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Kuliah Blok Urogenitalia

Brian Wasita,dr.,Sp.PA, Ph.D


BAGIAN PATOLOGI ANATOMI FK UNS
The clinical presentations of renal disease:
• Azotemiais a biochemical abnormality that refers to an elevation of blood
urea nitrogen (BUN) and creatinine levels, and is related largely to a
decreased glomerular filtration rate (GFR).

• Nephritic syndrome is due to glomerular disease and is dominated by the


acute onset of usually grossly visible hematuria (red blood cells in urine),
mild to moderate proteinuria, and hypertension (the classic presentation of
acute poststreptococcal glomerulonephritis)

• Rapidly progressive glomerulonephritis is characterized as a nephritic


syndrome with rapid decline (hours to days) in GFR.

• The nephrotic syndrome, also due to glomerular disease, is characterized


by heavy proteinuria (more than 3.5 gm/day), hypoalbuminemia, severe
edema, hyperlipidemia, and lipiduria (lipid in the urine).

• Acute renal failure is dominated by oliguria or anuria (reduced or no urine


flow), and recent onset of azotemia. It can result from glomerular,
interstitial, or vascular injury or acute tubular injury.
• Chronic renal failure, characterized by prolonged symptoms and signs of
uremia, is the end result of all chronic renal parenchymal diseases.

• Renal tubular defects are dominated by polyuria (excessive urine


formation), nocturia, and electrolyte disorders (e.g., metabolic acidosis).

• Urinary tract infection is characterized by bacteriuria and pyuria (bacteria


and leukocytes in the urine). The infection may be symptomatic or
asymptomatic, and it may affect the kidney (pyelonephritis) or the bladder
(cystitis).

• Nephrolithiasis (renal stones) is manifested by severe spasms of pain


(renal colic) and hematuria, often with recurrent stone formation.

• Urinary tract obstruction and renal tumors have varied clinical


manifestations based on the specific anatomic location and nature of the
lesion.
Renal Failure

Acute renal failure

• Acute renal failure implies a rapid and frequently reversible


deterioration of renal function.

• “Acute Kidney Injury (Acute Tubular Necrosis),” is the common


disorder.
chronic renal failure
• chronic glomerulonephritis is one of the most
common causes of chronic kidney disease in
humans

• Can be primary and secondary


Glomerular Disease
Structure of the Glomerulus
Immune mechanisms underlie most forms of primary glomerulopathy and many of
the secondary glomerular disorders.
Nephritic syndrome
• The nephritic patient clinical course: hematuria, red cell casts in the urine,
azotemia, oliguria, and mild to moderate hypertension. Proteinuria and
edema are common, but these are not as severe as those encountered in
the nephrotic syndrome,

• Typically caused by immune complexes. The inciting antigen may be


exogenous or endogenous.

• The prototypic exogenous antigen-induced disease pattern is


postinfectious glomerulonephritis, whereas an of an endogenous antigen-
induced disease is the nephritis of SLE.
Acute Proliferative (Poststreptococcal, Postinfectious) Glomerulonephritis

• Characterized histologically by diffuse proliferation of glomerular


cells, associated with influx of leukocytes.

• It usually appears 1 to 4 weeks after a streptococcal infection of


the pharynx or skin (impetigo).

• Skin infections are commonly associated with overcrowding and


poor hygiene.

• Poststreptococcal glomerulonephritis occurs most frequently in


children 6 to 10 years of age, but adults of any age can also be
affected.
Etiology and Pathogenesis:

• Only certain strains of group A β-hemolytic streptococci are nephritogenic,


more than 90% of cases being traced to types 12, 4, and 1.

• Young child : abruptly develops malaise, fever, nausea, oliguria, and


hematuria (smoky or cola-colored urine) 1 to 2 weeks after recovery from a
sore throat. The patients have red cell casts in the urine, mild proteinuria
(usually less than 1 gm/day), periorbital edema, and mild to moderate
hypertension.

• Adults : the onset is more likely to be atypical, such as the sudden


appearance of hypertension or edema, frequently with elevation of BUN
Nephrotic syndrome
The manifestations of the nephrotic syndrome include:

1.Massive proteinuria, with the daily loss of 3.5 gm or more of protein (less in
children).

2.Hypoalbuminemia, with plasma albumin levels less than 3 gm/dL

3.Generalized edema

4.Hyperlipidemia and lipiduria


• Membranous nephropathy is a common cause of the nephrotic syndrome
in adults.

• It is characterized by diffuse thickening of the glomerular capillary wall due


to the accumulation of electron-dense, Ig-containing deposits along the
subepithelial side of the basement membrane.
Membranous nephropathy. A,
Diffuse thickening of the
glomerular basement membrane
(periodic acid–Schiff stain). D,
Schematic diagram illustrating
subepithelial deposits, effacement
of foot pro-cesses, and the
presence of spikes of basement
membrane material between the
immune deposits.
Chronic glomerulonephritis

• Chronic glomerulonephritis is best considered a pool of end-


stage glomerular disease fed by several streams of specific
types of glomerulonephritis
Tubular and Interstitial Diseases

Two major groups of two major groups of processes:

1.Ischemic or toxic tubular injury, leading to acute kidney injury


(AKI) and acute renal failure.

2. Inflammatory reactions of the tubules and interstitium


(tubulointerstitial nephritis)
• AKI, a term increasingly favored over the often synonymously used terms
acute tubular necrosis (ATN) and acute tubular injury, is a clinicopathologic
entity characterized clinically by acute diminution of renal function and
often, but not invariably, morphologic evidence of tubular injury.

