YL6
Renal, Obstetrics, and GU Module [PATHOLOGY]
6 December 2010
PATHOLOGY OF THE LOWER URINARY TRACT
Alan T. Koa, MD
OUTLINE
I. Ureters
A. Congenital Anomalies
B. Inflammation
C. Tumors and tumor-like Lesions
D. Obstructive Lesions
II. Urinary Bladder
A. Congenital Anomalies
B. Inflammations
C. Metaplastic Lesions
D. Neoplasms
E. Obstruction
III. Urethra
A. Inflammation
B. Tumor and tumor-like Lesion
I.
A.
1.
URETERS
CONGENITAL ANOMALIES
Double Ureters

Associated with double renal pelvis or large kidney having
partially bifid pelvis

May pursue separate courses to the bladder but commonly
are joined within the bladder wall and drain through single
ureteral orifice

Majority of the cases are unilateral and have no clinical
significance
2.
Ureteropelvic Junction Obstruction

Congenital disorder that results in hydronephrosis
(hydronephrosis - dilatation of the pelvo-calyceal system)

Most common cause of hydronephrosis in infants and
children (commonly boys)

Left ureter is usually affected

Bilateral in 20% of cases and associated with other
congenital anomalies

In adults, ureteropelvic junction obstruction, obstruction is
more common in females and is often unilateral.
3.
Diverticula

Saccular outpouchings of the ureteral wall

Uncommon and asymptomatic

Incidental finding on imaging studies

Congenital or acquired defect

Implication: can cause stasis and secondary infections(due
to retrograde flow of the infected urine)

Counterpart of aneurysms (CVS)
4.
Hydroureter

dilation, elongation, tortuousity
a) Congenital hydroureter – neurogenic defect in the
innervation of the ureteral musculature
b) Megaloureter – massive enlargement due to functional
defect of ureteral muscle
Group 01
Figure 1. Most Common Causes of Ureteral Obstruction
B.
1.
INFLAMMATION
Ureteritis - Inflammation of the ureter
a) Ureteritis follicularis – accumulation or aggregation of
lymphocytes in the subepithelial region causing slight
elevations of the mucosa and granular mucosal surface
o Accumulation of lymphoid cells forming follicles with
germinal centers that elevate the mucosa
b) Ureteritis cystica – 1-5 mm cysts (modified transitional
epithelium) in mucosa that may aggregate to form small,
grape-like clusters
o Appear as vesicles (fluid-filled)
o Normal epithelium: transitional type of epithelium or
urothelium
C.
1.
TUMORS AND TUMOR-LIKE LESIONS
Fibroepithelial Polyps

Tumor-like lesion, often in children

Small mass projecting into lumen

Occur commonly in ureter (L>R), may be seen in bladder,
renal pelvis, urethra
Under microscopy, a polyp can be seen as a finger-like

growth with a fibrovascular core composed of fibroblasts
and thick-walled blood vessels
“Fibro”: refers to the central core; “Epithelial”: refer to the

covering
2.
Leiomyomas

Benign tumors composed of smooth muscle cells, which are
the mesenchymal elements

From the smooth muscle component of the ureter that
allows it to contract and dilate

not common, it is more prevalent in the female genital tract
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
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PATHOLOGY OF THE LOWER URINARY TRACT
PATHOLOGY
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3.
D.
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
1.
II.
A.
1.
Urothelial Carcinomas

6th to 7th decades of life

Occur concurrently with similar neoplasms in bladder or
renal pelvis

Cause obstruction of ureteral lumen

The most common malignancy (but not the only one)

Also called papillary transitional cell carcinoma

Can cause azotemia or elevation of BUN and creation then
lead to uremia

2.
Exstrophy

Presence of a developmental failure in the anterior wall of
the abdomen and in the bladder

Bladder either communicates directly through a large
defect with the surface of the body or lies as an opened sac

Bladder mucosa may undergo colonic glandular metaplasia
o Colonic epithelium - simple columnar with colonic
glands (i.e. large intestine has with goblet cells)

Mucosa is subject to the development of infections that
often spread to upper urinary tract

