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phonuclear leukocytes as well as some histiocytes indicating a chronic
purulent exudate.




Cardiac Diseases 67
A




B




C


68 Cardiac Diseases
1-97. Constrictive pericarditis due to healed tuber-
culosis. A. Heart is encased in a greatly thickened,
calci¬ed parietal pericardium. B. Transverse section
of another heart shows fused, ¬brosed parietal and
visceral layers of the pericardium with compression
of the cardiac chambers that are unable to ¬ll fully
A
in diastole.




B




Facing page:
1-96. Active tuberculous pericarditis. A. Recent active tuberculous pericarditis
with focal yellow tubercles visible on parietal pericardium. B. Healed tubercu-
lous pericarditis. In¬‚amed, densely adherent parietal pericardium has become
considerably thickened. Tuberculous infection had spread to the pericardium
from adherent mediastinal lymph nodes. C. Active granulomatous in¬‚ammation
with ¬brosis due to tuberculosis.


Cardiac Diseases 69
A B

1-98. Polyarteritis nodosa affecting the heart. A. Multiple aneurysms
of varying sizes lie along the course of the major epicardial coronary
arteries and their branches. B. Small epicardial coronary artery shows
arteritis with aneurysm formation and much of the lumen of the
aneurysm is ¬lled by organizing thrombus.




1-99. HeartMate left ventricular (LV) assist device
showing pump housing lying within the abdomen
and portion of liver and stomach prolapsing between
the afferent (right, attached to LV apex) and efferent
(left, terminates in aortic root) drive lines. Porcine
bioprosthetic aortic valves within the drive lines
assure unidirectional blood ¬‚ow.




70 Cardiac Diseases
DISEASES OF BLOOD VESSELS




A



1-100. Fatty streaks and dots on the aortic intima
may be precursor lesions of atherosclerosis. The
lesions are reversible and are commonly present in
young individuals, even babies. A. This ¬gure
shows two pictures of the same aorta of a young
person. The top picture shows a fair number of fatty
streaks and dots. In the lower ¬gure, the same aorta
has been stained with a fat stain (Oil Red O), and
this shows far more dots and streaks than were
observed in the natural aorta. B. The top histologic
section shows that a fatty streak comprises lipid-
laden histiocytes occupying the intima. The lower
section shows a “progressing fatty streak” in which
B
death of some of the histiocytes has led to release
of free lipid into the intima and formation of cho-
lesterol crystals. This event is an important stage in
the conversion of a fatty streak to early atheroscle-
rosis because the lipid evokes a further histiocytic
and ¬bromatous response in the intima.




Cardiac Diseases 71
1-101. Dystrophic calci¬cation of the aorta at the junction of the
sinus and tubular portion of the aorta (i.e., at the top lip of the
sinuses of Valsalva) should not be mistaken for atherosclerosis. The
condition has also been termed Stevenson™s bar. Elongated calci¬c
protrusions may occasionally obstruct the coronary ostia.




1-102. Ascending arch and descending thoracic aorta. Note that the
ascending aorta (bottom left) shows no signi¬cant atherosclerosis,
unlike the remainder of the aorta in which prominent atherosclero-
sis has developed. This is a common, unexplained phenomenon that
is fortunate because coronary arterial bypass grafting uses the ascend-
ing aorta.




72 Cardiac Diseases
*



A B




C



1-103. Due to the effects of gravity, atherosclerosis
tends to be most severe in the abdominal aorta. A.
Severe atherosclerosis with abundant superadded
surface thrombi. An atheroembolus (*) occludes the
ostium of the celiac artery. B. Severe atherosclero-
sis of the abdominal aorta below the renal arteries
with surface ulcerations and extensive associated
mural calci¬cation. C. The defect in the center of
this atherosclerotic plaque is the site of origin of an
atheroembolus. D. Atheromatous embolism has
occluded this artery within the pancreas.

