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A B




2-41. A. Early lung cancer arising from a left lower
lobe bronchus. B. Histology shows a poorly differ-
entiated neuroendocrine carcinoma.




Pulmonary Pathology 137
2-42. A. Small cell carcinoma that has arisen in the
right main bronchus (left side of picture) has also
in¬ltrated into the left main bronchus and the left
lung parenchyma. B. Histology shows a poorly pre-
A
served small cell carcinoma.




B




138 Pulmonary Pathology
A B



2-43. A. Squamous carcinoma has arisen in a
severely anthracotic lung. B. Histology shows a mod-
erately differentiated squamous carcinoma. C. Poorly
differentiated adenosquamous carcinoma arising in
the main bronchus of a lung. (continued on next
page)




C




Pulmonary Pathology 139
2-43. (Continued) D. Cartilage rings survive within
a bronchogenic carcinoma. E. By obstructing the
main bronchus, a large cell carcinoma has led to
multiple lung abscesses and pneumonic consolida-
tion. An illustration of the dictum that stasis favors
D
infection.




E



140 Pulmonary Pathology
A



2-44. A. Peripherally situated adenocarcinoma of
the lung. This tumor is less often associated with
cigarette smoking than is squamous carcinoma of
the lung. B. High-power view of a mucin-rich ade-
nocarcinoma.




B



Pulmonary Pathology 141
A




B

2-45. A. Bronchiolar-alveolar carcinoma of the lung macroscopically
mimics a pneumonic process. B. Histology of bronchiolar-alveolar
carcinoma shows alveoli lined by a well-differentiated adenocarci-
noma that is respecting the mural structure of the alveoli.




142 Pulmonary Pathology
2-46. Extensive necrotic lymphomatoid granulo-
matosis of the lung, now recognized as an extra-
nodal, angiocentric B cell lymphoma with a benign,
exuberant T cell response and having a predilection
for the lungs. The malignant B cells often contain the
Epstein-Barr virus.




Pulmonary Pathology 143
A



2-47. A. Metastatic carcinoma of the urinary bladder
in the lung lies in a subpleural position. B. Partially
necrotic metastatic thymic carcinoma in the lung.




B




144 Pulmonary Pathology
2-48. A. Diffuse lymphatic permeation of the lung
by carcinoma. This may present as a ˜crazy paving™
pattern on chest x-ray. B. Interlobular septal lym-
A
phatic contains metastatic carcinoma.




B




Pulmonary Pathology 145
A



2-49. A. Posttransplant lymphoproliferative dis-
ease. Note the solid white tissue in the upper lobe
and scattered nodules in the lower lobe and on the
pleural surface. B. Posttransplant B-cell lymphoma
in the hilar lymph nodes.




B




146 Pulmonary Pathology
A



2-50. Lymphangioleiomyomatosis of the lungs.
A. Cut surface of the lung has a reticulated, meaty
appearance due to diffuse involvement by lym-
phangioleiomyomatosis. B. Histology of pulmonary
lymphangioleiomyomatosis shows a marked dif-
fuse, smooth muscle cell proliferation in the pul-
monary interstitium.




B




Pulmonary Pathology 147
A



2-51. Malignant ¬brous tumor of the pleura. In the
past, this tumor was regarded as a form of mesothe-
lioma, but it is now believed to arise from non-
committed mesenchymal cells situated deep to the
mesothelial lining. A. Solid, ¬‚eshy tumor has arisen
on visceral pleura and lies outside the lung, pro-
truding into the pleural cavity. B. Histology shows
anaplastic, spindle-shaped cells arranged in an
interweaving pattern.




B




148 Pulmonary Pathology
2-52. Interstitial (surgical) emphysema. A. Appear-
ance of a lobe of lung affected by chronic intersti-
tial air trapping (surgical emphysema of the lung)
showing numerous rounded defects produced by air
trapped within the lung interstitium. B. Mediastinal
emphysema due to air leakage from the lung. C.
Interstitial emphysema of the mesentery: note the
numerous air bubbles present within the mesenteric
A
tissue.