In persistent chronic infections, mucosa is converted into
an ulcerated surface of granulation tissue
o granulation tissue: has fibroblasts, inflammatory
infiltrates, and blood vessels

Increased tendency for carcinoma later in life – mostly
adenocarcinoma of bladder (sir’s slides say colon)
3.
Miscellaneous Anomalies
a) Vesicoureteral reflux – most common and serious
anomaly; can cause renal infection and scarring
b) Congenital fistulas – Abnormal connections between
bladder and vagina, rectum or uterus
c) Persistent urachus – fistulous urinary tract that connects
bladder with umbilicus
o Depending on the patency of the urachus, it can give
rise to urachal cysts, lined by either transitional or
metaplastic epithelium.
o Adenocarcinomas may arise in such cysts
B.


INFLAMMATION: CYSTITIS
Women – shorter urethra (especially at reproductive age)
May be caused by:

E. coli, Proteus, Klebsiella, Enterobacter

Candida albicans and Cryptococcus – immunosuppressed
patients or on long-term antibiotics (usually involve the
lungs and the CNS)

Schistosoma haematobium

Adenovirus, Chlamydia, Mycoplasma

Cyclophosphamide – hemorrhagic cystitis (mucus of
bladder appears red and with blood clots)

Hemorrhagic cystitis – Umbrella cells on top (rounded topmost cells) of the urothelium are sloughed off

Tuberculous cystitis – sequel to renal TB

Radiation – radiation cystitis
1.
a.
ACUTE AND CHRONIC CYSTITIS
Morphology

Hyperemia of mucosa with exudate or hemorrhage
a) Hemorrhagic cystitis – follows radiation injury, antitumor
chemotherapy (ex. Cyclophosphamide), adenovirus
infection; accompanied by epithelial atypia
o Epithelial atypyia – atypical cells that can be due to a
reactive process secondary to the inflammation
OBSTRUCTIVE LESIONS
May obstruct the ureters and give rise to hydroureter,
hydronephrosis and pyelonephritis
Major causes of ureteral obstructions:
a) Intrinsic: calculi, strictures, tumors, blood clots, neurogenic
b) Extrinsic: pregnancy, periureteral inflammation (sclerosing
retroperitoneal fibrosis), endometriosis (presence of
endometrial glands and stroma outside the uterus), tumors
(cervical, uterine, bladder, rectal CA)
o Most common location: ovaries
Sclerosing Retroperitoneal Fibrosis

Fibrous proliferative inflammatory process encasing the
retroperitoneal structure s and causing hydronephrosis

Middle to late age

70% of cases idiopathic

Causes: drugs (beta-adrenergic blockers), adjacent
inflammatory conditions (vasculitis, diverticulitis, Crohn’s
disease), malignancy (lymphoma)

Systemic in distribution involving mostly the
retroperitoneum

Fibrotic changes are seen in other sites

Microscopic: prominent inflammatory infiltrate of
lymphocytes, with germinal centers, plasma cells and
eosinophils. Sometimes, there is a foci of fat necrosis and
granulomatous formation.

Beta blockers or “-olols” can cause this
URINARY BLADDER
CONGENITAL ANOMALIES
Diverticula

Consist of pouch-like eversion or evagination of the
bladder wall

Congenital or acquired from persistent urethral obstruction
o Congenital form may be due to focal failure of
development of the normal musculature or to some
urinary tract obstruction during fetal development
o Acquired diverticula are most often seen with
prostatic enlargement (hyperplasia or neoplasia)
wherein the increased pressure from the enlarged
prostate causes the diverticulum

May be clinically significant

Constitute sites of stasis and predispose to infection and
calculi formation

Predispose to vesicoureteral reflux as a result of
impingement on the ureter
Group 01
Carcinomas may arise rarely – more advanced in stage as a
result of thin or absent muscle wall of a diverticulum
When invasive cancers arise, they are more advanced in
stage as a result of the diverticula’s thin or absent muscle
wall of a diverticulum
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
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PATHOLOGY OF THE LOWER URINARY TRACT
b)
c)
PATHOLOGY
produced which comes from the infection
Suppurative cystitis
o Accumulation of large amounts of suppurative
exudate
o Accumulation of neutrophils in the bladder mucosa
Ulcerative cystitis
o sloughing off or denudation of the bladder mucosa
b.
Chronic Cystitis

