OS 215: Reproduction and Hormonal Regulation
Lec No. 2 Male Urologic Pathology
5
September 19, 2013
Dr. Karen Damian
OUTLINE
I. Penis
A. Penile Congenital Anomalies
B. Inflammation
C. Tumors of the Penis
II. Testis and Epididymis
A. Congenital Anomalies
B. Regression Changes
C. Testicular Inflammation
D. Vascular Changes
E. Spermatic Cord Tumors
F. Other Scrotal Swellings
G. Testicular Tumors
I. PENIS
A. PENILE CONGENITAL ANOMALIES
Most are extremely rare malformations of the urethral groove.

URETHRAL GROOVE MALFORMATION
 Associated with:
o failure of testicular descent
o malformation of urinary tract: constrictions with functional
obstruction (may be physiologic or hormonal, etc.)
o ascending urinary infection
o secondary sterility - complication
BENIGN TUMOR: CONDYLOMA ACUMINATUM
 papillary, keratinizing lesion caused by sexually transmitted HPV
types 6 and 11
 sexually transmitted
 aka genital warts/penile warts
 GROSS: Presents as warty exophytic (grows outward)/polyploid
or sessile (no stalk) lesions occurring on mucocutaneous areas,
external genitalia, perianal areas (scrotum, prepuce, etc.),
sometimes generalized up to several mm in diameter
 HISTO:
o koilocytosis – koilocytes are squamous epithelial cells, with
nuclear enlargement with a sunken or raisinoid appearance,
nucleus rimmed by clear cytoplasm and thickened membrane
o Hyperkeratosis
o Acanthosis / epidermal hyperplasia - stratified squamous
epithelium grow inwards or downwards without breaking
basement membrane
o Orderly maturation of epithelium, hence benign
URETHRAL GROOVE MALFORMATION: HYPOSPADIA
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urethral opening on the ventral surface
occurs 1 in 300 live male births (more common than epispadias)
results from the failure of fusion of the urethral folds
CLINICAL SIGNIFICANCE: urethral opening is constricted
resulting in urinary tract obstruction and risk for ascending urinary
tract infections
 CLINICAL SIGNIFICANCE: when the orifices are found near the
base of the penis, normal ejaculation and insemination may be
hampered or totally blocked causing sterility
URETHRAL GROOVE MALFORMATION: EPISPADIA
 abnormal opening of the urethra into the dorsal surface of the
penis
 a form of extrophy (failure of fusion of pubic bones so that the
bladder protrudes) of the urinary bladder
 less common than hypospadias
PHIMOSIS
 constricted prepuceal orifice prevents retraction of prepuce
over the corona
 frequently caused by repeated infection (in the foreskin) that
causes scarring, also due to anomalous development
 Interferes with hygiene infection and
scarring
(usu. A
complication of uncircumcised patients; bacteria entrapped in the
smegma)
 Interferes with hygiene because of constricted nature, smegma
entrapped, hence causing secondary infection. If left untreated it
can cause, scarring
 allows accumulation of secretions or debris under foreskin
(smegma), allowing secondary infection and possible squamous
cell carcinoma
 Paraphimosis – acute urinary retention and pain; tight prepuce of
the phimosis is forcibly retracted over the glans of the penis
causing constriction and edema (and even gangrene) behind the
glans penis
B. INFLAMMATION
 Specific – usually due to STD
o Syphilis, gonorrhea, chancroid, herpes, granuloma inguinale
 Non-specific
o Balanoposthitis – infection of the glans and prepuce
o C. albicans, anaerobes, Gardnerella, pyogenic bacteria
o Poor hygiene, uncircumcised males
 Accumulations of smegma secondary phimosis (acquired)
Figure 1. Condyloma Acuminatum
Branching, villous, papillary connective tissue stroma with thickening of
squamous epithelia, hyperkeratosis, and acanthosis (rete ridges). Viral
bodies (w/ koilocytic changes) are also present.
