atypia
Complex
hyperplasia
with atypia
Simple
hyperplasia
ENDOMETRIAL
CARCINOMA

78. 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

79. 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.

80. 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.

81.  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
* endometrial 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

82. RISK
FACTORS
NULLIPARITY
PCOS
EARLY
MENARCHE
LATE
MENOPAUSE
OBESITY
DIABETES
HYPERTENSION
LYNCH 2 /
HNPCC
TAMOXIFEN
HRT

83. These 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

84. 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

85. ESTROGEN-ONLY REPLACEMENT
THERAPY (ERT)
oestrogen
oestrogen + progestins .
TAMOXIFEN:SERM
potent antagonist in breast – RX OF CA BREAST
partial agonist in uterus-long term use- cause
endometrial proliferation,carcinoma

86. 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 exam
women 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 years
if there is atypical endometrial hyperplasia, treat and
reassess tamoxifen (ie. Consider hysterectomy)
*

87. 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,MSH6
early age of presentation
SCREENING after 35 years by
yearly colonoscopy, tvusg &
endometrial biopsy
*

89. 89
*Local
*Tubal
*Lymphatic
*Hematogenous

90. 90
LOCAL SPREAD
Slow invasion of the myometrium is the commonest spread. It
may produce considerable uterine enlargement; or spread may
involve the vaginal vault.

91. 91

*LYMPHATIC SPREAD

92. 92
*TUBAL SPREAD
Malignant 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

93. *
Type of patient:
Nullipara or low parity
Middle or upper social
class
Overweight and obese
patients
Early menarche and late
menopause
Hormone therapy
Age groups:
m.c age of presentation
is 55-70 years
75% after menopause.
20-25% perimenopausal.
Only 5% before age of 45

94. m.C symptom: post menopausal bleeding
Discharge per vaginum:
Abnormal pap smear
Difficult or painful urination
Urinary or rectal bleed
In later stages of the disease, women may feel
pelvic pain and experience unexplained weight loss
Abdominal distension

95. 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

96. *
There are four steps:
External Genital Exam
SpeculumExamination:
Per vaginum examination
The Bimanual Exam
The Rectovaginal Exam

97. *
*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
*

98. *Separate the labia and inspect
Labia minora
Clitoris
Urethral orifice
Vaginal orifice
Note the following:
 Discharge
 Inflammation
 Edema
 Ulceration
 Lesions

99. *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

100. *
*Performed prior to the bi-
manual exam.
*Always inserted with the
speculum blades warmed
with warm water and
closed

101. *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

102. *
*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

103. 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.

104. *
*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

105. 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):

106. *
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.

107. *
*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

109. *

110. *RADIOLOGICAL ANATOMY

111. *
#1 = Uterus
#2 = Bladder
#3 = Urethra
#4 = Vagina
#5 = Psoas
#6 = Iliacus
#7 = Obturator Internus
*

112. *#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

113. *

117. Nodes around the abdominal
aorta
1: DESCENDING AORTA
4: INFE RIOR VENACAVA

118. Nodes around the
abdominal aort
4 – inferior vena cava
26 – bifurcation of the
abdominal aorta at L4
*

119. *
COMMON ILIAC NODES
1 – right common iliac vein
2 – right common iliac artery
3 – left common iliac vein
4 – left common iliac artery
5 – psoas muscle
*

120. *
10 – left external iliac artery
11 – right external iliac vein
12 – right internal iliac vein
13 – right external iliac artery
14 – right internal iliac artery
17 – left external iliac vein
18 – left internal iliac
19 – iliopsoas muscle

121. *
10 – left external iliac artery
11 – right external iliac vein
13 – right external iliac artery
17 – left external iliac vein
19 – iliopsoas muscle
20 – piriformis muscle

122. 19 – iliopsoas muscle
21 – internal obturator muscle
22 – sartorius muscle
23 – right femoral vein
24 – right femoral artery
25 – left femoral vein
26 – left femoral artery

123. *
15 – Iliac musCle
16 – confluence of the left ext and
internal iliac vein
5 – psoas muscle
8 – confluence of the right external
and internal iliac veins
9 – left internal iliac artery
10 – left external iliac artery
11 – right external iliac vein
12 – right internal iliac vein
13 – right external iliac artery
14 – right internal iliac artery
17 – left external iliac vein
18 – left internal iliac

124. 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)

125. 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

126. *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)

127. *
*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.)

128. Ovarian adenocarcinoma involving both ovaries with ascites

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

130. *A 61-year-old woman with endometrial cancer.
*Note enlargement of the uterus (u)central area of hypodensity
*and the surrounding ascites (a)

131. *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

132. *ENDOMETRIAL CANCER

133. *thankyou