D




Cardiac Diseases 73
A B




C




1-104. A. Atherosclerotic abdominal aortic (AAA) aneurysm has a
fusiform shape due to circumferential weakening of the aortic wall
over a long area below the origin of the renal arteries. B. Thrombus
surgically removed from an AAA aneurysm; surgeons no longer
resect the wall of the aneurysm in performing a repair. C. Histology
of an “in¬‚ammatory variant” of AAA aneurysm shows a thicker than
usual aneurysmal wall due to nonspeci¬c chronic in¬‚ammation and
¬brosis.




Facing page:
1-105. A. Severe atherosclerotic narrowing of the left anterior descending coro-
nary artery and its diagonal branch. Atherosclerosis has more severe stenotic
effects in smaller arteries such as the coronaries than in the aorta. B. Histology
of coronary thrombosis (top) following rupture of the ¬brous cap of an athero-
matous plaque (bottom). C. Transmural rupture of artery with severe athero-
sclerosis following balloon angioplasty. Note the tear (arrow) at the bottom of
the transversely sectioned coronary artery.

74 Cardiac Diseases
A




B




C


Cardiac Diseases 75
A B

1-106. A. Transverse section of a stented coronary
artery that became thrombosed due to poor antico-
agulation. B. Histology of the same vessel shows
occlusive luminal thrombus in direct contact with
the bare metal posts that have no tissue overgrowth.



1-107. Thromboembolus (center) occludes a septal
perforator branch of the left anterior descending
coronary artery. The patient who had a mitral valve
prosthesis was clinically believed to have died of
an arrhythmia.




76 Cardiac Diseases
B
A




C




D

1-108. Dissecting aneurysm of the aorta may be due to systemic hyper-
tension or to weakening of the media by medionecrosis associated
with aging or Marfan syndrome. A. External rupture of the proximal
aorta due to a dissecting aneurysm led to the death of this patient by
cardiac tamponade. B. The false channel that has split the media is
clearly seen. C. Distal end of the traveling intramural hematoma is his-
tologically seen to be taking a line of least resistance by parting the
longitudinally orientated elastic lamellae. D. Double-barreled aorta
due to a chronic dissection in which the false channel containing the
plastic probe supplied the circulation to the right common iliac artery
via a reentry tear (tip of plastic probe).

Cardiac Diseases 77
1-109. Cystic medionecrosis. Aneurysmal dilatation
of the ascending aorta and the aortic arch (top) with
dissecting aneurysm that has arisen at probe site.
Bottom panel shows focal areas of loss of elastic
lamellar units on this elastic-stained section; such
areas are rich in acid mucopolysaccharides.




1-110. Chronic false aneurysm of the aorta that had
been previously transected due to an automobile
accident. The aortic adventitia and compressed sur-
rounding mediastinal tissues had maintained conti-
nuity of blood ¬‚ow between the severed ends of the
aorta. The patient died due to rupture of the thin-
walled false aneurysm.




78 Cardiac Diseases
1-111. Idiopathic aortitis (Takayasu disease) of
the aorta. A. The scarred aorta shows multiple
saccular aneurysms due to focal weakening of
its wall. B. Histology of Takayasu disease
showing two false aneurysms that have arisen
A
at sites of medial destruction.




B




Cardiac Diseases 79
1-112. A. Syphilitic aortitis with “tree bark” wrin-
kling of the intimal surface and multiple saccular
aneurysms, one of which contains a massive throm-
bus. B. Histology shows healed mesaortitis (top);
elastin stains black and collagen stains red. Bottom
panel shows a transverse section through aortic
route inclusive of one coronary arterial origin. Note
that the aortitis has spilled over as intimal thicken-
ing of the proximal coronary artery with resultant
A
stenosis.




B




80 Cardiac Diseases
1-113. A. Scaphoid facies of a child with Hurler
syndrome showing coarse features, prominent
supraorbital ridges, and depressed nasal bridge. B.
A montage of coronary arterial sections from a child
with Hurler syndrome showing marked intimal
thickening and severe luminal stenosis due to an
accumulation of Hurler cells, increased ¬brosis, and
accumulation of interstitial mucopolysaccharide.
Bone marrow transplantation may prevent the arte-
A
rial complications.