C
B




Pulmonary Pathology 149
2-53. Lung transplantation. A. Severe acute rejec-
tion of a donor lung is characterized by a hemor-
rhagic, devitalized appearance to the lung tissue.
B. Bronchial anastomosis lines in bilateral lung
A
transplantation. (continued on next page)




B




150 Pulmonary Pathology
C




E
D

2-53. (Continued) C. Chronic rejection of a 5-year-
old bilateral lung transplant. D. Bronchiolitis oblit-
erans in a lung transplant. Loss of small airways
may also occur in chronic rejection. E. Smooth mus-
cle actin immunostaining serves to delineate small
bronchioles ¬lled by loose ¬brous tissue in bron-
chiolitis obliterans.

Pulmonary Pathology 151
A



2-54. A. Macroscopic appearance of congenital lobar
emphysema is characterized by overdistention of the
affected lobe. The condition is a potentially
reversible life-threatening cause of neonatal respira-
tory distress. Absent bronchial cartilage may lead to
bronchial collapse during expiration, leading to air
trapping. B. Overdistention of alveoli, as seen in this
picture, may be associated with either hypoalveolar
or polyalveolar counts.




B




152 Pulmonary Pathology
2-55. Congenital cystic adenomatoid malformation
(CAM) is a hamartomatous malformation of the lung
that comprises about 25% of all congenital lung
lesions. CAM communicates with the tracheo-
bronchial tree and the pulmonary arterial and
venous circulations. A. Bisected CAM surgically
resected from a young child shows multiloculated
larger cysts and smaller cysts of varying size within
the lesion. B. Histology shows an adenomatoid pro-
liferation of structures and cysts resembling bron-
A
chioles.




B



Pulmonary Pathology 153
2-56. Pulmonary sequestration. A. Note the supply-
ing systemic artery (arrow) in the center top of the
section. B. Higher-power view showing cysts and
dilating spaces lined by bronchial epithelium.
Unlike cystic adenomatoid malformation, pulmonary
sequestration has no bronchial communication and
A
is supplied by anomalous systemic arteries.




B




154 Pulmonary Pathology
2-57. Solitary bronchogenic cyst was an incidental
¬nding in this lung.




2-58. Bochdalek hernia (arrow) behind left hemidi-
aphragm allowed stomach, small gut, spleen, and
portion of large gut to enter the left chest and to
compress the left lung (top right), which is much
smaller than the right lung.




*


Pulmonary Pathology 155
2-59. Bronchomalacia of right lung has led to
atelectasis and focal areas of consolidation due to
repeated lung infections.




156 Pulmonary Pathology
3 Kidneys, Ureters, and Urinary Bladder




A B

3-1. A. Kidney in acute tubular necrosis (ATN) show-
ing pale, swollen cortex and congested medulla. B.
Elongated, stretched out, regenerating proximal tubu-
lar lining cells encompass the necrotic epithelium. If
no regeneration is seen, then appearances are dif¬cult
to distinguish from postmortem autolysis. ATN may
result from ischemia, nephrotoxins, or circulating
heme proteins.




Kidneys, Ureters, and Urinary Bladder 157
A



3-2. A. Papillary necrosis (PN) associated with dia-
betes mellitus (DM) is seen in this bisected kidney.
The repetitive distribution of the necrosis limited to
the renal papillae is the key diagnostic feature of PN.
PN may occur with DM (often with pyelonephritis),
drugs (aspirin and phenacetin), hydronephrosis, and
sickle cell disease. In drug-induced PN, the papillae
may show necrosis of varying ages, unlike PN asso-
ciated with DM, in which the necrosis is all of the
same duration. PN in sickle cell disease may not
affect all papillae. B. Histology of PN. Note the pale-
colored necrotic papilla that is already showing
some blunting of its free surface. The necrotic area
may ultimately slough off and be excreted in the
urine.




