Male Genital System and Lower

Urinary Tract
Eric Mirandilla MD, DPSP
 MALE GENITAL SYSTEM
Penis
Congenital anomalies
Inflammations
Tumors
Testis and Epididymis
Congenital anomalies
Regressive changes
Inflammations
Vascular disturbances
Testicular tumors
Miscellaneous lesions of the Tunica Vaginalis
Prostate
Inflammations
Benign enlargement
Tumors
 Penis
Congenital anomalies
Hypospadias and Epispadias
Phimosis
Inflammations
Balanoposthitis
Tumors
Benign tumors
Condyloma Acuminata
Malignant tumors
Carcinoma in situ
Invasive Carcinoma
 PENIS
Congenital anomalies
Hypospadias and Epispadias
Malformations of the urethral groove and canal may produce
abnormal urethral orifices involving the ventral or dorsal aspects of
the penis, designated hypospadias or epispadias, respectively.
Phimosis
Abnormally small orifice in the prepuce
It may arise as a primary developmental defect but is more
frequently secondary to inflammation.
Predisposes to secondary infections and carcinoma, owing to chronic
accumulation of secretions and other debris under the foreskin
Paraphimosis
abnormal, painful swelling of the glans penis after forceful retraction of a
phimotic prepuce, it may cause urethral obstruction.
Epispadia Hypospadia
 PENIS
Congenital anomalies
Inflammations characteristically involve both the glans
penis and the prepuce.
Nonspecific inflammatory processes and specific sexually
transmitted diseases can occur.
Syphillis, gonorrhea, chancroid, lymphopathia venereum, genital
herpes, granuloma inguinale
Balanoposthitis
Refers to nonspecific infection of the glans penis and prepuce,
generally associated with phimosis or a redundant prepuce
There is chronic accumulation of smegma
Caused by a variety of bacteria, fungi, mycoplasmas, and chlamydiae.
Balanoposthitis
 PENIS
Benign Tumors
Condyloma Acuminata
Benign epithelial proliferation caused by HPV, types 6 and 11
May involve mucocutaneous genital surfaces of either sex;
sexual contact is the most common mode of transmission.
It occurs most frequently after puberty
Gross morphology: sessile or pedunculated papillary
excrescence, often involving the coronal sulcus or inner surface
of the prepuce
Histologic characteristics
Branching stromal papillae covered by hyperplastic stratified squamous
epithelium, associated with prominent hyperkeratosis.
Vacuolation of superficial epithelial cell is common
Maturation of epithelial cells is orderly, in contract to CIS
 PENIS

Benign Tumors
Condyloma Acuminata

Low magnification reveals the papillary (villous) architecture.

Epithelium shows vacuolization (koilocytosis), characteristic of

HPV infection
 PENIS
Malignant Tumors
Carcinoma in Situ
Bowen Disease
Occurs in the genial region in both men and women, generally over age 35
In men, the disease presents commonly as solitary or multiple thickened ,
gray-white or red shiny plaques over the penile shaft.
Microscopically there is marked epithelial atypia with complete loss of
normal surface maturation but no invasion of underlying stroma.
Transition to invasive squamous cell carcinoma occurs approximately 10%
of cases.
Bowenoid Papulosis
Presents as multiple, pigmented papular lesions on external genitalia;
It may grossly mimic condyloma acuminata
Patients are generally younger than those with Bowen disease
Indistinguishable from Bowen disease, but evolution into invasive
carcinoma is rare.
Carcinoma in situ (Bowen disease) of the penis
Bowen disease, gross
 PENIS
Malignant Tumors
Squamous Cell Carcinoma
Accounts for 1% of cancers in men in the US; prevalence is
higher in regions where circumcision is not routinely practiced
Most cases occur between ages 40 and 70
Potential causes include carcinogens within smegma
accumulation under the foreskin and HPV types 16 and 18
Typically presents as epithelial thickening on the glans or inner
surface of the prepuce, progressing to ulceroinfiltrative or
exophytic growth eroding the penile tip, shaft, or both.
Histologic appearance is identical to squamous cell carcinomas
involving other cutaneous sites.
 PENIS
Malignant Tumors
Squamous Cell Carcinoma
Clinical course is characterized by slow growth.
Metastases typically occur to regional (inguinal and iliac) lymph
nodes, and distant metastases are uncommon.
The 5-year survival rate is 66% for lesions confined to the penis
and 27% with regional node involvement.
Verrucous carcinoma is an uncommon well-differentiated form
of invasive squamous cell carcinoma with low malignant
potential.
Squamous cell Carcinoma
Verrucous carcinoma, microscopic
 TESTIS AND EPIDIDYMIS

