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complete info on ovarian tumours and their management.
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OVARIAN TUMOURS
III UNIT OG
Jagadeesh
lll OG
Anatomy of ovary
Situated in ovarian fossa near fimbrial end of fallopian tube
Almond shapedPearly grey colourMeasures about 35 mm length 25 mm width 18 mm thickness
OVARY - ANATOMY
Attached to lateral pelvic wall by INFUNDIBULOPELVIC LIGAMENT
Inner pole of ovary is attached to cornua of uterus by OVARIAN LIGAMENT
Attached to posterior surface of broad ligament by MESOVARIUM
Consists of 3 regions:1.Hilum:
Through which ovarian vessels,lymphatics & nerves pass into the ovary
Composed of connective tissue and unstriped muscle fibres
PARTS
2.Cortex:Outer layer, contains graffian follicles
Lined by a single layer of germinal epithelium
3.Medulla:
Central portion composed of connective tissue and blood vessels
Laterally – ovarian fossa
Medially – fimbria of fallopian tube
Anteriorly – obliterated umbilical artery & fallopian tube
Posteriorly - Ureter
RELATIONS
Ovarian artery:Arise from aorta just below renal arteryEnters hilum through infundibulopelvic
ligamentEnds by anastomosing with terminal part of
uterine artery
Uterine artery also give some branches to ovary
Arterial Supply
Left ovarian vein:Drains into left renal vein
Right ovarian vein:Drain into inferior venacava
Ovarian veins form PAMPINIFORM PLEXUS in infundibulopelvic fold
Venous Drainage
By ovarian plexus:Formed by coeliac,renal and hypogastric
plexusIt contains sympathetic(T10,T11) and
parasympathetic(S2,S3,S4) nerves
Lymphatic drainage:
Drain into lateral aortic and pre-aortic nodes
Nerve Supply:
Ovaries develop from the genital ridge which arise from medial side of mesonephros
Embryology
Primordial germ cells that are formed migrate to region of developing ovary
Sex cords proliferate from the germinal epithelium
Cords then surrounds primordial germ cell to form primordial follicle.
Epoophoron:Known as organ of RosenmullerRepresents the cranial end of wolffian bodyConsists of vertical tubules in mesovarium
and mesosalpinx
Paroophoron:Represents the caudal end of wolffian bodyContains vertical tubules
Its remnant Known as Gartner’s duct
Runs below and parallel to fall tube in mesosalpinx
Runs by the side of uterus upto internal os and enters the cervix
Then runs forwards to reach vaginal wall and hymen
Wolffian duct
Consists of 2 layers:
1.Theca interna:
Responsible for production of oestrogen and progesterone
Graffian follicle
These cells form projection into the cavity of graffian follicle called CUMULUS OOPHORUS
Spherical bodies scattered among the granulosa cells are called CALL EXNER BODIES
These cells secrete liquor folliculi and contains oestrogen
2.Granulosa cell layer:
1.Steroidal hormones:
OestrogenProgesteroneTestosteroneAndrostenedione
2.Non steroids:InhibinRelaxin
Secretes…
SCREENING: done for women with• Low parity• Low fertility• Delayed childbearing• Familial predisposition• BRCA-1 & BRCA-2 genes• Mumps prior to menarche• Multiple ovulation in IVF
Ovarian Tumours
SCREENING METHODS:Transvaginal USG:
Sensitivity - 95%
Tumour marker: CA 125
Sensitivity – 50% improves when combined with transvaginal USG
Surface Enhanced Laser Desorption Ionisation Time Of Flight (SELDI-TOF):
-Uses proteomic patterns to identify tumour
Sensitivity- 100% Specificity- 95%
NEWER METHODS:
-Involves measurement of plasma DNA levels and allelic imbalance
87% sensitive at stage I and II95% sensitive at stage III and IV
Digital Single Nucleotide Polymorphism (SNP) Analysis:
ETIOPATHOGENESIS, CLASSIFICATION AND PATHOLOGY
OF OVARIAN TUMOURS BY K JEEVITHARAJALAKSHMI
ETIOLOGYRISK FACTORS: NulliparityDecreased fertilityDelayed childbearingEarly menarche and late menopauseHeredity BRCA 1 BRCA2 ERB B2 –adenocarcinoma TP53 MutationFamily history
Multiple ovulation in IVF programme OTHER FACTORS Environmental factors: high fat diet use of talc on perineum industrial pollution White race and increasing age mumps prior to menarche
PROTECTIVE FACTORS: Multiparity breast feeding anovulation OCP’S
PATHOGENESIS Incessant ovulation theory: Repetitive ovulation
cyclic repair of ovarian surface epithelium p53 mutation carcinogenesis
5% to 10%- inherited predisposition loss of BRCA and P53 function Benign cyst
Low malignant potential tumours
Invasive carcinoma
BORDERLINE OVARIAN TUMOURSLow malignant potential10% to 20% of epithelial tumoursMitotic figure-<4/10 high field Characteristics:
High survival rateTypical indolent courseSpontaneous regression of peritoneal implantsDiagnosis based on examination Multiple section examination
CRITERIA: Epithelial proliferation with
papillary formation and pseudostratification
Nuclear atypia and increase mitotic activity
Absence of stromal invasion serous borderline tumor
Surface epithelial tumor
Germ cell tumors
Sex cord tumors
Metastais to ovary
origin Coelomic epithelium
Mullerian epithelium
Germ cells from yolk sac
Sex cord of stroma
Mullerian or extramullerian
Overall frequency
65% to 70% 15 to20%
5 %to10%
5%
Amongmalignancy
8o% to90% 3% to5%
2%to3% 5%
Age group 20+yrs 0-25yrs All ages variable
NORMAL OVARY
Surface epithelial germ cells sex cord
Cells stroma
WHO classificationSURFACE EPITHELIAL STROMAL TUMOURS Serous tumors -cystadenoma -borderline -cystadenocarcinoma Mucinous tumours -benign -borderline -malignant Endometriod tumours -adenosarcoma -mesodermal mixed tumour
Epithelial stromal tumours -benign
