OS 214 Excretory Module Pathology Department

Pathology Lab 2 part 2 Lab Exam & Exam 2

OUTLINE border are areas of necrosis), areas of

I. Gross Specimen hemorrhage (dark areas)
a. Renal Cell Carcinoma ** the bigger the tumor, the bigger the area of
b. Wilm’s Tumor necrosis
c. Renal Dysplasia - should always be correlated with clinical features
d. Chronic Pyelonephritis - clear cell CA – most common type
e. Nephrolithiasis ** the type of CA determines management and
f. Kidney Hydronephrosis
g. Benign Prostatic hyperplasia
prognosis
h. Transitional / urothelial cell ** the type of CA cannot be determined by just
carcinoma looking at the gross specimen lesion
II. Microscopic Specimen - during nephrectomy, blood vessel sample should
a. Chronic protatitis also be taken
b. NPH - invasion of gerota’s facia – malignant lesion
c. Prostatic adenocarcinoma
d. Papillary urothelial carcinoma
e. Chronic cystitis

GROSS SPECIMEN
A. Renal Cell Carcinoma
- May arise in any portion of the kidney
- Areas of ischemic, gray white necrosis; foci of
hemorrhage or discoloration; areas of softening
- Has a tendency to involve the renal vein

Figure 2. Due to gross yellow appearance, the

differential for this case is a xantho-granulomatous
pyelonephritis.

Figure 3. Fungating mass, nodular in appearance,

which has already invaded much of the normal kidney
tissue.

Figure 1. Renal Cell Carcinoma

Notes:
- when given a gross specimen, you have to
differentiate benign from a malignant lesion.
** malignant lesions: infiltrative, irregular border,
areas of necrosis, areas of hemorrhage
- specimen: infiltrative, irregular/ill-defined border,
necrotic areas (pale areas which can be found
either in the outer or inner part of the lesion, for
the gross specimen shown in the lab the outer
March 11, 2009 | WED Page 1 of 6
LEXI-ADI-GILLIAN-BUTCH
 OS 214 Excretory Module Pathology Department

Pathology Lab 2 part 2 Lab Exam & Exam 2

- due to an abnormality in metanephric

differentiation

Figure 4. The tumor has already spread to the

perirenal fat.

B. Wilm’s Tumor Figure 7. Renal Dysplasia

- Large, solitary, well circumscribed mass
- On cut sections, tumor is soft, homogenous, and
tan to gray with occasional foci of hemorrhage,
cyst formation and necrosis
- On microscopic sections, classic triphasic
combination of blastemic stromal and epithelial
cell types
Notes:
- congenital
- presence of islets of cartilage and immature
collecting tubules
D. Chronic Pyelonephritis
- kidneys are irregular scarred
- coarse, discrete, corticomedullary scar overlying
in a dilated, blunted or deformed calyx
- kidneys are smaller than usual
- ureter is dilated and thickened, a finding
consistent with chronic vesicoureteral reflux

Figure 5. Wilm’s Tumor

Notes:
- common in children
- specimen: smooth, homogenous lesion
occupying the entire renal parenchyma, foci of
hemorrhage (minimal areas of hemorrhage as Figure 8. Chronic Pyelonephritis
compared to the renal cell CA specimen) and Notes:
cyst - specimen: granular surface with scarring, small
- may be triphasic (classical type): composed of kidney, blunting of calyx (hallmark), thickening of
blastema, epithelial cells, stroma; biphasic; or ureter wall due to reflux
anaplastic - causes: recurrent UTI and chronic obstructive
diseases
- thyroidization – lumen filled with colloid-like
material
- kidney becomes nonfunctional requiring dialysis if
both kidneys are affected
-

Figure 6. Nephroblastoma, Differential is a

neuroblastoma, Triphasic: stromal, epithelial and
blastemic components, which can only be
differentiated under the microscope, Circumscribed,
well-demarcated, usually chromosomal, Common in
children<5 Figure 9. Inflammation is usually caused by
ascending infections due to E. coli. The cortico-
C. Renal Dysplasia medullary junction has been obliterated.
- irregular shaped, multicystic
- cysts vary in size E. Nephrolithiasis
March 11, 2009 | WED Page 2 of 6
LEXI-ADI-GILLIAN-BUTCH
 OS 214 Excretory Module Pathology Department