With chronicity, fibrous thickening in the muscularis
propria and consequent thickening and inelasticity of the
bladder wall
a) Follicular cystitis - collection of lymphocytes that tend to
form lymphoid nodules in the lamina propria
b) Eosinophilic cystitis- subacute inflammation aggregates of
eosinophils, sometimes associated with giant cells
c.
Clinical Presentation

Triad of symptoms:
1. Frequency
2. Lower abdominal pain
3. Dysuria

Fever, shills, malaise

Antecedents to pyelonephritis

A secondary complication of prostatic enlargement,
cystocele of bladder, calculi, tumors

b)
autoimmune disorders
Phases:
a. Early Phase (non-classic, non-ulcerative phase)
o Recent submucosal hemorrhages
b. Late Phase (classic, ulcerative)
o Chronic mucosal ulcers (Hunner ulcers)
o Inflammatory cells and granulation tissue involve
the mucosa, lamina propria, muscularis
o Transmural fibrosis – leading to a contracted
bladder
o Recall: Granulation tissue is composed of dead
cells, capillaries, BVs, fibroblasts, collagen,
inflammatory cells, mast cells ( granules that
secret histamine and heparin very similar to the
granules of basophils)
Malacoplakia

Characterized grossly by soft, yellow, slightly raised
mucosal plaques 3-4 cm in diameter

Infiltrates of large, foamy macrophages with multinucleate
giant cells and lymphocytes

Macrophages have granular cytoplasm – debris of bacterial
origin

Giant phagosomes point to defects in phagocytic or
degradative function of macrophages(overloaded with
undigested bacterial products)

Michaelis-Gutmann bodies present in macrophages and
between cells; laminated calcified material inside and
outside; huge macrophages with foamy cytoplasm

Related to chronic bacterial infection (E.coli, occasionally
Proteus)

Occurs with increased frequency in immunosuppressed
transplant recipients
Figure 2. Figure 5: Acute (left) vs. Chronic Cystitis (right): In acute, there is
microscopic foci of mucosal hemorrhage. In chronic, a nonspecific
inflammatory infiltrate composed of lymphocytes and plasma cells is present
in the edematous lamina propria.
2.
a)
SPECIAL FORMS OF CYSTITIS
Interstitial Cystitis (Chronic Pelvic Pain Syndrome, Hunner
Ulcer)

Persistent, painful form of chronic cystitis occurring
frequently in women

Associated with inflammation and fibrosis of all layers of
bladder wall

Intermittent, often severe, suprapubic pain, urinary
frequency, urgency, hematuria, dysuria, without evidence
of bacterial infections (Unlike in usual cystitis, when you
have infection you will be able to grow the organism to
identify)

Cystoscopic finding/s: fissures and punctuate hemorrhages
(glomerulations) in the mucosa

May clinically mimic flat carcinoma in situ

Unknown etiology but associated with SLE and other
Group 01
Figure 3. Cystitis with malacoplakia showing inflammatory exudates
and broad, flat plaques (L). Malacoplakia, PAS stain. Note the large
macrophages with granular PAS-positive cytoplasm and several
dense, round Michaelis-Gutmann bodies surrounded by artifactual
cleared holes in the upper middle field (R).
Figure 4. Malacoplakia. Inflammatory cells are composed principally of
macrophages, with fewer lymphocytes. (Inset) A Michaelis-Gutmann body
(arrow) is seen at high magnification
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
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PATHOLOGY OF THE LOWER URINARY TRACT
c)
Polyploid Cystitis

Inflammatory condition resulting from irritation to the
bladder mucosa

Indwelling catheters

Urothelium is thrown into broad, bulbous, polyploid
projections due to marked submucosal edema

May be confused with papillary urothelial carcinoma –
clinically and histologically
C.
1.
METAPLASTIC LESIONS
Cystitis Glandularis and Cystitis Cystica

Nests of transitional epithelium (Brunn nests) grow
downward into lamina propria and undergo transformation
of their central epithelial cells into cuboidal or columnar
epithelium (cystitis glandularis) or cystic spaces lined by
urothelium (cystitis cystica)