• It is the most common cause of acute renal failure which signifies rapid
reduction of renal function and urine flow, falling within 24 hours to less
than 400 mL per day.
Causes:

• Ischemia

• Direct toxic injury to the tubules (e.g., by drugs, radiocontrast


dyes, myoglobin, hemoglobin, radiation)

• Acute tubulointerstitial nephritis, most commonly occurring as a


hypersensitivity reaction to drugs

• Urinary obstruction by tumors, prostatic hypertrophy, or blood


clots (so-called postrenal acute renal failure)
Tubulointerstitial nephritis

• This group of renal diseases is characterized by histologic and


functional alterations that involve predominantly the tubules and
interstitium

• Tubulointerstitial nephritis can be acute or chronic.

• A rapid clinical onset and is characterized histologically by


interstitial edema, often accompanied by leukocytic infiltration of
the interstitium and tubules, and focal tubular necrosis.

• In chronic interstitial nephritis there is infiltration with


predominantly mononuclear leukocytes, prominent interstitial
fibrosis, and widespread tubular atrophy.
Pyelonephritis and UTI

• Pyelonephritis is a renal disorder affecting the tubules,


interstitium, and renal pelvis and is one of the most common
diseases of the kidney.

• Acute pyelonephritis is caused by bacterial infection and is the


renal lesion associated with urinary tract infection.

• Chronic pyelonephritis is a more complex disorder; bacterial


infection plays a dominant role, but other factors (vesicoureteral
reflux, obstruction) are involved in its pathogenesis
• The dominant etiologic agents (85%) of cases of UTI: gram-
negative bacilli that are normal inhabitants of the intestinal tract
(the most common is Escherichia coli, followed by Proteus,
Klebsiella, and Enterobacter).

• Streptococcus faecalis, also of enteric origin, staphylococci, and


virtually every other bacterial and fungal agent can also cause
lower urinary tract and renal infection.

• In immunocompromised persons, particularly those with


transplanted organs, viruses such as Polyomavirus,
cytomegalovirus, and adenovirus can also be a cause of renal
infection.

• There are two routes by which bacteria can reach the kidneys:
(1) through the bloodstream (hematogenous infection) and (2)
from the lower urinary tract (ascending infection)
•Acute pyelonephritis is an acute suppurative inflammation of the kidney caused by
bacterial and sometimes viral (e.g., polyomavirus) infection, whether hematogenous
and induced by septicemic spread or ascending and associated with vesicoureteral
reflux.
Morphology :

• The hallmarks of acute pyelonephritis


are patchy interstitial suppurative
inflammation, intratubular aggregates
of neutrophils, and tubular necrosis.
The suppuration may occur as
discrete focal abscesses involving
one or both kidneys, which can
extend to large wedge-shaped areas
of suppuration.
• The distribution of these lesions is
unpredictable and haphazard, but in
pyelonephritis associated with reflux,
damage occurs most commonly in the
lower and upper poles
• In the early stages, the neutrophilic infiltration is limited to the interstitial tissue.
Soon, however, the reaction involves tubules and produces a characteristic abscess
with the destruction of the engulfed tubules.
• Large masses of intraluminal neutrophils frequently extend along the involved
nephron into the collecting tubules. Characteristically, glomeruli seem to be
relatively resistant to the infection.
• Large areas of severe necrosis, however, eventually destroy the glomeruli, and
fungal pyelonephritis (e.g., Candida) often affects glomeruli.
Chronic pyelonephritis

• Chronic pyelonephritis is a disorder in which chronic


tubulointerstitial inflammation and renal scarring are associated
with pathologic involvement of the calyces and pelvis.

• Chronic pyelonephritis is an important cause of end-stage


kidney disease.

• an important cause of kidney destruction in children with severe


lower urinary tract abnormalities.
Macroscopic:

• The kidneys usually are irregularly scarred; if


bilateral, the involvement is asymmetric.
This contrasts with chronic
glomerulonephritis, in which both kidneys
are diffusely and symmetrically scarred.

• The hallmarks of chronic pyelonephritis are


coarse, discrete, corticomedullary scars
overlying dilated, blunted, or deformed
calyces, and flattening of the papillae.The
scars can vary from one to several in
number and may affect one or both kidneys.
Most are in the upper and lower poles,
consistent with the frequency of reflux in
these sites.
• The microscopic changes involve predominantly tubules and interstitium.

• The tubules show atrophy in some areas and hypertrophy or dilation in others. Dilated tubules with flattened epithelium may
be filled with colloid casts (thyroidization). There are varying degrees of chronic interstitial inflammation and fibrosis in the
cortex and medulla. In the presence of active infection there may be neutrophils in the interstitium and pus casts in the
tubules. Arcuate and interlobular vessels demonstrate obliterative intimal sclerosis in the scarred areas; and in the presence
of hypertension, hyaline arteriosclerosis is seen in the entire kidney. There is often fibrosis around the calyceal epithelium as
well as a marked chronic inflammatory infiltrate. Glomeruli may appear normal except for periglomerular fibrosis, or exhibit a
variety of changes, including ischemic fibrous obliteration and secondary changes related to hypertension.
Vascular Diseases
Congenital Abnormalities

• Congenital renal disease can be hereditary but is most often the


result of an acquired developmental defect that arises during
gestation.

• Agenesis, hipoplasia, ectopic, horseshoe kidney.

Horseshoe kidney:

• Fusion of the upper or lower poles of the kidneys produces a


horseshoe-shaped structure that is continuous across the midline
anterior to the great vessels.

• This anatomic anomaly is common and is found in about 1 in 500


to 1000 autopsies. Ninety percent of such kidneys are fused at the
lower pole, and 10% are fused at the upper pole.
Cystic diseases of the kidney

•Cystic diseases of the kidney are heterogeneous, comprising hereditary, developmental, and
acquired disorders.

Clinical course:

•Asymptomatic until renal insufficiency announces the presence of the disease.

•Hemorrhage or progressive dilation of cysts may produce pain.

