Lab reviewer

Ajmal sha
LECTURE 1
The relationship between normal, adapted, reversibly
injured, and dead myocardial cells. All three transverse
sections of the heart have been stained
with triphenyltetrazolium chloride, an enzyme substrate
that colors viable myocardium magenta. The cellular
adaptation shown here is myocardial hypertrophy
(lower left), caused by increased blood pressure
requiring greater mechanical effort by myocardial cells.
This adaptation leads to thickening of the left ventricular
wall (compare with the normal heart). In reversibly
injured myocardium (illustrated schematically, right),
there are functional alterations, usually without any
gross
or microscopic changes but sometimes with
cytoplasmic changes such as cellular swelling and fat
accumulation. In the specimen showing necrosis, a
form
of cell death (lower right), the light area in the
posterolateral left ventricle represents an acute
myocardial infarction caused by reduced blood flow
(ischemia
Physiologic hypertrophy of
the uterus during
pregnancy.
Atrophy
METAPLASIA
Morphologic changes in
reversible cell injury and
necrosis.
Coagulative necrosis
LIQUEFACTIVE NECROSIS
CASEOUS NECROSIS
FAT NECROSIS
APOPTOTIC BODIES IN THE
PANCREAS
Apoptosis of an epidermal
cell
Apoptosis of an epidermal cell in an
immune reaction. The cell is reduced in
size and contains brightly
eosinophilic cytoplasm and a condensed
nucleus
 Dystrophic
calcification of the
aortic valve.
DYSTROPHIC CALCIFICATION
IN ATHEROSCLEROSIS
CHOLESTEROLOSIS
Fatty liver

Fatty liver. High-power

detail of fatty change of
the liver. In most
cells the well-preserved
nucleus is squeezed into
the displaced rim of
cytoplasm
about the fat vacuole.
PROTIEN REABSORBPTION
DROPLETS IN THE RENAL
TUBULE

Protein reabsorption droplets in the

renal tubular epithelium
Lipofuscin granules in a
cardiac myocyte

Lipofuscin granules in a cardiac myocyte shown by (A) light

microscopy (deposits indicated by arrows), and (B) electron
microscopy
MALLORY BODIES IN LIVER
HEMATOCHROMATOSIS
 Hereditary
hemochromatosis

Hereditary
hemochromatosis. In
this Prussian blue-
stained
section, hepatocellular
iron appears blue. The
parenchymal
architecture is
normal.
Acute pneumitis

acute pumonary edema in alveolar spaces,

neutrophilic
appendix
Acute Appendicitis
Acute suppurative
inflammation
 Macrophage rich
chronic inflammation
 Esosinophil rich
inflammation- asthma
Gall bladder , chronic
colitis
Chronic inflammation in
the lung

Chronic inflammation in the lung, showing all three characteristic

histologic features: (1) collection of chronic inflammatory cells (*), (2)
destruction of parenchyma (normal alveoli are replaced by spaces lined by
cuboidal epithelium, arrowheads), and (3) replacement by connective tissue
(fibrosis, arrows). B, In contrast, in acute inflammation of the lung (acute
bronchopneumonia), neutrophils fill the alveolar spaces and blood vessels
are congested.
 Serous inflammation

Serous inflammation. Low-power view of a

cross-section of a
skin blister showing the epidermis
separated from the dermis by a focal
collection
of serous effusion.
 Fibrinous pericarditis

Fibrinous pericarditis. A, Deposits of fibrin on the pericardium. B,

A pink meshwork of fibrin exudate (F) overlies the pericardial
surface (P).
PURULENT INFLAMMATION
ULCER
Granulomatous
inflammation
 Typical tuberculous