Congenital anomalies Embryonal Carcinoma

Cryptorchidism Yolk sac Tumor
Regressive Changes Choriocarcinoma
Atrophy Teratoma
Mixed tumors
Inflammations
Tumors of Sex Cord-Gonadal Stroma
Non-specific Epididymits and Orchitis
Leydig (intestitial) Cell Tumors
Granulomatous (Autoimmunie) Orchitis
Sertoli Tumors (Androblastoma)
Specific inflammations
Gonadoblastoma
Gonorrhea
Testicular Lymphoma
Mumps
Tuberculosis Miscellaneous Lesions of the Tunica Vaginalis
Syphilis
Vascular Disturbances
Torsion
Spermatic Cord and Paratesticular Tumors
Testicular Tumors
Germ Cell Tumors
Seminoma
Spermatocytic Seminoma
Normal Testis
 TESTIS AND EPIDIDYMIS
Congenital Anomalies
Cryptorchidism
Synonymous with undescended testes and is found in
approximately 1% of 1-year-old boys
This anomaly represents a complete or incomplete failure of
the intra-abdominal testes to descend into the scrotal sac.
Most cases are idiopathic; other causes include
Genetic abnormalities (trisomy 13)
Hormonal abnormalities
 TESTIS AND EPIDIDYMIS

Congenital Anomalies
Cryptorchidism
Most cases are unilateral; 25% are bilateral
Histologic changes
Apparent as early as 2 years of age
Decreased germ cell development, thickening and hyalinization of
seminiferous tubular basement membrane, interstitial fibrosis and relative
sparing of Leydig cells.
Regressive changes may also occur in the contralateral descended testis.
Clinical significance is related to high prevalence of inguinal hernias,
sterility and an increased incidence of testicular neoplasms.
Surgical correction (orchiopexy) in most studies has been found to
decrease the likelihood of sterility if performed early.
Cryptorchidism
 TESTIS AND EPIDIDYMIS
Regressive Changes
Atrophy
Secondary to
cryptorchidism,
vascular disease, inflammatory disorders, hypopituitarism,
malnutrition, obstruction of outflow of semen, elevated levels of
female sex hormones (endogenous or exogenous),
persistently elevated levels of follicle-stimulating hormone,
exogenous androgenic steroids, radiation and chemotherapy.
Atrophy may also be encountered as a primary developmental
abnormality in patients with Klinefelter syndrome.
Morphologic alterations are identical to those seen in
cryptorchidism.
 TESTIS AND EPIDIDYMIS

Regressive Changes
Atrophy

A, Normal testis shows tubules with active spermatogenesis. B, Testicular atrophy. The tubules show Sertoli cells
but no spermatogenesis. There is thickening of basement membranes and an apparent increase in interstitial
Leydig cells
 TESTIS AND EPIDIDYMIS

Inflammations
Nonspecific Epididymitis and Orchitis
These conditions are often associated with infection of the urinary
tract, with secondary infection of the epididymis via vas deferens or
lymphatics of the spermatic cord. Causes vary with the age of the
patient and include:
Gram-negative rods associated with genitourinary malformations in
pediatric patients
Chlamydia trachomatis and Neisseria gonorrhea in sexually active men
younger than age 35
E. coli and Pseudomonas species in older men.
Nonspecific interstitial congestion, edema and neutrophilic infiltrates
occur in the early stages, with subsequent tubular involvement;
severe cases may progress to generalized suppuration of the entire
epididymis.
 TESTIS AND EPIDIDYMIS

Inflammations
Nonspecific Epididymitis and Orchitis
Inflammation can extend to the testis via efferent ductules or
local lymphatic channels.
Scarring of the testis and epididymis may occur with resultant
infertility.
Leydig cells are less severely affected, and sexual potency
generally is not disturbed.
 TESTIS AND EPIDIDYMIS