When the two conditions coexist – cystitis cystica et
glandularis
2.
Squamous Metaplasia

Response to injury – more durable lining
3.
Nephrogenic Adenoma

Results from shed renal tubular cells that implant in sites of
injured urothelium

Overlying urothelium may be focally replaced by cuboidal
epithelium, which can assume a papillary growth pattern

May clinically resemble cancer because of tubular
proliferation in the lamina propia and superficial detrussor
muscle

There is shedding of renal tubular cells
PATHOLOGY
keratin). D-cystitis glandularis. E-nephrogenic metaplasia (glands resemble
tubular glands)
D.
NEOPLASMS
1.

UROTHELIAL (TRANSITIONAL CELL) TUMORS
95% of neoplasms are of epithelial origin, the rest are
mesenchymal
Represent about 90% of all bladder tumors
Papillary to nodular or flat, invasive or non-invasive
Two distinct precursor lesions to invasive urothelial carcinoma:
a) Noninvasive papillary tumors – appear to arise from
papillary urothelial hyperplasia; demonstrate a range of
atypia (i.e. enlargement of nuclei, slight hyperchromasia,
infrequent mitosis)
o More common, non-invasive
o Majority are low grade arising from the lateral or
posterior wall at the bladder base
b) Flat noninvasive urothelial carcinoma – carcinoma in situ
(CIS)
o Majority are high grade
o “in situ”- malignant cells are confined to the
urothelium; no penetration of the basement
membrane; ”carcinoma” considered to be carcinoma
because of the presence of malignant-looking cells
o Major decrease in survival is associated with tumor
invading the muscularis propria (detrussor muscles) –
30% 5-yr mortality rate
Grading of Urothelial (Transitional Cell) Tumors: WHO/ISUP
Grades (International Society of Uroepithelial Pathology)
o Urothelial papilloma - benign
o Urothelial neoplasm of low malignant potential
o Papillary urothelial carcinoma, low grade – frank
malignancy
o Papillary urothelial carcinoma, high grade - frank
malignancy
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


Figure 6. Uroepithelial tumors. Papilloma - finger like villous projections; Flat
– does not penetrate the BM; Invasive papillary – penetrate the stroma; Flat
invasive- penetrate stroma but is flat not finger-like.
Figure 5. Proliferative and metaplastic changes of the bladder. Ahyperplasia. B-Brunn nests (straight arrow) and uteritis cystic (curved arrow)
protrude into the lamina propria. C-squamous metaplasia (squamous have
Group 01
PAPILLARY TUMORS
a) Papillomas

Younger patients

Benign
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
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PATHOLOGY OF THE LOWER URINARY TRACT
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Polyp – polypoid growth, fibrovascular growth with
uroepithelial core (columnar epithelium)
Lining epithelium of endocervix: simple columnar with
mucin (to provide lubrication)
Lining epithelium of ectocervix: stratified squamous
Helophytic Papillomas - Tumors arise singly as small (0.52.0 cm), delicate structures, superficially attached to the
mucosa by a stalk
o Papillae have a central core of loose fibrovascular
tissue covered by transitional epithelial cells
Inverted Papillomas - Benign lesions of inter-anatomising
cords of cytological bland urothelium extending down into
the lamina propria, no nodular ties or papilla
Figure 7. Papillary Tumor. Left – top section shows cross-section of bladder
with upper section showing a large papillary tumor; the lower section
demonstrates multifocal smaller papillary neoplasms. Right – under the
microscope (Lining: Transitional Epithelium)
b)
Papillary Urothelial Neoplasms of Low Malignant Potential
(PUNLMP)

Share many histologic features with papilloma

Thicker urothelium or diffuse nuclear enlargement

Rare mitotic figures

Not associated with invasion

May recur with the same morphology, not associated with
invasion, and rarely recur as higher-grade tumors
associated with invasion

Borderline lesions: neither benign nor malignant

Presents with enlargement of the nuclei
c)
Low-grade Papillary Urothelial Carcinomas

characterized by an orderly appearance architecturally and
cytologically

Cells are evenly spaced and cohesive cells

Minimal nuclear atypia with mitosis: scattered
hyperchromasia and mild pleomorphism

