Pathology Of Testes

1. Congenital

   1. absence

   2. synorchism, fusion of testes

   3. cryptorchidism, undescended testis. This could be unilateral or bilateral, but usually is unilateral. Until puberty, a man would not notice any problems. After puberty, undescended testis become fibrotic and atrophic. This also puts a man in risk for developing testicular malignancy later on in life.

   4. Atrophy (could be associated with chromosomal abnormalities), most commonly Kleinfelter’s Syndrome (XXY).

2. Inflammation, usually more common in epidydimus than in testis.

   1. gonorrhea, TB, inflammation in epidydimus (epidydimitis) first.

   2. syphilis, inflammation would actually affect testis first (orchitis)

   3. granulomatous orchitis (inflammation of testis) as a result of trauma (sperm flows out of the tubules into intersitum, setting up inflammatory reaction)

Vascular disturbances: torsion of sermaticord as a result of trauma, for example, will cut off venous drainage, resulting in congestion, and eventually in venous (hemorrhagic) infarct—this is an emergency.

3. Tumors

I. Germ cell tumors (95%)

A. Seminomas

These are the most common type of testicular tumors (50% of all tumors). They generally present as a painless testicular enlargement, arise in young men (peak incidence at age 30, with the exception of spermatocytic seminomas), are aggressive and spread both lymphatically (early) and hematogenously (late). However, they remain confined to the testes for a long time and are usually radiosensitive and fairly curable. There are three histologic types:

1)Classical—these consist of uniform-looking cells divided by fibrous stroma and increased lymphocyte response. The tumors are generally very radiosensitive and have a good prognosis.

2)Anaplastic—these are poorly differentiated and less uniform, with a prognosis that’s worse than that of typical seminoma.

3)Spermatocytic—this tumor is distinct in that its peak age of incidence is over 65 years and also because it is slow growing and histologically different from other seminomas, with very few metastases and excellent prognosis.

It is also important to note that pure seminomas are HCG and AFP negative (this will probably be tested in pathology, CPP, and perhaps on boards)

B.Non-seminomas (NSGST)

These tumors are different from seminomas in their cells of origin and prognosis. They metastasize much earlier, mostly by blood and are relatively radioresistant. There are various subtypes of non-seminomas, and most commonly, several different subtypes coexist within the same tumor, with the prognosis being determined by the prognosis of the most aggressive and treatment-resistant entity. If a seminoma and a non-seminoma are mixed in the same tumor, the prognosis will be determined by the seminoma.

1)Embryonal Carcinoma—these tumors occur mostly in 20-30 year olds and are more aggressive than seminomas. The tumor does not replace the testes and is poorly circumscribed and hemorrhagic. The tumor contains both HCG+ and AFP+ cells.

2)Yolk Sac Tumor—this is also known as infantile embryonal carcinoma and is the most common testicular tumor in boys under 3 years of age. In adults, pure forms of yolk sac tumor are rare, but elements of this tumor may be present within an adult embryonal carcinoma. The yolk sac tumor produces AFP exclusively and has a very good prognosis.

3)Choriocarcinoma—this is a highly malignant and rare tumor composed of both cytotrophoblast and syncytiotrophoblast. Rarely occurring on its own, nests of this tumor are common in mixed patterns. The choriocarcinoma cells produce HCG.

4)Teratoma—teratomas are an interesting group because these tumors are comprised of cells which are differentiated towards various organ lineages, such as bone, skin or nervous tissue, which can all be present in one tumor. They can occur at any age, with pure teratomas being more common in children. The teratomas can be mature, or well differentiated, or immature, or poorly differentiated. The mature teratomas occur more commonly in children are mostly benign, while the immature variant is more common in adults and have the potential for malignant transformation.

II. Non germ cell tumors (5%)

These originate from the non-germ cell components of the testes, which include Sertoli and Leydig cell tumors and lymphoma of the testes.

Sertoli cell—these are mostly benign and rarely secrete enough androgens to produce any morphological signs.

Leydig cell­—these mostly occur between ages 20-60 and usually present with testicular swelling. However, the tumor produces androgens which can then be converted to estrogens in the periphery, so gynecomastia might be the presenting complaint. Most of these tumors are benign.

Testicular lymphoma—the lymphomas constitute the most common form of testicular cancer in men over 60. The testicular tumor is usually part of disseminated disease and has a very poor prognosis.

Miscellaneous

The tunica vaginalis, a two-layered peritoneal remnant which surrounds the testes and can also be involved in some pathological states.

Hydrocele—this refers to accumulation of fluid between the layers of the tunica as a result of trauma, inflammation or for unknown reasons. The transillumination of the scrotum will show clear fluid with shadow of the testicle inside.

Hematocele—same as above, but in this case, the fluid is blood. This happens as a result of trauma or torsion.

Chylocele—accumulation of lymph in the tunica secondary to lymphatic obstruction.

Spermatocele—cystic accumulation of semen in the tunica.

Vericocele—a dilated vein in the spermatic cord, feels like a bag of worms, results from venous congestion. If found on the right, can be a presenting symptom of right renal carcinoma invading inferior vena cava (remember, right gonadal vein flows directly into IVC. Therefore, if there is a tumor blocking the inflow from the right testicular vein, this points to a right renal carcinoma).

Category: Pathology Notes