Inflammations
Gonorrhea
Most cases of gonorrhea represent retrograde extension of infection
from the posterior urethra to the prostate, seminal vesicles, and
epididymis.
Inflammatory pattern is identical to that seen in nonspecific
epididymitis and orchitis; infection may extend to the testis and
produce suppurative orchitis in untreated cases.
Mumps Orchitis
Uncommon in children, but develops in 20% to 30% of postpubertal
males infected with mumps
Orchitis typically develops about 1 week after onset of parotid
inflammation; it can precede parotitis or occur in the absence of
parotitis in a minority of patients.
 TESTIS AND EPIDIDYMIS

Inflammations
Tuberculosis
Inflammation almost always begins in the epididymis, with secondary
involvement of the testis
There is granulomatous inflammation associated with caseous necrosis,
identical to active tuberculosis in other sites.
Syphilis
Inflammation virtually always begins as orchitis, with secondary
involvement of the epididymitis; it may present as isolated orchitis, without
involvement of adnexal structures.
Orchitis can occur in both congenital and acquired syphilis.
Syphilis can produce gummas or diffuse interstitial inflammation.
Interstitial changes include edema, lymphoplasmacytic inflammatory cells
and typical obliterative endarteritis.
 TESTIS AND EPIDIDYMIS
Vascular Disturbances
Torsion, occur secondary to twisting of the spermatic
cord, with resultant venous obstruction; arteries may
also be occluded but often remain patent because of
thicker walls.
Neonatal torsion
Occurs either in utero or shortly after birth.
It lacks any associated anatomic defect to account for its occurrence
Adult torsion
Typically seen in adolescence presenting as sudden onset of testicular
pain.
Results from a bilateral anatomic defects where the testis has
increased mobility, called bell-clapper abnormality.
 TESTIS AND EPIDIDYMIS
Vascular Disturbances
Torsion
Occurs without any inciting injury; sudden pain heralding the
torsion may even occur during sleep.
Considered as one of the few urologic emergencies.
If the testis is explored surgically and manually untwisted
within approximately 6 hours after the onset of torsion, there
is a good chance that the testis will remain viable
In order to prevent the occurrence of subsequent torsion in
the contralateral testis, the testis unaffected by torsion is
surgically fixed to the scrotum (orchiopexy)
 TESTIS AND EPIDIDYMIS

Vascular Disturbances
Torsion
Changes range from
congestion and interstitial
hemorrhage to extensive
hemorrhagic necrosis,
depending on the duration
and severity of the process.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Divided into two major groups:
Germ cell tumors: accounting for approximately 95% of cases
Seminoma
Spermatocytic seminoma
Embryonal carcinoma
Yolk sac (endodermal sinus) tumor
Choriocarcinoma
Teratoma
Nongerminal tumors (stromal or sex cord tumors)
Leydig cell tumor
Sertoli cell tumor
 TESTIS AND EPIDIDYMIS
Testicular Tumors
Germ Cell Tumors
Incidence is approximately 6:100,000 men annually, with peak
incidence between ages 15 and 34.
Account for 10% of cancer deaths in this age group.
Testicular germ cell neoplasms may contain a single histologic
pattern (40% of cases) or a mixture of patterns (60% of cases).
Most tumors arise from a focus of intratubular germ cell
neoplasia (ITGCN)
Neoplastic germ cells may give rise to seminoma or transform
into a totipotential neoplastic cell (embryonal carcinoma)
capable of further differentiation.
Can be divided into seminoma and nonseminomatous tumors.
 TESTIS AND EPIDIDYMIS
Testicular Tumors
Germ Cell Tumors
Several risk factors are important:
Cryptorchidism: 10% of testicular tumors
Genetic factors: higher risk of testicular neoplasia among siblings of
patients with testicular tumors
Testicular dysgenesis includes testicular feminization and Klinefelter
syndrome.
Cytogenetic abnormalities involving chromosome 12 are common.
i(12p) is present in 90% of testicular germ cell tumors
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Seminoma
Accounts for 50% of all testicular germ cell tumors
Peak incidence is in the 30s
Variants include:
Classic seminoma (95% of seminoma)
Spermatocytic seminoma (5%)
Histologically identical tumors may occur in the ovary (dysgerminomas)
and CNS (germinomas)
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Seminoma
It presents as homogenous, lobulated,
gray-white mass, generally devoid of
hemorrhage or necrosis; the tunica
albuginea usually remains intact.