•Excretion of blood clots causes renal colic.

•The enlarged kidneys, usually apparent on abdominal palpation, may induce a dragging
sensation.

•The disease occasionally begins with the insidious onset of hematuria, followed by other
features of progressive chronic kidney disease, such as proteinuria (rarely more than 2
gm/day), polyuria, and hypertension
• Morphology. In gross appearance, the kidneys are usually bilaterally
enlarged and may achieve enormous sizes; weights as high as 4 kg for
each kidney have been reported. The external surface appears to be
composed solely of a mass of cysts, up to 3 to 4 cm in diameter, with
no intervening parenchyma.
Microscopic examination

•Reveals functioning nephrons dispersed between the cysts.

•The cysts may be filled with a clear, serous fluid or, more usually, with
turbid, red to brown, sometimes hemorrhagic fluid.

•As these cysts enlarge, they may encroach on the calyces and pelvis to
produce pressure defects.

•The cysts arise from the tubules throughout the nephron and therefore have
variable lining epithelia.

•On occasion, papillary epithelial formations and polyps project into the
lumen. Bowman capsules are occasionally involved in cyst formation, and
glomerular tufts may be seen within the cystic space.
Urinary obstruction
• Obstruction increases susceptibility to infection and to stone
formation, and unrelieved obstruction almost always leads to
permanent renal atrophy, termed hydronephrosis or obstructive
uropathy.

• Obstruction may be sudden or insidious, partial or complete,


unilateral or bilateral.

• May occur at any level of the urinary tract from the urethra to
the renal pelvis.

• Can be caused by lesions that are intrinsic to the urinary tract


or extrinsic lesions that compress the ureter.
The common causes are as follows :

1.Congenital anomalies: posterior urethral valves and urethral strictures, meatal stenosis, bladder
neck obstruction; ureteropelvic junction narrowing or obstruction; severe vesicoureteral reflux

2.Urinary calculi

3.Benign prostatic hypertrophy

4.Tumors: carcinoma of the prostate, bladder tumors, contiguous malignant disease


(retroperitoneal lymphoma), carcinoma of the cervix or uterus

5.Inflammation: prostatitis, ureteritis, urethritis, retroperitoneal fibrosis

6.Sloughed papillae or blood clots

7.Pregnancy

8.Uterine prolapse and cystocele

9.Functional disorders: neurogenic (spinal cord damage or diabetic nephropathy) and other
functional abnormalities of the ureter or bladder (often termed dysfunctional obstruction)
Hydronephrosis

• Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney
due to obstruction to the outflow of urine

• The kidney may be slightly to massively enlarged, depending on the degree and the
duration of the obstruction.

• The earlier features are those of simple dilation of the pelvis and calyces, but in addition
there is often significant interstitial inflammation, even in the absence of infection.

• In chronic cases the picture is one of cortical tubular atrophy with marked diffuse
interstitial fibrosis. Progressive blunting of the apices of the pyramids occurs, and these
eventually become cupped.

• In far-advanced cases the kidney may become transformed into a thin-walled cystic
structure having a diameter of up to 15 to 20 cm with striking parenchymal atrophy, total
obliteration of the pyramids, and thinning of the cortex.
Clinical course

• Acute obstruction may provoke pain attributed to distention of


the collecting system or renal capsule. Most of the early
symptoms are produced by the underlying cause of the
hydronephrosis. Thus, calculi lodged in the ureters may give
rise to renal colic, and prostatic enlargements may give rise to
bladder symptoms.

• Unilateral complete or partial hydronephrosis may remain silent


for long periods, since the unaffected kidney can maintain
adequate renal function.
• In bilateral partial obstruction the earliest manifestation is inability to
concentrate the urine, reflected by polyuria and nocturia. Some patients
have acquired distal tubular acidosis, renal salt wasting, secondary renal
calculi, and a typical picture of chronic tubulointerstitial nephritis with
scarring and atrophy of the papilla and medulla. Hypertension is common
in such patients.

• Complete bilateral obstruction results in oliguria or anuria and is


incompatible with survival unless the obstruction is relieved. Curiously,
after relief of complete urinary tract obstruction, postobstructive diuresis
occurs. This can often be massive, with the kidney excreting large
amounts of urine that is rich in sodium chloride.
Renal Stone
• Stones are of importance when they obstruct urinary flow or produce
ulceration and bleeding.

• They may be present without producing any symptoms or they may cause
significant renal damage.

• In general, smaller stones are most hazardous, because they may pass
into the ureters, producing colic, one of the most intense forms of pain, and
ureteral obstruction.

• Larger stones cannot enter the ureters and are more likely to remain silent
within the renal pelvis. Commonly, these larger stones first manifest
themselves by hematuria. Stones also predispose to superimposed
infection, both by their obstructive nature and by the trauma they produce.
Morphology. Stones are unilateral in about 80% of patients. The favored sites for
their formation are within the renal calyces and pelves and in the bladder. If formed
in the renal pelvis they tend to remain small, having an average diameter of 2 to 3
mm. These may have smooth contours or may take the form of an irregular, jagged
mass of spicules. Often many stones are found within one kidney.
Tumor of Kidney

• Benign : renal papillary adenoma, angiolipoma, oncocytoma.

• Malignant : renal cell carcinoma, Wilms tumor, urothelial


tumors of the calyces and pelves
Renal cell carcinoma

• The tumors occur most often in older individuals, usually in the sixth and
seventh decades of life, and show a 2 : 1 male preponderance.

• Because of their gross yellow color and the resemblance of the tumor
cells to clear cells of the adrenal cortex, they were at one time called
hypernephroma. It is now clear that all these tumors arise from tubular
epithelium and are therefore renal adenocarcinomas.