B




158 Kidneys, Ureters, and Urinary Bladder
A




B




C

3-3. A. Diffuse cortical necrosis of the kidney resulting from pro-
found hypotension. The hallmark feature is necrosis limited to the
renal cortex. B. Histology shows poor staining of the necrotic corti-
cal zone. C. Higher power shows a few tubules and glomeruli sur-
viving in a perivascular distribution (arrow), while the rest of the
cortex is diffusely necrotic.


Kidneys, Ureters, and Urinary Bladder 159
3-4. A. Pale, decolorized renal infarcts (circled)
affecting cortex and medulla. Renal infarcts are pale
because there is no open interstitium for blood to
percolate into (unlike the lung). B. Histologic junc-
tion of infarct (top) and surviving renal tissue
(arrows); note the subcapsular survival of scanty
A
renal tissue on the surface of the kidney (left).




B




160 Kidneys, Ureters, and Urinary Bladder
3-5. A. Healed renal infarct at upper pole of kidney
(circled). B. Histologic appearance of a healed
infarct. Note the V-shaped pro¬le of the healed
infarct compared to the U-shaped scar pro¬le of
A
healed pyelonephritis.




B




Kidneys, Ureters, and Urinary Bladder 161
3-6. A. Renal vein thrombosis has produced hem-
orrhagic infarction of the entire kidney. B. Histol-
ogy con¬rms renal infarction with massive intersti-
tial hemorrhage consistent with circulatory arrest
secondary to cessation of venous out¬‚ow from the
A
kidney.




B




162 Kidneys, Ureters, and Urinary Bladder
3-7. Triple renal arteries (a variation of normal
anatomy) supply this kidney.




3-8. The kidney on the left has suffered from (atherosclerotic) renal
artery stenosis (“Goldblatt kidney”) and has undergone atrophy with
symmetric reduction in size. This ischemic kidney caused systemic
hypertension via increased production of renin, angiotensin II, and
aldosterone, resulting in accelerated nephrosclerosis of the opposite
kidney (on the right of the picture). The narrowed renal artery sup-
plying the ischemic kidney protected it from hypertension; hence,
the nonscarred renal surface observed in the atrophied kidney.




Kidneys, Ureters, and Urinary Bladder 163
A




C
B

3-9. A. Fine surface granularity of benign nephroscle-
rosis due to aging or lower-level systemic hyperten-
sion tends to be more coarse than that seen in chronic
glomerulonephritis. B. Small intrarenal arteries show
intimal ¬broplasia plus replication of the elastic lam-
inae and hyalinization of the media. C. Wedge-
shaped area of slowly developed ischemic atrophy
due to the vascular narrowing.




164 Kidneys, Ureters, and Urinary Bladder
A



3-10. Malignant hypertension. A. Macroscopic
appearance of the kidneys in new-onset malignant
hypertension is characterized by normal-size kid-
neys showing focal small hemorrhages on the cap-
sular surfaces. B. Myxoid edema of intima in small
intrarenal artery is leading to further renal ischemia
and aggravation of the hypertension. (continued on
next page)




B




Kidneys, Ureters, and Urinary Bladder 165
3-10. (Continued) C. Concentric intimal onion peel-
like layering of intimal ¬brosis in a small intrarenal
artery. D. Fibrinoid necrosis of renal arterioles and
C
hemorrhage within a glomerulus.




D




166 Kidneys, Ureters, and Urinary Bladder
A



3-11. A. Nonsteroidal antiin¬‚ammatory drug
nephropathy. Both kidneys show cortical atrophy
and loss of several renal papillae due to prior pap-
illary necrosis, while other papillae show residual
evidence of necrosis. Expansion of the peripelvic fat
compensates for the parenchymal atrophy. B. Loss
of renal parenchyma is associated with endarteritic
thickening of small renal arteries.