Fairly well-circumscribed, pale, fleshy,

homogenous mass.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Seminoma
Microscopically, the mass is composed of large polyhedral seminoma
cells containing abundant clear cytoplasm, large nuclei and prominent
nucleoli
Cytoplasmic glycogen is typically present
Fibrous stroma of variable density divides the neoplastic cells into
irregular lobules
Lymphocytic infiltrates (usually T cell) is present in most cases
Human chorionic gonadotropin (hCG) is present in such cells and
presumably accounts for the minimally elevated serum hCG levels
demonstrable in some patients with pure seminoma
Classic seminoma cell do not contain AFP.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Seminoma

A, Low magnification shows clear seminoma cells divided into poorly demarcated lobules by delicate septa.
B, Microcopic examination reveals large cells with distinct cell borders, pale nuclei, prominent nucleoi, and a sparse lymphocytic infiltrate.
Seminoma
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Spermatocytic seminoma
Uncommon neoplasms, occurring in patients older than those with
classic seminoma
Indolent growths, with virtually no tendency to metastasize
Lesions tend to be larger than those of classic seminoma
Composed of a mixed population of cells, including smaller (6-8 mm)
cells resembling secondary spermatocytes designation), medium-
sized (15-18 mm) cells, and scattered giant cells.
In contrast to classic seminomas, spermatocytic seminomas arise
only in the testes and are not associated with other germ cell
tumors.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Embryonal carcinoma
Peak incidence between 20 and 30
years
More aggressive than seminoma
Lesions may be small and confined
to the testis; more examples are
poorly demarcated, gray-white
masses punctuated by foci of
hemorrhage, necrosis or both. They
may extend through the tunica
albuginea into the epididymis of
Embryonal carcinoma is a hemorrhagic mass
spermatic cord.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Embryonal carcinoma
Microscopically, they are
composed of primitive
epithelial cells with indistinct
cell borders, forming irregular
sheets, tubules, alveoli, and
papillary structures.
Mitotic figures and neoplastic Embryonal carcinoma shows sheets of
undifferentiated cells as well as primitive
giant cells are common glandular differentiation. The nuclei are large
and hyperchromatic
Syncytial cells positive for hCG
and AFP may be detected
Embryonal Carcinoma
 TESTIS AND EPIDIDYMIS
Testicular Tumors
Germ Cell Tumors
Yolk Sac Tumor
Most common testicular neoplasms in infants and young children
and endodermal sinus tumor.
Prognosis in children before 3 years is good
Most adult cases occur as a component of a mixed germ cell
neoplasm.
Pure forms present as infiltrative, homegenous, yellow-white
mucinous lesions.
Microscopically, they are composed of cuboidal neoplastic cells
arrayed in a lacelike (reticular) network; solid area and papillae may
also be seen
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Yolk Sac Tumor
Structures resembling
primitive glomeruli (Schiller-
Duval bodies) are seen in
50% of the cases.
Eosinophilic, hyaline
globules containing
immunoreactive AFP and
1-antitrypsin are present
within and around the
neoplastic cells.
Yolk Sac Tumor
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Choriocarcinoma
Highly malignant neoplasm composed of both cytotrophoblastic and
syncytiotrophoblastic elements.
Similar neoplasms may occur in the ovary, placenta or ectopic
pluripotential germ cell rests in other sites.
This neoplasm is rare in pure forms within the testis; it is more often
encountered as a component of a mixed germ cell neoplasm.
The primary testicular neoplasm is often quite small, even in the
presence of widespread systematic metastases.
The gross appearance ranges from a bulky, hemorrhagic mass to an
inconspicuous lesion replaced by a fibrous scar.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Choriocarcinoma
Histologically, it is composed of
polygonal, comparatively uniform
cytotrophoblastic cells growing in
sheets and cords, admixed with
multinucleated
syncytiotrophoblastic cells, Choriocarcinoma shows clear cytotrophoblastic
cells with central nuclei and
hCG is readily demonstrable syncytiotrophoblastic cells with multiple dark
nuclei embedded in eosinophilic cytoplasm.
within the cytoplasm of the Hemorrhage and necrosis is prominent
syncytiotrophoblastic elements.
Choriocarcinoma
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Teratoma
Neoplasm exhibiting evidence of simultaneous differentiation along
endodermal, mesodermal and ectodermal lines.
