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I.

Miscellaneous lesions of Tunica Vaginalis II.

Congenital anomaliesLesions Characteristics: Causes:

CRYPTORCHIDSM

HYDROCELE

- accumulation

serous fluid w/in

T.Vaginalis

- incomplete

closure processus

vaginalis- 2ry to generalized

edema @ infected

Incidence:

- incomplete descent of testis to scrotum

- 0.7% of male population- more in right

- 25% bilateral

HEM TOCELE

- accumulation

blood w/in

T.Vaginalis

- 2ry to trauma,

torsion,

hemorrhage,

generalized

bleeding diathesis,

malignt. Invasion

Pathogenesis :

- testis remain in body at its temp (37C)inhibit spermatogenesis

- BUT, testosterone still present

There4: they are infantile but develop 2ry male characteristics

CHYLOCELE

- accumulation

lymphatics w/in

T.Vaginalis

- lymphatic

obstruction

Causes(mostly idiopathic):

- hormonal abnorm. (decrease LHrh)

-genetic abnorm. (trisomy 13)

- short spermatic cord

- mechanicl obstruction in inguinal canal

SPERM TOCELE

- accumulation

semen w/in dilated

eff. Duct in head

epididymis

- obstruction in the

vas deferens

Morphology:

Grossly: early lifenormal

Pubertyatrophy

Micros: 6 yrsatrophy semin. Tubules, Leydig cell hyperplasia, interst. Fibrosis

Pubertyhyalinization of semin. tubules. Regressive changes in othr

testis

V RICOCELE

pampiniform

plexus elongated &dilated

Effects:

-asymptomatic- discovered at puberty (aftr testicular atrophy)

- Bilateralinfertility

- high incidence of malignancy compared to normal positioned testis


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I. Testicular atrophy II. Inflammatory disease of testis & epididymis III. Vascular disturbancesCauses:

- 1ry Klienfelterss syn.

- 2ry because of:

cryptorchidism

vascular diseaseinflammatory disease

hypopituitarism

malnutrition

obstruction semen outflow

increases female sex

hormones

persistant increase of FSH

radiation, chemotherapy

Types: Origin: Spread:

- torsion of testis

( precipitated with trauma @

violent movement )

Pathogenesis:

twisting of spermatic cordsevere venous

engorgement venous

infarction of testis (sac of soft,

necrotic, hemorrhagic tissue )

Risk factors:

- incompletely descended

testicles

- absence of scrotal ligament

- testicular atrophy

a) epididymo-

orchitis

Start: epididymitis

with inflmmtn of

testis proper

(orchitis)

- through ascendg infection via vas deferens by:

lymphatics of spermatic cord

hematogenous

b) nonspecific

epididymitis &orchitis

-1ry infection in

urinary tract-2ry infction of

epididymis &

testis

-2ry infction through ascend infction via:

vas deferenslymphatics of spermatic cord

- causative organisms:

E.coli

pseudomonas

gramve rods

Chlamydia trachomatis

c) autoimmune

(granulomatous)

orchitis

-obscure (not clearly seen)

- trauma & autoimmune

d) specific

inflammation

i- gonorrhoeal

infection

ii- mumps

iii- tuberculosis

iv- syphilis

- STD because of

N. Gonorrhea

-Childrentesticular involvement uncommon

-Postpubertalorchitis (20-30%)

testicular involvement, 70% unilateral

-hematogenous spread to lung, kidney

- congenital @ acquired

- reaction maybe:

localized (gamma)

diffuse (diffuse syphilitic granulation tissue)

- 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


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IV. TESTICULAR NEOPLASMSCharacteristics:

-most imp. cause of firm, painless, enlargement of testis

- Peak incidence15-35 years

- 95% from germ cells (ALL malignant)

- 5% from Leydig cells @ Sertoli cells ( benign, characterized by endocrine abnorm. )

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) B) Sex cord-gonadal stroma