• Risk factor: tobacco, obesity (particularly in women); hypertension;


unopposed estrogen therapy; and exposure to asbestos, petroleum
products, and heavy metals
• The three classic diagnostic features of renal cell carcinoma are
costovertebral pain, palpable mass, and hematuria, but these are seen in
only 10% of cases.

• The most reliable of the three is hematuria, but it is usually intermittent


and may be microscopic; thus, the tumor may remain silent until it attains a
large size.

• Often associated with generalized constitutional symptoms, such as fever,


malaise, weakness, and weight loss.

• This pattern of asymptomatic growth occurs in many patients, so the tumor


may have reached a diameter of more than 10 cm when it is discovered.

• Paraneoplastic syndromes : ascribed to abnormal hormone production,


including polycythemia, hypercalcemia, hypertension, hepatic dysfunction,
feminization or masculinization, Cushing syndrome, eosinophilia,
leukemoid reactions, and amyloidosis
• One of the common characteristics of this tumor is its tendency
to metastasize widely before giving rise to any local symptoms
or signs.

• In 25% of new patients with renal cell carcinoma, there is


radiologic evidence of metastases at the time of presentation.
The most common locations of metastasis are the lungs (more
than 50%) and bones (33%), followed in frequency by the
regional lymph nodes, liver, adrenal, and brain.

• The average 5-year survival rate of persons with renal cell


carcinoma is about 45% and as high as 70% in the absence of
distant metastases

• Nephrectomy has been the treatment of choice, but partial


nephrectomy to preserve renal function is being done with
increasing frequency and similar outcome.
Morphology:

• Renal cell carcinomas may arise in any


portion of the kidney, but more commonly
affects the poles.

• Clear cell carcinomas arise most likely


from proximal tubular epithelium, and
usually occur as solitary unilateral lesions.
They are spherical masses, which can
vary in size, composed of bright yellow-
gray-white tissue that distorts the renal
outline. The yellow color is a consequence
of the prominent lipid accumulations in
tumor cells. There are commonly large
areas of ischemic, opaque, gray-white
necrosis, and foci of hemorrhagic
discoloration. The margins are usually
sharply defined and confined within the
renal capsule
Clear cell carcinoma the growth pattern varies from solid to trabecular (cordlike) or tubular (resembling tubules). The tumor cells
have a rounded or polygonal shape and abundant clear or granular cytoplasm, which contains glycogen and lipids). The tumors
have delicate branching vasculature and may show cystic as well as solid areas. Most tumors are well differentiated, but some
show marked nuclear atypia with formation of bizarre nuclei and giant cells.
Papillary carcinoma is composed of cuboidal or low columnar cells arranged in papillary formations. Interstitial foam cells are
common in the papillary core. Psammoma bodies may be present. The stroma is usually scanty but highly vascularized.
Chromophobe renal carcinoma is made up of pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a
concentration of the largest cells around blood vessels.
Wilms Tumor

• The peak incidence for Wilms tumor is between 2 and 5 years of age, and
95% of tumors occur before the age of 10 years.

• Approximately 5% to 10% of Wilms tumors involve both kidneys, either


simultaneously (synchronous) or one after the other (metachronous).

• Bilateral Wilms tumors have a median age of onset approximately 10


months earlier than tumors restricted to one kidney, and these patients are
presumed to harbor a germline mutation in one of the Wilms tumor–
predisposing genes.
Most children with Wilms tumors present with a large abdominal
mass that may be unilateral or, when very large, may extend
across the midline and down into the pelvis.

Hematuria, pain in the abdomen after some traumatic incident,


intestinal obstruction, and appearance of hypertension are other
patterns of presentation.

In a considerable number of these patients, pulmonary


metastases are present at the time of primary diagnosis.
Grossly :

• Wilms tumor tends to present as a


large, solitary, well-circumscribed
mass, although 10% are either bilateral
or multicentric at the time of diagnosis.

• On cut section, the tumor is soft,


homogeneous, and tan to gray with
occasional foci of hemorrhage, cyst
formation, and necrosis.
Microscopically, Wilms tumors are characterized by recognizable attempts to recapitulate
different stages of nephrogenesis.

The classic triphasic combination of blastemal, stromal, and epithelial cell.Sheets of small
blue cells with few distinctive features characterize the blastemal component. Epithelial
differentiation is usually in the form of abortive tubules or glomeruli. Stromal cells are
usually fibrocytic or myxoid in nature, although skeletal muscle differentiation is not
uncommon.
ANATOMI
KELAINAN KONGENITAL
HIPOSPADIA

Hipospadia
 orifisium uretra yang
abnormal disepanjang
aspek ventral penis
 1 dari 300 kelahiran
hidup bayi laki-laki
EPISPADIA

Epispadia
 Orifisium uretra di
aspek dorsal penis
FIMOSIS

Lubang preputium terlalu


kecil sehingga tidak bisa
diretraksi

Dapat akibat perkembangan


yang abnormal tapi juga bisa
dari infeksi yg menyebabkan
jaringan parut cincin preputium
LESI NON NEOPLASTIK
Balanoposthitis

Infeksi pada glans penis dan


preputium oleh berbagai
macam organisme
(Candida albicans,Gardnerrella sp,
bakteri piogenik Staphylococcus aureus)

Pada umumnya disebabkan


oleh kurangnya kebersihan pd
pria yang tidak disirkumsisi,
dimana smegma sebagai
local irritant
Balanoposthitis

Infeksi yang menetap dapat menyebabkan jaringan parut, dimana sebagai


penyebab umum fimosis
PRIMARY SYPHILIS
(CHANCRE)
Infeksi seksual yang disebabkan Spirokaeta, Treponema pallidum

Sifilis di glans penis


PRIMARY SYPHILIS
(CHANCRE)

Mikroskopis:
Epidermis yang tipis dan
kadang-kadang ulcerasi disertai
infiltrat padat limfosit dan sel plasma
Pembuluh darah mengalami hipertrofi
dan proliferasi sel endotel, infiltrasi sel
inflamasi di dinding pembuluh darah
Spirochetes dapat ditunjukkan dengan
pengecatan Warthin-Starry silver stain
TUMOR
Condyloma acuminatum
Penyakit menular seksual
yg disebabkan HPV tipe 6
kadang2 tipe 11
Pertumbuhan pedunculated,
sessile, papiler merah pd meatus
penis atau fossa navicularis
atau bagian lain di glans penis
Condyloma acuminatum, low power.