Can occur at any age
Composed of a haphazard array of differentiated mesodermal (muscle,
cartilage, adipose tissue), ectoderm (neural tissue, skin) and endodermal
(gut, bronchial epithelium) elements.
In the child, differentiated mature teratomas are may be expected to
behave as benign tumors and almost all these patients have a good
prognosis.
In the postpubertal male, all teratomas are regarded as malignant and
capable of metastatic behavior regardless of whether the elements are
mature or immature.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Teratoma
Teratoma with malignant
transformation is characterized
by non-germ cell malignancy
(carcinoma, sarcoma,
neuroblastoma, Wilms tumor)
developing within a teratoma
When the non-germ cell
component spreads outside Teratoma of the testis consisting of disorganized
the testis it does not respond collection of glands, cartilage, smooth muscle and
to chemotherapy and the only immature stroma.
hope for cure resides in the
local resectability of the tumor.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Germ Cell Tumors
Mixed Tumors
Account in aggregate for approximately 50% of germ cell neoplasms
Histologic patterns are variable
Most common includes mixture of teratoma, embryonal carcinoma,
yolk sac tumor, and hCG-containing giant cells
Teratomacarcinoma designates neoplasms containing both teratoma
and embryonal carcinoma.
Metastases from such lesions may contain virtually any germ cell
element, including elements not present in the primary tumor.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Clinical features of Germ Cell Neoplasms
Most cases present with painless enlargement of the testis;
neoplasia should be considered in the differential diagnosis of all
testicular masses, even those that are painful.
Biopsy of a testicular neoplasm is associated with a risk tumor
spillage which would necessitate excision of the scrotal skin in
addition to orchiectomy.
Consequently, the standard management of a solid testicular mass is
radical orchiectomy based on the presumption of malignancy.
Lymphatic metastases most commonly go to retroperitoneal para-
aortic nodes but may occur in more distant sites (mediastinal and
supraclavicular nodes)
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Clinical features of Germ Cell Neoplasms
Lungs are the most common site for hematogenous metastases,
followed by liver, brain, and bone.
The histologic appearance of metastases may be identical to that of
the primary tumor or may contain other germ cell elements
Biological behaviour of NSGCTs is, in general, more aggressive than
that of seminomas.
Roughly 70% of seminomas present with localized (clinical stage I); in
contrast, 60% of NSGCTs present with advanced (stage II or III)
disease.
Extensive metastases may be present even with small primary
lesions, particularly in the case of choriocarcinoma.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Clinical Staging
Stage I: tumor confined to the testis
Stage II: Metastases limited to retroperitoneal nodes below the
diaphragm.
Stage III: metastases outside the retroperitoneal nodes or
above the diagphragm
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Several peptides can be produced by germ cell neoplasms and
can be detected in body fluids by sensitive assays.
AFP and hCG are the most common
Lactate dehydrogenase, not specific for testicular tumors, is
produced by tumor cells, and the degree of elevations provides
a rough measure of tumor burden.
Serum markers are of value to
Evaluate testicular masses
Stage germ cell tumors
Assess tumor burden
Monitor the response of germ cell tumor therapy
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Sex Cord-Stromal Tumors
Leydig (Interstitial Cell Tumors)
Relatively uncommon neoplasms, accounting for 2% of all testicular tumors
Most occur between the ages 20 to 60 years, but they may be found at any
age.
Tumors may elaborate androgens or mixtures of androgen and other
steroids (estrogen, corticosteroids).
Clinical manifestations include a testicular mass and changes referable to
hormonal abnormalities (e.g., gynecomastia, sexual precocity in
prepubertal boys)
Tumors are grossly circumscribed nodules with a homegenous, golden
brown cut surface.
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Sex Cord-Stromal Tumors
Leydig (Interstitial Cell Tumors)
Microscopically, they are composed of polygonal cells with abundant
granular, eosinophilic cytoplasm and indistinct cell borders.
Lipochrome pigment, lipid droplets and eosinophilic Reinke crystalloids
are commonly present.
10% of tumors invade or metastasize.
Leydig cell tumor
 TESTIS AND EPIDIDYMIS