Pathology Lab 2 part 2 Lab Exam & Exam 2

- favoured sites of formation are within the renal
calyces and pelvis, thus causing dilatation and if
multiple, may thin out the renal parenchyma
- most stone (75%) are calcium containing
(calcium oxalate, calcium phosphate); 15% are
so-called triple stones (magnesium ammonium
phosphate).
- weighs between 60 to 100 grams; even up to 200
or more
- may show a well defined bulge
- almost exclusively occurs in the inner aspect of
the gland, in the transitional and periurethral
zones
- Nodular enlargement may encroach the lateral
walls of the urethra to compress it into a slitlike
orifice
-

Figure 10. Nephrolithiasis

Notes:
- specimen: dilated calyx, atrophic renal
parenchyma which is replaced with fat
- types of stone: (1) calcium, (2) triple
phosphate/magnesium ammonium
phosphate/struvite stone
- treatment: laser to convert the stone into powder
- type of necrosis: coagulative necrosis wherein
the original morphology is retained
- urinalysis: presence of blood (hematuria) and
crystals
** renal cell CA may also present with hematuria
** how to differentiate renal cell CA and
nephrolithiasis? conduct urine cytology (low
sensitivity)
** urine cytology: centrifuge urine sample → get
the sediments → stain with hematoxylin eosin
(H&E)
- ureterolithiasis – kidney is still intact

F. Kidney Hydronephrosis
- enlargement may be slight or massive
- kidney transformed into a thin-walled cystic
structure
- striking parenchymal atrophy
- blunting of apices of the pyramids

Figure 12. BPH

Notes:
- can weigh up to 200g
- usually occur in the older age group
- specimen: nodular lesion which may displace the
urethra, dilated urethra may be due to obstruction
but usually the urethra is slit-like due to
impingement

H. Transitional / urothelial cell carcinoma

- gross pattern vary: may be papillary to nodular or
flat
- heterogenous gross appearance
Figure 11. Kidney Hydronephrosis
- may fungating, necrotic or ulcerative that have
Notes:
unmistakably invaded deeply
- specimen: atrophy of parenchyma replaced with
fatty tissue
- cause: chronic obstruction
- kidney may rupture from trauma which may lead
to peritonitis since urine is detected as a foreign
body
- treatment: pathologic kidney is usually removed

G. Benign Prostatic hyperplasia

March 11, 2009 | WED Page 3 of 6

LEXI-ADI-GILLIAN-BUTCH
 OS 214 Excretory Module Pathology Department

Pathology Lab 2 part 2 Lab Exam & Exam 2

Figure 15. Hyperplasia of the median lobe of the

prostate produces a polypoid mass that protrudes in
the bladder lumen.

Figure 13. Transitional / urothelial cell carcinoma

Notes:
- normal bladder wall – smooth or trabeculated
- specimen: fungating lesion (papillary), infiltrating
into the smooth muscle, black areas are due to Figure 16. The luminal contour shows tufts and
India Ink stain which is used to determine the papillary infoldings of glands. The tall secretory
depth of infiltration microscopically and as epithelial cells have pale clear cytoplasm and uniform
surgical lining of the section; along with the round or oval nuclei. Prominent nucleoli are not seen.
specimen is the an atrophied uterus which is Fibromuscular stroma and any basal cells can be
means the specimen came from a 50-60 year old identified.
female
- management: surgical removal of the bladder
and creation of a neobladder from the ilium

MICROSCOPIC SPECIMEN
A. Chronic protatitis

Figure 17. BPH can involve both glands and stroma,

though the former is usually more prominent. Here, a
large hyperplastic nodule of glands is seen.

Figure 14. A dense inflammatory infiltrate has

replaced glandular epithelium which has been largely
destroyed. Some cases of granulomatous prostatitis
may closely mimic high-grade cancer. Small foci of
cancer adjacent to foci of inflammation may
sometimes be overlooked.

