TUMOR TRACTUS

UROGENITAL

Dr. Resti Arania Sp.PA

WILMS' TUMOR
= Nephroblastoma
= , umur median 2 th 11 bln
Ka = Ki, 5 % bilateral
15 % + kelainan kongenital :
Anomali UG
Hemihipertrofia
Aniridia
ETIOLOGI : Diduga kongenital

KLINIS :

Flank mass
Flank pain
Trias
Hematuria
Hipertensi
Anorexia, Nausea, Vomiting
Kelainan kongenital lain

LABORATORIUM :
Hematuri
Anemia

RADIOLOGIS :
BNO

: - Kesuraman salah satu sisi perut

- Usus terdesak oleh massa

IVP

: Collecting sytem terdesak massa /

distorsi

USG

: Massa padat dalam ginjal

PATOLOGI :
Campuran Epithelial, Stromal, Blastematous
( Immature Mesenchyma )
2 kelompok :
- Favorable histology
- Unfavorable H

89 %
11 %

Prognosa kurang baik

STAGING ( Menurut NWTS ) :

I.

Terbatas dalam ginjal, eksisi sempurna

II.

Keluar ginjal, eksisi sempurna

III. Sisa tumor dalam abdomen

IV. Metastase jauh
V.

Bilateral

DD :

Neuroblastoma
Teratoma
Hamartoma
Hidronefrosis
Cystic kidneys

TERAPI :
Radical nephrectomy
Chemotherapy : vincristine + Actinomycin D
( adriamycine)
Radiasi

PROGNOSA
Stage
I
II
III
IV
V

2Y Relapse free

2 YSR

88 %
78 %
70 %
49 %

95 %
90 %
84 %
54 %
87 %

GRAWITZ' TUMOR

Renal cell Ca
Adeno Ca ginjal
Hypernephroma = Clear cell Ca

Pria : Wanita = 2 : 1
Sering pada dekade 5 -6
Penyebab ?
Faktor resiko : - merokok
- analgesik
- dll

Tanda dan Gejala :

Trias :- Gross hematuria
- Flank pain
- Flank mass

Laboratorium :
- Hematuria
- Anemia
- LED

Radiologi :
- IVP
: distorsi PCS
- USG
: massa di ginjal
- CT Scan : massa di ginjal

Terapi :
- Nefrektomi Radikal

Terapi Ajuvan :
- Radiasi
- Hormonal
- Kemoterapi

TUMOR BULI-BULI
Tumor yang tumbuh dari epitel buli-buli
Jenis : - Transitional cell Ca
90 %
- Epidermoid Ca/ KSS
5 - 10 %
- Adeno Ca
2%
Pria : Wanita = 2,7 : 1

Penyebab : Belum jelas

Faktor resiko :
Merokok
Pekerja yang berhubungan dengan ;
Bahan kimia

Cat
Karet
Bensin
Kulit

Trauma fisik :
Infeksi
Instrumentasi
Batu

Tanda dan Gejala :

Painless, gross hematuria 90 %
Polakisuria, dysuria, urgency
Nyeri tulang, nyeri pinggang
Massa supra pubis

Diagnosis :
Urinalysis

: hematuria

Sitologi urine
IVP

: klas IV - V

: filling defect dalam buli-buli

Komplikasi :
Anemia
Gagal ginjal kronis

Penatalaksanaan :
TUR Buli
Sistektomi partial
Sistektomi total
Kemoterapi intravesikal
Radiasi
Kemoterapi

Overview of organogenesis of the urogenital organs

Urinary and reproductive systems are
Cr.
closely associated in
D
V
topography,function and development.
Ca.
Two systems have common origin
from the urogenital ridge(UGR) and
have homologous structures.
Internal genital duct system is derived
from the foetal urinary system.
Malformation of one system affects the
other.
Mesonephros
Gonad
(nephrogenic
The UGR is longitudinal swelling in
Plate)
(genital ridge)
dorsolateral side of the abdomen
UGR--> formed mostly from
--non-segmented intermediate mesoderm
Mesonephric
Lateral UGR(nephrogenic plate) forms
Duct
urinary organs and internal genital
Paramesonephric
ducts.
duct
Ventromedial UGR is genital ridge,
forms gonads.
The Urogenital ridge

SEX DETERMINATION
Mullerian/
Paramesonephric
duct

Red arrows shows gene regulation

DAX
Wnt 4
Gonadal ridge

Ovary

Bipotential
gonad
SRY

Testis

Primary sex determination at fertilisation

(i) genetic sex: XY, XX
(ii).Y chromosomes encodes testisdetermining
factorSRYgonadogenesis
secretion of foetal hormones by
interstitial cells[(Sertoli and
Leydig(M),theca cells(F)]
secondary sex(phenotypic sex)

