| What is hydrocele? | ➢ Most common cause of scrotal swelling
➢ Idiopathic or arise in response to neighboring infections or tumors
➢ Caused by an accumulation of serous fluid within the tunica vaginalis.
➢ The clear fluid of a hydrocele allows light to pass through (transluminescence), distinguishing it from collections of blood, pus, or lymph, all of which are cloudy or opaque.
➢ Accumulation of blood or lymphatic fluid within the tunica vaginalis, termed hematocele and chylocele, respectively, also may cause scrotal enlargement.
➢ In extreme cases of lymphatic obstruction, caused, for example, by filariasis, the scrotum and the lower extremities may enlarge to grotesque sizes—a condition termed elephantiasis |
| What is varicocele? | ➢ Common cause of male infertility
➢ Up to 20% of men and in 40% of infertile men
➢ Prominent dilation of the pampiniform plexus of veins
posterior to the testis
➢ Asymptomatic
➢ Palpation with the feel of “a bag of worms ”
➢ The increased blood flow makes this lesion a radiant heat
device that increases the temperature of testicular tubules,
inhibiting normal spermatogenesis |
| What is cryptorchidism? | ➢ Cryptorchidism is a failure of testicular descent into the scrotum.
➢ Normally, the testes descend from the abdominal cavity to the scrotum
during the last 2 months of intrauterine life.
➢ Diagnosis is only established with certainty after 1 year of age,
particularly in premature infants (testicular descent into the scrotum is
not always complete at birth).
➢ Undescended testes become atrophic
➢ It is Associated with a 3- to 5-fold increased risk for testicular cancer,
which arises from foci of germ cell neoplasia
➢ in-situ within the atrophic tubules.
➢ Microscopically, tubular atrophy begins to appear by 5 to 6 years of
age, and is usually advanced by the time of puberty.
➢ Early orchiopexy reduces the risk for sterility and cancer. |
| How is cryptorchidism and testicular atrophy? | ➢ Atrophic, small residual tubules with no spermatogenesis, and pale surrounding stroma.
➢ A cryptorchid testis fails to develop normal spermatogenesis unless placed in the scrotum, because deterioration leading to the appearance shown begins by age 2.
➢ If unilateral, spermatogenesis in the remaining normal testis may prevent infertility. Cryptorchidism carries an increased risk for testicular carcinoma in either testis.
➢ Leydig cells (not shown here) still retain their function. |
| What is testicular atrophy? | ➢ Atrophic changes similar to those in cryptorchid testes may be
caused by other insults :
o chronic ischemia
o Trauma
o irradiation
o anti-neoplastic chemotherapy
o conditions associated with chronically elevated estrogen levels (e.g.,
cirrhosis)
➢ Normal size early in life, but some degree of atrophy usually is
evident by the onset of puberty
➢ Microscopically, tubular atrophy begins to appear by 5 to 6 years of
age, and is usually advanced by the time of puberty |
| How is cryptorchidism and testicular cancer? | ➢ 3- to 5-fold increased risk for testicular cancer
➢ Patients with unilateral cryptorchidism also are at increased risk for
the development of cancer in the contralateral, normally descended
testis
➢ Some intrinsic abnormality, rather than simple failure of descent,
underlies the increased cancer risk
➢ Germ cell neoplasia in-situ may be present in cryptorchid testes and
is a likely precursor of subsequent germ cell tumors except in
Spermatocytic tumor
➢ Treatment : Surgical placement of the undescended testis into the
scrotum = Orchiopexy
➢ Recommended by 18 months of age to decrease the likelihood of
testicular atrophy, infertility, and testicular cancer |
| How is inflammatory lesions of testicles? | ➢ More common in the epididymis than in the testis proper
➢ Sexually transmitted infectious disorders
➢ Nonspecific epididymitis and orchitis, mumps, and TB
➢ Nonspecific epididymitis and orchitis :
usually begin as a primary urinary tract infection that spreads to the testis through the vas deferens or the lymphatics of the spermatic cord.
The involved testis is swollen and tender, and histologic examination reveals numerous neutrophils. |
| What are other types of inflammatory lesions of testicles ? | ➢ Mumps infection involving the testes : Rare in male children but occurs in roughly 20% of infected adults. Affected testes are edematous and congested, and contain a lymphoplasmacytic inflammatory infiltrate. Severe mumps orchitis may lead to extensive necrosis, loss of seminiferous epithelium, tubular atrophy, fibrosis, and sterility.
➢ Granulomatous inflammation : many causes of which TB is the
most common. Testis TB generally begins as an epididymitis, with secondary
involvement of the testis. Histologically, there is granulomatous inflammation and caseous necrosis identical to that seen in active TB in other sites |
| What are vascular diturbances of testicles? | ➢ Torsion, or twisting of the spermatic cord, typically results in obstruction of testicular venous drainage while leaving the thick-walled and more resilient arteries patent.