There is thickening of the epidermis


with rounded thickened rete ridges,
with little or no thickening of the
stratum corneum. There may be focal
areas of parakeratosis.

Condyloma acuminatum, high


power.

There are koilocytotic changes of virally


affected keratinocytes, including
hypergranulosis, perinuclear vacuoles,
and irregular nuclear membranes.
Low magnification reveals
the papillary (villous)
architecture, and thickening
of the epidermis

The epithelium shows


vacuolization
(koilocytosis)
characteristic of human
papillomavirus infection
Carcinoma in Situ
(CIS)

BOWENOID
Bowen disease PAPULOSIS
BOWEN DISEASE

Biasanya pada usia >35 tahun


Infeksi HPV,paling sering tipe 16
Pada pria  kulit batang penis
dan scrotum
10%  infiltrating squamous cell
carcinoma
Secara makroskopis
tampak sebagai plak solid,
menebal, abu-abu putih, opak.
Dapat juga muncul di glans penis
& preputium sebagai plak merah
terang tunggal atau multipel

Penile Bowen disease. Bowen disease


appearing as a well demarcated reddish
plaque on the inner aspect of the foreskin.
BOWEN DISEASE

Mikroskopis . Tampak proliferasi epidermis dengan banyak


mitosis, atipia. Sel mengalami displasi dengan inti besar,
hiperkromatis dan maturasi yang tidak teratur
Membran basalis masih utuh
There is full-thickness atypia,
with pleomorphism and high
mitotic activity

Note the hyperchromatic,


dysplastic dyskeratotic
epithelial cells with scattered
mitoses above the basal layer.
The intact basement
membrane is not readily seen
in this picture.
Bowenoid papulosis

Pada orang dewasa aktif secara seksual.


Perbedaan dengan Bowen disease adalah umur
yang lebih muda dan gambaran klinis yaitu adanya
lesi papular berwarna merah coklat yang mutipel
Bowenoid papulosis

Secara Histologi
 bowenoid papulosis tidak dapat
dibedakan dengan Bowen disease
 terkait dengan HPV type 16.

Tidak berkembang menjadi


invasive carcinoma & dalam
banyak kasus regresi spontan.
Clinical appearance of bowenoid papulosis in the skin
of the scrotum. The lesions are small, multiple
hyperpigmented.
Squamous cell carcinoma

Resiko karsinoma sel skuamous dapat dikurangi dengan dilakukannya sirkumsisi


sesegera mungkin, karena berhubungan dengan smegma
Berhubungan juga dengan infeksi HPV
 ditemukan HPV DNA pada 50% kasus SCC
Paling banyak timbul di glans penis, preputium dan sulcus corona
Squamous cell carcinoma

Pola pertumbuhan dapat menyebar superifisial,


exophytic (fungating verruciform) atau endophytic
(infiltartif, ulcerating, vertical).
Dapat pola campuran
Pola pertumbuhan exophytic lebih baik
differensiasinya daripada endophytic

The glans penis is


deformed by a firm,
ulcerated, infiltrative
mass
Outer aspect (A) and cut surface (B) of squamous cell carcinoma of penis showing a papillomatous pattern of growth.
Penile squamous cell carcinoma with extensive
involvement of prepuce.
Squamous cell carcinoma

Pada gambaran mikroskopis, dibagi menjadi tipe usual, warty(condylomatous),


verrocous dan papillary NOS.
Hanya pada bentuk warty (condylomatous) yang terdapat atipia koilocitosis difus
Verrucous carcinoma  varian exophytic well-differentiated squamous cell
carcinoma
low malignant potential.
locally invasive, but they rarely metastasize.
SQUAMOUS CELL CARCINOMA

The boundaries between stroma Deeply invasive carcinomas may focally show spindle,
and tumour are irregular or finger pleomorphic, acantholytic, giant, basaloid or clear cells.
like.
SCROTUM
LESI NON NEOPLASTIK

HIDROKEL
Akumulasi cairan serosa dalam tunika vaginalis
 Akumulasi darah (hematokel), cairan limfe (kilokel)
 Bedakan spermatocele (asal epididimis) ada sperma
dalam cairan kista.

Outer appearance of hydrocele. The wall is translucent and the content had a serous quality.
NEOPLASMA