-borderline -malignantTransitional cell tumours brenner tumourSEXCORD STROMAL TUMOURS Granulosa stromal cell tumour granulosa cell tumour thecoma cell tumour Sertoli leydig cell tumour Gyndroblastoma Lipid cell tumour
GERM CELL TUMOURTeratoma mature immature monodermalDysgerminoma Yolk sac tumour Mixed germ cell tumourMETASTATIC TUMOURSKrukenberg tumourOthers
TYPES RESEMBLANCESEROUS TUMOUR ENDOSALPHINXMUCINOUS TUMOUR ENDOCERVIX
ENDOMETRIOIDTUMOUR ENDOMETRIUM
CLEAR CELL TUMOUR CLEAR CELL CA OF ENDOMETRIUM
BRENNER TUMOUR
URINARY TRACT
GERM CELL TUMOUR GERM CELL
ENDODERMAL SINUS TUMOUR
EMRYONAL TISSUE OF YOLK SAC
GRANULOSA TUMOUR GRANULOSA CELL OF GRAFFIAN FOLLICLE
THECOMA TUMOUR THECA LUTEIN CELL OF GRAFFIAN FOLLICLE
PATHOLOGY OF OVARIAN TUMOURSRATIONALE FOR HISTOTYPING: DIAGNOSTIC CRITERIACARCINOMA GRADINGTHERAPEUTIC RELAVANCEPROGNOSTIC SIGNIFICANCE
TUMOURS OF SURFACE EPITHELIUMSEROUS TUMOURS Most common Tall columnar epithelium resemble
endosalphinx 50% bilateralGross:Cystic lesions-intracystic or papillary projections
from surface
TYPE GROSS
Benign smooth glistening wall with no or less papillary projection
Borderline more papillary projections
malignant Irregular large solid mass with nodularity and fixation
SEROUS -TYPES MICROSCOPIC FEATURE
BENIGN Columnar epithelium with abudant cilia and microscopic papillae
BORDERLINE More complexity of stromal papillae with stratification and nuclear atypia
MALIGNANT More complexity and stromal infiltration
Mucinous tumoursResemble endocervixUsually unilateral,5%bilateral12%-25% of ovarian neoplasmGROSS:Multiple cyst without surface involvementMultiloculated with sticky gelatinous fluidHoney combed appearance
MUCINOUS TYPES
MICROSCOPIC FEATURES
BENIGN Tall columnar epithelium with mucin and absence of cilia
BORDERLINE
Abudant gland like with stratification without stromal invasion
MALIGNANT More solid growth ,Epithelial cell atypia, loss of gland like, necrosis ,stromal invasion
EndometrioidResemble endometrium lining10% of ovarian neoplasmGROSS:Partly cystic and partly solid with foci of hemorrhageMICROSCOPIC FEATURE:Typical glandular patternLike endometrium
CLEAR CELL CARCINOMA Highly malignantResemble clear cell carcinoma of endometriumGROSS:Large partly cystic and solid MICROSCOPIC FEATURE: Large cuboidal cell with abudant clear cytoplasmHobnail cells
BRENNER TUMOURResemble transitional cell of urinary tract1%-2% of neoplasmGROSS: Solid yellow grey firm mass90% UnilateralMICROSCOPIC FEATURE:Epithelial cell nest- puffed wheat& Coffee
bean nuclei
GERM CELL TUMOURSTeratoma:MATURE- BENIGN:GROSS:Unilocular cyst with hair and cheesy sebaceous material,teeth,bone…MICROSCOPIC FEATURE:Stratified squamous epithelial with Hairshaft,sebaceous gland &skinAdnexal structureKaleidoscopic appearanceEX:Dermoid cyst
IMMATURE –MALIGNANTGROSS:BULKY solid mass with variegated appearanceMICROSCOPIC FEATURE:Immature tissue differentiating towards gland ,nerve ,muscle ,CartilageStruma ovarii- contain thyroid tissueCarcinoid tumour-argentaffinoma
Dysgerminoma80% 90%-Unilateral GROSS:Solid mass, elastic rubber consistencyPink ,lobulated, soft &fleshyMICROSCOPIC FEATURE:Large cells in bunchesDark staining nuclei, clear translucent cytoplasmLmphocytic infiltration of fibrous stroma
Endodermal sinus tumourGROSS:Solid with cystic degeneration MICROSCOPIC FEATURE:Glomerulus like structureSchiller duval bodies- germ cellsCentral blood vessels
CHORIOCARCINOMAVery vascular, highly malignantMICROSCOPIC APPEARANCE:Dimorphic population of syncytotrophoblast
and cytotrophoblast in necrotic& hemorrhagic pattern
SEX CORD STROMAL TUMOURS- mesenchymomasGRANULOSA TUMOURS:Resemble granulosa cell of graffian follicleGROSS:U/L yellowish brown oval,Soft, lobulatedMICROSCOPIC FEATURE:Rosette like call exner bodies contain Central amphorous pink materialSurronded by granulosa cells
FibrothecomaResemble theca lutein cells of graffian follicleGROSS:U/L Solid white firm massMICROSCOPIC FEATURE:Spindle shaped fibroblast & Collagen with fat laden polyhedral cells
SERTOLI LEYDIG CELLS:GROSS: SOLID grey to golden brownMICROSCOPIC FEATURE: Well differentiated tubules – tubules
composed of sertoli and leydig cells interspesed with stroma
TUMOUR FROM CONNECTIVE TISSUE OF OVARYOVARIAN FIBROMA:3% Of ovarian neoplasmGROSS:Oval with smooth surface with large vein in capsule,Firm and harder in consistencyCalcerous degeneration occursMICROSCOPIC APPEARANCE:Uniform spindle shaped cells inFeather stitched patternResemble ovarian cortexMEIG SYNDROME
KRUKENBERG TUMOUR:
Almost BilateralGROSS:Smooth surfaceSolid waxy consistency with cystic spacesMICROSCOPIC FEATURE:Mucin producing large signet ring cells in cellular
stroma
BENIGN OVARIAN ENLARGEMENTS
- KARTHIK. M
Causes of ovarian enlargement:
• Retention cysts- distention cysts• Lutein cysts
• Endometriosis•Hypertrophy- cong. & acquired•Corpus luteum hematoma•Ovarian pregnancy•Oophoritis- acute, chronic•Luteoma of pregnancy•1ᵒ neoplasm- benign, malignant•2ᵒ neoplasm
Retention cysts:Cystic changes greater than normal range.
1. Atretic cysts2. Germinal inclusion cysts3. Follicular cysts4. Theca lutein cysts
Atretic cystsGraffian follicle, corpus luteum, corpus albicans, corpus fibrosum.
All these may remain cystic prior to replacement by fibrous tissue.
Cysts- small and multiple
Lined by granulosa cells, granulosa lutein, theca lutein, connective tissue or hyaline tissue.
Germinal inclusion cystsWalthard inclusions
Microscopic cysts found in ovaries of older women.
Importance- origin of cystadenoma, Brenner tumor
It is lined by epithelium similar to that on surface of ovary.