Can recur and invade infrequently (10%)

Frankly malignant
Figure 8. Low-grade papillary urothelial carcinoma with an overall orderly
appearance, a thicker lining than papilloma, and scattered hyperchromatic
nuclei and mitotic figures pointed by the arrows.
Group 01
PATHOLOGY
d)
High-grade Papillary Urothelial Carcinomas

Dyscohesive cells with large hyperchromatic nuclei

Some tumor cells show frank anaplasia

Frequent mitosis, some atypical

Disarray with loss of polarity

Higher incidence of invasion (80%) into muscularis layer

Higher risk of progression than low-grade with significant
metastatic potential

40% of invasive tumors metastasize to regional lymph
nodes

Hematogenous spread to liver, lungs, bone marrow, occurs
late with highly anaplastic tumors
CARCINOMA IN SITU (CIS OR FLAT UROTHELIAL CA)

Presence of cytologically malignant cells within a flat urothelium

May range from full thickness cytologic atypia to scattered
malignant cells in an otherwise normal urothelium (pagetoid
spread) – but no involvement of the basement layer
Lack of cohesiveness (a common feature with high grade
urothelial carcinoma) leads to shedding of malignant cells into
the urine (seen in urinalysis)

Grossly, appears as an area of mucosal reddening, granularity,
or thickening without an intraluminal mass

Multifocal

May involve most of bladder surface and extend

Into ureters and urethra

If untreated, 50-75% progress to muscle-invasive cancer
Figure 9. Urothelial carcinoma in situ. The urothelial mucosa shows nuclear
pleomorphism and lack of polarity from the basal layer to the surface,
without evidence of maturation. Lining epithelium: Transitional epithelium
Figure 10. Normal uroepithelium (L) and Flat carcinoma in situ (R). L –
uniform nuclei and well-developed umbrella cell layer. R – cells with enlarged
and pleomorphic nuclei
INVASIVE UROTHELIAL CANCER
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
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PATHOLOGY OF THE LOWER URINARY TRACT
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
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Associated with high grade papillary cancer or CIS
Extent of invasion is of prognostic significance. The extent of
spread at the time of initial diagnosis is the most important
factor in determining the prognosis of the patient.
Staging, in addition to grade, is critical in the assessment of
bladder neoplasms
o Only malignancies are staged (not benign ones)
AJCC/UICC
Depth of Invasion
Noninvasive, papillary
Ta
CIS (noninvasive, flat)
Tis
Lamina propria invasion
T1
Muscularis propria invasion
T2
Microscopic extravesicle invasion
T3a
Grossly apparent extravesicle
T3b
invasion
Invades adjacent structures
T4
AJCC/UICC, American Joint Commission on Cancer/Union
Internationale Contre le Cancer.
NOTE: MEMORIZE THIS! (T = tumor staging)
PATHOLOGY

c)
Small Cell Carcinoma

Indistinguishable from the small cell CA’s of the lungs
3.
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EPIDEMIOLOGY OF BLADDER CARCINOMA
Men>women (3:1 urothelial tumors)
50-80 years
Industrialized nations
Not familial
4.


FACTORS IMPLICATED IN THE CAUSATION OF UROTHELIAL CA:
Cigarette smoking – most important influence
Industrial exposure to arylamines (2-naphthylamine) – cancers
appear to 15-40 years after exposure
Schistosoma haematobium – ova deposited in bladder wall
incite chronic inflammatory response; 70% are SCCa, remainder
urothelial
Long term use of analgesics
Heavy long term exposure to cyclophosphamide – induces
hemorrhagic cystitis
Prior exposure of bladder to radiation: occurs many years after
irradiation




Figure 11. Staging of urothelial carcinoma of the urinary bladder. Stage T0
tumors (carcinoma in situ) are limited to the epithelium of the mucosa. T1
tumors show invasion of the lamina propria. T2 tumors invade the muscle
layer superficially. T3 tumors invade the perivesical tissue. T4 tumors invade
into the adjacent organs or show local and distant metastases (if male:
muscularis layer, then seminal vesicle, then prostate.)
2.
OTHER TYPES OF CARCINOMA
a)
Squamous Cell Carcinomas