B




Cardiac Diseases 81
1-114. Kawasaki disease is the most common cause
of acquired coronary arterial disease in children in
North America. It is an acute multisystemic vas-
culitis of infancy and early childhood, which pres-
ents with fever, rash, conjunctivitis, mucosal
in¬‚ammation, erythema of palms and soles, and
cervical lymphadenopathy. In this patient, healed
Kawasaki disease has produced a coronary arterial
aneurysm (left and top right) that subsequently
became totally thrombosed. Histology of the
aneurysm wall (bottom right) shows no active
arteritis at this time.




82 Cardiac Diseases
A




1-115. Cystic adventitial disease of a joint-related
B
artery is an idiopathic, cystic accumulation of muci-
nous material in the adventitia of an artery possibly
related to trauma, ectopic ganglion cyst, or “dyspla-
sia.” A. Macroscopic appearance of a resected seg-
ment of popliteal artery shows an adventitial cyst
whose expansion is compressing the arterial lumen.
Both levels show luminal thrombosis that was the
indication for surgical resection and grafting, instead
of the usual adventitial drainage therapy. Angio-
plasty is not used for this lesion. B. Histology of the
adventitial cyst (top) and recent thrombus is seen
within the compressed arterial lumen (bottom).




Cardiac Diseases 83
A



1-116. Segmental mediolytic arteriopathy (SMA) is
de¬ned as a peculiar, nonin¬‚ammatory lesion of
visceral and/or coronary arteries characterized by
focal medial lytic changes that may lead to hemor-
rhage, dissection, or thrombosis. Theories of cau-
sation include vasospastic response to shock or
¬bromuscular dysplasia. This author believes that
the condition results from overactivity of serum
elastase. A. SMA is manifesting as multiple longi-
tudinal tears in the terminal aorta and both com-
mon iliac arteries. B. Histology shows evolving tears
at focal areas of mediolysis.
B




1-117. Fatal stab wound in the heart. A. Left panel
shows transverse slice of both ventricles with
hematoma enveloping left anterior descending (LAD)
coronary artery. B. Right panel (histology) shows that
the knife has cut open the LAD coronary artery.




B
A




84 Cardiac Diseases
1-118. Mycotic aneurysm of the aorta (left panel) shows friable
thrombus merging with outer more compact thrombus. The wall of
this small aneurysm is dif¬cult to discern, accounting for the propen-
sity for early rupture of a mycotic aneurysm. Right panel shows the
histologic feature of masses of neutrophils separating the aortic
lamellae.




1-119. Fibromuscular dysplasia (FMD) of the renal artery. The two
pictures on the left show a renal artery exhibiting the most common
form of FMD, namely medial hyperplasia. Note the segmental, irreg-
ular string of beads or corkscrew pattern comprising the ridges that
separate the outpouching of the lumen. The histologic section (right)
shows a ridge that has been demonstrated by a longitudinal section
of the artery. Contrary to most arterial conditions, longitudinal sec-
tioning is the best way to demonstrate the histology of FMD.




Cardiac Diseases 85
A




B

1-120. A. Congenital stenosing arteriopathy (CSA),
so-called macaroni arteries, is a unique form of con-
genital arterial dysplasia affecting the aorta and its
major branches. Branches of the aortic arch are seen
(center) and the descending aorta is present (top
right). B. Transverse section of carotid artery (left)
and its elastic-stained histology (right) shows that
arterial mural thickening results from a hyperplasia
of medial lamellar units with an outer medial dis-
array pattern.




86 Cardiac Diseases
A


B




C




1-121. Venous thrombosis. A. Transverse section of
D
a thrombosed large vein shows lines of Zahn (arrow)
indicative of an antemortem thrombus derived from
¬‚owing blood. B. Histology con¬rms that the pale
lines correspond to deposits of ¬brin and platelets
between the masses of coagulated erythrocytes. C.
Clockwise from top left: bilateral iliofemoral venous
thrombosis with embolization of the thrombus from
the top vein (portion of thrombus is missing); major
thromboemboli occlude the left and right pulmonary
arteries; and histology of a web in a pulmonary
artery “ the web results from an old organized
thromboembolus. D. In both males and females, the
pelvic veins may be the source of cryptic throm-
boembolism. This picture shows massive thrombo-
sis (X) of the periprostatic venous plexus.