Oestrogen

Female genital
ducts

Anti-Mullerian hormone
(Sertoli cells)
Regression of Mullerian
duct
Testosterone
(Leydig cells)
Differentiation of Wolffian duct into
Male genital ducts
Descent of testis

Gonadogenesis(2). The bipotential gonad

4 Gonadogenesis occurs at the genital ridge initiated by 2

simultaneous events:(i).Formation of gonadal cords

4 Epithelium from degenerate mesonephric nephrons invade genital
ridge.And form network of epithelial cords
(ii).Migration of primordial germ cells.
4 PGC are endodermal cells, migrate from the yolk sac into the
bipotential gonad.The gonad has a central medulla and a peripheral
cortex, surrounded by coelomic epithelium.
PGC arrive at the genitalMesonephric/Wolffian
Dorsal aorta
duct
Glomerulus Arteriole
ridge at 21 days cat and
proliferate.
Epithelial incorporate
PGC, forming gonadal
cords.
Gonadal differentiation
begins.
Mesonephric
tubule

Dorsal
Genital mesentery
ridge

Migratiing
PGC

PROSTATE NEOPLASIA
BENIGN PROSTATIC
HYPERPLASIA
AND
PROSTATE CANCER

PROSTATE ANATOMY

fibromuscular tissue (30-50%)

glandular epithelial cells (50-70%)
peripheral zone (most cancers)
central zone
transition zone (BPH,low grade cancers)

BENIGN PROSTATIC
HYPERPLASIA

17% of men age 50-59 (require Rx)

27% of men age 60-69 (require Rx)
35% of men age 70-79 (require Rx)
Similar crosscultural prevalence
Some genetic and racial susceptibility to symptom
severity (autosomal dominant)
Diet high in saturated fats, zinc and low in fruits
and vegetables.
Sedentary life style.

BPH
Proposed Etiologies
Reawakening of the urogenital sinus to
proliferate
Change in hormonal milieu with alterations
in the testosterone/estrogen balance
Induction of prostatic growth factors
Increased stem cells/decreased stromal cell
death

BPH
Pathophysiology
Slow and insidious changes over time
Complex interactions between prostatic
urethral resistance, intravesical pressure,
detrussor functionality, neurologic integrity,
and general physical health.

BPH
Pathophysiology
Initial hypertrophydetrussor
decompensationpoor tonediverticula
formationincreasing urine
volumehydronephrosisupper tract
dysfunction

PENIS KARSINOMA

TESTICULAR TUMOUR
1% of all Malignant Tumour
Affects young adults - 20 to 40 yrs - when
Testosterone Fluctuations are maximum
90% to 95% of all Testicular tumours from
germ cells
99% of all Testicular Tumours are malignant.
Causes Psychological & Fertility Problems in
young

Survival in Testicular
Tumours

Improved overall survival in last 15 to 20

years due to -

Better understanding of Natural History

and Pathogenesis of disease
Reliable Tumour Markers
Cis-platinum based chemotherapy

CROSS SECTION OF TESTIS

Testis
Stroma

Seminiferous Tubules
(200 to 350 tubules)

Interstitial Cells
Supporting
Spermatogonia
Leydig
or
(Androgen)
Sertoli Cell

EPIDEMIOLOGY
Incidence :

1.2 per 100,000 (Bombay)

3.7 per 100,000 (USA)
Age : 3 Peaks
- 20-40 yrs. Maximum
- 0 - 10 yrs.
- After - 60 yrs.

Bilaterality : 2 to 3% Testicular Tumour

CLASSIFICATION
I. Primary Neoplasma of Testis.
A. Germ Cell Tumour
B. Non-Germ Cell Tumour
II. Secondary Neoplasms.
III. Paratesticular Tumours.

