I.

Miscellaneous lesions of Tunica Vaginalis

Lesions

Characteristics:
- accumulation
serous fluid w/in
T.Vaginalis

Causes:
- incomplete
closure processus
vaginalis
- 2ry to generalized
edema @ infected

HEMATOCELE

- accumulation
blood w/in
T.Vaginalis

CHYLOCELE

- accumulation
lymphatics w/in
T.Vaginalis

- 2ry to trauma,
torsion,
hemorrhage,
generalized
bleeding diathesis,
malignt. Invasion
- lymphatic
obstruction

SPERMATOCELE

- accumulation
semen w/in dilated
eff. Duct in head
epididymis

HYDROCELE

VARICOCELE

- obstruction in the
vas deferens

pampiniform
plexus elongated &
dilated

II.
Congenital anomalies
CRYPTORCHIDSM
Incidence:
- incomplete descent of testis to scrotum
- 0.7% of male population
- more in right
- 25% bilateral
Pathogenesis :
- testis remain in body at its temp (37C) inhibit spermatogenesis
- BUT, testosterone still present
There4: they are infantile but develop 2ry male characteristics

Causes(mostly idiopathic):
- hormonal abnorm. (decrease LHrh)
-genetic abnorm. (trisomy 13)
- short spermatic cord
- mechanicl obstruction in inguinal canal
Morphology:
Grossly: early life normal
Puberty atrophy
Micros: 6 yrs atrophy semin. Tubules, Leydig cell hyperplasia, interst. Fibrosis
Puberty hyalinization of semin. tubules. Regressive changes in othr
testis
Effects:
-asymptomatic
- discovered at puberty (aftr testicular atrophy)
- Bilateral infertility
- high incidence of malignancy compared to normal positioned testis

I. Testicular atrophy
Causes:
- 1ry Klienfelterss syn.
- 2ry because of:
cryptorchidism
vascular disease
inflammatory disease
hypopituitarism
malnutrition
obstruction semen outflow
increases female sex
hormones
persistant increase of FSH
radiation, chemotherapy

II. Inflammatory disease of testis & epididymis

Types:
a) epididymoorchitis

b) nonspecific
epididymitis &
orchitis

c) autoimmune
(granulomatous)
orchitis
d) specific
inflammation

Origin:
Start: epididymitis
with inflmmtn of
testis proper
(orchitis)
-1ry infection in
urinary tract
-2ry infction of
epididymis &
testis

-2ry infction through ascend infction via:

vas deferens
lymphatics of spermatic cord
- causative organisms:
E.coli
pseudomonas
gram ve rods
Chlamydia trachomatis
-obscure (not clearly seen)
- trauma & autoimmune

i- gonorrhoeal
infection

- STD because of
N. Gonorrhea

ii- mumps

- viral infection
commonly affects
school age
-begins in
epididymis
-2ry involvement
of testis
- begins as orchitis
-2ry invlvmnt of
epididymis
* mostly orchitis
not assoc. With
epididymitis

iii- tuberculosis

iv- syphilis

Spread:
- through ascendg infection via vas deferens by:
lymphatics of spermatic cord
hematogenous

-Children testicular involvement uncommon

-Postpubertal orchitis (20-30%)
testicular involvement, 70% unilateral
-hematogenous spread to lung, kidney

- congenital @ acquired
- reaction maybe:
localized (gamma)
diffuse (diffuse syphilitic granulation tissue)

III. Vascular disturbances

- torsion of testis
( precipitated with trauma @
violent movement )
Pathogenesis:
twisting of spermatic cord
severe venous
engorgement venous
infarction of testis (sac of soft,
necrotic, hemorrhagic tissue )
Risk factors:
- incompletely descended
testicles
- absence of scrotal ligament
- testicular atrophy

IV. TESTICULAR NEOPLASMS

Characteristics:
-most imp. cause of firm, painless, enlargement of testis
- Peak incidence 15-35 years
- 95% from germ cells (ALL malignant)
- 5% from Leydig cells @ Sertoli cells ( benign, characterized by endocrine abnorm. )

1- seminoma
* confined to testis
* common
metastasize by
lymphatics to
paraaortic & iliac L.N
* radiosensitive

