Kuliah Urogenitalia 2013

7/25/2019 Kuliah Urogenitalia 2013

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BAGIAN PATOLOGI ANATOMI FK UNS

Kuliah Blok Urogenitalia


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The clinical presentations of renal disease:

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 urineflow), 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.


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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 thelesion.


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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.


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chronic renal failure

chronic glomerulonephritis is one of the mostcommon causes of chronic kidney disease in

humans

Can be primary and secondary


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Clinical manifestation


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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 ispostinfectious glomerulonephritis, whereas an of an endogenous

antigen-induced disease is the nephritis of SLE.


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Acute Proliferative (Poststreptococcal,

Postinfectious) Glomerulonephritis

Characterized histologically by diffuse proliferation ofglomerular 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 beaffected.


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Etiology and Pathogenesis:

Only certain strains of group A -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 froma 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


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Nephrotic syndrome

The manifestations of the nephrotic syndrome include:

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

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

3. Generalized edema

4. Hyperlipidemia and lipiduria


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Membranous nephropathy is a common causeof the nephrotic syndrome in adults.

It is characterized by diffuse thickening of the

glomerular capillary wall due to theaccumulation of electron-dense, Ig-containing

deposits along the subepithelial side of the

basement membrane.


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Chronic glomerulonephritis

Chronic glomerulonephritis is best considered a pool of end-stage glomerular disease fed by several streams of specific

types of glomerulonephritis


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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 lessthan 400 mL per day.


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Causes:

Ischemia

Direct toxic injury to the tubules (e.g., by drugs, radiocontrastdyes, 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)


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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.


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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)


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Acute pyelonephritis is an acute suppurative inflammation of the kidney caused bybacterial and sometimes viral (e.g., polyomavirus) infection, whether hematogenous

and induced by septicemic spread or ascending and associated with vesicoureteral

reflux.


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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 isunpredictable and haphazard, but in

pyelonephritis associated with reflux,

damage occurs most commonly in

the lower and upper poles


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In the early stages, the neutrophilic infiltration is limited to the interstitial tissue.

Soon, however, the reaction involves tubules and produces a characteristic abscesswith 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.


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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 withsevere lower urinary tract abnormalities.


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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 scarsoverlying 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 ofreflux in these sites.

The microscopic changes involve predominantly tubules and interstitium


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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.


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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.


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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


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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.


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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, andglomerular tufts may be seen within the cystic space.


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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 tothe renal pelvis.

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

or extrinsic lesions that compress the ureter.


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Clinical co rse


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Clinical course

Acute obstruction may provoke pain attributed to distention ofthe 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 maintainadequate renal function.


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In bilateral partial obstruction the earliest manifestation is inability to

concentrate the urine, reflected by polyuria and nocturia. Some patientshave 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.


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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 causesignificant 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.


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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.


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Tumor of Kidney

Benign : renal papillary adenoma,angiolipoma, oncocytoma.

Malignant : renal cell carcinoma, Wilms

tumor, urothelial tumors of the calyces andpelves


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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


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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


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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.


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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 ofbright 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 ofhemorrhagic discoloration. The margins

are usually sharply defined and confined

within the renal capsule


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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 tumorpredisposing genes.


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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.


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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


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p y, y g p

recapitulate different stages of nephrogenesis. The classic triphasic combination of

blastemal, stromal, and epithelial cell types is observed in the vast majority of lesions,

although the percentage of each component is variable. 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 usuallyfibrocytic or myxoid in nature, although skeletal muscle differentiation is not

uncommon. Rarely, other heterologous elements are identified, including squamous or

mucinous epithelium, smooth muscle, adipose tissue, cartilage, and osteoid and

neurogenic tissue. Approximately 5% of tumors reveal anaplasia, defined as the

presence of cells with large, hyperchromatic, pleomorphic nuclei and abnormal mitoses


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Male Genitourinary System


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Scrotum Testis & Epididymis

Neoplasms of the Scrotum are uncommon

Invariably they are squamous cell carcinomas

Sir Percival Pott (Mid 1700s) observed amarked increase in scrotal cancer among the

Chimney Sweeps

These fellows bathed once year need it or not

The scrotum was exposed to the tars and soot arising

The clothing was greasy with this material


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Scrotum Testis & Epididymis

Hydrocele

Most common cause of scrotal enlargement

Accumulation of serous fluid in the tunicavaginalis


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Cryptorchidism & Testicular

Atrophy Complications

Bilateral = sterility

Increased risk of testicular malignancyOrchiopexy does not guarantee fertility nor

does it decrease the risk of testicular

malignancy


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Inflammatory lesions of the

Testes Epididymis much more affected than testes

proper

Mumps orchitis - rare in children15-20% of adults with mumps get orchitis

Walkers Law :-)