Testicular Tumors
Sex Cord-Stromal Tumors
Sertoli Cell Tumors (Androblastoma)
These tumors are uncommon neoplasms, composed of Sertoli cells.
Tumors may elaborate androgens or estrogen but rarely in sufficient
quantity to produce precocions masculinization or feminization.
Tumors present as homogenous gray-white to yellow masses of
variable size.
Microscopic picture is dominated by cells with tall, columnar
cytoplasm, often forming cords reminiscent of immature seminiferous
tubules.
Most are benign: 10% demonstrate invasion or metastases.
 MALE GENITAL
TESTIS SYSTEM
AND EPIDIDYMIS

Miscellaneous Lesions of the Tunica Vaginalis

Hydrocele: accumulation of serous fluid within the tunica
vaginalis, either secondary to generalized edema or due to
incomplete closure of the processus vaginalis.
Hematocele: accumulation of blood within the tunica vaginalis
secondary to trauma, torsion, or hemorrhage; a generalized
bleeding diathesis; or rarely, invasion of the tunica by neoplasms.
Chylocele: accumulation of lymphatic fluid within the tunica
vaginalis, secondary to lymphatic obstructions (e.g., in patients
with elephantiasis)
Spematocele: local accumulation of semen in the spermatic cord,
generally within a dilated duct in the head of the epididymis.
Varicocele: local accumulation of blood within a dilated vein in the
spermatic cord,
 PROSTATE

Inflammations
Acute bacterial prostatitis
Chronic bacterial prostatitis
Chronic abacterial prostatitis
Granulomatous prostatitis
Benign Enlargement
Nodular Hyperplasia (Benign Prostatic
Hyperplasia)
Tumors
Adenocarcinoma
Miscellaneous Tumors and Tumor-like conditions
 PROSTATE

In the normal adult, prostate weighs approximately 20 grams

It is a peritoneal organ encircling the neck of the bladder and
urethra and is devoid of a distinct capsule.
Prostatic parenchyma can be divided into 4 zones:
Peripheral
Central
Transitional zones
Region of proliferative lesions are different in each region
Types of proliferative lesions are different in each region.
Most hyperplasias arise in the transitional zone
Most carcinomas originate in the peripheral zone
PROSTATE
Normal prostate Normal Seminal Vesicle
 PROSTATE
Inflammations
Acute Bacterial Prostatitis
Most cases are caused by organisms associated with UTI (E. coli
and other gram-negative rods), Enterococcus, or S. aureus.
Organisms reach the prostate via direct extension from the
urethra or urinary bladder or by lymphatic or hematogenous
seeding from more distant sites. This may follow
catheterization or surgical manipulation of the urethra or
prostate.
It presents with fever, chills, dysuria and a boggy, markedly
tender prostate.
Diagnosis is based on clinical features and urine culture.
 PROSTATE

Inflammations
Chronic Bacterial Prostatitis
It may be asymptomatic or associated with low back pain,
suprapubic and perineal discomfort, and dysuria
It is frequently associated with a history of recurrent UTI
caused by the same organism.
Diagnosis is established by demonstration of leukocytes in
expressed prostatic secretions and positive bacterial cultures in
prostatic secretions and urine; most cases are caused by
organisms similar to those responsible for acute prostatitis.
Most cases appear insidiously, without a history of prostatitis.
 PROSTATE

Inflammations
Chronic Abacterial Prostatitis
Most common form of prostatitis, typically affecting sexually
active men
Manifestations are similar to those of chronic bacterial
prostatitis but without a history of recurrent urinary tract
infections.
Expressed prostatic secretions contain more than 10
leukocytes per high-power field, but cultures are uniformly
negative.
 PROSTATE

Benign Enlargement
Nodular Hyperplasia (Benign Prostatic Hyperplasia)
Present in approximately 20% of men at age 40 years, increasing to
70% by age 60 years and to 90% by age 70 years.
Only 50% of those who have microscopic evidence of nodular
hyperplasia have clinically detectable enlargement of the prostate; of
those individuals only 50% develop clinical symptoms.
Dihydrotestosterone (DHT), a metabolite of testosterone, is the
ultimate mediator of prostatic growth.
It is synthesized in the prostate from circulating testosterone by the
action of the enzyme 5-reductase, type 2. Enzyme is localized
principally in stromal cells; these cells are the main site for DHT
synthesis.
 PROSTATE