Cardiac Diseases 87
1-122. Inferior venal caval umbrella has success-
fully detained multiple thrombi that were on their
way to the lungs. Flat thrombi have also developed
on the struts of the umbrella.



1-123. A. Thrombosis of the superior mesenteric
(bottom arrow) and portal (top arrow) veins inferior
to the liver (top). B. Resultant venous infarction of
the small intestine has occurred.




B




A


88 Cardiac Diseases
1-124. Greatly dilated splenic vein (probe) in cir-
rhosis-induced portal hypertension. Rupture of the
splenic vein may rarely occur, and although the
resultant retroperitoneal hemorrhage may be less
dramatic than an arterial rupture, it may still kill
the patient.




1-125. Idiopathic aneurysm of the inferior vena in
a young girl who died of thromboembolism as a
result of massive thrombus detaching from the
aneurysm and traveling to her pulmonary arteries.




Cardiac Diseases 89
2 Pulmonary Pathology




2-1. Atelectasis (alveolar collapse due to absence of
air) has produced a zone of lung tissue that is
depressed below the surrounding aerated lung tis-
sue and has a redder and more solid appearance.




90 Pulmonary Pathology
2-2. Localized ¬brinous pleurisy (arrow) over
parenchymal lesions due to Aspergillosis. The ¬b-
rin deposit produces a roughened appearance to the
pleural surface.



2-3. Anthracosis of the lung: pleural lymphatics around lobules are
outlined by carbon deposits. See also Figs. 2-26A and 2-43A, which
each show marked anthracosis in addition to a malignancy.




Pulmonary Pathology 91
2-4. Lobar pneumonia. A. Consolidation affects the
entire left lower lobe of lung. This is typical of a
pneumococcal (Streptococcus pneumoniae) infec-
tion in which hypersensitivity leads to an outpour-
ing of ¬‚uid within the lung. The infection spreads
to all alveoli via the pores of Kohn. Klebsiella pneu-
moniae may also cause a lobar pneumonia, but the
cut surface of the affected lobe usually has a more
mucoid appearance due to the organisms™ thick,
gelatinous capsule. B. Stage of red hepatization:
low-power histology shows congestion, and alveoli
are ¬lled with neutrophils. C. Grey hepatization:
A
intraalveolar exudate compresses the capillaries.




C

B




92 Pulmonary Pathology
2-5. Bronchopneumonia. A. Extensive bronchop-
neumonia in upper lobe of lung is seen as areas of
yellow-white consolidation centered on bronchi
and bronchioles against a congested pulmonary
parenchyma. Overall, bronchopneumonia occurs
more commonly in the lower lobes of the lungs.
B. Focal area of acute bronchopneumonia with sur-
rounding edema. Air bubbles are present within the
intraalveolar edema ¬‚uid. Bacterial colonies are
seen on the left of the picture. C. High-power view
A
of bronchopneumonia.




C
B




Pulmonary Pathology 93
2-6. A. Nearly the entire upper lobe of the lung
shows consolidation. Such a pattern of subtotal
consolidation may be noted with lobar pneumonia
that has been treated with antibiotics, or it may
occur with a Klebsiella infection and has been
termed “lobular pneumonia.” Rarely, con¬‚uent
bronchopneumonia may produce extensive consol-
idation mimicking lobar pneumonia. B. Histologic
appearance of bronchiolitis obliterans organizing
pneumonia (BOOP) in which the lumens of many
A
bronchioles are obstructed by loose ¬brous masses.




B




94 Pulmonary Pathology
2-7. A. Surgical resection of portion of lung with
lung abscesses caused by staphylococcal bronchop-
neumonia. B. Histologic appearance of a lung
abscess ful¬lling the criterion of a localized area of
destruction of the lung parenchyma, with the space
being occupied by polymorphonuclear leukocytes.
A
(continued on next page)




B




Pulmonary Pathology 95
2-7. (Continued) C. Chronic lung abscess shows
residual pus attached to pulmonary artery that spans
the abscess cavity. The pulmonary arteries are much
more resistant to destruction by an abscess than are
the bronchioles, veins, and lung parenchyma.
D. In¬‚amed granulation tissue lines a chronic
C
abscess cavity.