Enlarged testicle, edema and chronicinflammation

May lead to testicular atrophy and scarring

If bilateral, can cause infertility


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Inflammatory lesions of the

Testes Non-specific epididymitis and orchitis

Secondary bacterial infection, ascending

Neutrophilic infiltrate

Granulomatous Orchitis

Tuberculosis


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Testicular Neoplasms

Most important cause of painless testicular

enlargement

Peak Incidence 15-34 years of age Virtually all testicular neoplasms are

MALIGNANT

Walkers Law for Surviving Females - Regular breast self exam

Males - Regular testicular self exam


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Pathogenesis Cryptorchidism increases the risk 10-40

fold

Testicular dysgenesis increases the riskKlinefelter syndrome

Testicular feminization

Siblings of patients with testicular cancerare at increased risk

Caucasians >>> African Americans


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Classification >95% of all testicular neoplasms arise from

the germ cells


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Testicular NeoplasmsClassification - One Histologic Pattern

Table 18-1 p 581 Seminoma

Embryonal carcinoma

Yolk sac tumor

Choriocarcinoma

Teratomas

Mature

Immature

With Malignant Transformation


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G C ll


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Germ Cell

Seminoma

Mature testicular

cell type

Embryo and Embryo

Related Cells

Choriocarcinoma

Embryonal

Cell Carcinoma

Yolk Sac

Tumor

Teratoma


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Seminoma

Same as dysgerminoma in Ovary

Large, soft, well demarcated gray-white

lesions that bulge from the cut surface Usually NO hemorrhage

Microscopic

Large cells with clear cytoplasm

Fibrous septae

Mild lymphocytic infiltrate


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Teratoma

Somatic cell differentiation arising in

totipotential germ cells

Usually involve all three germ lines Skin with cartilage and gut

If you see more than one recognizable germ

layer type -- it is a teratoma


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More than onegerm layer type

TERATOMA

Fi 18 8 583 T


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Teratoma Micro

Figure 18-8 p 583 Teratoma

Glands Squamous CellsCartilage


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Teratoma Morphology

Mature

Fully differentiated tissues

ImmatureFetal type tissues


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Teratoma Morphology

Teratoma with malignant transformation

teratomatous elements

often squamous cell carcinoma or adenocarcinoma

Teratocarcinoma

Teratoma combined with Embryonal

CarcinomaPost pubertal teratomasALLhave an associated

germ cell neoplastic component


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Mixed Germ Cell Tumors

50-60% of all testicular neoplasms

Walkers Law :-)

The most common is the teratocarcinomaCombination of Teratoma and Embryonal

Carcinoma


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Germ Cell

Seminoma

Mature testicularcell type

Embryo and Embryo

Related Cells

Choriocarcinoma

Embryonal

Cell Carcinoma

Yolk Sac

Tumor

Teratoma

Testic lar Neoplasms


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Testicular NeoplasmsClinical

Painless enlargement of the testis

Some present as metastases

Seminoma -- Iliac and para-aortic lymph nodes

Other types -- lymph nodes, liver, lung

Tumor markers in the blood (Table 18-2 p 584)

hCG in Choriocarcinoma

Alpha fetoprotein in yolk sac tumor

Helpful in diagnosis and followup


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Prostate

Inflammatory lesions - Prostatitis

Nodular Hyperplasia

Adenocarcinoma


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Prostatitis

Acute bacterial prostatitis

E. coli or other gram negative rods

The same organisms causing most UTIs

Chronic Prostatitis

Follow obvious episodes of acute prostatitis

Develop insidiously

Most are abacterial

Chlamydia trachomatis

Ureaplasma urealyticum


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Prostatitis Morphology

Acute Prostatitis - PMN infiltrate

Chronic Prostatitis - Variable mononuclear

infiltrate Granulomatous Prostatitis

TB

Fungi

Sarcoid

Round-up the usual suspects


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Prostatitis Clinical

Dysuria

Urinary frequency

Low back pain

Pelvic pain

Fever

Leukocytosis


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Normal Prostate

There are anatomic zones

Different pathologic processes arise in

different zones more frequently Lets look at the zones 2 ways

First the books way


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Normal

Prostate

Sagittal

Section

CZ = Central Zone

TZ = Transitional Zone

PZ = Peripheral Zone


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Urethra

Now Walkers Way


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Urethra

Walkers Way #2

N d l H l i f th


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Nodular Hyperplasia of the

Prostate Forever, since Hippocrates it has been

referred to as

BPH or Benign Prostatic Hypertrophy BUT it is not hypertrophy it is hyperplasia

Better term is Nodular Hyperplasia


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NodularHyperplasia

GrossFigure 18-10p 586

NodulesHyperplastic


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Nodular

HyperplasiaGross with

arrowsFigure 18-10

p 586


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Nodular Hyperplasia

Arises in the central zone most often

Hyperplasia involves glands & stroma

Present in 15-20% of 40 y/o

Present in 85-90% of 70 y/o

Walkers Law :-)

Central Zone location ----> Bladder

Obstruction!!!!