PREMALIGNANT LESION: CARCINOMA IN SITU (CIS)
 Cytologically malignant cells confined to the epithelium, no
orderly maturation, no local invasion, no break in the basement
membrane,
 seen as cells with dysplastic changes and disorganized
pleomorphism
 ETIOLOGIC AGENT: HPV 16 in 80% of cases of CIS
 May involve into an invasive malignancy
 2 lesions displaying histologic features of CIS (Bowen’s disease,
Bowenoid papulosis)
Table 1. Bowen’s Disease and Bowenoid’s Papulosis
BOWEN’S DISEASE
BOWENOID PAPULOSIS
GROSS: Multiple red> 35yo
GROSS: solitary, thickened,
brown popular lesions
gray-white opaque papule/plaque
seen
Sexually active young
on the penile shaft, sometimes
adults
HISTO: same as Bowen
on scrotal skin, may also appear
(distinguished from
shiny red and velvety on the
Bowen by gross)
glans and prepuce
HISTO: epidermal proliferation
with mitosis, dysplasia, no
invasive CA
maturation. Intact BM
Spontaneous
regression in most
10%
cases
Associated with visceral
malignancies (colon and breast
CA) in 1/3 of cases
C. TUMORS OF THE PENIS
 uncommon
 carcinomas predominate
 Benign > pre-malignant > malignant
MAC, THEA, LARIE
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Urologic Pathology (Lecture)
OS 215
CLINICAL FEATURES OF CARCINOMA
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Figure 2. Premalignant Lesion
There is proliferation and numerous mitoses, some atypical, of the
epidermis. Cells are also markedly dysplastic with large hyperchromatic
nuclei and lack of orderly maturation but with a sharp delineated dermalepidermal border and basement membrane.
slow growing
locally invasive
non painful until there is ulceration and infection
prognosis – stage of CA
I. TESTIS AND EPIDIDYMIS
 Involves
o Congenital anomalies o Regressive changes
o Inflammation
o Vascular Disorders
o Neoplasms
A. CONGENITAL ANOMALIES
 Extremely rare except for disorders of descent:
o Synorchism- fusion of testes
o Aplasia- no testes
o Cryptorchidism – undescended testis
CRYPTORCHIDISM
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Figure 3. Bowen Disease & Bowenoid Papulosis
MALIGNANT: CARCINOMA
 Uncommon
 Circumcision confers protection (better hygiene, reduced exposure
from carcinogens, decreases infection from oncogenic HPV)
 HPV 16, 18 in 50% of cases
 Smoking increases risk
 Squamous Cell Carcinoma and Verrucous Carcinoma
 SQUAMOUS CELL CARCINOMA
o Most common malignancy of the penis
o Disease of older men (40-70 years old)
o Smoking is a risk factor in its development
o Can involve the entire organ (Usual sites: glans, prepuces,
coronal sulcus)
o GROSS:
o Papillary lesions-fungating cauliflower like
o Flat lesions - ulceration, thickened patch, mucosal fissuring
o HISTO: well differentiated (islands of squamous cells, onion-skin
keratin pearls; intercellular bridges; invading the stroma)
o CLINICAL COURSE: painless, slow-growing
o Inguinal lymph node metastasis
o Distant metastasis is rare
o 66% 5-yr survival rate in early lesions (w/o lymph node
metastasis)
o 27% 5-yr survival rate if with LNM (lymph node metastasis)
 VERRUCOUS CARCINOMA
o Solitary, bulky and large exophytic mass
o Locally invasive and recurrent but does not metastasize
o Very well differentiated often benign-looking squamous cells
 May be confused with condyloma acuminata
o aka Giant condyloma of Butschke and Lowenstein
o How to differentiate it with squamous cell CA histologically?