Tumor jinak&ganas jarang terjadi sebagian besar dari


adneksa kulit
Leiomioma tumor jinak
mesenkimal paling umum
Karsinoma sel skuamosa
 neoplasma tersering,
berkaitan dgn faktor lingkungan
(pekerja cerobong asap,parafin,
tar,pabrik kapas)
Leiomyoma of tunica dartos.
TESTIS DAN EPIDIDIMIS
KELAINAN KONGENITAL
CRIPTOCHIDISM
• Kegagalan turunnya testis ke kantong scrotum
• Pada 1% bayi usia 1 tahun
• Asimptomatik, ditemukan oleh pasien atau
pemeriksa ketika kantong scrotum tidak berisi
testis
• Kebanyakan unilateral, 25% bilateral
• Perubahan histologis mulai usia 2 tahun,
hambatan perkembangan sel germinal yang
berhubungan dengan hialinisasi dan
penebalan membran basal tubulus
spermatikus
• Tubulus tampak sebagai berkas padat jaringan
ikat yang dibatasi membran basal
• Peningkatan stroma interstitial
• Atrofi tubulus, testis kecil dan lunak
A. Normal testis shows tubules with active spermatogenesis.
B. Testicular atrophy in cryptorchidism. The tubules show Sertoli cells but no
spermatogenesis. There is thickening of basement membranes and an apparent
increase in interstitial Leydig cells.
REGRESSIVE CHANGES
Atrophy and Decreased Fertility
• Beberapa penyebab atrofi :
– Aterosclerosis pada usia tua
– Orchitis tahap akhir
– Cryptochidism
– Hipopituitari
– Malnutrisi berat
– Radiasi
– Pemberian anti-androgen jangka panjang
– Exhaustion atrophy (pemberian folikel stimulating
pituitary hormon dosis tinggi)
INFLAMASI
Nonspecific Epididymitis and Orchitis
• Berhubungan dengan infeksi di traktus
urinarius (cystitis, urethitis, prostatitis)
• Pada pria usia <35 tahun, paling sering oleh C.
Trachomatis dan N. Gonorrhea
• Pada usia>35 tahun, paling sering E. Coli dan
pseudomonas
• Edema, infiltrasi leukosit PMN, makrofag, dan
limfosit

Acute epididymitis caused by gonococcal infection. The


epididymis is replaced by an abscess. Normal testis is seen on the
right
• Gonorrhea
– Perluasan infeksi dari uretra posterior-prostat-
vesika seminalis-epididimis. Gambaran sama
dengan infeksi nonspesifik
• Mumps
– Penyakit virus sistemik yang paling mengenai anak
usia sekolah
• Tuberculosis
– Di epididimis dan dapat menyebar ke testis.
Muncul reaksi inflamasi kaseosa granulomatosus
• Sifilis
VASCULAR DISORDERS
TORSI TESTIS
• Torsi menyebabkan putusnya drainase vena
dari testis
• Arteri yang berdinding tebal tetap utuh
menyebakan infark hemoragik
• Dua tipe torsi: neonatal dan dewasa; neonatal
torsion pada waktu bayi belum lahir atau baru
lahir karena defek anatomik, adult torsion
karena cedera
Depending on the duration of the process, the morphologic changes
range from intense congestion to widespread extravasation of blood
into the interstitial tissue to hemorrhagic testicular infarction ( Fig.
21-22 ). In these late stages the testis is markedly enlarged and is
converted virtually into a sac of soft, necrotic, hemorrhagic tissue
TUMOR
SPERMATIC CORD AND
PARATESTICULAR TUMORS
• Lipomas, benign neoplasia, matur white adipose
origin
• Adenomatoid tumor, mesothel origin, biasanya
berupa nodul kecil, biasanya terjadi di dekat
epididimis bagian atas. Merupakan salah satu
tumor jinak yang terjadi di dekat testis
• Malignant paratesticular tumors, mesenkhimal
tumor yang paling sering terjadi di ujung distal
dari spermatic cord, rhabdomyosarcomas pada
anak-anak dan liposarcomas pada dewasa
TESTICULAR TUMORS

• 95% dari tumor testis


adalah dari germ cell.
• Kebanyak germ cell
tumor adalah kanker
yang agresif dan cepat
menyebar walaupun
dapat disembuhkan.
• Sex cord stromal tumor
secara umum jinak
GERM CELL TUMOR
SEMINOMA TESTIS
• Germ cell tumor yang paling sering
• Insidensi tertinggi pada usia 30an, hampir
tidak pernah terjadi pada infant.
• 25% dari tumor ini mempunyai mutasi yang
mengaktivasi c-KIT
• Marker: PLAP, OCT 3/4 dan NANOG
Seminoma of the testis appears as a fairly well-circumscribed, pale,
fleshy, homogeneous mass.
Kadang-kadang 10x ukuran testis normal, permukaan homogen, abu-abu
putih, berlobus-lobus, tanpa perdarahan atau nekrosis
Seminoma Klasik

Seminoma
A. Low magnification shows clear seminoma cells divided into poorly demarcated lobules by
delicate septa.
B. Microscopic examination : large cells with distinct cell borders, pale nuclei, prominent
nucleoli, and a sparse lymphocytic infiltrate. Cells are large, round-polyhedral with distinct
cell membranes, abundant clear/watery cytoplasm (glycogen), large central nuclei, 1-2
prominent often elongated and irregular nucleoli. Usually minimal mitotic figures.
Granulomatous inflammation with Langhans type multinucleated giant cells present in
20%
Yolk Sac Tumor
• Tumor testis yang paling sering terjadi pada bayi dan anak-
anak < 3 tahun
• 50% tumor dapat terlihat endodermal sinuses (Schiller-Duval
Bodies): inti mesodermal dengan papiler di tengah dan lapisal
sel visceral dan parietal seperti glomelurus primitif
• Schiller–Duval bodies mirip dengan glomelurus, mempunyai
inti mesodermal dengan papiler di tengah, dilapisi oleh sel
pipih baik sel visceral dan sel parietal
• Adanya PAS dan AFP staining positif untuk hialin globul
Germ Cell tumor (GCT) Non Seminomatous tumor

Yolk sac tumor


• Tumor sinus endoderm
• Anak : tumor testis tersering
anak umur < 3 thn
• Dewasa : sering ditemukan
bercampur dgn embrional
carcinoma
• Makroskopis: tidak berkapsul, pada pembelahan tampak homogen kuning-
putih, mucinous.
Yolk sac tumor

Primitive tumor cells, which are relatively small and less pleomorphic relative to embryonal carcinoma.
Majority cases of these tumors is microcystic structure, which is characterized by the presence of a
spider-weblike network formed by vacuolated cytoplasm of tumor cells, similar to a honeycomb.
Schiller Duval bodies (Yolk sac tumor)