B




Kidneys, Ureters, and Urinary Bladder 167
A




3-12. Tubulointerstitial nephritis. A. The ¬brotic
nature of the renal interstitium is easily discerned
in this gross photo; ¬brous tissue appears gray-white
in the picture. B. Histologic section: trichrome stains
collagen blue between atrophic tubules.



B




168 Kidneys, Ureters, and Urinary Bladder
A B



3-13. Acute pyelonephritis may occur via hematoge-
nous spread of infection to the kidney or by ascend-
ing infection via cystitis with vesicoureteral re¬‚ux or
due to hydronephrosis (e.g., due to a renal stone).
A. Acute on chronic pyelonephritis with numerous
septic foci present in an already scarred kidney.
B. Acute pyelonephritis with coccal organisms (arrow)
and neutrophils. C. Acute pyelonephritis is present
(top left) with incipient subcapsular abscess forma-
tion. (continued on next page)




C


Kidneys, Ureters, and Urinary Bladder 169
3-13. (Continued) D. Very severe acute (“emphyse-
matous”) pyelonephritis with spaces in the infected
renal parenchyma due to the action of gas-produc-
ing microorganisms. Papillary necrosis is also noted.
E. Xanthogranulomatous pyelonephritis: the yellow-
ish areas contain foamy macrophages in addition to
the usual in¬‚ammatory cells. The patient had mod-
erate hydronephrosis that was complicated by a Pro-
D
teus infection.




E




170 Kidneys, Ureters, and Urinary Bladder
A



3-14. Obstructive uropathy results from structural or
functional abnormalities of the urinary tract that
impede urine ¬‚ow, which may cause renal dysfunc-
tion (obstructive nephropathy) and dilatation of the
collecting system (hydronephrosis). A. Bilateral
hydronephrosis with acute on chronic pyelonephritis
in a child due to urinary tract obstruction. Note the
dilated ureters and renal pelves. B. Hydronephrosis
with thinned renal parenchyma in an adult kidney.




B




Kidneys, Ureters, and Urinary Bladder 171
A B




D

3-15. Healed pyelonephritis is characterized by parenchymal
C
scarring plus distortion of the calyceal system. A. Broad U-
shaped scar of healed pyelonephritis. B. Healed pyelonephritis
associated with vesicoureteral re¬‚ux has produced scarring of
both poles of the kidney with calyceal distortion due to infec-
tion of the peripheral compound papillae. (Obstruction produces
infection of the papillae.) C. Histology of healed pyelonephritis
scar shown in A shows the ¬brosis extends from the capsule to
the calyx. D. End-stage chronic pyelonephritis with shrunken
scarred kidney exhibiting multiple, small acquired cysts.




172 Kidneys, Ureters, and Urinary Bladder
B
A


3-16. Hematogenous disseminated Candida albi-
cans infection. A. Renal surface is studded with
multiple small fungal abscesses. B. Cut surface
shows cavitation of some of the lesions due to loss
of the contents of the abscess. C. Histology shows
Candida pseudohyphae (top) in an area of tissue
destruction and in¬‚ammation.




C




Kidneys, Ureters, and Urinary Bladder 173
3-17. Renal tuberculosis secondary to hematoge-
nous spread of tubercle bacilli. The renal pelvis, the
calyces and the ureters are lined by shaggy, caseous-
looking material. From the kidney, the infection
may spread down the ureters and reach the blad-
der, the male sexual glands, and the epididymis.




3-18. Bilateral partial double ureters. No renal
pathology is present.




174 Kidneys, Ureters, and Urinary Bladder
3-19. Staghorn calculus in pelviureteric junction. 3-20. Bilateral catheters (“stents”) pass from blad-
Kidney shows dilated, distorted calyces and areas der to both renal pelves to relieve bilateral ureteral
of healed pyelonephritis. stenosis.


3-21. Kidney of a young child with acute prolifer-
ative glomerulonephritis appears slightly mottled.
The gross appearance cannot be used to make the
diagnosis of glomerulonephritis; renal histology is
used for this purpose.