Follicular cystsEnlargement of immature unruptured graffian follicle.Anovulation.Ovum degenerates but granulosa and theca cell layer may persist. Single or multiple size-3 to 5cm
Due to accumulation of more follicular fluid, follicles increase in size lining epithelium flattens and disappear.
• Excessive normal Gn stimulus- ovulation of other follicles not arrested
Abnormal Gn stimulus- ovulation arrested
Single follicular cyst- secrete estrogenPolycystic ovaries in PCOD- secrete androgens Triad- anovulation, hirsutism,
Rx- disappear spontaneouslyovulation induction- MDPA, Clomiphene citrateCyst persisting more than 2 months- neoplastic
Theca lutein cystsLess common usually B/L multicystic large upto 25 cm
•Endogenous causes- molar pregnancy, chorioCa, multiple pregnancy•Exogenous causes- ovulation induction
High output of GnIncrease in hCG
Excessive leutinisation
Rx- disappears spontaneously when cause is removed
Symptoms•POLYMENNORHEA, POLYMENNORHAGIA- multiple small cysts ass. with condns causing ovarian hyperemia.
•AMENNORHEA OR OLIGOMENNORHEA- when cystic ovaries are androgenic.
•INFERTILITY- anovulation or decreased ovulation.
•PAIN - in iliac fossa When associated with Hemorrhage, pelvic adhesions. Tunica albuginea of ovary ill defined and nonresistant to distension. Pain arises only when blood leaks into peritoneum from hematoma. Cystic ovaries that are buried in peritoneal adhesions – resistant to enlargement – pain.
Treatment
If associated with PID- treat the causeIn absence of other disease
•Spontaneous regression•Surgical removal of cystic portion of ovary or whole of ovary.
Corpus luteum cystGreater than 3cm
Corpus luteum of pregnancy- forms cyst- degenerates b/w 2nd n 3rd month, it is symptomless
Corpus luteum of menstruation- may become cystic.
Lining layers of granulosa lutein and paraleutin continuously produces progesterone and estradiol.
Endometrium is in secretory phase.
Excretion of pregnanediol is increased.
• Symptoms- delayed menstruation, pain, adnexal mass.
• Complications- rupture, torsion
• Rx- if ruptured, it leads to hemoperitoneum. It requires surgical treatment.
Luteoma of pregnancyHyperplastic conditions
8 to 20cm large cut section- orange yellow in color
Solid multiple foci of luteal tissue- in one or both the ovaries during
pregnancy. Usually asymptomatic. Arises from theca or stromal cells.
Due to the action of hCG.
It disappears spontaneously after pregnancy.
Occasionally some androgenic action – causes virilisation of mother or her
female child.
BENIGN OVARIAN TUMOURS
M . Kiruthika III OG
BENIGN OVARIAN TUMOURS
Predominantly occur in premenopausal women.
Benign neoplastic cystic tumours of germ cell origin are most common in young women.
Benign ovarian tumours are usually slow growing .
Surface epithelium
Corpus luteumTheca cell
Granulosa cell
Ovum
Germ cell tumours• Benign cy stic teratoma
• S truma ovarii• Gonadoblastoma
Sex cord stromal Tumours• Fibroma• Theca cell tumour
Surface epithelial tumours• Serous cystadenoma• Mucinous cystadenoma
• Endometroid cystadenoma
• Brenner tumour
Classification of benign ovarian tumours
BENIGN SURFACE EPITHELIALTUMOURS
Serous cystadenoma• Women aged between 30 – 50 years.• 30 % Bilateral.• Moderate sizes ranging from 10 – 15 cm.• Clear yellow fluid present.• TYPES Simple serous cysts. Multilocular serous cysts. Papillary serous cystadenoma.• No specific symptoms.
Mucinous cystadenoma Common in 30 – 50 age group. Unilateral. May reach huge size & Multilocular. Bluish or yellowish transparent colour. Filled with mucinous material which is sticky, slimy, viscid. Rupture may cause pseudomyxoma peritoni.
Endometroid cystadenoma
Rare tumour Median age of occurrence 57 years Usually unilateral , 17 % Bilateral Median diameter – 10 cm External surface – smooth, Cyst contains clear or yellowish fluid.
Brenner tumour Rare tumour Prevalent in women > 40 years. Usually small ( < 2 cm ) to moderate size. Solid in consistency. Probably arise from Wollfian metaplasia of
surface ovarian epithelium
BENIGN GERM CELL TUMOURS
Benign cystic teratoma
• Common.• Encountered below 20 years, during
pregnancy & during child bearing period.• Usually of moderate size ( 8 – 10 cm ) &
bilateral.• Most have a long pedicle.• Greyish in colour• Mostly unilocular.
• Consists of combination of well differentiated ectoderm, mesodermal & endodermal elements.
Skin & skin appendages Sebaceous glands Sweat glands Hair follicles Muscle fibers Cartilage, bone ,teeth Respiratory & gastrointestinal epithelium.• 50 % asymptomatic
STRUMA OVARI
Monodermal teratoma composed of harmonally active thyroid tissue.
1 – 4 % of cystic teratomas. Only 5 % produce sufficient thyroid harmone
to produce symptoms.
GONADOBLASTOMA
Composed of germ cells mixed with other cells resembling granulosa & sertoli cells.
Patients have an abnormal gonad with a Y chromosome in 90 % of cases.
Predispose to development of dysgerminoma or other malignant germ cell tumours..
BENIGN SEX CORD STROMAL TUMOURS
FIBROMA Around age of 50 years. Usually mobile with a long pedicle. Lobulated glistening white surface. Firm ,hard tumour . Associated with ascites and hydrothorax MEIG’S SYNDROME
THECA CELL TUMOUR ( THECOMA)
Occurs in postmenopausal women. unilateral encapsulated tumour Many are functioning tumours producing
oestrogen.
CLINICAL FEATURES
SYMPTOMS
ABDOMINAL SWELLING
Pressure symptoms
Respiratory embarassment
Frequency of micturition Edema
Ovarian Cachexia
ASCITES – MEIG‘ S SYNDROME
Ascites
Hydrothorax
Dull ache lower abdominal pain , low back pain.
Peritonitis, shock due to rupture of large cyst. Dyspareunia
Menstrual disorders
Menorrhagia
Amenorrhoea
Post menopausalBleeding.