Schiller-Duvall body. A Schiller-Duvall body is a structure resembling the endodermal sinus,


characterized by the presence of a central vessel, surrounded by fibrous tissue and epithelial tumor
cells, in a space lined by flat tumor cells.
Choriocarcinoma
• Tumor testis yang sangat ganas
• Sering tidak menyebabkan pembesaran testis
dan hanya sebagai nodul kecil
• Kecil, umumnya <5cm
• Sering ditemukan perdarahan dan nekrosis
• Mengandung 2 tipe sel : Syncytiotrohosblast
dan cytotrophoblast
• Sel cytotrophoblast lebih regular dan
cenderung poligonal, dengan batas jelas dan
sitoplasma jernih, mereka tumbuh sebagai
cord atau massa dan mempunyai inti tunggal
dan seragam
• Sel syncytiotrophoblast besar dan banyak inti
hiperkromatis ireguler atau lobular dan
banyak sitoplasma eosinofilik bervakuola.
HCG mudah diperlihatkan di sitoplasma
Choriocarcinoma shows clear cytotrophoblastic cells (arrowhead) with
central nuclei and syncytiotrophoblastic cells (arrow) with multiple dark
nuclei embedded in eosinophilic cytoplasm. Hemorrhage and necrosis
are seen in the upper right field
Teratoma
• Kelompok tumor testis yang mempunyai bermacam-
macam sel atau komponen organ dari lebih satu
lapisan germinal.
• Dapat terjadi pada usia berapapun
• Makroskopis : besar, diameter 5-10 cm, dari
bermacam-macam jaringan, tampak ada yang solid,
kartilago, dan daerah kistik
• Teratoma terdiri dari berbagai macam differensiasi sel
dan struktur organ, seperti jaringan saraf, otot,
kartilago, kelompok epitel squamous, struktur seperti
kelenjar tiroid, epitel bronkus atau bronkiolus, dan
sedikit dinding usus atau otak, semua menempel pada
jaringan ikat atau jaringan miksoid
• Teratoma ada tiga :
– Teratoma mature
– Teratoma immature
– Malignant transformation of teratoma
Teratoma of testis. The variegated
cut surface with cysts reflects the
multiplicity of tissue found
histologically

Teratoma of the testis consisting of


a disorganized collection of glands,
cartilage, smooth muscle, and
immature stroma
Teratoma
Tumors of Sex Cord–Gonadal Stroma
Sertoli Cell Tumors
• Most Sertoli cell tumors are hormonally silent
and present as a testicular mass
• Tumor ini tampak sebagai nodul kecil, lunak dan
pada pembelahan tampak berwarna abu-abu
putih sampai kuning
• Mikroskopis, sel tumor tersusun dalam trabekula
yang membentuk struktur tali(cord) dan tubulus
• Kebanyak tumor sel sertoli adalah jinak, tapi
sekitar 10% adalah ganas
Tumor sel sertoli (Androblastoma)

• Terkadang berhubungan
dengan ginekomastia
• Melepaskan hormon
androgen ,estrogen
• Sebagian besar bersifat
jinak
• 10% Metastasis
• Mitosis
• Pleomorphis
• Ukuran sel besar
• Nekrosis
Tumor sel sertoli

sel tumor tersusun dalam trabekula yang membentuk struktur tali(cord) dan tubulus
LIMFOMA TESTIS

• NHL, diffuse large B-cell


lymphoma
• 5% dari tumor testis
• Sering pada usia > 60 thn
• Prognosis buruk
Limfoma testis
Limfoma testis
MISCELLANEOUS LESIONS OF TUNICA
VAGINALIS
• Hydrocele : akumulasi cairan serosa di tunica
vaginalis, menyebabkan pembesaran scrotum
• Hematocele : adanya darah di tunica vaginalis
• Chylocele : akumulasi limfa di tunica
• Spermatocele : kista kecil, akumulasi semen di
ductus eferen yang berdilatasi atau di ductus
rete testi
• Varicocele : dilatasi vena di spermatic cord.
ANATOMI PROSTAT
• fibromuscular tissue
(30-50%)
• glandular epithelial cells
(50-70%)
• peripheral zone (>>
cancer)
• central zone
• transition zone
(BPH,low grade cancer)
PROSTAT
• Berat prostat hampir 20 gram
• Prostat merupakan organ retroperitoneal yang
mengelilingi kandung kemih dan uretra, tanpa
kapsul yang jelas.
• Parenkimprostat dapat dibagi dalam 4
zona/bagian: perifer,central,transisional, dan
bagian stroma fibromuskular anterior
• Tipe lesi proliferasi berbeda disetiap bagian
(hiperplasia terjadi sering di bagian transisional,
sedang carsinoma pada bagian perifer)
KELENJAR PROSTAT NORMAL
PROSES PATOLOGI

• 1. INFLAMASI
• 2. HIPERTROFI NODULAR JINAK→ >>
• 3. TUMOR
1. INFLAMASI
Prostatitis bakterialis akut
Prostatitis bakterialis kronik
Prostatitis non-bakterialis kronik
Prostatitis granulomatosa
PROSTATITIS BAKTERIAL AKUT
- >> Karena E.coli
- biasanya akibat intraprostatik reflux urin
dari uretra posterior atau kandung kemih,
bisa juga merupakan penyebaran
limpohematogen dari fokus infeksi yang jauh
- akibat dari manipulasi pada uretra atau prostat
(kateterisasi,cystoscopy,dilatasi uretra, reseksi
prostat)
PROSTATITIS BAKTERIAL AKUT
• Gejala klinis prostatitis bakterial akut berupa
panas, disuria, menggigil.
• Pemeriksaan prostat : lembek,nyeri tekan
• Diagnosis : kultur urin dan pemeriksaan klinis
PROSTATITIS BAKTERIAL AKUT