D


96 Pulmonary Pathology
A



2-8. A. Early bronchiectasis with ectasia of a small
bronchus (arrows) near the periphery of the lung. It
is unusual to see a bronchial structure of this size
in such a peripheral position. B. Histology of the
small bronchus shows chronic in¬‚ammation with
dilatation of its lumen and loss of both cartilage and
much of the smooth muscle coat.




B




Pulmonary Pathology 97
2-9. A. Active bronchiectasis in a patient with cys-
tic ¬brosis (CF). All stages of bronchiectasis are
noted, and the multicentric peribronchial whitish-
colored consolidation is due to lymphoid hyper-
plasia. B. Bronchial casts comprising dense, viscid
A
sputum expectorated from a patient with CF.




B




98 Pulmonary Pathology
2-10. End-stage bronchiectasis with almost no resid-
ual functioning lung parenchyma.




Pulmonary Pathology 99
2-11. A. Bilateral, patchy, ill-de¬ned areas of con-
solidation due to infection with Pneumocystis
jiroveci. Such infections are more common in
immunocompromised individuals, including per-
sons with acquired immunode¬ciency syndrome
(AIDS). B. Microscopically, the alveoli are seen to
contain a foamy exudate, and the thickened inter-
stitium contains a mononuclear cellular in¬ltrate.
C. Grocott methenamine silver stain shows an
intraalveolar collection of helmet-shaped cysts of
A
Pneumocystis.




B C




100 Pulmonary Pathology
2-12. A. Ill-de¬ned, diffuse pneumonic consolida-
tion due to Cryptococcus neoformans (Torula)
infection in a patient with systemic lupus erythe-
matosus. B. Mucin-stained section shows abundant
yeast-like organisms with a mucin-positive capsule
A
consistent with Torula.




B



Pulmonary Pathology 101
2-13. A. Pneumonitis with a bronchopneumonic
pattern in areas due to cytomegalovirus (CMV)
pneumonia. B. Typical CMV inclusions are seen
within several greatly enlarged alveolar lining cells.
C. Positive immunohistochemical staining of the
A
viral inclusions by a speci¬c antibody to CMV.




B C




102 Pulmonary Pathology
2-14. A. Upper and middle lobes of right lung con-
tain multiple infarct-like lesions, some of which
appear hemorrhagic due to Aspergillus niger infec-
tion of the lung. B. Early Aspergillus lesion (bottom
arrow) in the lung shows fungal elements in¬ltrat-
ing through the wall (top arrow) of a small pul-
monary vessel and into its lumen. The angioinva-
sive nature of the fungus with secondary thrombosis
accounts for the ischemic nature of its resultant tis-
A
sue lesions. (continued on next page)




B




Pulmonary Pathology 103
2-14. (Continued) C. Aspergillus hyphae growing
within infarcted and in¬‚amed lung tissue. D. Silver
stain shows 45-degree branching of septate hyphae
C
characteristic of Aspergillus fungus.




D




104 Pulmonary Pathology
A



2-15. A. Diffuse consolidation of both lungs due to
diffuse alveolar damage (DAD) (adult respiratory
distress syndrome). B. Many alveoli are lined by
deposits of ¬brin lying on areas that have lost their
alveolar lining cells. (continued on next page)




B




Pulmonary Pathology 105
2-15. (Continued) C. Later stage of DAD with organ-
ization of intraalveolar ¬brin. D. Late stage of non-
fatal DAD with ¬brosis and cystic change due to air
C
trapping in the lung.




D




106 Pulmonary Pathology
A



2-16. A. Hemorrhagic appearance of the posterior
aspect (inferior aspect in a reclining patient) of both
lungs due to inhalation of blood following a
hematemesis due to a bleeding gastric ulcer. B. Alve-
oli are ¬lled with blood, and reactive changes are
noted in the alveolar septa.




B




Pulmonary Pathology 107
2-17. Diffuse intrapulmonary hemorrhage in a patient
with Goodpasture syndrome.