PHYSICAL SIGNS
INSPECTION • Abdominal swelling.• Symmetrical enlargement of abdomen.• On deep inspiration the abdominal wall can
be seen to move over the swelling.PALPATION• Mass – central or to one side.• Well defined upper & lateral border.• Smooth or lobulated surface
MOBILE from above downwardsCONSISTENCY – tense & cystic fluid thrill elicited
PERCUSSION
AUSCULTATION silent
BIMANUAL EXAMINATION GROOVE’S SIGN
MALIGNANT OVARIAN TUMORs
by
Madhu maetha .R III O & G
SECOND MOST COMMON ( 10-15%) GYNAECOLOGICAL CANCER
HIGH MORTALITY RATE
80-85% WOMEN WITH OVARIAN CANCER DIE
CLASSIFICATION
SEROUS CYSTADENOCARCINOMA MUCINOUS CYSTADENOCARCINOMA ENDOMETROID CYSTADENOCARCINOMA CLEAR CELL CARCINOMA MALIGNANT BRENNER TUMOUR UNDIFFERENTIATED CARCINOMA
DYSGERMINOMAENDODERMAL SINUS
TUMOURCHORIOCARCINOMAMALIGNANT TERATOMAEMBRYONAL CELL
CARCINOMAPOLYEMBRYOMA MIXED TUMOURS
GRANULOSA CELL TUMOR
SERTOLI LEYDIG CELL TUMOR
MALIGNANT GERM CELL TUMOURS
MALIGNANT SEX CORD STROMAL TUMOURS
OVARIAN EPITHELIAL CARCINOMA
Classification
EPITHELIAL OVARIAN CANCER INCIDENCE
*60-70% of all Ovarian Tumors *90% of all Ovarian Malignances
AETIOLOGY
*Nulliparous or Infertile women
*Hereditary genetic factors -5-10% genetic predisposition -younger age -defective BRCA 1 and BRCA 2
Macroscopically
Microscopically ADENOCARCINOMAWhich might be, commonly
SEROUS ADENOCARCINOMA (75%) MUCINOUS ADENOCARCINOMA(20%) ENDOMETROID ADENOCARCINOMA(2%)
Serous cystadenocarcinoma
Mucinous cystadenocarcinoma
Endometroid carcinoma
Clear cell carcinoma
RARELY, malignant brenner tumor
Transitional cell carcinoma
SMALL CELL CARCINOMA
NON-EPITHELIAL OVARIAN CANCER
MALIGNANT GERM CELL
TUMORS
MALIGNANT SEX-CORD STROMAL
TUMORS
UNCOMMON OVARIAN TUMORS
Malignant germ cell tumorsINCIDENCE *20-30% of all ovarian tumors
*5% of germ cell tumors- MALIGNANT
CLASSIFICATION
SPECIAL FEATURES OF GERM CELL TUMORS Lower age incidence
Tends to grow rapidly
Most tumors produce TUMOR MARKERS
TUMOR MARKERSDYSGERMINOMA ALKALINE
PHOSPHATASE & LACTATE
DEHYDROGENASE
ENDODERMAL SINUS TUMOR ALPHA
FETOPROTEIN
CHORIO CARCINOMA HUMAN CHORIONIC
GONADOTROPIN
DYSGERMiNOMA Commonest Malignant Germ cell
tumor
Younger age (10-20 years)
secretes ALKALINE PHOSPHATASE & LACTATE DEHYDROGENASE
dysgerminoma
MALIGNANT TERATOMA 2nd commonest Germ Cell Malignancy
contains elements resembling tissues derived from Embryo - ABNORMAL MATURATION producing Undisciplined growth
occur in combination with other Germ cell tumors- MIXED GERM CELL TUMOR
Malignant change in Benign cystic teratoma-0.5% to 2%- commonly Squamous cell carcinoma
ENDODERMAL SINUS TUMOR from Multipotent Embryonal tissue –
SELECTIVE DIFFERENTIATION OF YOLK SAC STRUCTURES
Young age ( 16-18 years)
secretes ALPHA FETOPROTEIN
clinical presentation- Abdominal pain & Pelvic mass
endodermal sinus tumor
Chorio carcinoma Rarely occurs in Pure form, generally it is a part of
Mixed Germ Cell Tumor
its origin as a Teratoma- confirmed in Pre- pubertal girls
secretes HUMAN CHORIONIC GONADOTROPIN
Highly malignant- metastasis to Liver, Lungs, Brain,Bones and other viscera
choriocarcinoma
MALIGNANT SEX CORD STROMAL TUMORS arises from Functioning or Non-Functioning
stroma of ovary Functioning sex cord tumors may be
* Estrogenic- GRANULOSA CELL TUMOR * Androgenic- SERTOLI-LEYDIG CELL TUMOR * Both Estrogenic and Androgenic(very rare) - GYNANDROBLASTOMA
Non-functioning stroma may very rarely give rise to Fibrosarcoma of ovary
Granulosa cell tumor functioning- secrete ESTROGEN
associated with Endometrial carcinoma in 5-10% of cases & with Endometrial hyperplasia in 25-50% of cases
causes Irregular bleeding, Precocious puberty, menstrual irregularities, postmenopausal bleeding
Granulosa cell tumor
Sertoli leydig cell tumors many are Functioning- secrete
ANDROGENS
Defeminisation followed by masculinisation
Primary modes of spread of ovarian cancer
DIRECT EXTENSION
TRANSCOELOMIC SPREAD
LYMPHATIC SPREAD
HEMATOGENOUS SPREAD
METASTATIC OVARIAN CANCER 5-6% of Ovarian tumors
PRIMARY
GENITAL EXTRA GENITAL
KRUKERNBERG TUMOR accounts for 30-40% of Metastatic
cancers of ovary
Bilateral solid ovarian tumor Microscopically- SIGNET RING CELLS
CEA markers increase
arise by RETROGRADE LYMPHATIC SPREAD
KRUKERNBURG TUMOR
CLINICAL PICTURESYMPTOMS- “SILENT KILLER”EARLY STAGE DISEASE- asymptomatic
Non specific GIT symptoms
PRESSURE SYMPTOMSUrinary frequency
Constipation
ABDOMINAL PAIN
ABDOMINAL SWELLING
ABNORMAL UTERINE BLEEDIND especially
POST-MENOPAUSAL BLEEDING
PHYSICAL SIGNS Palpation of a Pelvic mass
Bilateral Solid Fixed masses
suggest MALIGNANCY
CLINICAL FEATURES SUGGESTING malignancy in ovarian tumors
Extremes of Age Rapid
growth of tumor
In HISTORY,
Loss of weightPain
Post menopausal bleeding & symptoms of Virilisation
On general examination, Malignant Cachexia
Palpable Supraclavicular nodes
Pleural Effusion
Any asssociated Breast mass
On abdominal examination,INSPECTION
Abdominal enlargement
PALPATION Bilateral solid fixed mass
PERCUSSION
Presence of
Ascites
On pelvic examinationNodules in the Pouch of Douglas
Frozen Pelvis
At laparotomy Ascites especially if altered blood stained ascites
Bilaterality,fixation & invasion of capsule
Extracystic papillae & ADHESION to surrounding structures
Peritoneal nodules or Secondary deposits in omentum, intestine or liver
Variable consistency of tumor & cut section showing Haemorrhage and Necrosis OMENTAL
DEPOSITS
BENIGN TUMORS
MALIGNANT TUMORS
unilateral bilateral
cystic solid
mobile fixed
smooth irregular
*Ascites*Cul-de-sac nodules*Rapid growth rate
COMPLICATIONS AND DIFFERENTIAL DIAGNOSIS
COMPLICATIONSTORSIONRUPTUREPSEUDOMYXOMA OF THE PERITONIUM INFECTIONEXTRAPERITONEAL DEVELOPMENTSECONDARY MALIGNANCY
TORSION It occurs
• commonly in ovarian cyst. • when size of the cyst is 10 cm or more in
diameter. As a result of rotation • anterior surface of tumor turns towards the
patient’s right side. •the veins in pedicle becomes occluded. The increased tension causes severe abdominal pain
and peritoneal irritation. Rotation of an ovarian cyst is hemodynamic. Rare in chocolate cysts and malignant ovarian tumors.