Pure SCCA associated with chronic bladder irritation and
infection (Schistosomiasis)

Mixed urothelial cell carcinomas with squamous
carcinoma are more frequent than pure SCCa

Invasive, fungating tumors or infiltrative and ulcerative

Level of cytologic differentiation varies widely

May be keratinizing or non-keratinizing
b)
Adenocarcinomas

Rare

Arise from urachal remnants or in association with
extensive intestinal metaplasia

Arises from metaplastic foci: intestinal metaplastic areas
because they are glandular

Variants: signet-ring cell Ca and mixed adenocarcinoma
and urothelial cell carcinomas

Epidemiology of Bladder Carcinoma
Group 01
Man>Women (3:1 for urothelial tumors)
5. PATHOGENESIS OF UROTHELIAL CANCER
“Read up on this” – Dr. Koa

Genetic alterations

Chromosome 9 monosomy or deletions of 9p and 9q

Deletions of 17p, 13q, 11p, 14q

Chromosome 9 deletions – only genetic changes present
frequently in superficial papillary tumors and occasionally in
noninvasive flat tumors

The 9p deletions (9p21) involve the tumor suppressor gene p16
(ink4a) which encodes and inhibitor of a cyclin-dependent
kinase, and also the related tumor suppressor gene p15

Many invasive urothelial cell carcinomas show deletions of 17p
and mutations in p53 gene (also seen in flat CIS)

13q deletions involve the retinoblastoma gene present in
invasive tumors

14q deletions seen in flat lesions or invasive tumors but not in
papillary tumors

Model for bladder carcinogenesis (2 pathway model)
o First pathway is initiated by deletions of tumor suppressor
genes on 9p and 9q, leading to superficial papillary tumors,
few may have p53 mutations and progress to invasion
o Second pathway is initiated by p53 mutations, leads to CIS,
with loss of chromosome 9, progresses to invasion
6.
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
CLINICAL COURSE OF BLADDER CANCER
Bladder tumors classically present with painless hematuria (Q:
How can there be painless hematuria if there is dysuria? Dr. Koa
will check on this.)
Frequency, urgency and dysuria
With ureteral orifice involvement: pyelonephritis and
hydronephrosis
Urothelial tumors have a tendency to develop new tumors after
excision, recurrence may be high grade
Most important factors for progression-free survival: grade,
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
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PATHOLOGY OF THE LOWER URINARY TRACT
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E.
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III.
A.
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presence of lamina propria invasion, associated CIS
Papillomas, PUNLMP, lg Papillary Urothelial CA yield 98% 10-yr
survival rate regardless of the number of recurrence
Hg Papillary Urothelial CA: invade and lead to death in 35% of
cases, 40% 10-yr survival rate
Patients with primary (de novo) CIS as opposed to CIS
associated with infiltrating urothelial carcinoma, are less likely
to progress to muscle -invasive cancer (28% vs. 59%) or die of
disease (7% vs. 45%)
SCCa: 70% dead within a year
Invasive urothelial carcinoma: 30% mortality rate once tumor
invades into the lamina propria
Overall, SCCa and adenocarcinoma are associated with worse
prognosis than urothelial carcinoma, yet stage for stage they are
similar
Clinical challenge is early detection and adequate follow up.
Cystoscopy and biopsy for diagnostics (flexible tube inserted in
the urethra to the bladder and may do biopsy if tumor is
present)
Cytologic exam and urine markers (h-related protein,
telomerase, etc)
Treatment depends on grade, stage, whether lesion is flat or
papillary
Small, localized low grade papillary tumors: transurethral
resection followed with periodic cystoscopies and urine
cytology
Multifocal tumors: instillation of topical chemotherapy into
bladder post-op can reduce recurrence
Patients who are at high risk of recurrence and/or progression
receive topical immunotherapy of intravesical installation of an
attenuated strain of > tuberculosis (bcg): works by eliciting local
cell-mediated immune reaction that destroys tumor cells
Radical cystectomy – remove the entire bladder tumor invading
the muscularis propria, CIS or hg papillary cancer refractory to
bcg, CIS extending into prostatic urethra and extending down
prostatic ducts beyond reach of bcg
Chemotherapy: advanced bladder cancer
OBSTRUCTION
Obstruction to bladder neck is important because it has its
effects on the kidneys
A variety of intrinsic and extrinsic diseases of bladder can
narrow urethral orifice and cause partial or complete vesical
obstruction
In males, enlargement of prostate
In females, cystocele of bladder
Morphology: Thickening of bladder wall due to hypertrophy of
smooth muscle and trabeculation of bladder wall
(“trabeculation” because looks like trabeulae carnae of the
heart)
URETHRA
INFLAMMATION: URETHRITIS
Gonococcal : manifestation of a venereal infection
Non-gonococcal: E.coli, Chlamydia, Mycoplasma
Accompanied by cystitis in women and by prostatitis in men
One component of Reiter syndrome (arthritis, conjunctivitis,
urethritis)
Group 01
PATHOLOGY
B.
1.
TUMORS AND TUMOR-LIKE LESIONS
Urethral Caruncle