Borders are bulging to the stroma unlike in squamous cell CA
where borders are invasive
Mac, Thea, Larie

 Undescended testis (complete or incomplete failure of intraabdominal testes to descend into the scrotal sac)
 One or both of the testes is/are undescended in the scrotal sac
 Affects 0.8% of the general male population, greater incidence in
in 1 yr old boys – 1% (allow appropriate time for descent)
 Unilateral in most cases, 25% present bilaterally
Most often are isolated cases but may accompany other
genitourinary defects like hypospadias
Frequent sites of arrest: intra-abdominal and inguinal
CAUSES or ASSOCIATIONS:
o Mostly idiopathic
o Other genetic abnormalities like trisomy 13 or Patau Syndrome
o Hormonal factors (remember that testosterone is responsible for
descent)
GROSS:
o Atrophic testes
o Appear small and fibrotic
HISTOLOGY:
o Testicular atrophy: small and fibrotic
o Maturation arrest of germ cells
o marked hyalinization and thickening of the basement membrane
o increase in stroma
o Leydig cells appear prominent (only because of the paucity of
the germ cells)
o Histologic changes appear at two years of age
COMPLICATIONS:
o Inguinal hernia in 10-20% of cases
o Sterility: Contralateral descended testes may also show paucity
of germ cells (atrophy)  results to sterility bec of no viable
germ cells on both testes
o If undescended testes is located in inguinal canal, it is more
o susceptible to trauma prone to crushing against ligaments and
bones
o Increased risk of testicular tumors (5-10x)
 TREATMENT:
o Orchiopexy by 2 years age – involves putting the testes into the
scrotal sac
o Must be done before two years of age if you want to improve
fertility
B. REGRESSION CHANGES
TESTICULAR ATROPHY
 Regressive changes that affect the scrotal testes
 CAUSES
o Cryptorchidism
o Vascular disease – atherosclerotic narrowing of testicular
arteries
o Hypopituitarism - decreased hormonal stimulation of testis
o End-stage orchitis - persistent infection in epididymis and testis
o Malnutrition or cachexia
o Irradiation (persistent exposure to radiation)
o Prolonged exposure to anti-androgens (homosexuals taking
estrogen therapy are at a higher risk)
o Exhaustion atrophy due to persistent stimulation by FSH
o Primary failure of genetic origin (Klinefelter syndrome)
 GROSS and HISTOLOGY: similar to atrophic cryptorchid testes
(see cryptorchidism)
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Urologic Pathology (Lecture)
Figure 4. Testicular Atrophy
Peritubular and interstitial fibrosis of the testis. On gross appearance,
appears small. Ideally, all stages if germ cell maturation can be seen.
However, in atrophic testes, not all stages can be seen (some only have
primordial germ cells left). In the normal testis, spermatids can be seen.
Also the Leydig cells are prominent as compared to non-prominent
Leydig cells in a normal testis.
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o Neonatal torsion
o Occurs in utero or shortly after birth;
o Absence of anatomic defect that accounts for its occurrence
o
Idiopathic
o Adult torsion
 Appears in adolescence

May occur even without previous injury
 Bilateral anatomic defect where the testis has increased
mobility (usually caused by bell-clapper abnormality –
defective or loose attachment of spermatic cord to tunica
vaginalis; very mobile testishigh tendency to twist)
 Morphology:
o Congestions
o Extreme Hemorrhagic infarctions in all layers
o Necrosis – no more blood supply
C. TESTICULAR INFLAMMATION
 More common in the epididymis
 Begins as epididymitis then with direct extension to the testes
(epididymoorchitis), e.g. TB, gonorrhea
NON-SPECIFIC INFECTION
 Associated with urinary tract infection via the vas deferens or
via the lymphatic route
 In children and the elderly: predominated by Gram (-) rods
 Sexually active young adults (<35): sexually transmitted
(Chlamydia. N. gonorrhea)
 Adults >35 yo: predominated by E. coli and Pseudomonas
 HISTOLOGY:
o Non-specific acute inflammation with predominance of
neutrophils
o Abscess formation – neutrophils or PMNs
o Suppurative necrosis
o Congestion, edema
o Fibrous scarring – if there is repeated infection present
 COMPLICATIONS: Sterility
SPECIFIC INFECTION
 Associated with infections of the genital tract (posterior urethra,
prostate, etc.)