Kidneys, Ureters, and Urinary Bladder 175
3-22. A. Hemorrhagic biopsy site in a kidney with
membranoproliferative glomerulonephritis (GN).
Patient died of shock from massive hemorrhage
from the biopsy site. B. Poststreptococcal prolifera-
tive GN. C. Rapidly progressive GN with crescent
formation within Bowman™s capsule. (continued on
A
next page)




B C




176 Kidneys, Ureters, and Urinary Bladder
D




E F

3-22. (Continued) D. IgA nephropathy with mesangial
thickening (M). E. Membranous GN. Note the diffuse
thickening of the basement membranes. F. Macro-
scopic appearance of chronic GN with blurring of the
demarcation between the thinned pale cortex and the
medulla.



Kidneys, Ureters, and Urinary Bladder 177
3-23. Diabetic nephropathy (glomerulosclerosis)
accounts for about one-third of cases of chronic
renal failure. A. Narrowed renal cortex due to dia-
betic nephropathy. B. Histology of advanced diabetic
glomerulosclerosis with prominent Kimmelstiel-
Wilson nodules (increased mesangial matrix) within
sclerosing glomeruli. C. Finely granular surface
of end-stage renal failure of undetermined cause “
glomerulonephritis or diabetic glomerulosclerosis
A
may lead to a similar end-stage kidney.




C
B




178 Kidneys, Ureters, and Urinary Bladder
3-24. Congenital nephrotic syndrome (CNS). This
kidney appears pale and slightly sclerotic macro-
scopically. CNS occurs in the ¬rst 3 months of life.
Histology is needed to distinguish subtypes (e.g.,
Finnish CNS, diffuse mesangial sclerosis-type CNS).



3-25. Primary oxaluria due to de¬ciency of hepatic
enzymes leading to decarboxylation of glyoxylate
has led to oxalate nephropathy. The kidney is
reduced in size and shows diffuse scarring, and
oxalate stones are present within the calyceal sys-
tem at both renal poles.




Kidneys, Ureters, and Urinary Bladder 179
3-26. Bile nephrosis: acute renal failure of uncertain
cause may occur in patients with jaundice. A. Bile-
stained kidney in patient with cirrhotic liver failure.
B. Bile plugs (arrows) are noted within the lumen of
A
some renal tubules.




B




180 Kidneys, Ureters, and Urinary Bladder
3-27. Pericalyceal hemorrhage is a useful indicator
of a bleeding tendency and occurs around the
mobile, contractile renal pelvis from disruption of
small capillaries that normally seal off by platelet
coagulation. A. Pericalyceal hemorrhage in a kidney
bearing some old vascular scars. B. Histology con-
A
¬rms the pericalyceal situation of the hemorrhage.




B




Kidneys, Ureters, and Urinary Bladder 181
A B

3-28. A. Kidney with ischemic atrophy also bears
very small subcapsular adenomas near to each pole.
B. Histology of a subcapsular papillary adenoma
shows tubules arranged in a papillary fashion. All
such “adenomas” are presently regarded as early
cancers.




182 Kidneys, Ureters, and Urinary Bladder
3-29. A. Surgically removed angiomyolipoma (AML)
of the kidney shows a macroscopic predominance of
adipose tissue. Histology may also show vessels and
smooth muscle. AML has an incidence of 25% to
50% in patients with tuberous sclerosis. B. Histology
of another AML in which smooth muscle prolifera-
tion predominates and some cellular atypism and
A
mitotic activity is noted.




B




Kidneys, Ureters, and Urinary Bladder 183
3-30. Mesoblastic nephroma of the kidney is a con-
genital benign neoplasm or hamartoma that is
encountered in the ¬rst 3 months of life. A. Partially
necrotic, ¬‚eshy-looking mesoblastic nephroma
replacing most of the kidney has to be distinguished
from a Wilms™ tumor by histology. B. Histology of
mesoblastic nephroma shows two surviving
glomeruli within a proliferation of myo¬broblastic
A
spindle cells.