➢ This leads to intense vascular engorgement and infarction unless the torsion is relieved.
➢ There are two types of testicular torsion :
✓ Neonatal torsion
✓ Adult torsion |
| How is testicular torsions? | Neonatal torsion
➢ occurs either in utero or shortly after birth
➢ There is no associated anatomic defect to account for its occurrence.
Adult torsion
➢ Adolescence
➢ Sudden onset of testicular pain
➢ May even awaken the patient from sleep
➢ In contrast with neonatal torsion, adult torsion results from a bilateral congenital anomaly whereby the testis is abnormally anchored in the scrotal sac giving rise to increased mobility (bell clapper abnormality)
➢ Occurs without any inciting injury |
| How is tx of testicular torsions? | ➢ Immediate (within 6 hours) treatment by surgically untwisting and suturing the cord in place to prevent future torsion prevents infarction and loss of function
➢ Sometimes only the little appendix testis undergoes torsion, producing acute pain
➢ To prevent the catastrophic occurrence of torsion in the contralateral testis, the unaffected testis typically is surgically fixed within the scrotum |
| What are testicular neoplasms? | ➢ Occur in roughly 6 per 100,000 males.
➢ In the 15- to 34-year-old age group, when these neoplasms peak in incidence, they are the most common tumors in men.
➢ heterogeneous and include germ cell tumors and sex cord–stromal tumors.
➢ In postpubertal males, 95% of testicular tumors arise from germ cells, and almost all are malignant.
➢ By contrast, sex cord-stromal tumors derived from Sertoli or Leydig cells are uncommon and usually benign |
| How is epidemiology of testicular neoplasms? | ➢ More common in whites than in blacks
➢ Incidence has increased in white populations
➢ Cryptorchidism is associated with a 3- to 5-fold increase in the risk for cancer in the undescended testis, as well as an increased risk for cancer in the contralateral descended testis
➢ Family history is important, as brothers of males with germ cell tumors have an 8- to 10-fold increased risk.
➢ Extra copies of the short arm of chromosome 12, usually due to the presence of an isochromosome 12 [i(12p)], are found in virtually all germ cell tumors |
| How is pathogenesis of testicular neoplasms? | ➢ In addition to cryptorchidism Intersex syndromes, including androgen
insensitivity syndrome and gonadal dysgenesis, are also associated
with an increased frequency of testicular Kc.
➢ Brothers of males with germ cell tumors have an 8- to 10-fold
increased risk, presumably owing to inherited factors.
➢ The development of cancer in one testis also is associated with a
markedly increased risk for neoplasia in the contralateral testis.
➢ Extra copies of the short arm of chromosome 12, are found in
virtually all germ cell tumors.
➢ Point mutations that create oncogenes are relatively rare in germ cell
tumors, occurring at the lowest frequency of any solid tumor in adults.
➢ Among these are oncogenic mutations in KIT which are found in up
to 25% of tumor |
| How is pathogenesis of testicular cancer germ cell neoplasia? | ➢ Germ cell neoplasia in situ is a precursor lesion present in conditions
associated with a high risk for developing germ cell tumors
➢ GCN exhibits the same abnormality of chromosome 12 that is
characteristic of fully developed germ cell tumors.
➢ As might be expected, germ cell neoplasia in situ often is found in
“normal” testis adjacent to full-blown germ cell tumors.
➢ Testicular germ cell tumors are subclassified into seminomas and
nonseminomatous germ cell tumors
➢ Seminomas are most common, accounting for about 50% of Testicular
Germ Cell Neoplasm .
➢ They are histologically identical to tumors called dysgerminomas, which
occur in the ovary, and germinomas, which occur in the central nervous
system and other extragonadal sites. |
| What are neoplasms in situ? | ➢ Most testicular tumors in postpubertal males arise from germ
cell neoplasia in situ.
➢ This precursor lesion is present in conditions associated with a
high risk for developing germ cell tumors (e.g.,
cryptorchidism, dysgenetic gonads)
➢ Exhibits the same abnormality of chromosome 12 that is
characteristic of fully developed germ cell tumors.