I. PRIMARY NEOPLASMS OF TESTIS

A. Germinal Neoplasms : (90 - 95 %)
1. Seminomas - 40%
(a) Classic Typical Seminoma
(b) Anaplastic Seminoma
(c) Spermatocytic Seminoma
2. Embryonal Carcinoma - 20 - 25%
3. Teratoma - 25 - 35%
(a) Mature
(b) Immature
4. Choriocarcinoma - 1%
5. Yolk Sac Tumour

I. PRIMARY NEOPLASMS OF
TESTIS
B. Nongerminal Neoplasms : ( 5 to 10% )
1. Specialized gonadal stromal tumor
(a) Leydig cell tumor
(b) Other gonadal stromal tumor
2. Gonadoblastoma
3. Miscellaneous Neoplasms
(a) Adenocarcinoma of the rete testis
(b) Mesenchymal neoplasms
(c) Carcinoid
(d) Adrenal rest tumor

II. SECONDARY NEOPLASMS OF TESTIS

A. Reticuloendothelial Neoplasms
B. Metastases
III. PARATESTICULAR NEOPLASMS

A. Adenomatoid
B. Cystadenoma of Epididymis
C. Mesenchymal Neoplasms
D. Mesothelioma
E. Metastases

AETIOLOGY OF TESTICULAR
TUMOUR
1.

Cryptorchidism

2.

Carcinoma in situ

3.

Trauma

4.

Atrophy

CRYPTORCHIDISM & TESTICULAR

TUMOUR

Risk of Carcinoma
developing in
undescended testis is
14 to 48 times the normal
expected incidence

CRYPTORCHIDISM & TESTICULAR

TUMOUR

The cause for malignancy are as follows:

Abnormal Germ Cell Morphology
Elevated temperature in abdomen &
Inguinal region as opposed to scrotum
Endocrinal disturbances
Gonadal dysgenesis

Requirements for staging

To properly Stage Testicular Tumours following
are pre-requisites:
(a)Pathology of Tumour Specimen
(b)History
(c) Clinical Examination
(d)Radiological procedure - USG / CT /
Bone Scan
(e)Tumour Markers - HCG, AFP

MRI /

Investigation
1. Ultrasound - Hypoechoic area
2. Chest X-Ray - PA and lateral views
3. CT Scan
4. Tumour Markers
- AFP
- HCG
- LDH
- PLAP

CLINICAL FEATURES
Painless Swelling of One Gonad
Dull Ache or Heaviness in Lower Abdomen
10% - Acute Scrotal Pain
10% - Present with Metatstasis
- Neck Mass / Cough / Anorexia / Vomiting /
Back Ache/ Lower limb swelling
5% - Gynecomastia
Rarely - Infertility

Tumour Markers
TWO MAIN CLASSES
Onco-fetal Substances : AFP & HCG
Cellular Enzymes : LDH & PLAP
( AFP - Trophoblastic Cells
HCG - Syncytiotrophoblastic Cells )

AFP ( Alfafetoprotein )
NORMAL VALUE: Below 16 ngm / ml
HALF LIFE OF AFP 5 and 7 days
Raised AFP :
Pure embryonal carcinoma
Teratocarcinoma
Yolk sac Tumour
Combined Tumour

REMEMBER: AFP Not raised is Pure Choriocarcinoma or Pure Seminoma

HCG ( Human Chorionic

Gonadotropin )
Has and polypeptide chain
NORMAL VALUE: < 1 ng / ml
HALF LIFE of HCG: 24 to 36 hours
RAISED
100 % 60%
55%
25%
7%
-

HCG Choriocarcinoma
Embryonal carcinoma
Teratocarcinoma\
Yolk Cell Tumour
Seminomas

ROLE OF TUMOUR MARKERS

Helps in Diagnosis - 80 to 85% of Testicular
Tumours have Positive Markers
Most of Non-Seminomas have raised markers
Only 10 to 15% Non-Seminomas have normal
marker level
After Orchidectomy if Markers Elevated means
Residual Disease or Stage II or III Disease
Elevation of Markers after Lymphadenectomy means
a STAGE III Disease

ROLE OF TUMOUR MARKERS cont...

Degree of Marker Elevation Appears to be Directly
Proportional to Tumour Burden
Markers indicate Histology of Tumour:
If AFP elevated in Seminoma - Means Tumour has
Non-Seminomatous elements
Negative Tumour Markers becoming positive on follow
up usually indicates Recurrence of Tumour
Markers become Positive earlier than X-Ray studies

PRINCIPLES OF
TREATMENT
Treatment should be aimed at one stage above
the clinical stage
Seminomas Radiotherapy.

Radio-Sensitive.

Treat

with

Non-Seminomas are Radio-Resistant and best

treated by Surgery
Advanced Disease or Metastasis - Responds
well to Chemotherapy

CONCLUSION
Improved Overall Survival of Testicular
Tumour due to Better Understanding of
the Disease, Tumour Markers and Cisplatinum based Chemotherapy
Current Emphasis is on Diminishing
overall Morbidity of Various Treatment
Modalities

SEMINOMA

Terima Kasih