108 Pulmonary Pathology
2-18. A. Yellow-colored areas of pneumonic consol-
idation due to histoplasmosis pneumonia. B. His-
tology shows a tuberculoid granulomatous in¬‚am-
mation due to histoplasmosis. (continued on next
A
page)




B

Pulmonary Pathology 109
2-18. (Continued) C. Healed, caseous lesion of
histoplasmosis with ¬brous capsule in lung
parenchyma is reminiscent of a tuberculous infec-
tion. The proximity to the lung hilum (note adja-
cent major pulmonary artery branch) means one
cannot exclude the process occurring in an intra-
pulmonary lymph node. D. Histology shows coagu-
lative necrosis (caseation). E. Methenamine silver
stain shows yeast-like histoplasmosis organisms
C
within the caseous material.




D E




110 Pulmonary Pathology
2-19. A. Coagulative necrosis and granulomatous
in¬‚ammation of the lung in a case of infection with
Coccidioides immitis (coccidioidomycosis). Unlike
histoplasmosis, these granulomas seldom calcify.
B. A spherule of C. immitis containing numerous
endospores is seen in the lower half of the picture,
and free-lying endospores are seen in the upper por-
A
tion of the picture.




B

Pulmonary Pathology 111
* 2-20. A. Primary tuberculosis (TB) with midlung
parenchymal (Ghon complex) (*) and hilar nodal
involvement (arrow) by TB combine to produce a
Ranke complex. B. Progressive primary pulmonary
TB in a young child showing massive caseation of
hilar lymph nodes and widespread tuberculous
bronchopneumonia secondary to bronchogenic
A
spread of the disease. (continued on next page)




B




112 Pulmonary Pathology
C



2-20. (Continued) C. Miliary TB of both lungs due
to blood spread of tubercle bacilli via the thoracic
duct or following erosion of a tuberculous node into
a pulmonary vein or venule. (Photos courtesy of Dr.
R.M. Bowen.) D. Histology of subacute military TB
of the lung showing multiple, small discrete tuber-
culous granulomas, a few of which show early cen-
tral necrosis.




D




Pulmonary Pathology 113
A



2-21. A. Adult, reinfective tuberculosis (TB) show-
ing massive cavitation (pulmonary arteries span
cavities) and marked pleural ¬brosis and minimal
lymph nodal involvement. The difference from pri-
mary TB is due to the greater rigidity of the adult
bronchi, as well as the presence of immunity and
hypersensitivity. Immunity limits spread of tubercle
bacilli to the regional lymph nodes, and hypersen-
sitivity favors necrosis and cavitation following
expectoration of necrotic material from eroded
bronchi. (Photo courtesy Dr. R.M. Bowen.) B and C.
Coagulative necrosis with surrounding epithelioid
histiocytes and Langhans giant cells plus lympho-
cytes comprising the in¬‚ammatory response to
active TB infection. (continued on next page)




B



114 Pulmonary Pathology
2-21. (Continued) D. Mycobacterium tuberculosis
acid-fast bacilli are characterized by a beaded and
C
slightly curved appearance.




D




Pulmonary Pathology 115
2-22. A. Pulmonary ¬brosis in steroid-treated sar-
coidosis. B. Noncaseating, tuberculoid granuloma of
sarcoidosis in the lung. The granulomas are cen-
tered on venules in about 80% of cases and involve
arteries to a much lesser degree. In parts of the
world where tuberculosis (TB) is common, the
pathologist is not in a position to make the differ-
ential diagnosis between TB and sarcoidosis on a
A
biopsy without clinical input.




B


116 Pulmonary Pathology
2-23. A. Wegener granulomatosis (WG): note the
pale area in the upper lobe due to a combination of
necrosis (yellow areas) and reparative ¬brosis
(white areas). B. Pulmonary cavitation in WG may
mimic tuberculosis, and Langhans-type giant cells
may be observed in both conditions. (continued on
A
next page)




B


Pulmonary Pathology 117
2-23. (Continued) C. Treated WG. The presence of
a small vessel vasculitis, a mixed in¬‚ammatory
in¬ltrate, and parenchymal serpiginous necrosis
(not seen here) is characteristic of WG. D. Small
C
pulmonary arterial vasculitis in WG.