Typical tuberculous granuloma showing an area of central

necrosis surrounded by multiple Langhans-type giant cells,
epithelioid cells, and lymphocytes.
Granulomatous tissue-
tissue granulitis
HEALING OF SKIN ULCERS
Keloid collagen bunds
GRANULATION TISSUE
LECTURE 2
 1 LIVER WITH CHRONIC PASSIVE
CONGESTION
This is a nutmeg liver with chronic passive
congestion. Note the dark-red congested
regions that represent accumulation of red
blood cells within centrilobular regions.
The nutmeg pattern results from
congestion around the central veins,
usually from right-sided heart failure. If the
passive congestion is pronounced and
heart failure leads to ischemia, there can
be centrilobular necrosis because the
oxygenation in zone 3 of the hepatic lobule
i s d i m i n i s h e d , a n d t h e A S T a n d A LT
i n c r e a s e . R a r e l y, c h r o n i c p a s s i v e
congestion leads to fibrosis extending
between central veins—a “cardiac
cirrhosis.” Extensive hepatic congestion
can accompany disseminated intravascular
coagulation and hemoglobinopathies such
as sickle cell diseasea
 MICROSCOPIC VIEW OF A
NUTMEG LIVER
Hepatic congestion, the central vein and
sinusoids are distended with blood, and
there may even be necrosis of centrally
located hepatocytes. The periportal
hepatocytes, better oxygenated because of
their proximity to hepatic arterioles,
experience less severe hypoxia and may
develop only reversible fatty change.
In chronic passive congestion of the liver,
the central regions of the hepatic lobules,
viewed on gross examination, are red-brown
and slightly depressed (owing to cell loss)
and are accentuated against the surrounding
zones of uncongested tan, sometimes fatty,
liver (nutmeg liver) (Fig. 4.1A). Microscopic
findings include centrilobular hepatocyte
necrosis, hemorrhage, and hemosiderin-
laden macrophages
 MUCOSA OF THE INTESTINE
Petechiae are minute (1 to 2 mm in diameter)
hemorrhages Into skin, mucous membranes, or
serosal surfaces (Fig. 4.4A); causes include low
platelet counts
(thrombocytopenia), defective platelet function,
and loss of vascular wall support, as in vitamin
C deficiency
(Chapter 8). Purpura are slightly larger (3 to 5
mm) hemorrhages. Purpura can result from the
same disorders that cause petechiae, as well as
trauma, vascular inflammation (vasculitis), and
increased vascular fragility.
• Ecchymoses are larger (1 to 2 cm)
subcutaneous hematomas (colloquially called
bruises). Extravasated red cells are
phagocytosed and degraded by macrophages;
the characteristic color changes of a bruise
resul t fro m t h e e n z y m a t i c c o n v e r s i o n o f
hemoglobin (red-blue color) to bilirubin (blue-
green color) and eventually hemosiderin
(golden-brown).
CEREBRAL HEMORRHAGE
 Embolus derived from a lower-
extremity deep venous thrombus
lodged in a pulmonary artery branch.
 Unusual types of emboli-
Bone marrow embolus
Bone marrow embolus. The embolus
is composed of hematopoietic marrow and
marrow fat cells (clear spaces)
attached to a thrombus.

Soft tissue crush injury or rupture of marrow

vascular sinusoids (eg, due to a long bone
fracture) release microscopic
fat globules into the circulation. Fat and
marrow emboli are common incidental
findings after vigorous cardiopulmonary
resuscitation but probably are of little clinical
significance. Similarly, although fat and
marrow embolism occurs in some 90% of
individuals with severe skeletal injuries (Fig.
4.16A), less than 10% show any clinical
findings.
 INFRACTS
RED INFRACT WHITE INFRACT

Hemorrhagic, Sharply demarcated pale infarct in the spleen

roughly wedge-shaped pulmonary infarct (white
(red infarct). infarct).
Infarcts are classified based on their color (reflecting the amount of
hemorrhage) and the presence or absence of microbial infection. Thus,
infarcts may be either red (hemorrhagic) or white (anemic) and may be
either septic or bland. Red infarcts (Fig. 4.17A) occur (1) as a result of
venous occlusions (such as in ovarian torsion); (2) in loose tissues (e.g.,
lung)where blood can collect in infarcted zones; (3) in tissues with dual
circulations such as lung and small intestine, where partial, albeit
inadequate perfusion by collateral arterial supplies is typical; (4) in
previously congested tissues (as a consequence of sluggish venous
outflow); and (5) when flow is reestablished after infarction has
occurred (e.g., after angioplasty of an arterial obstruction).White infarcts
occur with arterial occlusions in solid organs with end-arterial circulations
(e.g., heart, spleen, and kidney), and where tissue density limits the
seepage of blood from adjoining patent vascular beds (Fig. 4.17B).
Infarcts tend to be wedgeshaped, with the occluded vessel at the apex
and the organ periphery forming the base (Fig. 4.17); when the base is a
serosal surface, there is often an overlying fibrinous exudate. Lateral
margins may be irregular, reflecting flow from adjacent vessels. The
margins of acute infarcts typically are indistinct and slightly hemorrhagic;
with time, the edges become better defined by a narrow rim of hyperemia
attributable to inflammation.
 LUPUS NEPHTITIS