torsion
Ordinary people think merely of spending time, great people
think of using it.
RUPTURETRAUMATIC SPONTANEOUSDirect violence to
abdomenDuring labour Bimanual
examination
Malignant ovarian tumors-papillomatous type
Pappilomatous serous cystadenomas
Actively growing mucinous cystadenomas
rupture
Tumors Mechanism of ruptureMalignant ovarian tumors Pappillomatous serous tumours
Carcinoma cells infiltrate through the connective tissue capsule to ulcerate into the peritoneal cavity
Actively growing mucinous cystadenomas
The epithelial elements of the growth grow so rapidly that the connective tissue of the capsule are unable to keep up with them.
First thing in the human personality that dissolves in alcohol is dignity.
PSEUDOMYXOMA OF PERITONEUM Coagulated mucinous material adherent to
omentum and intestines.Boiled sago pudding.At operation , the material cannot be removed
completely.Usually occurs with mucinous cystadenoma and
also reported in mucocele of appendix and carcinoma of large intestine.
Mesothelium of peritoneum secretes mucinous material because of its conversion into columnar cells.
Bad prognosis.
Pseudomyxoma of peritoneum
INFECTION InfrequentMost cases follow acute salpingitis and
torsion.Uncommon through bloodstream. Infected ovarian tumors are always adherent
to adjacent viscera.
EXTRAPERITONEAL DEVELOPMENT Burrow extraperitoneally during their
development. It may spread upwards into the perinephric
region.Removal-extremely difficult , •danger of injuring the ureter. •large vessels may be torn.
SECONDARY MALIGNANCY50% in serous cystadenomas.5% in mucinous cystadenomas.1.7% in dermoid cysts.
Never drive faster than your guardian angel can fly.
DIFFERENTIAL DIAGNOSIS FULL BLADDERPREGNANT UTERUSMYOMAASCITESOTHER ABDOMINAL TUMORS
FULL BLADDERTense and tender ,fixed in position ,anterior to
the uterus ,projecting anteriorly more than an ovarian cyst.
A catheter should be passed to establish the diagnosis.
PREGNANT UTERUS It should be thought of whenever a tumour
is found arising from the pelvis.Exclude pregnancy by •careful bimanual examination •signs of pregnancy •ultrasonic examination and
pregnancy tests Mistakes-unmarried girl who denies history
of amenorrhoea.
MYOMAUsually hard or firm ,without the tense cystic
consistency of atypical ovarian cystPedunculated and degenerated fibroid may
however mistaken for an ovarian cyst.
Don’t dig ur grave with ur own knife and fork
ASCITES Sometimes , it is difficult to distinguish between a
large ovarian cyst and ascites. With a large ovarian cyst • percussion note over the tumour is dull •both flanks are resonant In ascites •note is dull over the flanks •abdomen is tympanitic in the midline •physical signs of shifting dullness may
be obtained.
OTHERS TUMOURSA large hydronephrosis •penetrates back into the loin and
situated high up in the abdomen ,well above the
pelvis. •intravenous or retrograde pyelography
will establish the diagnosis.Enlarged spleen , mesenteric cyst , mucocele
of appendix or gallbladder , hydatid cysts and pancreatic cysts should be considered if physical signs of an ovarian cysts are atypical.
INVESTIGATIONS
M.MARIMUTHU
1.ULTRASOUNDTransabdominal ultrasound If tumour is abdominalTransvaginal ultrasound It gives more details about the
tumour(>95%sensitivity) Normal size of ovary is 2*1.5*1cm volume is 8.8ml. More than this is
suspicious of an ovarian growth.
Normal ovary
In benign lesions-
The tumour is mostly unilateral , unilocular or multilocular with septa is <5mm in thick.
The cavity is non ecogenicThe dermoid cyst shows solid areas in cystic
tumour occasional presence of a tooth
Benign solid mass
Benign cystic ovarian mass
In malignant lesions –
The tumour is bilateral or may be unilateral and multiloculated with septa is greater than 5mm thickness
Solid tumours with echogenic or cystic area In Meigs syndrome ascites is characteristic of
benign tumour The endometrial lining more than 4mm in
thickness with papillary projections in a perimenopausal women is seen in feminizing tumour and if endometrial secondaries are present
Malignant ovary
Malignant ovarian mass
2.Colour dopplerNeovascularisation, Increased blood flow,Low pulsatile index <1 andResistance index <0.4 are suggest
malignancy
Colour doppler
3.X-Ray
Abdomen and pelvis demonstrate soft tissue shadow or teeth in
dermoid cystChest To rule out pulmonary metastasis and Hydrothorax- rt sided in Meigs syndromeBarium meal To exclude a GI primary carcinoma
4.Breast examination To rule out pregnancy and primary growth
5.CT and MRI To identifying a dermoid cyst , haemorrhagic
cyst , fibroma , endometriosis, hydro salpinx In malignant tumour – to rule out the spread
of tumour , enlargement of pelvic and para aortic lymph nodes >1cm to planning surgery , post operative radiotherapy and chemotherapy .