 Gonorrhea
o infection via extension from posterior urethra, prostate, seminal
vesicles to the epididymis
o neglected gonococcal infection
o Abscess formation in the in the epididymis which may lead to its
destruction
o Spread to the testis will produce suppurative orchitis
 Mumps orchitis
o Systemic viral disease
o Uncommon in childhood mumps
o Occurs in 20-30% of post-pubertal cases of mumps
o Manifests one week after parotid swelling
o Unilateral 70% of the time
o HISTOLOGY:
Lymphoplasmocytic
patchy
interstitial
infiltration (nonspecific feature) – where lymphocytes and
plasma cells diffuse
 Tuberculous epididymo-orchitis
o Secondary spread from other genitor-urinary tract TB
o HISTOLOGY: Caseating granulomata
 Syphilitic orchitis
o Involves the testis at the onset, NOT accompanied by
epididymitis
o Tertiary and congenital syphilis
o HISTO: Diffuse lymphoplasmocytic infiltrate, gummatous
inflammation
o May lead to the production of gummas or diffuse interstitial
inflammation characterized by edema and lymphocytic and
plasma cell infiltration
D. VASCULAR DISEASES
Testicular torsion – a urologic emergency
 Twisting of the spermatic cord and vessels lead to hemorrhagic
infarction of the testis and your epididymis
 Sudden onset of intense pain
 Two types:
Mac, Thea, Larie
Figure 5. Adult testicular Torsion
E. SPERMATIC CORD/PARATESTICULAR TUMORS
 Lipoma
o Most common in the proximal spermatic cord, probably
represents retroperitoneal fat that has been pulled into
(entrapment) the inguinal canal along with the hernia sac
o Not true neoplasm/tumor
 Adenomatoid
o Most common benign paratesticular tumor - adjacent to testis
not within
o Mesothelial; small nodules in the upper pole of epididymis
 Malignant Paratesticular Tumors
o Rhabdomyosarcoma (children)

Most common malignant paratesticular tumor at the distal end
of the spermatic cord in children
o Liposarcoma (adult)
 Most common malignant paratesticular tumor at the distal end
of the spermatic cord in adults
F. TESTICULAR TUMORS
 Divided into two categories: germ cell tumors and sex cordstromal tumors
 Most common are mixed germ cell tumors
 95% of the tumors found in the testis are malignant germ cell
tumors
 Sex cord-stromal tumors are benign but secrete steroids
GERM CELL TUMORS
 Risk Factors
o Cryptorchidism: most important RF
o 10% of germ cell tumors
o Intratubular germ cell neoplasia – develops when dormant
atypical cells in a cryptorchid testis are stimulated by
carcinogens
o higher the location, greater risk
o Genetic factors
o Familial clustering without a defined mode of inheritance
o Father and sons- 4x higher than normal
o Siblings of affected individuals- 8-10x at risk
o Testicular dysgenesis syndrome
 Includes cryptorchidism, hypospadias, poor sperm quality
 May be influenced by in utero exposures to pesticide and nonsteroidal estrogens
 Clinical Features
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Urologic Pathology (Lecture)
o Painless testicular enlargement
o Lymphatic spread - retroperitoneal para-aortic first to be
affected/involved  mediastinal LN  supraclavicular LN
(ascends upward)
o Hematogenous spread - lungs, liver, brain, bones
o Seminomas: through LN Metastasis
o NSGCTS- hematogenous spread, metastasizes earlier
Table 2 Seminoma versus NSGCTS
Seminoma
70 % Stage1 (majority are
detected at Stage 1)
Lymphatic
Radiosensitive
Less aggressive
Good prognosis
Arise from primordial cells
NSGCTS
60% Stage II, III
Hematogenous
Radioresistant, chemotherapy
Vry aggressive
Poor prognosis
Tumor cells usually arise from
undifferentiated cells
 Biologic markers- used for evaluation of tumor, monitoring
response to therapy, tumor burden, staging
o LDH- mass of tumor cells, asses tumor burden
o AFP- Yolk sac tumor
o HCG- choriocarcinoma, seminomas with syncitiotrophoblasts
 Staging (nice to know)
o Stage I- confined within testes, epididymis or spermatic cord
o Stage II- spread to retroperitoneal nodes below diaphragm
o Stage III- spread to retroperitoneal nodes above the diaphragm
or other node groups
o Stage IV – distant metastasis
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necrosis or hemorrhage
o HISTO: germ cells divided by fibrous bands with interspersed
lymphocytes
o Seminomal cell: large, round distinct cell membrane, clear
cytoplasm, large central nucleus with 1-2 nucleoli o (+) c-KIT,
OCT4, PLAP
o May extend to epididymis, spermatic cord, scrotum; ill-defined
granulomas with giant cells may be seen in 15% of cases,
syncitiotrophoblasts are seen  (+) HCG
o Lymphocytes in fibrous septa - pathognomonic
o Sometimes with caseating granuloma
o Multinucleated giant cells
o Male counterpart of dysgerminoma in women
o Closely resembles young spermatocytes
o Tumor are soft and yellow
o Almost never occurs in infants. They peak in the 30s.
o Least differentiated among the germ cell tumors
o Cancer that closely resembles young spermatocytes o Positive
for placental alkaline phosphatase (PLAP)
o There is greater cellularity and nuclear irregularity with
anaplastic seminoma
o Placental AP for seminoma as tumor marker
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

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Pure GC tumors are more common in the young
Painless, non-tender masses in the testis
The primary may be occult, e.g. pure choriocarcinoma
60% present two or more histologic patterns while 40% have a
single histologic pattern
 Germ cell tumors arise from pre-malignant intratubular germ cell
neoplasia (ITGCN)
o Carcinoma in situ wherein the germ cells look malignant but they
are confined to tubules
o Where most tumors arise from
o Usually seen in cryptorchid testis
 Also includes Non-Hodgkin’s tumor
Figure 7. Gross morphology of a seminoma
Large, homogenous, soft and yellowish (or gray-white) lobulated cut
surface devoid of hemorrhage, cystic changes, and necrosis.