Pathogenesis:
- unknown
Risk factors:
1. cryptorchidism ( 10% testicular tumor )
2. testicular feminization & Klienfelters syndrome (XXY)
3. genetic factors

A) Germ cell tumor (one histologic pattern)

2- non-seminoma
* may have metastases during diagnosis in absence palpable mass
* metastasize early by lymphatics & hematogenous
* radioresistant more aggressive, poor prognosis

Incidence:

- most common germ

cell tumor in adult
- 30% of testicular
germ cell tumor
th
- peak incidence ( 4
decade )

Morphology:

Grossly:
- large, soft, well
demarcated, graywhite, bulges from cut
surface of affected
testis
- large tumor contain
foci of coagulative
necrosis
- confined to testis
only by an intact T.
Albuginea

a.Embroyonal
carcinoma
-aggressive
than seminoma
- peak
incidence
20-30 years

b.yolk sac
tumor
- most
common in
infants &
children
-In adults,
occurs as
mixed
germ cell
neoplasm

B) Sex cord-gonadal stroma

1. Leydig
2. Sertoli cell tumor
(interstitial) cell
(androblastoma)
tumor

c.choriocarcinoma

d.teratomas

- highly malignant
- hematogenous
metastasis to liver &
lung
- component of
mixed germ cell
tumor
- peak incidence
20-30 years

-differentiation of
endoderm, mesoderm,
ectoderm
- occur at any age

- uncommon
- occurs at any
age, mostly 20-60
yrs
- secretes
androgen,
estrogen,
corticosteroids

- uncommon

Grossly:
- firm consistency
- cut surface contain
cysts & cartilaginous
areas

- painless
testicular mass
with hormonal
changes
- gynecomastia in
adults
- precocious
puberty in children

- composed of Sertoli
cells @ mix. Sertoli &
granulose cells
- secretes androgen,
estrogen but
insufficient to
produce feminization
@ precocious
puberty
- mostly benign
- 10% only spread &
infiltrate

Microscopically:
1. classic (typical)
85%
- large cells with
distinc borders
- clear glycogen-rich
cytoplasm
- rounded nucleus
with prominent
nucleoli
- cells in small lobules
separated by fibrous
septae containg
lymphocytic infiltrate
- some cases contain
giant cells
2. anaplastic (10%)
3. spermatocytic (5%)

Testicular Lymphoma
- not 1ry tumor. Affected patient may present with
only testicular mass
- 5% of all testicular neoplasms
- most common tumor of testis in men over 60 yrs
- diffuse, large cells, non-Hodgkins lymphoma,
disseminates widely
- poor prognosis

Micros:
1. mature teratomas
common in children
(benign)
adult (malignant)
-fully differ. tissues:
-ectoderm (skin, neural
tissue)
-mesoderm (muscle,
cartilage, blood cells)
-ectoderm (gut,
bronchial epithelium)
2. immature teratomas
-incomplete stages of
differ.
-malignant esp. In
adults
3. teratomas with
malignant
transformation
-frank malignancy
develop in mature
teratoma
- occurs in adult

Clinical staging:
-achieved by physical exam. Radiographic
imaging, studying tumor markers.
Stage I: confined to testis
Stage II: metastases limited to retroperitoneal
nodes below diaphragm
Stage III: metastases outside peritoneal nodes
@ above diaphragm

Prognosis:
- 90% benign
excellent
prognosis
- 10% malignant
infiltrative &
spreading
tendency

Tumor markers value in:

a) evaluation testicular masses
b) staging of germ cell tumors
c) monitor response of therapy
d) diagnosis of recurrence during follow up
Exp:
--feto protein increases in yolk sac tumor
- human chorionic gonadotropin increases in germ
cell neoplasm containing syncytio. elements

DISEASES OF PROSTATE
I) Inflammation of prostate (prostatitis)
A- Acute prostatitis
- associated with acute
bacterial urinary tract
infection
Ex: E.coli, gram-ve rods,
enterococci, gonococci,
staph.aureus
- fever, chills, dysuria, low
backache
- prostate enlarged, tender,
spongy, soft