Benign Enlargement
Nodular Hyperplasia (Benign Prostatic Hyperplasia)
Estrogens also participate in mediating prostatic hyperplasia
and stromal-epithelial interactions mediated by peptide
growth factors also contibute.
Clinical symptoms of lower urinary tract obstruction are due to
smooth muscle mediated contraction of the prostate.
The tension of prostate smooth muscle is mediated by the 1-
adrenoreceptor localized to the prostatic stroma.
 PROSTATE

Benign Enlargement
Nodular Hyperplasia (Benign
Prostatic Hyperplasia)
Prostate weighs 60 and 100 gm
Nodular hyperplasia of the
prostate originates almost
exclusively in the inner aspect of
the prostate gland, in the
transition zone.
Nodules arising lateral to the
urethra may compress the
urethral lumen to a slit-like
orifice
 PROSTATE

Benign Enlargement
Nodular Hyperplasia
(Benign Prostatic
Hyperplasia)
Nodules are composed of
variable mixtures of
proliferating glands and
fibromuscular stroma
Cystic dilation of glandular Shows nodules of hyperplastic glands on both
sides of the urethra
elements is common and
contributes to the nodularity
Prostatic Hyperplasia
 PROSTATE

Benign Enlargement
Nodular Hyperplasia (Benign Prostatic Hyperplasia)
Urinary frequency, nocturia, and difficulty starting and stopping the
stream of urine
Acute urinary retention
Chronic urinary stasis with resultant bacterial overgrowth and
urinary tract infection
Chronic obstruction resulting in a variety of secondary structural
alterations, including:
Hypertrophy of the urinary bladder
Urinary bladder diverticula
Hydronephrosis
 PROSTATE

Tumor
Adenocarcinoma
Prostatic carcinoma is the most common form of cancer in men;
currently, it is the second leading cause of cancer death among men.
Occurs predominantly in men over age of 50
Rare in Asians; more common in blacks than in whites
Etiology remains unknown; clinical and epidemiologic data suggest
that advancing age, race, hormonal influences, genetic factors, and
environmental factors all contribute.
Most cases (70%) arise in the peripheral zone of the prostate,
particularly in the posterior region, facilitating palpation during
rectal examination
Primary lesions characteristically are grossly poorly demarcated, firm
and yellow.
 PROSTATE

Tumor
Adenocarcinoma
Locally advanced cases may infiltrate the seminal vesicles and
urinary bladder; invasion of the rectum is uncommon.
Lymphatic metastases occur initially in obturator nodes,
followed by spread to perivesical, hypogastric, iliac, presacral
and para-aortic nodes.
Hematogenous dissemination occurs primarily to bone, most
often in the form of osteoblastic metastases
 Tumor
Adenocarcinoma
Pathogenesis
Androgens: Prostate cancer cells depend on androgen
interactions with AR to activate pro-growth and pro-survival
genes.
Germline genes: Risk increases with the number of first-
degree relatives with prostate cancer (one relative two-
fold increased risk; two relatives five-fold increased risk)
and the onset of disease occurs at an earlier age.
BRCA2 mutations increase risk 20-fold, but most familial prostate
cancers are associated with loci that only modestly affect risk.
 Tumor
Adenocarcinoma
Pathogenesis
Acquired mutations and epigenetic changes:
Chromosomal rearrangements that juxtapose an ETS family transcription
factor gene next to the androgen-regulated TMPRSS2 promoter lead to
overexpression of the ETS transcription factors and make prostate epithelial
cells more invasive.
Hypermethylation of the glutathione S-transferase gene down regulates its
expression and leads to increased susceptibility to a variety of carcinogens
normally modified by the enzyme.
Reduced expression of the adhesion molecule E-cadherin is associated with
increased expression of the EZH-2 transcriptional repressor
Precursor lesions: Prostatic intraepithelial neoplasia (PIN) is now
identified as a precursor on the spectrum to prostatic carcinoma; it
contains many of the molecular changes seen in malignancy.
Prostatic Adenocarcinoma
Primary lesions
characteristically are
poorly demarcated,
gritty, firm, and yellow.
Locally advanced cases
may infiltrate the
seminal vesicles and
urinary bladder;
invasion of the rectum
is uncommon.
Prostatic Adenocarcinoma
Most are well-
differentiated
adenocarcinomas with
small, crowded glands
lined by a single layer of
epithelium (lacking the
outer basal layer of cells);
nuclei are large and often
exhibit nucleoli.
Perineural invasion is a
sign of malignancy.
Gleason scoring
 It is used to describe how aggressive a
prostate cancer tumor is, and how likely
it is to spread
Used only for adenocarcinoma, the most
common type of prostate cancer.
Reflects how different the tumor tissue is
from normal prostate tissue.
 It uses a scale from 1 to 5.
The doctor gives the cancer a number
based on the patterns and growth of
the cancer cells.
The lower the number, the more
normal the cancer cells look and the
lower the grade.
The higher the number, the less
normal the cancer cells look and the
higher the grade.
 Grades 1 and 2 are not commonly
used because the tumor tissue looks
and acts like normal tissue.
Most prostate tumors are grade 3 or
higher.
 Pattern 1
The cancerous prostate closely
resembles normal prostate tissue. The
glands are small, well-formed, and closely
packed. This corresponds to a well
differentiated carcinoma.