Figure 8. Histology of a seminoma
Seminoma cells are divided into poorly-demarcated lobules by delicate
septa of fibrous tissue, infiltrated with lymphocytes and plasma cells.
Seminoma cells are round or polyhedral with a distinct cell membrane,
glycogen-rich clear cytoplasm, central nucleus with one or more
prominent nucleoli. Presence of abnormal mitotic figures
Figure 6. Mechanism of testicular tumors.
A. Seminomatous Tumors
 most undifferentiated class of tumors
 Seminoma (Classical)
o Most common type of germinal tumor (50% of all GCT) and the
most likely to produce a uniform population of cells.
o 3rd decade of life
o GROSS: large, homogenous, gray-white surface without
Mac, Thea, Larie
 Spermatocytic seminoma
o One of two not arising from ITGCN (the other one is teratoma)
o Not so common
o 1-2% of population with age involvement around 65 years old
o Slow growing with good prognosis; no evidence of metastasis
o Lack of lymphocytes, granulomas, syncitiotrophoblasts, extra
testicular sites of origin, admixture with other GCTs association
with ITGCN
o What’s left are the round seminoma cells
o Gross: soft, pale gray, may contain mucoid cysts
o Intermixed three cell populations:
 Small
cells resembling secondary spermatocytes: 6-8
micrometers
 Medium-sized cells: 15-18 micrometers
 Scattered Giant cells: 50-100 micrometers
o Tumor cells show nuclear and cytoplasmic features of
spermatocytic maturation
o Grossly appear as pale gray, soft with friable cut surface
o Good response to radiation or chemotherapy (radiosensitive) o 5
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Urologic Pathology (Lecture)
year survival rate of 95%
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and necrosis).
Figure 12. Histology of an embryonal CA.
Undifferentiated cells, primitive glandular differentiation. Tumor cells
grow in alveolar, tubular and papillary patterns. Nuclei are large and
hyperchromatic with indistinct borders, with mitotic figures with
variation in cell and nuclear size and shape.
Figure 9. Spermatocytic seminoma (gross & histo)
Small, hemorrhagic sites, homogenous cells.
 Intratubular Germ Cell Neoplasia (ITGCN)
o
Type of “carcinoma in situ”
o
Atypical germ cells are confined within the lumens of the
seminiferous tubules
o
Occur in utero and stay dormant until puberty
o
Presumed precursor of germ cell tumors except pediatric
YST, teratoma and adult spermatocytic seminoma
 Yolk Sac Tumor
o Most common testicular tumor of children < 3 years old
o Good prognosis in children (usually seen in its pure form)
o In adults, usually seen in mixed forms of GCT
o GROSS: non-encapsulated, yellow-white, very soft and
mucinous to gelatinous tumors
o HISTO: loose, lace like (reticular) appearance, other patterns
seen (papillary, solid, etc.): Hyaline globules, Schiller-Duval
Bodies (50% of tumors) appear glomeruloid
o (+) AFP (alpha fetoprotein)
o Also called endodermal sinus tumor, orchioblastoma, infantile
embryonal carcinoma; Usually cystic
o Usually occurs "pure" rather than mixed
o Tends to be a component of an embryonal cell CA in adults.
o Composed of papillary structures (Schiller Duval bodies seen in
50% of cases) with extracellular globules of AFP (alpha
fetoprotein)
o Metastasizes hematogenously.
o Response to chemotherapy: better in children and less in adults
Figure 10. Intratubular Germ Cell Neoplasia
Fibrotic tubules (if the testis is cryptorchid). Clear cytoplasm due to
glycogen. Enlarged nuclei and prominent nucleoli with no ongoing
spermatogenesis. Seminiferous tubules and basement membranes are
thickened, and walls are becoming fibrotic.