B




184 Kidneys, Ureters, and Urinary Bladder
A




3-31. Renal cell carcinoma is the most common pri-
mary renal tumor in adults and may be occult. It is
more common in males and affects the upper pole
of the kidney more often than elsewhere. Etiology
includes tobacco exposure and von Hippel-Lindau
disease. A. Small clear cell renal cell carcinoma
(hypernephroma, Grawitz tumor) is spreading into
perirenal adipose tissue. Note the very abundant
peripelvic and pericapsular ¬broadipose tissue.
B. Histology shows a clear cell-type renal carcinoma
comprising rounded cells with a translucent cyto-
plasm. C. Typical lobulated, whorled, tan-colored cut
surface of a renal cell carcinoma. (continued on
next page)



B C




Kidneys, Ureters, and Urinary Bladder 185
D




3-31. (Continued) D. Abundant lipid within the
tumor cells as well as necrosis may give the tumor
a yellow color, as in this case. E. Invasion of the
renal vein (*) and inferior vena cava (arrow) by
renal cell carcinoma.



E




*




186 Kidneys, Ureters, and Urinary Bladder
3-32. Papillary urothelial (transitional cell) carcinoma of renal
pelvis. Note the exophytic, multifronded nature of the tumor.
The resection lines have been marked with ink. Urothelial car-
cinomas comprise about 5% to 10% of primary renal tumors.




Kidneys, Ureters, and Urinary Bladder 187
A




3-33. Wilms™ tumor (nephroblastoma) of the kidney
is the most common intraabdominal solid tumor in
children younger than 10 years. It is a malignant
tumor composed of embryonal nephrogenic ele-
ments, including blastemal, stromal, and epithelial
tissues. Not all elements are present in all tumors.
A. Solid, bulging, ¬‚eshy tan-white, partially necrotic
tumor has replaced much of the kidney and is
encompassed by a thin rim of renal tissue. B. This
Wilms™ tumor appears whiter due to formalin ¬xa-
tion and has extended beyond the con¬nes of the
kidney. Foci of necrosis and hemorrhage appear as
darker zones within the tumor. C. Histology shows
hypercellular areas comprising undifferentiated
blastema, loose stroma with undifferentiated mes-
enchymal cells and immature tubules and a
glomeruloid body (bottom).



B C




188 Kidneys, Ureters, and Urinary Bladder
3-34. Metastatic poorly differentiated adenocarci-
noma at inferior pole of kidney.




Kidneys, Ureters, and Urinary Bladder 189
3-35. Renal transplantation. A. Note the two end-
stage native kidneys in normal position, the
atrophic ¬rst donor kidney (lower left), and the
larger second donor kidney (lower right). B. Subto-
tal renal infarction due to hyperacute (antibody-
A
mediated) rejection. (continued on next page)




B




190 Kidneys, Ureters, and Urinary Bladder
C D

3-35. (Continued) C. Severe acute rejection of donor
kidney. Focal infarcts are present. D. Severe chronic
rejection (graft arteriopathy). Note the severe
parenchymal atrophy and the thick-walled arteries.




Kidneys, Ureters, and Urinary Bladder 191
3-36. Opened fetal abdomen with bowel removed showing a horse-
shoe kidney (arrows) due to congenital fusion of both lower poles ante-
rior to the great vessels.




192 Kidneys, Ureters, and Urinary Bladder
3-37. Hypoplastic kidney. A. Note the small size of
the kidney relative to the pelvis and ureter, plus the
reduced number of renal lobes (renunculi).
B. Bisected hypoplastic kidney showing scanty
A
renal parenchymal tissue.