MRI malignant ovary
MRI malignant ovary
6.Tissue markersCA 125 It is a glycoprotein More than 30 U/ml suggest malignant Not produced by normal ovarian
epithelium may be produced by both benign and malignant ovarian tumour
It is synthesized within affected ovarian epithelial cells and secreted in to the cysts.
In benign tumours , excess antigen is released in to and may accumulate within cyst fluid.
Hypothetically , abnormal tissue architecture associate with malignant tumours may allow antigen release into the vascular circulation .
90% of women presenting with malignant non mucinous tumours , CA125 levels are elevated .
FALSE NEGATIVE : Half of stage 1 ovarian cancers will
have a normal CA 125 measurement
FALSE POSITIVE : Pelvic inflammatory disease,
endometriosis, leiomyomas, abdominal TB, pregnancy and even menstruation
CEA(Carcino Embryonic Antigen) CEA more than 5ng/ml (normal 2.5-5ng/ml)
is reported in endometrioid, brenner tumour, mucinous tumour, colonic, liver, breast and lung metastasis.
Alpha fetoprotein, hCG, NB/70k, placental alkaline phosphatase and lactate dehydrogenase are tissue markers for germ cell tumours.
In mucinous tumour – Tumour marker is CA 19-9 CEA may be better indicators of disease than
CA125
7.Cytological study Ascitic fluid or aspirated cystic fluid may
reveal malignancy. False negative is high.
STAGING LAPAROTOMY
AND
SURGERY FOR OVARIAN CANCER
- MURUGESAN. V
WHAT IS
STAGING LAPAROTOMY ?
STAGING LAPARATOMY:FIGO staging of ovarian cancer
TECHNIQUE: Incision – Midline or Paramedian
abdominal incision. If Ovarian malignancy is present and the tumor is apparently confined to the ovaries or the pelvis, thorough surgical staging to be done.
STAGING STEPS:
Any free fluid in the pelvic cul-de-sac - Cytological evaluation.
If no free fluid-Peritoneal washing
Peritoneal washing:Instilling and recovering 50 – 100ml of saline
fromPelvic cul-de-sac,
Right and left paracolic gutter and
Beneath each hemi-diaphragm
Then send it for Cytological evaluation
A systematic exploration of all intra abdominal surfaces and viscera – clockwise fashion.
Caecum
Rt. Paracolic gutter
Ascending Colon
Transverse Colon
Descending Colon
Lt. Paracolic gutter
Recto Sigmoid
Colon
Small intestine
& mesentery
Any suspicious areas or adhesions on the peritoneal surfaces - sampled for biopsy.
Eg: peritoneum over the bladder,
peritoneum of the pelvic cul-de-sac and both the paracolic gutters and intestinal mesenteries.
The diaphragm – biopsyscrapping with a tongue depressor
Infra colic omentectomy- Omentum is resected from the
transverse colon, after ligating the branches of gastro epiploic vessels that feed the infra colic omentum.
If the Gastrocolic ligament is palpably normal, it does not need to be resected.
Exploration of retroperitoneal spaces- Pelvic and para aortic lymph nodes.
Enlarged lymph nodes should be resected and sent for frozen section.
FIGO STAGING FOR
Ca OVARY
STAGE I – Tumour restricted to one or both ovaries
I A – Tumour restricted to one ovary No tumour on external surface Capsule intact, no Malignant ascites I B – Tumour limited to both ovaries No tumour on external surface Capsule intact, no Malignant ascites I C – Tumour IA or IB Positive for surface malignant growth Capsule ruptured Malignant ascites or positive peritoneal
washings
STAGE II – Tumour involves one or both ovaries with pelvic extensions
II A – Extension/Metastasis to uterus, fallopian tubes or pelvic
extensions. No Malignant cells in
ascites/washings.II B – Extension to other pelvic organs No Malignant cells in
ascites/washings.II C - Tumour II A or II B with surface
growth Capsule ruptured at/or prior to
surgery. Malignant ascites/positive
peritoneal washings
STAGE III – Tumour involving one/both ovaries with microscopic implants outside
the pelvis with positive nodes(inguinal, retroperitoneal)
Tumour limited to true pelvis but
with histological evidences of spread to bowel, omentum,
presence of superficial metastasis on the
liver.
III A – Tumour grossly limited to the pelvis Nodes negative, but microscopic seedlings of peritoneum of the
abdominal wall.
III B – Tumour with abdominal peritoneal implants of less than 2cm size and nodes negative.
III C – Abdominal implants of more than 2cm
size and positive nodes.
STAGE IV – Growth involving one or both ovaries with distant
metastasis in liver, lungs and pleura.
Tap fluid for cytology.
SURGERY
Early stage disease( STAGE I AND II)Post menopausal women: Total Abdominal Hysterectomy with Bilateral Salphingo-oophorectomy with Infracolic Omentectomy.Reproductive Age group: Unilateral Oophorectomy Preserve Uterus and contralateral
ovary Follow up with CA-125 After completion of child bearing, other
ovary and uterus should be removed.
ADVANCED STAGE DISEASE(STAGE III AND IV) Cyto Reductive Surgery: Removal of as much of the tumour and its metastasis as possible. Debulking Surgery: Total Abdominal Hysterectomy with Bilateral Salphingo- Oopherectomy Omentectomy Resection of metastatic lesions from the peritoneal surfaces or the intestines.
Second look surgeryTo detect presence of any residual tumor
following a planned course of chemotherapy.
Following a 3 to 6 months of chemotherapy, in an inoperable case- Total abdominal hysterectomy with Bilateral salpingo oophorectomy or debulking procedure.
CHEMOTHERAPY
N.NIRANJANA JOY
Prolongs remission and survival
Also used for palliative treatment in advanced and recurrent disease
Administered in all cases beyond stage Ia
Earlier single agents were used, nowadays combination therapy is favoured
No chemotherapeutic agent kills all cancer cells in one treatment , treatment needs to be repeated several times
All agents used should be active against that particular tumor
should have different modes of action to avoid drug resistance and should have different mechanisms of toxicity.