B. Nonseminomatous Tumors
 Embryonal Carcinoma
o 20-30 YO
o More aggressive than seminoma
o GROSS: small, hemorrhagic, necrotic mass that destroys tunica
albuginea
o HISTO: sheets of undifferentiated cells with areas that show
alveolar and tubular structures; mitosis; giant cells frequent
o (+)cytokeratin, CD30
o may be (+)OCT3/4 or(+)PLAP o (-)cKIT
o Many contain differentiated structures of a coexisting teratoma
(Teratoma + Embryonal cell Carcinoma = Teratocarcinoma)
o Embryonal carcinoma component of the teratocarcinoma
metastasize to the retroperitoneum and disseminate, embryo
carcinoma is the malignant portion
o Presence of areas of hemorrhage and necrosis (rarely seen in
seminoma)
Figure 11. Gross morphology of an embryonal carcinoma.
Appear as grayish white masses with hemorrhage and necrosis,
smaller than a seminoma and usually does not replace the whole
testis (recall that a seminoma is a bulky mass devoid of hemorrhage
Mac, Thea, Larie
Figure 13. Gross morphology of a yolk sac tumor
Complete replacement of normal testicular parenchyma with a lobulated,
gelatinous mass. It presents with homogenous yellow-white mucinous
appearance on the cut surface.
Figure 14. Histology of a yolk sac tumor.
It is composed of papillary structures (Schiller-Duval bodies) with
extracellular globules of α-fetoprotein (AFP); glomeruloid appearance,
central blood vessel surrounded by yolk sac cells.
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Urologic Pathology (Lecture)
 Choriocarcinoma
o Rare in pure forms, most are part of mixed GTCs
o Very aggressive and widely metastasizing (lungs)
o GROSS: small, extensively hemorrhagic tumor
o HISTO: syncytiotrophoblasts, cytotrophoblasts; (+)hCG
levels in the thousands (really very high as compared to
pregnancy
o Composed of cytotrophoblastic and syncytiotrophoblastic cells
(biphasic)
o Lot of hemorrhage and necrosis
o Bloody tumor with few solid areas
o hCG levels are always elevated (in serum, urine)
o Most are composed of necrotic tissues and bloody elements
o Histologically:
 LPO: alternating layers of cytotrophoblast and
syncytiotrophoblast in areas of necrosis, with some
inflammatory cells
 HPO: biphasic appearance of dysplastic trophoblasts
 Syncytiotrophoblasts form a ‘cap’ around clusters of
cytotrophoblasts in an attempt to mimic the architecture of
immature placental villi
o Can occur as an occult (non-palpable) neoplasm, discovered
only after metastasizing
o Often a component of teratocarcinoma but may be pure or mixed
with any other germ cell tumor component (very rare to be pure)
Figure 15. Histology of a choriocarcinoma.
Clear
cytotrophoblastic
cells
have
central
nuclei
while
syncytiotrophoblastic cells have multiple dark nuclei embedded in
eosinophilic cytoplasm.
 Teratoma
o Ectodermal. Mesodermal, endodermal components
o Pure form common in children (2nd most common testicular
tumor), rare in adults
o Teratomas mixed with other GCT: 45%
o GROSS: large heterogenous solid and cystic with cartilaginous
ad myxoid areas
o HISTO: variants
o
Mature- resemble adult tissue
o Immature- fetal or embryonal tissue
o Teratoma with malignant transformation: non-GCT arising
from the derivatives of the germ cell layers (usually squamous
cell CA)
o Organoid components from more than one germ layer
o Pure teratomas common in children, rare in adults
o Dermoid cysts are rare in the testis (but relatively common in the
ovaries)
o Mixed germ cell tumors – 60% prognosis worsened by
aggressive elements (e.g. choriocarcinoma even if it’s just 10%)
o In postpubertal male; all teratomas are regarded as malignant
(unless proven otherwise by histology) and capable of metastatic
behavior regardless of whether the elements are mature or
immature
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choriocarcinoma, or both.
Figure 17. Histology of a teratoma
Mature Teratomas are composed of a heterogeneous, helter-skelter
collection of differentiated cells or organoid structures. Immature
teratomas can be viewed as intermediate between mature teratoma and
embryonal carcinoma.
