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DISEASES OF TESTIS & EPIDIDYMIS

I.
Lesions

Miscellaneous lesions of Tunica Vaginalis


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

Causes:
- incmplte closure
processous
vaginalis
- 2ry to generalized
edema @ infected

b)hematocele

- accumulation
blood w/in
T.Vaginalis

c)chylocele

- accumulation
lymphatics w/in
T.Vaginalis

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

d)spermatocele

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

a)hydrocele

e)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 bcoz of Klienfelterss
syndrome
- 2ry bcoz of:
cryptorchidism
vascular disease
inflammatory disease
hypopituitarism
malnutrition
obstruction outflow of
semen
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

Origin:
Strts by
epididymitis
with inflmm. Of
testis proper
(orchitis)
-1ry infection in
urinary tract
-2ry infction of
epididymis &
testis

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

d) specific
inflammation
i- gonorrhoeal
infection

- STD bcoz of N.
Gonorrhea

ii- mumps

- viral infection
commonly
affects school
age.

-Children testicular involvement


uncommon
-Postpubertal orchitis (20-30%)
testicular
involvement, 70% unilateral

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

iii- tuberculosis

-begins in
epididymis
-2ry involvement
of testis

iv- syphilis

- begins as
orchitis
-2ry invlvmnt of
epididymis
* mostly orchitis
not assoc. With
epididymitis

-hematogenous spread to lung, kidney

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

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. )

Incidence:

Morphology:

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)


1- seminoma
2- non-seminoma
* confined to testis
* may have metastases during diagnosis in absence palpable mass
* common
* metastasize early by lymphatics & hematogenous
metastasize by
* radioresistant more aggressive, poor prognosis
lymphatics to
paraaortic & iliac
L.N
* radiosensitive
a.Embroyonal b.yolk sac c.choriocarcinoma
d.teratomas
carcinoma
tumor
- most common
-aggressive
- most
- highly malignant
-differentiation of
germ cell tumor in
than
common
- hematogenous
endoderm,
adult
seminoma
in infants metastasis to liver
mesoderm,
- 30% of testicular
- peak
&
& lung
ectoderm
germ cell tumor
incidence
children
- component of
- occur at any age
- peak incidence (
20-30 years
-In adults, mixed germ cell
4th decade )
occurs as tumor
mixed
- peak incidence
germ cell 20-30 years
neoplasm
Grossly:
Grossly:
- large, soft, well
- firm consistency
demarcated, gray- cut surface contain
white, bulges from
cysts & cartilaginous

B) Sex cord-gonadal stroma


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

- uncommon
- occurs at any
age, mostly 2060 yrs
- secretes
androgen,
estrogen,
corticosteroids

- uncommon

- painless
testicular mass
with hormonal
changes

- composed of
Sertoli cells @ mix.
Sertoli & granulose
cells

cut surface of
affected testis
- large tumor
contain foci of
coagulative necrosis
- confined to testis
only by an intact T.
Albuginea
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%)

areas
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

- gynecomastia
in adults
- precocious
puberty in
children
Prognosis:
- 90% benign
excellent
prognosis
- 10% malignant
infiltrative &
spreading
tendency

- secretes
androgen, estrogen
but insufficient to
produce
feminization @
precocious puberty
- mostly benign
- 10% only spread
& infiltrate

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

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

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

--> 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

etiology

morphology

-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

-most common visceral cancer in males


- 2nd most common cause of cancer-related death after lung cancer (in men older than 50 yrs)
- Peak incidence 65-75 years
- 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.

morphology

Grading
(Gleason
system)
spread

staging

Clinical
features

diagnosis

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)