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Nodular Hyperplasia


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Nodular Hyperplasia

Morphology Prostate is enlarged

Multiple nodules

Urethral compression is common

Gland and stromal proliferation


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N d l H l i


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Nodular HyperplasiaClinical

Of all patients with nodular hyperplasia

Only 10-15% have symptoms

Walkers Law :-) Symptoms are those of lower urinary tract

partial obstruction

N d l H l i


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Partial obstruction of lower urinary tract

Difficulty initiating urine stream (hesitancy)

Interruption of streamFrequency

Urgency

Nocturia (think of CHF also) Rectal exam - soft and boggy prostate

Nod lar H perplasia


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Complete Obstruction

Painful bladder distension

HydronephrosisAnuria

Nodular Hyperplasia


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Nodular HyperplasiaComplications

Residual Urine increases risk of UTI

Nodular Hyperplasia DOES NOT increase

the risk of developing prostate carcinoma


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Carcinoma of the Prostate

Most common visceral cancer in Males

Second most common cause of cancer

related deathLung cancer is most common in males

Older men over the age of 65

Latent cancer (no symptoms) occurs in asmany as 50% of men > 80 y/o

Walkers Law :-)


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Cause is unknown

But genetic, hormonal and environmental

factors are importantCarcinoma growth can be inhibited by

orchiectomy or use of estrogen therapy

Symptomatic CA is more common in African-

Americans than in Caucasians, Asians or

Hispanics



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Morphology The majority of prostate carcinomas arise

in the peripheral zone and are thus

palpable! Less likely to cause Urinary Obstruction

Because it is PERIPHERAL not central

Ill-defined, Non-nodular mass, grey-whiteto yellow


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Morphology Metastases to regional lymph nodes is not

uncommon

Invasion of seminal vesicles is notuncommon

Invasion of the bladder is more common

than invasion of the rectum

Prostate Carcinoma


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Prostate Carcinoma

Morphology Adenocarcinomas

Back to Back Glands

Lined by a single layerNormal prostate has a flat basal layer with a

columnar epithelium overlying

Histologic grading schemes are HELPFULin predicting prognosis


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Prostate Carcinoma Microscopic

Figure 18-13 p 587 Back-to-Back glands

Single layer of lining cells

Prostate Carcinoma


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Prostate Carcinoma

Clinical Often silent

They are peripheral not central so do not cause

obstruction 15-20% are discovered in TURPs

TURP = TransUrethral Resection of the

Prostate

TURPs are done for Nodular Hyperplasia not

for cancer!

Walkers Law :-)

Prostate Carcinoma


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Prostate Carcinoma

Clinical - Often silent Autopsy studies of men older than 80

50-60% have occult prostate cancer

Walkers Law :-) A digital rectal exam is critically important

Prostate Carcinoma


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Prostate Carcinoma

Clinical - Often silent May present primarily with Metastases

Bone mets are frequently OsteoBLASTIC

and present in the axial skeleton OsteoBLASTIC (not lytic) mets in a male

are virtually diagnostic of Prostatic

Carcinoma

Prostate Carcinoma


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Prostate Carcinoma

Clinical - Often silent Screening with PSA (Prostate Specific

Antigen)

Produced by both normal and neoplasticcells

Elevated in

Nodular hyperplasiaProstatitis

Adenocarcinoma of Prostate


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Prostate Carcinoma


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Prostate Carcinoma

Clinical - Often silent Serial follow-up of PSA in patients with

prostate cancer is useful to monitor disease

Recurrence orProgression

Prostate Carcinoma


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Prostate Carcinoma

Clinical - Often silent 85-90% 10 year survival in patients with

limited disease

Walkers Law :-) 10-15% 10 year survival in patients with

disseminated disease

Walkers Law :

-)


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REFERENCES

1. Kumar V, Abbas A, Fausto N. Robbin

and Cotran Pathologic Basis of Disease

8th

edition. Elsevier Saunders,Philadelphia, 2010.

2. Mudjahid A, 2004. Kuliah Male

Genitourinary System.

Kuliah Urogenitalia 2013

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