D




118 Pulmonary Pathology
2-24. A. Asbestos (ferruginous) body (AB) in the
lung comprises a thin, almost invisible, colorless,
nonbirefringent, needle-like ¬ber of asbestos that is
rendered visible by deposits of iron (hemosiderin)
and protein on its surface in a beaded fashion. The
ABs are most numerous toward the bases of the
lungs due to the effect of gravity and may pass
through the lungs. Dense structures such as bone
(e.g., ribs) and very dense collagen (e.g., central ten-
don of the diaphragm) may arrest the asbestos
¬bers™ passage in the body, and the outcome is local
irritation and ¬brogenesis, resulting in the follow-
ing distribution for ¬brous plaques due to asbestos
¬bers. B. Fibrous plaques (*) on the parietal pleura
are distributed along the inner aspect of the ribs,
while sparing the intercostal muscles that failed to
arrest passage of the asbestos ¬bers. Fibrous plaques
may occur with asbestos exposure in the absence of
A
asbestosis. (continued on next page)




B



Pulmonary Pathology 119
C



2-24. (Continued) C. Similarly, on the upper surface
of the diaphragm, the plaques are con¬ned to the
pleura overlying the central tendon of the
diaphragm and are rarer on its muscular portion.
D. Asbestosis may lead to obliteration of the pleu-
ral space due to the parietal pleura becoming ¬rmly
attached to the visceral pleura. Note the rib mark-
ings on the exterior of the parietal pleura that is
covering most of the lung.




D




120 Pulmonary Pathology
2-25. A. Asbestosis has produced widespread, patchy
interstitial pulmonary ¬brosis and cyst formation
(“honeycomb” lung) due to air trapping in the lung.
B. Histologic appearance of advanced asbestosis with
A widespread ¬brosis and cystic dilatation of airspaces.




B


Pulmonary Pathology 121
2-26. A. Malignant mesothelioma on the pleural surface
and spreading into the interlobar ¬ssures of an extremely
anthracotic lung. B. Malignant mesothelioma entirely
encases the left lung and is in¬ltrating into the lung from
the exterior. C. Histology of a malignant mesothelioma
exhibiting a spindle-cell pattern in a prominent ¬brous
A
stroma.




B C




122 Pulmonary Pathology
A




B C

2-27. A. Whole lung section shows pan-acinar
emphysema of lung in a patient with ±-1-antitrypsin
de¬ciency. B and C. Histology shows destruction of
alveolar walls in a diffuse fashion.




Pulmonary Pathology 123
A B


2-28. Centrilobular emphysema of the lungs, com-
monly related to cigarette smoking, is most severe
in the upper portions of the lungs. A. Centrilobular
carbon deposits in the lung. B. Early centrilobular
emphysema in left upper lobe of lung. C. Whole
lung section of moderate centrilobular emphysema.
(continued on next page)




C




124 Pulmonary Pathology
D




F
E

2-28. (Continued) D. More severe centrilobular emphysema is
most noticeable in both upper lobes. E. Whole lung section of
severe centrilobular emphysema. F. Centrilobular emphysema
histology shows maximal alveolar destruction in the center of
the lobule closest to the bronchiolar and lobular pulmonary
arterial branches.
Pulmonary Pathology 125
2-29. Bullous emphysema of the lung in a 6-year-
old child with Marfan syndrome resulting from
intrapulmonary de¬ciency of elastin.




126 Pulmonary Pathology
A




B C

2-30. Silicosis is a form of pneumoconiosis due to inhalation of silicon
dioxide (silica) (e.g., due to sand blasting). A. Note the pale, large,
rounded silicotic nodules against a black background due to severe asso-
ciated anthracosis. B and C. Histologic appearance of multiple, coalesc-
ing silicotic nodules composed of concentrically arranged collagen ¬bers
with surrounding aggregates of lymphocytes and ¬broblasts.



Pulmonary Pathology 127
B
A




C D




128 Pulmonary Pathology
A



2-32. A. Bilateral patchy pulmonary consolidation
and early honeycombing due to Langerhans cell his-
tiocytosis (a proliferation of dendritic cells or
macrophages also called “histiocytosis X” or
“eosinophilic granuloma”). B. Numerous eosinophils
lie scattered between aggregates of large phagocytes
with foamy cytoplasm and grooved nuclei (Langer-
hans cells). Because not all tumor cells contain Bir-
beck granules on electron microscopy, staining for S-
100 and CD1a may assist in the diagnosis.