Inflammatory lesion

Small, red, painful mass in external urethral meatus in
women

Morphology: may be covered by mucosa but extremely
friable and trauma may cause ulceration and bleeding

Histology: vascularized, fibroblastic connective tissue
infiltrated with leukocytes and overlying transitional or
squamous epithelium
2.
Benign Epithelial Tumors

Squamous and urothelial papillomas

Inverted urothelial papillomas

Condylomas – due to HPV; like a wart (“verucca” not wart –
if found elsewhere)
3.
Carcinoma of the Urethra

Uncommon; occur in advanced age in women

Proximal urethra: urothelial differentiation

Distal urethra: squamous carcinoma
IV. Test Yourself
1.
2.
3.
4.
5.
6.
Which of the following is not a congenital anomaly?
a. Diverticula
b. Hydroureter
c. Malacoplakia
d. Exstrophy
Urothelium is otherwise known as
a. Transitional Epithelium
b. Squamocolumnar Epithelium
c. Tranpository Epithelium
d. Stratified Columnar Epithelium
Which of the following structures is not lined by the histologic
feature in No. 2?
a. Ureter
b. Rectum
c. Bladder
d. Renal Pelves
Ureteropelvic Junction Obstruction is the most common cause
of ____ in children
a. Dilatation
b. Hydronephrosis
c. Congenital anomaly
d. Carcinoma
Sheila has a Stage 3 carcinoma of the lungs. She is taking
cyclophosphamide as an antitumor drug. What is the most likely
side effect of this drug in the genito-urinary system?
a. Nephrotoxicity
b. Vesicoureteral reflux
c. Hemorrhagic cystitis
d. Infertility
Juan is 10 pack-year smoker who drinks alcohol every other day
in the nearby sari-sari store. He was recently been diagnosed to
have bladder cancer after taking purgatives for his Schistosomal
infection. The likely cause of his bladder cancer is
a. Schistosoma
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
Page 7 of 8
PATHOLOGY OF THE LOWER URINARY TRACT
7.
8.
PATHOLOGY
b. Smoking
c. Alcohol drinking
d. Being male
Interstitial Cystitis is –
a. More common in men
b. More common in women
c. Frequency and pain
d. Proteinuria and hematuria
e. A and C
f. B and C
g. A and D
A peek of the histologic pictures of Low-grade papillary
urothelial carcinoma and High-grade papillary urothelial cancer
and you would be able to differentiate the two because of
a. The number of nucleus
b. The obscured white spaces in high-grade
c. The dyscohesiveness of the high-grade
d. The diverticula produced by high-grade
Answers: 1C, 2A, 3B, 4B (not just dilatation (A) but dilatation of the
pelvo-calyceal system aka Hydronephrosis) 5C, 6B (even though
Schistosoma can increase the risk and most patients are male,
smoking is 50-80% strongly associated with bladder cancer), 7F, 8C
(Low grade CA are cohesive and evenly spaced)
Group 01
Carissa, Maxine, Glenn, Danize, Leslie, Clarissa, Ralph, Nerisse, Ramon, Armand, Bernadette
Page 8 of 8