Focal proliferative glomerulonephritis, with two focal necrotizing

lesions at the 11 o’clock and 2 o’clock positions (H&E stain).
Extracapillary proliferation is not prominent in this case
 GLOBAL /DIFFFUSE PROLIFERATIVE
GLOMERULONEPHRITIS

Diffuse proliferative glomerulonephritis. Note the marked increase in

cellularity throughout the
glomerulus (H&E stain).
 LUPUS NEPHRITIS WITH WIRE
LOOP LESIONS

Lupus nephritis showing a glomerulus with several “wire-loop” lesions

representing extensive subendothelial deposits of immune
complexes (periodic acid-Schiff stain).
Electron micrograph of a renal glomerular capillary loop from a
patient with SLE nephritis. Subendothelial dense
deposits (arrowheads) on basement membrane (arrow)
correspond to “wire loops” seen by light microscopy
 Enlargement of the
salivary gland.
GLAND- PAROTID GLAND

SJÖGREN SYNDROME
Sjögren syndrome is an inflammatory
disease that primarily affects the
salivary and lacrimal glands, causing
dryness of the mouth and eyes.
• The disease is believed to be caused
by an autoimmune T-cell reaction
against an unknown self antigen
expressed in these glands, or immune
reactions against the antigens of a virus
that infects the tissues.
 PAROTID GLAND
PAROTID DUCT LINED BY
COLOUMNAR CELLS

HYPERPLASTIC PROLIFERATION OF
THE PAROTID DUCT SURROUNDED BY
LYMPHOCYTES (B) AND PLASMA
CELLS

Intense lymphocytic and plasma cell

infiltration with ductal epithelial hyperplasia
in a salivary gland.
 SYSTEMIC SCLEROSIS

Systemic sclerosis. (A) Normal skin. (B) Skin biopsy from a patient with
systemic sclerosis. Note the extensive deposition of dense collagen in
the dermis, the virtual absence of appendages (e.g., hair follicles), and
foci of inflammation (arrow).
 subcutaneous fibrosis

The extensive subcutaneous fibrosis has virtually immobilized

the fingers, creating a clawlike flexion deformity. Loss of blood supply
has led to cutaneous ulceratio
 Colonic polyp

An aedonmatous (glandular) polyp is

projecting into the colonic lumen and is
attached to the mucosa by a distinct stalk.
Gross appearance of several colonic polyps.
 MIXED TUMOR

This mixed tumor of the parotid gland contains

epithelial cells forming ducts and myxoid stroma that
resemble cartilage
TERATOMA OF THE OAVARY

Gross appearance of an opened cystic

teratoma of the ovary. Note the
presence of hair, sebaceous material,
and tooth
MICROSCOPIC VIEW OF TUMOR

microscopic view of a similar tumor

shows skin, sebaceous glands, fat cells,
and a tract of neural tissue (arrow).
 Leiomyoma of the uterus

Leiomyoma of the uterus. This benign, well-differentiated tumor

contains interlacing bundles of neoplastic smooth muscle cells that
are virtually identical in appearance to normal smooth muscle cells
in the myometrium.
FOLLICULAR ADENOMA OF THE
THYROID

Benign tumor (adenoma) of the thyroid.

Note the normal-looking
(well-differentiated), colloid-filled
thyroid follicles
squamous cell carcinoma
of the skin

Well-differentiated squamous cell carcinoma of the

skin. The tumor cells are strikingly similar to normal
squamous epithelial cells, with intercellular bridges
and nests of keratin pearls (arrow).
ADENO CARCINOMA OF THE
colon

Malignant tumor (adenocarcinoma) of the colon.

the cancerous glands are irregular in shape and
size and do not resemble the normal colonic glands.
This tumor is considered differentiated because gland
formation is seen. The malignant glands have invaded
the muscular layer of the colon.
 Anaplastic tumor

Anaplastic tumor showing cellular and nuclear

variation in size and shape. The prominent cell in the
center field has an abnormal tripolar spindle.
 Carcinoma in situ
EPITHELIAL LINING WITH
DYSPLASIA