B



Facing Page:
2-31. A. Macroscopic appearance of ¬brosing alveolitis; note the tendency toward
involvement of the more peripheral portions of the lung parenchyma. B. Sub-
pleural ¬brosis and early honeycombing in ¬brosing alveolitis. C. End-stage hon-
eycomb lung due to ¬brosing alveolitis. D. External appearance of honeycomb
lung shows a cobble stone-like pattern.


Pulmonary Pathology 129
A




B




C




130 Pulmonary Pathology
A



2-34. A. Wedge-shaped lung infarct with base on the
pleural surface (arrow indicates thromboembolism).
The lung has a dual blood supply, and pulmonary
arterial occlusion may only produce infarction (as
opposed to incomplete/subinfarction) if cardiac fail-
ure negates the protective effect of the bronchial cir-
culation. B. Histologic edge of pulmonary infarct is
seen in lower left. (continued on next page)




B




Facing Page:
2-33. A. Massive, fatal pulmonary thromboembolism (TE) of main pulmonary
artery extending into its bifurcation due to TE from iliofemoral segment venous
thrombosis. Note the coiled up thrombus ¬lling the pulmonary artery. B. Unrav-
eled thrombus from another patient™s massive TE reveals a venous thrombus with
thrombotic extensions from side branches of the venous system. C. Right main
pulmonary artery is ¬lled by a thromboembolus.


Pulmonary Pathology 131
C



2-34. (Continued) C. The darker-colored infarct
situated subpleurally on the right is surrounded by
an extensive area of hemorrhagic-looking lung
parenchyma exhibiting incomplete (sub)infarction in
which the alveolar walls are viable and intraalveolar
hemorrhage has occurred. D. Histology of incomplete
(sub)infarct showing intraalveolar hemorrhage, but
viability of the alveolar walls is maintained by the
bronchial circulation.




D




132 Pulmonary Pathology
A



2-35. The lung has an excellent healing capacity, so
healed infarcts of the lung are seldom observed;
sometimes, only a wafer-thin scar remains as a tes-
tament to the previous infarct. A. Healing bland
(noninfected) infarct of the lung is seen as a slightly
hemorrhagic, shrunken, scarred area (arrow) beneath
the pleural surface. B. Healing septic (infected)
infarct of the lung showing cavitation of the infarct
close to the pleural surface. Yellow color is due to
the presence of neutrophils within the infarct.




B




Pulmonary Pathology 133
2-36. Gross morphology indicative of pulmonary
hypertension may be observed in the right ventricle
and main pulmonary arteries. A. Disproportionate
right ventricular hypertrophy and dilatation. B. Ath-
erosclerosis of the main pulmonary artery and its
branches occurs predominantly with pulmonary
hypertension, and the only other cause is extreme
old age (e.g., older than 90 years). In pulmonary
hypertension, the arteries appear thicker than nor-
mal and are more protuberant on the cut surface of
A
the lung.




B




134 Pulmonary Pathology
A B

2-37. A. Surgically removed chondroid hamartoma
of the lung. B. Histology of chondroid hamartoma
shows compressed epithelial structures overlying a
rounded mass of benign cartilaginous tissue.



2-38. Pulmonary blastoma showing focal areas of
necrosis and hemorrhage on its cut surface.




Pulmonary Pathology 135
A B


2-39. A. Carcinoid tumor of lung in a lobectomy
specimen. B. Carcinoid tumor expanding and in¬l-
trating the wall of a large bronchus and compress-
ing the adjacent pulmonary artery. C. Typical his-
tology of a carcinoid tumor comprising small nests
of uniform-looking small, dark cells.




C


136 Pulmonary Pathology
2-40. Sputum cytology from a patient with lung
cancer shows highly atypical, anaplastic malignant
epithelial cells encompassed by acute in¬‚ammatory
cells (polymorphonuclear leukocytes).

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