Infiltrat radang dalam lumen, area nekrosis, stroma sembab (gambaran abses)
PROSTATITIS BAKTERIAL KRONIS

• gejala klinis: low back pain,disuria, rasa tidak


nyaman pada perineal dan suprapubik
• simptomatik
• sering mempunyai riwayat infeksi saluran
kemih berulang (cystitis,urethritis)
• Diagnosis : berdasar gambaran leukositosis
pada sekresi prostat,dengan kultur bakteri
positif
Dense lymphocytic infiltrate in prostatic stroma with focal
infiltration into the epithelium
PROSTATITIS NON BAKTERIAL KRONIS

• Paling sering ditemukan saat ini


• Gejala klinis seperti prostatitis bakterial
kronis, tanpa riwayat ISK
• Diagnosa : sekret prostat (>10 neutrofil/LPK),
kultur bakteri negatif
PROSTATITIS GRANULOMATOSA

• Granulomatosa prostatitis nonspesifik muncul


ditandai dengan reaksi sekresi dari duktus dan
acini prostat yg rusak
• Bisa dikarenakan ISK,fungal, tuberculosa
sistemik
PROSTATITIS GRANULOMATOSA

Granulomatous prostatitis. The inflammatory infiltrate,


which contains scattered multinucleated cells, is
characteristically centered on a prostatic acinus
BENIGN PROSTATIC HYPERPLASIA (BPH)

• Pembesaran nodus kelenjar prostat


karena hiperplasi dari komponen stroma
dan kelenjarnya
BPH
• Lesi non neoplastik yang sering ditemukan
pada laki-laki usia lanjut.
• normal 20-30 gram,BPH→60-100 gram
• 20% (40 th), 70% (60 th), 90% ( 80 th)
• Nodul bervariasi pada peri urethral zone.
• 10% kasus, simptomatik.
PATOGENESIS
• Imbalance hormonal pada usia tua.
• Estrogen sensitif pada periurethral (trans)
zone.
• Akumulasi dihydrotestosterone (DHT) pada
prostat merangsang dan menumbuhkan efek
andogenik
• Finasteride menghambat dihydrotestosterone
dan mengurangi pembesaran prostat.
GEJALA KLINIS
• Sering kencing, nocturia, sukar memulai dan
menghentikan panc.urin
• Retensi urin yg akut
• Stasis urin yang kronik
• Obstruksi kronik, perubahan struktur
 Hipertropi pd bladder
 Divertikulum pada bladder
 Hidronefrosis
MAKROSKOPIS BPH
• Nodul bervariasi konsistensi dan warnanya.
• Pada nodul yang sebagian besar berisi
kelenjar konsistensi kenyal, warna merah
jambu, keluar cairan seperti susu dari area ini
• Pada nodul yang terutama terdiri dari stroma
fibromuskular,setiap nodul pucat,tidak
mengeluarkan cairan,berbatas tegas dengan
jaringan sekitar.
MIKROSKOPIS BPH
• Noduler (nodul fibromuskular dan
fibroepitelial) dengan predominan kelenjar
• Proliferasi kelenjar terbentuk dari aggregasi
dilatasi kelenjar kecil sampai besar, dibatasi 2
lapis, kolumnair pada bagian dalam dan
kuboid pada bagian luar.
Pembesaran nodus kelenjar prostat karena hiperplasi
dari komponen stroma dan kelenjarnya
Dapat ditemukan Corpora amylacea (massa eosinofil di dalam lumen
kelenjar)
Adenokarsinoma prostat
• Kanker yang paling banyak dijumpai pada laki-
laki diatas 50 thn
• Jarang pada orang asia
• Orang kulit hitam lebih banyak dp org kulit
putih
• Etiologi masih belum jelas
• Merupakan kanker dengan insidensi no 8 di
Indonesia (Oemiati et al, 2007).
Faktor resiko
• Umur
Puncaknya 65-70 thn

• Genetik
• Allelic lost pada tumor suppressor gene (8p, 10q, 13 q, 16q dan 17p)
• Fusi TMPRSS2 gene dan ETS transcription factor gene (ERG)
• Gene silencing (PTEN, RB, p16/INK4a, MLH1, MSH2 dan APC).

• Ras
Banyak di derita ras Afroamerican

• Diet
Diet tinggi lemak hewani
• Hormonal
Tidak terjadi pada laki-laki yang dikastrasi sbl pubertas atau
pada populasi dengan ekskresi rendah-5 alpa-reductase,
insidensinya sangat rendah
• Aktivitas seksual
Seksual aktivitas yang dini, mempunyai banyak partner sex,
meningkatkan insidensi, kemungkinan infeksi STD dan ekses
dari testosterone
• Hipotesa viral infeksi
Sejak thn 1970, herves virus dicurigai, tapi blm ada konfirmasi
• Lingkungan.
Radiasi gamma, konsentrasi kadmium yg tinggi.
Grossly, the tumor may be difficult to see but usually can be identified as a gray or
yellowish, poorly delineated, firm area
Histopatologi adenokarsinoma prostat

• Asinus berukuran kecil yang infiltratif diantara


kelenjar normal.
• Satu lapisan sel epithel, tanpa sel basal
• Basophilic mucin.
• Eosinophilic cristalloid.
• Perineural invasion  lymphovascular
invasion.
• Collagenous nodule (mucinous fibroplasia)
periganglional/neural invasion
Metastasis
• Penyebaran lokal :
seminal vesicles , vesica urinaria, prostatic
urethra, rectum (jarang).
• Metastasis jauh :
Tulang (Lumbar spine, sacrum, dan pelvis ),
paru/pleura, liver, kelenjar adrenal, limfonodi
dan testis.
References

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