➢ Often found in “normal” testis adjacent to full-blown germ cell
tumors. |
| What are germ cell tumors? | ➢ Subclassified into seminomas and nonseminomatous
➢ Seminomas remain confined to the testis for a long time and spread mainly to paraaortic nodes; distant spread is rare
➢ Nonseminomatous tumors tend to spread earlier, by both lymphatics and blood vessels
➢ Pure (Composed of a single histologic type)
➢ Mixed (seen in 40% of cases)
➢ Painless testicular mass
➢ Nontranslucent (unlike enlargements caused by hydroceles)
➢ Biopsy of a testicular neoplasm is associated with a risk for tumor spillage, which would necessitate excision of the scrotal skin in addition to orchiectomy
➢ Standard management of a solid testicular mass is radical orchiectomy, based on the presumption of malignancy |
| What is seminoma? | ➢ Most common
➢ 50% of testicular germ cell neoplasms
➢ Histologically identical to tumors called dysgerminomas, which occur in the ovary, and germinomas, which occur in the central nervous system and other extragonadal sites.
➢ Soft, well-demarcated
➢ Gray-white tumor that bulges from the cut surface of the affected testis
➢ Large tumors may contain foci of coagulative necrosis
➢ Usually without hemorrhage |
| How is seminoma morphology? | ➢ Large, uniform cells with distinct cell borders, clear, glycogen-rich cytoplasm, round nuclei, and conspicuous nucleoli
➢ Small lobules with intervening fibrous septa
➢ Lymphocytic infiltrate usually is present
➢ Granulomatous reaction
➢ 15% of cases, syncytiotrophoblasts are present – (elevated serum HCG)
➢ Often remain confined to the testis for long periods and may reach considerable size before diagnosis
➢ Metastases most commonly are encountered in the iliac and paraaortic lymph nodes, particularly in the upper lumbar region
➢ Hematogenous metastases occur late
➢ Sensitive to radiation and chemotherapy
➢ Good prognosis |
| What are spermatocytic seminoma? | ➢ Uncommon
➢ Older men
➢ Beyond 50 years of age
➢ Lack lymphocytic infiltrates, granulomas, and syncytiotrophoblasts
➢ Not admixed with other germ cell tumor histologies
➢ Not associated with germ cell neoplasia in-situ
➢ Do not metastasize
➢ Polygonal cells of variable size
➢ Arranged in nodules or sheets |
| What are non seminomatous tumors? | ➢ Tend to metastasize earlier, by lymphatic as well as hematogenous routes
➢ Hematogenous metastases are most common in the liver and lungs
➢ Metastatic lesions may be identical to the primary testicular tumor or may contain elements of other germ cell tumors |
| How is embryonal carcinoma? | ➢ Second most common
➢ Ill-defined, invasive
➢ Foci of hemorrhage and necrosis
➢ Small, even in patients with systemic metastases
➢ In most cases admixed with other germ cell tumors (e.g., yolk sac tumor, teratoma, choriocarcinoma)
➢ Pure embryonal carcinomas account for only 2% to 3% of all testicular germ cell tumors
➢ Large cells with large hyperchromatic nuclei
➢ Basophilic cytoplasm, indistinct cell borders, large nuclei, and prominent nucleoli
➢ Undifferentiated, solid sheets or may form primitive glandular structures and irregular papillae |
| What are yolk sac tumors? | ➢ Most common primary testicular neoplasm in children younger than 3 years of age
➢ In this age group, it has a very good prognosis
➢ In adults, yolk sac tumors most often are seen admixed with embryonal carcinoma
➢ Large and may be well demarcated
➢ Low cuboidal to columnar epithelial cells that form microcysts, lacelike (reticular) patterns, sheets, glands, and papillae
➢ A distinctive feature is the presence of structures resembling primitive glomeruli called schiller-duval bodies
➢ Often have eosinophilic hyaline globules containing α1-antitrypsin and alpha fetoprotein (AFP), which can be demonstrated by immunohistochemical techniques |
| How is choriocarcinoma? | ➢ Tumor in which the pluripotential neoplastic germ cells
differentiate into cells resembling placental trophoblasts
➢ Primary tumors often are small and nonpalpable, even in
patients with extensive metastatic disease
➢ Composed of sheets of small cuboidal cytotrophoblast like cells that are irregularly intermingled with or capped by large, eosinophilic syncytiotrophoblast like cells containing multiple dark, pleomorphic nuclei
➢ HCG can be identified in the syncytiotrophoblastic cells by immunohistochemical staining |
| How is teratoma? | ➢ They may occur at any age from infancy to adult life : Teratoma, postpubertal-type : Malignant tumor Teratoma, prepubertal-type : Almost always exhibits benign behaviour Teratoma, postpubertal-type
➢ Malignant germ cell tumour derived from germ cell neoplasia in situ (GCNIS) and composed of several tissue types arising from one or more germ layers (endoderm, mesoderm, and ectoderm).