 Mixed Tumor
o 60% of testicular tumors: composed of more than one of the
pure patterns
o Prognosis is worsened by aggressive elements
o Composed of two or more tumor cell lines
o Barricaded appearance
o Heterogenous appearance
o Comprises 60% of testicular tumors
o Prognosis follows the histologic type which has the worst
prognosis
o Good sampling technique would involve getting a piece of tissue
every 1 cm2, so that you can determine the different tissue
components of this tumor.
o Simply means that complete evaluation reveals more than one
histologic type
SEX CORD-STROMAL TUMORS
 Indolent
 endocrine abnormalities like gynecomastia, precocity
 Leydig Cell Tumors or Interstitial Cell Tumors
o Golden brown cut surface, Reinke crystals in 25% of cases, 90%
benign
o Occur at any age, are usually benign o Not very common
o Can produce precocious puberty or gynecomastia
o Circumscribed nodules – 5cm, contains Reinke cells
o Can be virilizing
o May present as testicular swelling, gynecomastia or sexual
precocity in children
Figure 18. A Leydig cell tumor
These neoplasms form circumscribed nodules, usually less than 5 cm
in diameter. They have a distinctive golden brown, homogeneous cut
surface.
Figure 16. Gross morphology of a teratoma.
Usually large, (5-10 cm) in diameter. Heterogeneous with solid,
sometimes cartilaginous and cystic areas. Hemorrhage and
necrosis. usually indicate admixture with embryonal carcinoma,
Mac, Thea, Larie
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Urologic Pathology (Lecture)
Figure 19. Histology of a Leydig cell tumor
Tumorous Leydig cells usually are remarkably similar to their normal
forebears in that they are large and round or polygonal, and they have
an abundant granular eosinophilic cytoplasm with a round central
nucleus. Cell boundaries are often indistinct. The cytoplasm frequently
contains lipid granules, vacuoles, or lipofuscin pigment, but, most
characteristically, rod-shaped crystalloids of Reinke occur in about 25%
of the tumors.
 Sertoli Cell Tumors or Androblastoma
o White yellow cut surface, tumor arranged in cord and tubules,
90% are benign
o May be composed of entirely Sertoli cells
o Masculinization or feminization
o Either estrogens or progesterones are elaborated
TESTICULAR LYMPHOMA
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Figure 21. Hematocele
VARICOCELE
 dilated vein in pampiniform plexus
 Varicosities in the pampiniform plexus of veins found in the
testis
 Common in young men
 May present as a ‘bag of worms’ during palpation
 May be asymptomatic but may cause infertility problems because
of the increased temperature brought about by the increased
circulation of warm blood
 Can be corrected by surgical repair
 Most common testis malignancy >60yo
 Non-Hodgkins lymphoma, Diffuse Large B cell type
 Poor prognosis
RANKING OF TUMORS BASED ON AGGRESSIVENESS
1. Choriocarcinoma
2. Embryo carcinoma
3. YST and seminoma (radiosensitive)
4. Teratomas (benign)
G. OTHER SCROTAL SWELLING
 Maybe caused by:
o Inflammation, serous, lymphatic fluid, blood
Figure 22. Varicocele
CHYLOCELE
HYDROCELE
 Serous fluid
 Fluid in the tunica vaginalis
o Serosa-lined sac adjacent to testis and epididymis o Maybe
affected by anything affecting either organ
o Scrotal enlargement by fluid/blood may be mistaken for testicular
pathology
 Usually idiopathic
 May contain 100cc or more of serous fluid
 Frequently lined by mesothelial cells
 Rarely, malignant mesotheliomas may also arise
 Diagnosed by transillumination, which distinguishes it from tumor
mass (which would appear opaque), and by palpation (fluctuant
looking mass)
 lymph, seen in elephantiasis
 accumulation of lymph in the tunica
 almost always found in patients with elephantiasis who have
widespread, severe lymphatic obstruction
SPERMATOCELE
 small cystic accumulation of semen in dilated efferent ducts
or ducts of the rete testis
END OF TRANSCRIPTION
MAC: Let’s watch Lady Med bukas! Support Snow White and her
lovable 7 Dwarfs! Haha.Hi DDY!
THEA: Hi Mac! Ang cute mo! Hehe.
LARIE: Hi MTJMDNAJNAME!  AFTG!
Figure 20. Clear fluid accumulates in a sac of tunica vaginalis.
HEMATOCELE
 blood, due to trauma or torsion
 Blood in the tunica vaginalis
 Possible causes
o Direct trauma to the testis
o Can arise from torsion with hemorrhagic suffusion into the
surrounding tunica vaginalis
o Hemorrhagic diseases associated with widespread bleeding
diatheses
Mac, Thea, Larie
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