Drugs are given at 3 weeks intervals
TYPES OF CHEMOTHERAPY
Intravenous chemotherapy
Intraperitoneal chemotherapy
Neoadjuvant chemotherapy
RECOMMENDED REGIMENINTRAVENOUS CHEMOTHERAPY
DRUGS DOSE(mg/sq.m)
ROUTE INTERVAL(Weeks)
CYCLES
PACLITAXELCARBOPLATIN
175AUC=5-6
IV 3 6-8
PACLITAXELCISPLATIN
13575
IV 3 6-8
CYCLOPHOSPHAMIDECISPLATIN
75075
IV 3 6-8
DRUGS DOSE(mg/sq.mm)
ROUTE
INTERVAL(Weeks)
DOXORUBICIN,LIPOSOMAL
35-50 IV 3-4
TOPOTECAN 1-1.254
IVIV
13(DAILY*3-5DAYS
ETOPOSIDE 50 PO 3,DAYS 14-21
INTRAPERITONEAL CHEMOTHERAPY
DRUGS DOSE(mg/sq.m)
ROUTE INTERVAL(Weeks)
CYCLES
PACLITAXEL 135 IV 3,DAY 1 6
CISPLATIN 50-100 IP DAY 2
PACLITAXEL 60 IP DAY 8
Platinum Compound
Carboplatin Cisplatin
Taxol (Paclitaxel)
STAGE 1 EPITHELIAL TUMOUREarly stage,low risk NO adjuvant therapy is requiredEarly stage,high risk Adjuvant therapy is required Carboplatin and paclitaxel given for 3-6
cycles
ADVANCED STAGE EPITHELIAL TUMOURAdvanced epithelial ovarian cancer is very
sensitive to chemotherapy with responses in the range of 70-80% to first-line chemotherapy. The majority, however, relapse and ultimately die of chemotherapy-resistant disease.
Major advance in the treatment of advanced stage tumour is the introduction of paclitaxel as one of the chemotherapeutic agents
Carboplatin has less toxicity compared with cisplatin
Preferred regimen carboplatin and paclitaxel
DOCETAXEL AND CARBOPLATIN Docetaxel has efficacy similar to
paclitaxel regimen produced significant
myelosuppressionFIVE ARM TRIAL Addition of either
gemcitabine,topotecan or doxorubicin to the standard regimen does not enhance survival rate
INTRAPERITONEAL CHEMOTHERAPY
Ideal anticancer agentVery effective systemically against ovarian
cancerPenetrate deep into the tumorStays in the peritoneal cavity for prolonged
period Low incidence of systemic adverse effect
but providing satisfactory drug concentrations in the inner core of tumor
Cisplatin
The peritoneal lining had 2.5-8 times higher levels of drug after IP administration
Intraperitoneal chemotherapy might increase the therapeutic index for small tumors confined to the peritoneal cavity
IP cisplatin-based chemotherapy has been shown to have a survival benefit over IV cisplatin-based chemotherapy for advance ovarian cancer patients with optimal debulking
Strengths of Intraperitoneal chemotherapyAchieve dose intensification (as ‘high-dose’)
Treats both intraperitoneal tumor bed and extraperitoneal tumor via systemic recirculation
Reaches sites that may not be reached by Intravenous route.
Toxicity
More bonemarrow suppressions, Gastrointestinal effects, neurologic symptoms, and infections
Complications of CatheterBlockadeLeakageInfectionDiarrheaBowel perforationFistula formation
Patient selection issuesPatient characteristics
eg.: renal function ; neuropathy (DM –associated)
Significant peritoneal adhesionOngoing abdominal infection, or indwelling IP
catheter becomes infected or malfunction, will be unable to treated by this route of drug delivery
NEOADJUVANT CHEMOTHERAPYIn stage 3 and stage 4 disease chemotherapy
can be given to ‘downstage the disease’ prior to chemotherapy
Helpful in patients with massive ascitis ,pleural effusion.
REGIMEN FOR NON-EPITHELIAL TUMORS
Germ cell tumors are treated with surgery and multi-agent chemotherapy in most cases VAC Vincristine
ActinomycinCyclophosphamide
BEP BleomycinEtoposideCisplatin
VBC VincristineBleomycinCisplatin
SIDE EFFECTSWhile chemotherapy drugs kill cancer cells,
they also damage some normal cells, causing side effects. These side effects will depend on the type of drugs given, the amount taken, and how long treatment lasts. Temporary side effects might include the following:• nausea and vomiting • loss of appetite • hair loss • hand and foot rashes • kidney or nerve damage
• mouth sores
bleeding or bruising after minor cuts (from a shortage of platelets)
an increased chance of infection (from a shortage of white blood cells)
tiredness (from low red blood cell counts)
Ca Ovary IIIcInoperable –
BiopsyNeodjuvant
chemoCisplatin +
PaclitaxelComplete
responseSec.
Cytoreductive surgery done now
Palliative and Adjuvant Therapy
ByR.Pani MalarIII OG MMC
Palliation
From Latin palliare to cloakAny form of medical care or
treatment that concentrates on reducing the severity of disease
symptoms, rather than striving to halt, delay, or reverse progression of the disease itself or provide a
cure.