➢ These tumors form firm masses that often contain cysts and recognizable areas of cartilage
➢ Pure forms of teratoma are fairly common in infants and children being second in frequency only to yolk sac tumors
➢ In adults, pure teratomas are rare, constituting 2% to 3% of germ cell tumors, and the remaining tumors are seen in combination with other histologic types |
| How is composition of teratoma? | ➢ Teratomas are composed of a heterogeneous, collection of differentiated cells or organoid structures,
➢ Such as neural tissue, muscle bundles, islands of cartilage, clusters of squamous epithelium, structures reminiscent of thyroid gland, bronchial epithelium, and bits of intestinal wall or brain substance,
➢ All embedded in a fibrous or myxoid stroma
➢ Elements may be mature (resembling various tissues within the adult) or immature (sharing histologic features with fetal or embryonal tissues)
➢ Regardless of whether they are composed of mature or immature elements, postpubertal males teratomas are malignant, being capable of metastasis. |
| How is teratoma with malignant transformations? | ➢ Rarely, non–germ cell tumors may arise in teratoma—a phenomenon referred to as teratoma with malignant transformation
➢ Such neoplasms include squamous cell carcinoma, adenocarcinoma, and various sarcomas
➢ These non–germ cell malignancies do not respond to therapies that are effective against metastatic germ cell tumors thus, the only hope for cure in such cases resides in surgical resection |
| What are tumor markers of testicular neoplasms? | ➢ Secreted by germ cell tumors
➢ Are helpful diagnostically and very valuable in following the response of tumors to therapy after the diagnosis
➢ HCG is always elevated in patients with choriocarcinoma and may be minimally elevated in individuals with other germ cell tumors containing syncytiotrophoblastic cells (seminoma)
➢ Increased AFP in the setting of a testicular neoplasm indicates a yolk sac tumor component
➢ The levels of lactate dehydrogenase (LDH) correlate with the tumor burden |
| How is therapy of testicular neoplasms? | ➢ Seminoma is extremely radiosensitive and tends to remain localized for long periods
➢ Has the best prognosis
➢ More than 95% of patients with early-stage disease can be cured
➢ Among nonseminomatous germ cell tumors, the histologic subtype does not influence the therapy
➢ Approximately 90% of patients achieve complete remission with aggressive chemotherapy, and most are cured
➢ The exception is choriocarcinoma, which is associated with a poorer prognosis |
| What is leydig cell tumors? | ➢ May elaborate androgens and in some cases both androgens and estrogens, and even corticosteroids.
➢ Any age, most cases between 20 and 60 years of age.
➢ Testicular swelling, gynecomastia may be the first symptom.
➢ In children, hormonal effects, manifested primarily as sexual precocity, are the dominant features.
➢ Circumscribed nodules, usually less than 5 cm in diameter.
➢ They have a distinctive golden brown, homogeneous cut surface.
➢ Approximately 10% of the tumors in adults are invasive and produce metastases; most are benign |
| How is morphology of leydig cell tumor? | ➢ Neoplastic Leydig cells have an appearance that is similar to their normal counterparts.
➢ Large in size, round or polygonal cell outlines, abundant granular eosinophilic cytoplasm, and a round central nucleus.
➢ Nests and clusters
➢ The cytoplasm frequently contains lipid droplets, vacuoles, or lipofuscin pigment, and, most characteristically, rod-shaped crystalloids of Reinke, (25% of the tumors).
➢ Many intervening capillaries, typical of endocrine tissue |
| How are sertoli cell tumors? | ➢ Most Sertoli cell tumors are hormonally silent and present as a testicular mass.
➢ These neoplasms appear as firm, small nodules with a homogeneous gray-white to yellow cut surface.
➢ Histologically the tumor cells are arranged in distinctive trabeculae that tend to form cordlike structures and tubules.
➢ Most are benign, but about 10% pursue a malignant course. |
| What are gonadoblastoma? | ➢ Gonadoblastomas are rare neoplasms.
➢ In situ form of malignant germ cell tumour consisting of germ cell neoplasia in situ (GCNIS), seminoma, or dysgerminoma cells, and incompletely differentiated sex cord cells reminiscent of Sertoli or granulosa cells.
➢ In some cases the germ cell component becomes malignant, giving rise to seminoma. |
| What are testicular lymphomas? | ➢ Aggressive non–Hodgkin lymphomas account for 5% of testicular neoplasms.
➢ The most common form of testicular neoplasms in men older than age 60 years.
➢ Affected patients may present with only a testicular mass, mimicking other, more common, testicular tumors.
➢ In most cases, the disease is already disseminated at the time of detection.
➢ The most common testicular lymphomas, in decreasing order of frequency, DLBCL, Burkitt, and EBV-positive extranodal NK/T cell lymphoma.
➢ Testicular lymphomas have a higher propensity for central nervous system involvement than do similar tumors arising at other sites.
➢ With all testicular tumors, recurrences, typically in the form of distant metastases, usually occur within the first 2 years after treatment |
