TESTICULAR TUMORSNILOY SHARMA SHUVO

Faridpur medical college, Bangladesh

Topics

Introduction Etiology Classification Pathophysiology Clinical Feature Investigation Differential Diagnosis Treatment

Introduction

Although rare, is the most common malignancy in men in 15-35 yr age group

Delayed diagnosis Has become one of the most curable

solid tumour Associated with accurate tumour markers Origin in germ cells Capacity to differentiate into histologically

more benign forms Predictable, systematic pattern of spread Occurrence in young individuals

What is Testicular Tumour

Cancer of the testicles, also known as testicular cancer, is one of the less common cancers. It usually affects younger men between the ages of 15 and 49. The most common symptom is a painless lump or swelling in the testicles.

Etiology

 The exact cause of most cases of testicular tumour is not known.

Congenital Causes: Cryptorchidism Klinefelter’s syndrome

Age: 20-35 years highest risk group Hormones

Maternal hormone ingestion during pregnancy History of mumps orchitis, inguinal hernia, hydrocele

in childhood - Atrophy High socioeconomic status Testicular cancer contralateral testis HIV positive.

Classification

I. Primary Neoplasma of Testis A.Germ Cell Tumour (90-95%) B.Non-Germ Cell Tumour (5-10%) II. Secondary Neoplasms.

III. Paratesticular Tumours.

PRIMARY NEOPLASMS OF TESTIS

Germinal Neoplasms : (90 - 95 %)

Seminomas - 40% (a) Classic Typical Seminoma (b) Anaplastic Seminoma (c) Spermatocytic Seminoma Teratoma - 25 - 35% (a) Mature (b) Immature Embryonal Carcinoma - 20 - 25% Choriocarcinoma - 1% Yolk Sac Tumour

Nongerminal Neoplasms : ( 5 to 10% )

Specialized gonadal stromal tumor (a) Leydig cell tumor (b) Sertoli’s cell tumour (c) Granulosa cell tumour (b) Other gonadal stromal tumor Gonadoblastoma Miscellaneous Neoplasms (a) Adenocarcinoma of the rete

testis (b) Mesenchymal neoplasms (c) Carcinoid

SEMINOMA Typical : 82-85%

ThirtiesSlow growth

Anaplastic: 5-10%More aggressive, potentially more lethalGreater metastatic potential

Spermatocytic Seminoma: 2-12 %Cells closely resemble different phases of maturing spermatogoniaB/L tumours have been reportedExtremely low metastatic potentialFavourable prognosis

Seminoma

Teratoma

Contains more than one germ cell layers in various stages of maturation and differentiation

Grosssly large, lobulated, nonhomogenous tumours

Microscopically, cystic & solid componenets

Pathophysiology

The malignant transformation of carcinoma in situ is characterised by growth beyond the basement membrane, eventually replacing most of the testicular parenchyma. Spontaneous regression is rare; therefore, any growth of the testis should be regarded as malignant and managed accordingly. The tunica albugenia is a natural barrier to local metastasis so it should not be compromised by direct diagnostic scrotal needle biopsy.

Pathophysiology

Lymphatic spread is the most common cause of metastasis and commonly occurs through spermatic cord lymphatics to the retroperitoneal lymph node chain. One exception is pure choriocarcinoma, which may disseminate more frequently through vascular invasion. On rare occasions a direct communication exists between testicular lymphatics and the thoracic duct, causing a thoracic (sternal) metastasis without retroperitoneal involvement. Scrotal invasion may present with inguinal metastasis. Germ cell cancers may also present with extranodal distant metastasis following direct vascular invasion or tumour embolisation through lymphatico-venous communications. This accounts for most regional treatment failures despite radical orchiectomy and retroperitoneal surgical clearance.

Pathophysiology

Non-seminoma doubling time ranges from 10 to 30 days. This is reflected by alterations in the serum tumour markers. Most treatment failure cases followed by mortality occur within the first 2 to 3 years of diagnosis. Seminoma usually has a much slower doubling time and may recur 2 to 10 years after initial treatment because of its indolent course. Based on the natural history of the disease, curability after multimodality treatment regimens is often declared after 5 years. However, relapse has been reported 10 years after treatment.

CLINICAL FEATURES

Nodule/Painless Swelling of One Gonad Dull Ache or Heaviness in Lower

Abdomen 10% - Acute Scrotal Pain 10% - Present with Metatstasis

- Neck Mass / Cough / Anorexia / Back Ache

5% - Gynecomastia Infertility

Investigation

Ultrasound - Hypoechoic area Chest X-Ray - PA and lateral views CT Scan MRI 4. Tumour Markers - AFP - HCG - LDH - PLAP(placental alkaline

phosphatase)

Staging of testicular tumour

Stage 1-Testis lesion-No spread Stage 2-Nodes below the Diaphragm only Stage 3-Nodes above the diaphragm Stage 4-Pulmonary or Hepatic metastases

Differential Diagnosis

Torsion Epididymitis Epididimo-orchitis Hydrocele Hernia Haematoma Spermatocele Syphilitic gumma

Treatment

Staging is an essential step in planning treatment Blood is collected to enable the levels of tumours

markers (HCG,Alpha fetoprotein and LDH) to be measured. Tumour marker level can be used to monitor the response to treatment.

A chest radiograph shows whether there are pulmonary deposit.

Orchidectomy is essential to remove the primary tumour and to obtain histology

Computerised tomography (CT) and MRI are the most useful means of detecting secondary and for monitoring the response to therapy

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