Palliative Radiotherapy•In advanced ovarian cancer
shrinks the tumor and reduces the symptoms
•Dysgerminoma•Nodal metastasis
Intra peritoneal radiotherapy
•Provides local radioactivity•Treats all peritoneal
surfaces•Uses Au-198 and P-32
Method•10 – 15 mCi of P-32 mixed
with 1 to 2 L of saline injected intra peritonealy
•Positional changes every 15 to 30 min
External radiation MOVING STRIP TECHNIQUE
•Hypofractionation technique•12 to 14 strips of 2.5 cm height
are marked•Treated for 5 - 6 weeks
•180 to 200 cGy
Open Field Technique•Larger treatment field of 45
cm•Treated daily
•Liver and kidneys shielded•25 to 45 Gy
Nutrition•Calories 2000-2400
kcal/day•Adequate protein vitamins
and minerals•Fluid intake 1500 – 2000 ml
•Blood transfusion for anemia
Relief of Pain
•Opiates – Morphine•Muscle spasm – Diazepam
•Bone pain – NSAIDs•Nerve pain – Sod Valproate
carbamazepine•Bowel and bladder pain –
anticholinergics
Steroids•Promotes the feeling of well
being•Increases appetite
•Relieves the pressure of metastasis in brain and liver
•Also effective in bladder and bowel pain
Relief of symptoms•Vomiting - Haloperidol
Metoclopramide•Cerebral vomiting - Cyclizine
Domperidone
•Constipation - laxatives
•Thrush - fluconazole
•Ascites - tapping•Pleural effusion -
pleurodesis
thoracocentesis•Intestinal obstruction –
Surgery
Psychological Impact•Decreased sex libido
•Dyspareunia•Menopausal symptoms – HRT
•Mental depression due to oestrogen deficiency
Follow up•Clinical Examination•Radiological – USG
•Serology – tumor markers
Prognostic factors •Pathology-Histology
-grade- well differentiated - good
poorly differentiated - bad
•Biology-Low stage - diploid-good High stage-aneuploid-bad
•Clinical featuressmall disease volume prior to
surgerysmall residual disease after
surgeryabsence of ascites have good
prognosis
5 yr SurvivalFIGO Staging
5 year survival
Stage 0 90 – 100%
Stage I 70%Stage II 25 – 30%Stage III 10%Stage IV 0 - 5%
OVARIAN TUMOURSAND
PREGNANCY
BYX.A.PRASANNA
III UNIT OG
COMMON TUMOURSDYSGERMINOMAMATURE CYSTIC TERATOMAPARAOVARIAN CYSTSEROUS CYSTADENOMACORPUS LUTEAL CYST OF PREGNANCYFIBROMA
MATURE CYSTIC TERATOMA
Mostly asymptomaticShooting pain down thighs, pain abdomenPressure effects
DyspnoeaPrecordial pain
DyspepsiaFrequency
Constipation
CLINICAL FEATURES
Uterus larger than gestational ageMass pushed behind uterus Or to 1flank
StagingSimilar to non-pregnancy stateUsually stage 1 – low grade
Examination
•INCIDENTAL FINDING•MALIGNANT –IRREGULAR SEPTA,SOLID AREAS,PAPILLARY EXCRESCENCESUSG•USED AS A SCREENING PROCEDURE•NOT SPECIFICCA 125•MATERNAL SERUM•ENDODERMAL SINUS TUMOURAFP
INVESTIGATIONS
DIFFERENTIAL DIAGNOSISUterine leiomyomasPelvic kidneyRetroperitoneal
tumourEctopic pregnancyRetroverted gravid
uterusNon pregnant horn
of bicornuate uterus
HINGORANI SIGN
Effects of pregnancy on tumourTorsion
InfectionIncarceration
Effects of tumour on pregnancyUrinary retention
UTI Malpresentation
Rupture -peritonitis
COMPLICATIONS
TORSION OVARY
Effect of tumour on labourObstructed labour
Uterine inertiaRupture
Effect on tumour in puerperiumTorsion (25%)
Why– Rapid involution of uterusLax abdominal walls
Mobility of abdominal viscera
Large solid massesComplications –torsion, incarceration in cul de sacMore lymphatic spreadTreatment – unilateral oopherectomy
+Ipsilateral pelvic & para aortic node dissection
15% bilateral10% recurs
DYSGERMINOMA
Click icon to add picture
Rare Complicated by
Rupture 19% haemoperitoneum
14% dystocia
Edema ,prominent luteinisation ,lacks recognizable differentiation
SEX CORD STROMAL
Similar to non pregnant casesIndividualize treatment
Total abdominal hysterectomyOR
Cytoreduction
Gestational age , fetal viability ,demand
EPITHELIAL TUMOURS
MANAGEMENTSurgery – II trimesterEven then , risk of preterm labor , IUGR ,IUD common
Chemotherapy – controversial .II , III trimester
Radiotherapy – contraindicated
TIMING OF TUMOR
I TRIMESTER
CYSTECTOMY
OVARIECTOM
Y
> 28 WKS
PTLNORMAL DELIVERY
REMOVE TUMOR 1 WK AFTER DELIVERY
WAIT TILL AAA16 WKS
Complicated tumours
< 10 CM •USG – CYST•LUTEAL CYST –RESOLVES BY 12 -16 WKS•IF NOT ,SURGICAL REMOVAL AFTER PUERPERIUM
OBSTRUCTS LABOR
•CAESARIAN FIRST, •TUMOUR REMOVAL
TORSION •IMMEDIATE SURGERY•LAPAROTOMY
1. Sedatives – 48 to72 hours
2. 25 mg progesterone –parenterally 1 week
3. Gentle & minimal handling of pregnant uterus
Survival not different from non pregnant cases
POSTOPERATIVE CARE
Ovarian enlargements, solid/cystic may occur at any age
Functional and inflammatory enlargements develop during child bearing years
Second most common site for development of gynaecological malignancy (10-15% gynaecological cancers)
Easy screening methods not avilablePrognosis poor
HIGHLIGHTS
Mostly resolve spontaneously PCOS - Anovulation, hirsutism
USG findings – ‘Necklace appearance’↑E2, LH, androgens
Treatment – Metformin 500 mg tds./Surgery – Lap. punctures
Non neoplastic enlargements
Commonest 80% - epithelial cell tumours (90 % malignant)
Tumour in adolescent and post menopausal women – more often malignant
Boderline ovarian tumours /LMPDon’t invade stroma
Mitotic figures <4/10 high field
OVARIAN TUMOURS
ORIGIN OF TUMOURS TUMOURS
ENDOSALPINX SEROUS EPITHELIAL CELL TUMOUR
ENDOCERVIX MUCINOUS EPITHELIAL TUMOUR
ENDOMETRIUM ENDOMETRIOID TUMOUR
TRANSITIONAL CELL BRENNER TUMOUR
CLEAR CELL Ca ENDOMETRIUM CLEAR CELL CARCINOMA
TOTIPOTENT CELLS TERATOMA
MESENCHYMAL CELLS GRANULOSA CELL TUMOUR
BRCA 1 ,BRCA 2 mutations in 5 – 10%
Yolk sac tumour -↑ AFP , ↑ alpha 1 antitrypsin
Choriocarcinoma - ↑ hCG
Embryonal cell carcinoma - ↑ AFP ,↑hcg
Metastasis – pylorus
Krukenburg’s tumour – myxomatous stroma ,signet ring cells, retrograde lymphatic spread .
MALIGNANT TUMOURS
Ascites + mass , bilateral , rapidly growing – malignant
Except – meig’s ,fibroma ,brenner tumour
Complications – TorsionRupture
Pseudomyxoma peritonei Infection
Retroperitoneal haematoma
CLINICAL FEATURES & COMPLICATIONS
GOLD STANDARD - INVESTIGATIONTransvaginal ultrasound
– BENIGN
Unilateral , unilocular ,thin wall, thin septa <5mm
Non -echogenic
malignant – bilateral ,solid tumour
Ascites Septa >5mm
Papillary projections
BENIGN - Total abdominal hysterectomy with bilateral salpingo oopherectomy ,
Unilateral ovariotomyCystectomy
Laparoscopic /USG guided aspiration
Stage I , II – Total abdominal hysterectomy and bilateral salpingo oopherectomy , omentectomy
Stage III,IV –Debulking , postoperative chemotherapy , radiotherapy .
TREATMENT
SCREEN BY TRANSVAGINAL
ULTRASOUND
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