B




Kidneys, Ureters, and Urinary Bladder 193
A




C
B




3-38. Cystic renal dysplasia (CRD) is an abnormal-
ity in metanephric differentiation that may be uni-
lateral or bilateral and is usually cystic. Histology
shows immature collecting ductules, undifferenti-
ated mesenchyme, and even focal cartilage.
A. Bisected kidney shows a less severe form of CRD
with multiple cysts and focally a signi¬cant degree
of disorganization of parenchymal architecture. B.
Histology of bisected kidney shows portions of
cysts, variably dilated epithelial-lined ducts,
periductal myxoid stroma, and an immature
glomerulus. C. Severe multicystic, unilateral CRD
with markedly de¬cient renal parenchyma that pre-
sented as a ¬‚ank mass.



194 Kidneys, Ureters, and Urinary Bladder
A




3-39. A. Autosomal recessive (infantile) polycystic
B
disease (ARPKD). Elongated streaks represent dilated
tubules. B. Histology of ARPKD shows dilated col-
lecting tubules extending to the capsular surface
(top).




Kidneys, Ureters, and Urinary Bladder 195
3-40. A. Simple cyst occupies upper pole of kidney.
B. Dialysis-related multiple small cysts in a coarsely
A
scarred kidney.




B


196 Kidneys, Ureters, and Urinary Bladder
3-41. A. Early stage of autosomal dominant (adult)
polycystic kidney disease (ADPKD). A signi¬cant
amount of renal parenchyma is still present. B. Late
stage of ADPKD showing greatly enlarged renal pro-
¬les due to innumerable cysts of varying size
replacing the renal parenchyma. (continued on next
A
page)




B




Kidneys, Ureters, and Urinary Bladder 197
3-41. (Continued) C. Cut surface of ADPKD show-
ing variable-size, irregular cysts with no recogniza-
ble intervening normal parenchyma. Most cysts
contain clear ¬‚uid and the pelvis is distorted. D.
Histology of ADPKD shows a single glomerulus
C
alongside several cysts.




D




198 Kidneys, Ureters, and Urinary Bladder
3-42. A. Kidney of a young child showing glomeru-
locystic kidney disease (GCKD) with numerous sub-
capsular cysts. In about 50% of cases, GCKD is an
early manifestation of ADPKD. B. Histology of
GCKD shows cysts arising due to dilatation of Bow-
man™s space and the ¬rst part of the proximal con-
A
voluted tubule.




B




Kidneys, Ureters, and Urinary Bladder 199
3-43. Multiple acquired diverticula (arrows) lie
between hypertrophied muscular bundles in a
hypertrophied bladder of a patient who had severe
prostatic hyperplasia. Congenital diverticulum of
the bladder tends to be a solitary lesion.




200 Kidneys, Ureters, and Urinary Bladder
A




B




3-44. Acute in¬‚ammation of the urinary bladder.
A. Acute hemorrhagic cystitis showing a greatly
reddened, in¬‚amed bladder mucosa with areas of
hemorrhage breaching the mucosal surface. B. Fol-
licular cystitis shows focal pale nodules elevating
the in¬‚amed mucosa from below due to the pres-
ence of lymphoid follicles as part of a more chronic
in¬‚ammatory response.




Kidneys, Ureters, and Urinary Bladder 201
A



3-45. Cystitis cystica of the bladder results from
(Brunn) nests of urothelial cells growing downward
into the lamina propria and developing cystic
spaces lined by urothelium. A. Numerous thin-
walled cysts elevate the bladder mucosa. B. Histo-
logic appearance of the cystic Brunn nests.




B




202 Kidneys, Ureters, and Urinary Bladder
3-46. Bladder perforation (arrow) due to pressure of
tip of a Foley catheter in a patient with graft-
versus-host disease after bone marrow transplant.


3-47. A. Urothelial (transitional cell) carcinoma in
situ of the urinary bladder. If untreated, up to 75%
of cases go on to invasive cancer. B. Histology of
carcinoma in situ (surface is to the right).