Pattern 2
The tissue still has well-formed glands,
but they are larger and have more tissue
between them, implying that the stroma
has increased. This also corresponds to a
moderately differentiated carcinoma.
 Pattern 3
The tissue still has
recognizable glands,
but the cells are
darker.
At high magnification,
some of these cells
have left the glands
and are beginning to
invade the
surrounding tissue or
having an infiltrative
pattern.
This corresponds to a
moderately
differentiated
carcinoma.
 Pattern 4
The tissue has few
recognizable
glands.
Many cells are
invading the
surrounding tissue
in neoplastic
clumps.
This corresponds
to a poorly
differentiated
carcinoma.
 Pattern 5
The tissue does
not have any or
only a few
recognizable
glands.
There are often
just sheets of
cells throughout
the surrounding
tissue.
This corresponds
to an anaplastic
carcinoma.
 A pathologist then assigns a grade to the
observed patterns of the tumor specimen.

Primary grade - assigned to the

dominant pattern of the tumor (has to
be greater than 50% of the total pattern
seen).
 Secondary grade - assigned to the next-
most frequent pattern (has to be less than
50%, but at least 5%, of the pattern of the
total cancer observed).

Tertiary grade - increasingly, pathologists

provide details of the "tertiary"
component. This is where there is a small
component of a third (generally more
aggressive) pattern.
 The pathologist then sums the pattern-
number of the primary and secondary
grades to obtain the final Gleason score
If only two patterns are seen, the first
number of the score is that of the
tumor's primary grade while the second
number is that of the secondary grade,
as described in the previous section.
 If three patterns are seen, the first
number of the score would be the primary
grade and the second number the pattern
with the highest grade

For example, if the primary tumor grade was 2 and

the secondary tumor grade was 3 but some cells
were found to be grade 4, the Gleason score would
be 2+4=6. This is a slight change from the pre-2005
Gleason system where the second number was the
secondary grade (i.e., the grade of the second-most
common cell line pattern).
 Gleason scores range from 2 to 10, with 2
representing the most well-differentiated
tumors and 10 the least-differentiated tumor.
Gleason scores have often been categorized
into groups that show similar biologic
behavior
low-grade (well-differentiated),
intermediate-grade, moderate to poorly
differentiated or high-grade.
 PROSTATE

Tumor
Most common form of staging is TNM
Stage T1 refers to cancer found incidentally either on transurethral
resection (TURP) done for BPH symptoms (T1a and T1b depending
on the extent and grade) or on needle biopsy typically performed for
elevated serum PSA levels (stage T1c)
Stage T2 is organ-confined cancer
Stage T3a and T3b tumors show extraprostatic extension, with and
without seminal vesicle invastion, respectively.
Stage T4 reflects direct invasion of contiguous organs.
Any spread of tumor to the lymph nodes regardless of extent is
eventually associated with a fatal outcome, such that the staging
system merely records the presence or absence of this finding
(N0/N1)
Thank you