B- Chronic prostatitis
-bacterial @ non bacterial
-bacteria origin occur on top
of acute prostatitis @ -nonbacteria develop insidiously
w/out previous acute
infection
- asymptomatic but
chronic prostatitis may
serve as reservoir causing
urinary tract infection

II) Senile prostatic hyperplasia (nodular@benign prostatic hyperplasia)

incidence

clinically

etiology

morphology

--> will not cause prostate carcinoma

- hyperplasia of prostatic glands & its stroma
- 20% males age 40 years
- 70 % age 60 years
- 90% by 80 years

Occur in 10% of cases. Almost all are lower urinary tract affection:
1. frequency, urgency, nocturia (due to urinary bladder irritation)
2. diff. In staring & stopping urinary system
3. painful distention of urinary bladder
4. infection (cystitis, pyelonephritis) due to residual urine in bladder & chronic obstruction
5. stone formation (due to stasis + infection)
6. hypertrophy, dilatation, urinary bladder diverticulae
7. bilateral hydronephrosis chronic renal failure
-uncertain (related to hormonal changes)
Old age androgen drop estrogens action unopposed estrogen increase sensitization of
androgen mainly at central portion of prostate increase sensitivity to dihydrotestosterone
Grossly:
- affects periurethral glands
- prostate enlarged
- cut surface shows multiple well circums. Nodules (solid @ contain cystic spaces)
- urethra compressed
- hypertrophied gland bulge in urinary bladder lumen as pedunculated mass ball-valve type
urethral obstruction
Microscopically:
- glands lined by 2 cell layer (inner tall columnar & outer flattened basal cells)
- glands show:
intraluminal papillae & cystically dilated gland
- others still contain proteinaceous material (corpora amylacia)
- glands separated each other by proliferated fibromuscular stroma
- in hugely enlarged cases areas of infarcts & sq. metaplasia

III) Carcinoma of the prostate (occult carcinoma----- small in size & hidden)
incidence

pathogenesis

morphology

Grading
(Gleason
system)
spread

staging

Clinical
features

diagnosis

-most common visceral cancer in males

- Peak incidence 65-75 years
- 2nd most common cause of cancer-related death after lung cancer (in men older than 50 yrs)
- occult cancer are more common than clinically apparent
cause unknown but related with:
1. hormonal factors ( no prostatic carcinoma in males castrated b4 puberty)
- also its growth inhibit by orchiectomy & admin. Of estrogen (ex: dihydrostilbosterol)
2. genetic influence increase incidence in 1st degree relatives patient with prostatic cancer
3. environmental factors in certain industrial settings & significant geographic diff.
Grossly:
- ill defined masses beneath capsule in outer peripheral part of prostate
- Cut section foci appearing as firm, gray-white to yellow masses with ill defined margins
Microscopically (variable degree of diff.) :
well differentiated:
-small glands infiltrate stroma irregularly in haphazard fashion
- glands in back to back appearance & not lining by collagen @ stromal cells
- lining by single layer of cuboidal cells with prominent nucleoli
- basal layer absent
- epithelial cells of adjacent glands show dysplastic changes
5 grades:
Grade 1 most well diff. ( neoplastic gland uniform & rounded & packed into well-circumscribed nodules)
Grade 5 no glandular diff, tumor cells infiltrate stroma in the form of cords, sheets & nests
1. direct to seminal vesicles, wall of urinary bladder. Extension to rectum rare
2. lymphatic to regional L.N (early)
3. blood esp. to bones
Stage T1 : incidentally found cancer
Stage T2 : organ-confined cancer
Stage T3 : extra prostatic extension
Stage T4 : direct invasion of contagious organ
- minority are asymptomatic & diagnosed at autopsy @ removal of prostate in senile hyperplasia
- advanced cases cause symptoms of prostatism:
lower urinary tract obstruction, local discomfort, dysuria, hematuria, frequency
back pain in advance cases
- bone osteoblastic metastases occur in late cases
- > 70 % found peripherally & can be palpated in DIGITAL RECTAl EXAM.
- using: transrectal ultra sonography CT scan MRI
tumor markers ( serum acid phosphatise & prostatic specific antigen
immunohistochemical localization (verification of origin of metastatic tumors)