B
A


Kidneys, Ureters, and Urinary Bladder 203
*




3-48. A. Invasive urothelial carcinoma (*) of the
bladder is invading the muscle coat on the right
side of the picture. B. Moderately differentiated
A
urothelial carcinoma of bladder.




B




204 Kidneys, Ureters, and Urinary Bladder
3-49. Bladder stones lie in a small recess alongside
a ¬‚eshy-looking squamous carcinoma.




Kidneys, Ureters, and Urinary Bladder 205
A



3-50. A. Advanced urothelial cancer of the bladder
has spread posteriorly (arrow) to invade the uterus.
B. Poorly differentiated urothelial carcinoma.




B




206 Kidneys, Ureters, and Urinary Bladder
4 Liver, Biliary System, and Pancreas




A




C
B

4-1. A. Fatty liver due to malnutrition in a child
shows multifocal necroses, each surrounded by a
hemorrhagic ring due to disseminated herpesvirus
simplex infection. B. Cowdry type A intranuclear
inclusions due to herpes simplex viral infection.
Note the marginated chromatin at the edge of the
affected nuclei. C. Close-up view of focal necroses
in a formalin ¬xed liver due to herpesvirus infec-
tion in an immunocompromised adult. Note that
each randomly distributed area of necrosis is sur-
rounded by a localized zone of hemorrhage, giving
a targetoid appearance to the lesions.




Liver, Biliary System, and Pancreas 207
A




B C




4-2. Adenovirus infection of the liver. A. Multiple
areas of focal necrosis, some becoming con¬‚uent,
are scattered throughout the liver. B. Histology
shows intranuclear inclusions. C. Positive intranu-
clear immunoperoxidase staining using a speci¬c
antibody for adenovirus.



208 Liver, Biliary System, and Pancreas
A




C

4-3. A. Multiple abscesses within the liver second-
ary to portal pyemia derived from a septic focus in
the portal vein drainage territory. B. Histologically,
the abscess comprises central remnants of necrotic
liver tissue interspersed and surrounded by poly-
morphonuclear leucocytes. Outside this lies a zone
of compressed liver parenchyma. C. The pus has
been washed out of this large liver abscess to reveal
blood vessels spanning the abscess cavity.



B




Liver, Biliary System, and Pancreas 209
4-4. Multiple amebic abscesses of the liver show
the characteristic roughened, necrotic inner lining
to the abscesses. Note the absence of signs of acute
in¬‚ammation around the lesions because the ame-
bae produce substances to reduce the in¬‚ammatory
response. Hemorrhage into an abscess may produce
“anchovy sauce” pus. The abscesses may erode
through the diaphragm to produce intrapulmonary
lesions or pericardial tamponade. (Photo courtesy of
Dr. R.M. Bowen.)




210 Liver, Biliary System, and Pancreas
A




B C




4-5. Intrahepatic cholestasis. The green color in both macro-
scopic pictures (A and C) is due to the reduction of bilirubin
to biliverdin by the formaldehyde ¬xative. A. Total parenteral
nutrition-induced hepatic cholestasis and hepatic ¬brosis,
which might have proceeded to cirrhosis had the patient sur-
vived longer. B. The bile stasis, as evidenced by bile ¬lled
canaliculi, is well demonstrated histologically in this hema-
toxylin-only stained section. C. Cholestasis due to systemic
bacterial infection. Multiple focal yellow granulomata due to
histoplasmosis are also present.




Liver, Biliary System, and Pancreas 211
A B

4-6. Acetaminophen toxicity. This young man took
large doses of acetaminophen in combination with
excessive ethanol “ a lethal combination because
chronic ethanol consumption increases the 3A4 iso-
form of cytochrome P450, which increases the
metabolism of acetaminophen. A. Close-up view of
liver shows centrilobular zonal necrosis (paler
green areas), with sparing of the peripheral portions
of the lobules (brown-colored areas). B. Histology
shows that centrilobular zonal necrosis has
expanded to affect much of this lobule.



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