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• Testicular tumors


  Most common cause of firm painless enlargement of the testis
• Causes of increased risk of testicular cancer


  • Cryptorchidism
  • Testicular feminization
  • Klinefelter syndrome
  • Having a sibling with testicular cancer
  • Development of cancer in one testis increases risk in the other
• Testicular tumors are more common in white people than blacks
• Major histogenetic groups of testicular tumors


  • Germ cell tumors (>90%)
  • Gonadal stromal/sex cord tumors
• Seminoma


  Neoplastic primitive germ cells may differentiate along the gonadal lines
• Embryonal carcinoma


  Primitive germ cells transform into totipotential cells which largely remain undifferentiated
• Yolk sac tumor


  Totipotential cells may differentiate into extraembryonic cell lines
• Choriocarcinoma


  Differentiation of pluripotential neoplastic germ cells along trophoplastic lines
• Teratoma


  Totipotential cells may differentiate along the somatic cell lines
• Classic seminoma


  • About 90% of all seminomas
  • Solid, gray-white, poorly demarcated growth that bulges from the cut surface of the testis
  • May replace the entire testis in more than half of cases
  • Histologically: solid nests of proliferating tumor cells with lymphocytic infiltration
  • 5-year survival with radiotherapy is 85-90%
• Spermatocytic seminoma


  • About 5% of all seminomas
  • Arises in older patients (>50 years)
  • Variable size up to 15cm
  • Poorly demarcated, soft yellow-gray, gelatinous with small cystic areas
  • Histologically: 3 cell populations - small, intermediate, and scattered large cells
  • Lack the lymphocytic infiltration characteristic of classic seminoma
• Seminomas may reach a large size and show late metastases by lymphatic spread, while other germ cell tumors show early metastases even without a palpable testicular lesion, by both lymphatic and hematogenous routes
• Hematogenous metastases of testicular tumors are most common to the liver and the lung
• Seminoma


  • Most common type
  • Occurs in young men
  • Curable
  • Arises from sperm producing cells
  • Several histologic types
  • Lymphocytic infiltration
  • No production of Beta-HCG or Alpha-fetoprotein
• Anaplastic seminoma


  • About 5% of all seminomas
  • More marked nuclear pleomorphism and increased mitoses
  • Tends to be at a higher stage at diagnosis than classic seminoma
• Embryonal carcinoma


  • Second most common testicular germ cell tumor (15-35%)
  • Occurs between 20-35 years
  • Ill-defined invasive masses with foci of hemorrhage and necrosis
  • Primary lesion is small even with systemic metastases
  • Histologically: large, primitive cells with basophilic cytoplasm, often mixed with other germ cell tumor elements
  • Cure rate with chemotherapy is 95-98%
• Yolk sac tumor


  • Most common primary testicular neoplasm in children <3 years
  • In adults, mostly seen mixed with embryonal carcinoma
  • Grossly: typically large and well-demarcated
  • Histologically: cuboidal/columnar epithelial cells forming sheets, glands, papillae, and microcysts with eosinophilic hyaline globules and Schiller-Duvall bodies
  • Alpha-fetoprotein positive
• Choriocarcinoma


  • Grossly: very small, nonpalpable lesions even with extensive metastases
  • Histologically: sheets of small cuboidal cells with large eosinophilic syncytial cells (cytotrophoblasts and syncytiotrophoblasts)
  • No well-formed placental villi
  • Beta-HCG positive
• Variants of pure teratoma


  • Mature teratoma
  • Immature teratoma
  • Teratoma with malignant transformation
• Mature teratoma


  • Contains fully differentiated tissues from one or more germ cell layers in a haphazard array
• Immature teratoma


  • Contains immature somatic elements resembling developing fetal tissue
• Teratoma with malignant transformation


  • Develops frank malignancy in preexisting teratomatous elements, such as squamous cell carcinoma or adenocarcinoma
  • Most common in adult patients, while pure teratomas in prepubertal males are usually benign
• Leydig cell tumor


  • Rare neoplasm arising from interstitial Leydig cells
  • Functionally active, secreting testosterone or estrogen or both
  • Occurs in boys >4 years and men in 3rd-6th decades
  • May cause precocious puberty or feminization
  • Cured by orchiectomy
• Sertoli cell tumor


  • Less frequent than Leydig cell tumor
  • 20% are malignant
  • Cured by orchiectomy
• Prostatitis


  Inflammation of the prostate, may be acute or chronic, manifested by dysuria, urinary frequency, and lower back pain
• Diagnosis of prostatitis


  1. Clinical feature

  2. Microscopic exam

  3. Culture of urine specimen before and after prostatic massage
• Acute prostatitis


  • Most commonly associated with LUTI such as urethrocysitis caused by E. coli and other G-ve organisms
  • Organisms may reach the prostate by either direct extension or by vascular channels from more distant sites
• Microscopically, acute prostatitis is characterized by acute neutrophilic infiltration with stromal congestion and edema, with destruction of the glandular epithelium and microabscess formation in severe infection
• Grossly, visible abscesses are uncommon in acute prostatitis but may develop in extensive tissue destruction, as in patients with DM
• Chronic prostatitis


  Follows recurrent episodes of acute prostatitis, with an increase in leukocytes in prostatic secretion but negative bacteriological culture, caused by non-bacterial agents such as Chlamydia trachomatis
• Microscopically, chronic prostatitis shows acute inflammatory changes with lymphoid infiltration, more glandular tissue destruction, and fibroblast proliferation
• Chronic granulomatous prostatitis


  • Associated with systemic inflammatory processes such as disseminated TB, fungal infection, sarcoidosis, Wegener granulomatosis
• Benign prostatic hyperplasia (BPH)


  Prostatic parenchyma consists of glandular and stromal elements, divided into specific regions, with most hyperplastic lesions arising in the inner transitional and central zones, while most carcinomas arise in the peripheral zones
• Benign prostatic hyperplasia (BPH) is not a precursor or risk factor for prostate cancer
• Pathogenesis of BPH


  • Estrogens and androgens have both been implicated, with androgens playing a permissive role, and inhibitors of 5α-reductase (which converts testosterone to dihydrotestosterone) being effective in management
  • Elevated prostate dihydrotestosterone concentrations, increased 5 alpha-reductase activity, and prostate atrophy following castration suggest a significant role for dihydrotestosterone
  • An increasing plasma estrogen/testosterone ratio with age, and the presence of estrogen receptors in the prostatic stroma, indicate that estrogen may also be involved

  
• Clinical features of BPH


  • Increased bladder outlet resistance
  • Lower urinary tract symptoms (LUTS) including obstructive symptoms (hesitancy, intermittent stream, straining) and urinary bladder irritation symptoms (frequency, urgency, urge incontinence)
  • Urinary retention (acute or chronic)
• Diagnosis of BPH


  1. Clinical history

  2. Physical examination (including digital rectal exam, assessment of bladder)

  3. Laboratory tests (urinalysis, PSA)

  4. Imaging (to rule out other causes of LUTS)
• Gross description of BPH: Variably sized nodules with a gray to yellow color and a granular appearance bulge above the cut surface of a prostate section
• Microscopically, BPH is characterized by epithelial hyperplasia with nodular lesions composed of variably sized glandular structures, glandular dilatation with papillary infoldings and cysts, and stromal nodules composed of bland spindle cells