Figure 18. At higher magnification, the enlarged

prostate has glandular hyperplasia. The glands are
well-differentiated and still have some intervening
B. Nodular prostatic hyperplasia stroma. The small laminated pink concretions within

March 11, 2009 | WED Page 4 of 6

LEXI-ADI-GILLIAN-BUTCH
 OS 214 Excretory Module Pathology Department

Pathology Lab 2 part 2 Lab Exam & Exam 2

the glandular lumens are known as corpora - invasive urothelial CA – no need to grade
amylacea. because regardless of a low or high grade,
prognosis and management are still the same
C. Prostatic adenocarcinoma - LM: fibrovascular core

a. Low-grade

Figure 19. High-grade prostatic intraepithelial

neoplasia (PIN) consists of intermediate to large size
preexisting glands with proliferative changes resulting
in hyperchromatic appearance. Note the small foci of
cancer adjacent to PIN on the upper left and lower
right.
Figure 21. These tumors show more architectural
disorder and nuclear atypia than urothelial tumors of
low malignant potential. The nuclear size, shape,
polarity, and chromatin show greater variability.
Mitoses are still infrequent. Umbrella cells can still be
seen.

b. High-grade

Figure 20. Prostatic CA

Note:
- gross pic: asymmetrical, multilobulated
- nodular hyperplasia due to proliferation of stromal Figure 22. These tumors display total architectural
or/and glandular elements; glandular hyperplasia disorganization and significant cytologic atypia of
grossly appear as cystic spaces urothelium. There is loss of nuclear polarity;
- adenocarcinoma – cells are trying to form glands considerable variation in nuclear size, shape, and
which fuse together chromatin content; mitoses are frequent and may be
- gleason grading: grades 1-3 = distinct glands abnormal. Umbrella cells are usually absent.
grade 4 = fused glands
grade 5 = no glands visible E. Chronic cystitis
score = predominating grade + second most
predominant grade
- LM pic: pleomorphic hyperchromatic nuclei

D. Papillary urothelial carcinoma

Figure 23. Inflammation of the sub mucosa

Notes:
- gross: unilaterally dilated ureter due to stones
impacted at the outlet
- when evaluating the urothelium look for: number
Figure 21. Urothelial Carcinoma of cell layers (normal is 7 layers but if the section
Notes: is tangentially cut there may be more than 7
- gross pic: thick, stiff, nodular wall (may be layers), polarity, crowding of nuclei
malignant) - pic: stones caused inflammation of the
submucosa

March 11, 2009 | WED Page 5 of 6

LEXI-ADI-GILLIAN-BUTCH
 OS 214 Excretory Module Pathology Department

Pathology Lab 2 part 2 Lab Exam & Exam 2

a. Papillary Cystitis

Figure 27. The presence of edema fluid and

inflammatory cells can be better appreciated in this
Figure 24. Proliferation of vessels and accumulation image. The majority of the patients with polypoid
of edema fluid and inflammatory cells in the lamina cystitis have history of indwelling catheters.
propria has created papillary configuration focally.
Distinction from papillary urothelial carcinoma is
important.

Figure 28. The lamina propria contains eosinophils,

Figure 25. Another example of papillary cystitis. The
urothelium is hyperplastic. The lamina propria
contains numerous plasma cells and delicate vessels.
plasma cells, lymphocytes, and rare neutrophils. The
overlying urothelium is unremarkable. On cystoscopic
examination, papillary and polypoid cystitis are
frequently mistaken for neoplasms. Microscopic
examination reveals their true nature.

b. Polypoid Cystitis
- (Robbin’s) an inflammatory condition resulting
from irritation to the bladder mucosa. Although
indwelling catheters are the most commonly cited
culprits, any injurious agent may give rise to this
lesion. The urothelium is thrown into broad,
bulbous, polypoid projections as a result of
marked submucosal edema. Polypoid cystitis
may be confused with papillary urothelial
carcinoma both clinically and histologically
-

Figure 26. The term polypoid cystitis is applied for

broad-based lesions enclosing large amounts of
edema fluid with scattered inflammatory cells. If the
lesions are even more broad-based and larger, the
term bullous cystitis may be applied.

March 11, 2009 | WED Page 6 of 6

LEXI-ADI-GILLIAN-BUTCH