1- seminoma

* confined to testis

* common

metastasize by

lymphatics to

paraaortic & iliac L.N

* radiosensitive

2- non-seminoma

* may have metastases during diagnosis in absence palpable mass

* metastasize early by lymphatics & hematogenous

* radioresistantmore aggressive, poor prognosis

1. Leydig

(interstitial) cell

tumor

2. Sertoli cell tumor

(androblastoma)

Incidence: - most common germ

cell tumor in adult

- 30% of testicular

germ cell tumor

- peak incidence ( 4th

decade )

a.Embroyonal

carcinoma

b.yolk sac

tumor

c.choriocarcinoma d.teratomas

- uncommon

- occurs at any

age, mostly 20-60

yrs

- secretes

androgen,

estrogen,

corticosteroids

- uncommon-aggressive

than seminoma- peak

incidence

20-30 years

- most

common ininfants &

children

-In adults,

occurs as

mixed

germ cell

neoplasm

- highly malignant

- hematogenousmetastasis to liver &

lung

- component of

mixed germ cell

tumor

- peak incidence

20-30 years

-differentiation of

endoderm, mesoderm,ectoderm

- occur at any age

Morphology: Grossly:

- large, soft, well

demarcated, gray-

white, bulges from cut

surface of affected

testis

- large tumor contain

foci of coagulative

necrosis

- confined to testis

only by an intact T.

Albuginea

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


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Microscopically:

1. classic (typical)

85%

- large cells with

distinc borders

- clear glycogen-rich

cytoplasm

- rounded nucleuswith prominent

nucleoli

- cells in small lobules

separated by fibrous

septae containg

lymphocytic infiltrate

- some cases contain

giant cells

2. anaplastic (10%)

3. spermatocytic (5%)

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

Prognosis:

- 90% benign

excellent

prognosis

- 10% malignant

infiltrative &

spreading

tendency

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


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DISE SES OF PROST TE

I) Inflammation of prostate (prostatitis) II) Senile prostatic hyperplasia (nodular@benign prostatic hyperplasia)

--> will not cause prostate carcinomaA- Acute prostatitis B- Chronic prostatitis

- associated with acute

bacterial urinary tractinfection

Ex: E.coli, gram-ve rods,

enterococci, gonococci,

staph.aureus

-bacterial @ non bacterial

-bacteria origin occur on topof acute prostatitis @ -non-

bacteria develop insidiously

w/out previous acute

infection

incidence - hyperplasia of prostatic glands & its stroma

- 20% males age 40 years- 70 % age 60 years

- 90% by 80 years

- fever, chills, dysuria, low

backache

- prostate enlarged, tender,

spongy, soft

- asymptomaticbut

chronic prostatitis may

serve as reservoir causing

urinary tract infection

clinically 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 diverticulae7. bilateral hydronephrosischronic renal failure

etiology -uncertain (related to hormonal changes)

Old ageandrogen dropestrogens action unopposedestrogen increase sensitization of

androgen mainly at central portion of prostateincrease sensitivity to dihydrotestosterone

morphology 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 casesareas of infarcts & sq. metaplasia


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

incidence -most common visceral cancer in males - Peak incidence65-75 years

- 2ndmost common cause of cancer-related death after lung cancer (in men older than 50 yrs)

- occult cancer are more common than clinically apparent

pathogenesis 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 influenceincrease incidence in 1stdegree relatives patient with prostatic cancer

3. environmental factorsin certain industrial settings & significant geographic diff.

morphology Grossly:

- ill defined masses beneath capsule in outer peripheral part of prostate

- Cut sectionfoci 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 cellswith prominent nucleoli

- basal layer absent

- epithelial cells of adjacent glands show dysplastic changes

Grading

(Gleason

system)

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

spread 1. direct to seminal vesicles, wall of urinary bladder. Extension to rectum rare

2. lymphatic to regional L.N (early)

3. bloodesp. to bones

staging Stage T1 :incidentally found cancer

Stage T2 : organ-confined cancer

Stage T3 : extra prostatic extension

Stage T4 : direct invasion of contagious organ

Clinical

features

- 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

diagnosis - > 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)


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