Carcinoma in situ. A low-power view shows that the epithelium

is entirely replaced by atypical dysplastic cells. There is no
orderly differentiation of squamous cells. The basement
membrane is intact, and there is no tumor in the subepithelial
stroma.
 MICROSCOPIC VIEW OF
CARCINOMA

A high-power view of another region shows failure

of normal differentiation, marked nuclear and cellular
pleomorphism, and numerous mitotic figures extending
toward the surface.
Fibroadenoma of the breast

Fibroadenoma of the breast. The tan-

colored, encapsulated small tumor is
sharply demarcated from the whiter
breast tissue
MICROSCOPIC SECTION OF
BENIGN FIBROADENOMA

Microscopic view of fibroadenoma of the breast seen in

Figure 7-11. The fibrous capsule (right) delimits the tumor
from the surrounding tissue
 COLON CARCINOMA

Colon carcinoma invading pericolonic

adipose tissue.
 METASTATIC
ADENOCARCINOMA

Axillary lymph node with metastatic breast

carcinoma. Note the aggregates of tumor cells
within the substance of the node and the dilated
lymphatic channel.
LIVER WITH METASTATIC
CANCER

A liver studded with metastatic

cancer.
Microscopic view of lung metastasis

Microscopic view of lung metastasis. A

colonic adenocarcinoma
has formed a metastatic nodule in the lung.
LECTURE-3
Bronchopneumonia.

Bronchopneumonia. Section of lung

showing patches of consolidation
LOBAR PNEUMONIA

Lobar pneumonia—gray hepatization.

The lower lobe is uniformly
consolidated.
 ACUTE PNEUMONIA

Acute pneumonia. The congested septal

capillaries and numerous intra-alveolar
neutrophils are
characteristic of early red hepatization. Fibrin
nets have not yet formed.
Primary pulmonary
tuberculosis

Primary pulmonary tuberculosis, Ghon

complex. The gray-white parenchymal focus is
under the pleura in the lower part of the upper
lobe. Hilar lymph nodes with caseation are seen
on the left.
 THE MORPHOLOGIC SPECTRUM
OF TUBERCULOSIS
The morphologic spectrum of
tuberculosis. Characteristic tubercle at
low magnification (A) and high
magnification (B) shows central granular
caseation surrounded by epithelioid and
multinucleate giant cells. This is the
usual response in people who have
developed cell-mediated immunity to the
organism. Inset: Acid-fast stain shows
rare positive (red) organisms. C,
Occasionally, even in immunocompetent
patients, tubercular granulomas may not
show central caseation; hence
regardless of the presence or absence
of caseous necrosis, use of special stain
for acid-fast organisms is indicated
when granulomas
are present. D, In this specimen from an
immunocompromised patient, sheets of
foamy macrophages packed with
mycobacteria are seen (acid-fast stain).
 MEASELS PNEUMONIA

Measles giant cells in the lung. Note the glassy

eosinophilic intranuclear inclusions. The blotchy,
reddish brown rash of measles virus infection on
the face, trunk, and p r o x i m a l e x t r e m i t i e s i s
produced by dilated skin vessels, edema, and a
mononuclear perivascular infiltrate. Ulcerated
mucosal lesions in the oral cavity near the opening
of the Stensen ducts (the pathognomonic Koplik
spots) are marked by necrosis, neutrophilic
exudate, and neovascularization.
The lymphoid organs typically have marked
follicular hyperplasia, large germinal centers, and
randomly distributed multinucleate giant cells,
c a l l e d Wa r t h i n - F i n k e l d e y c e l l s , w h i c h h a v e
eosinophilic nuclear and cytoplasmic inclusion
bodies. These are pathognomonic of measles and
are also found in the lung and sputum (Fig. 8-8).
The milder forms of measles pneumonia show the
same peribronchial and interstitial mononuclear
cell infiltration that is seen in other nonlethal viral
infections.
 HERPES VIRUS

A herpesvirus blister showing glassy

intranuclear viral inclusion bodies.
Skin lesion of chickenpox
(varicella-zoster virus)

Skin lesion of chickenpox (varicella-

zoster virus) with intraepithelial vesicle.
Candida infections

Severe candidiasis of the distal

esophagus.
MICROSCOPIC SECTION OF
CANDIDA ALBICANS

Characteristic pseudohyphae and

budding yeast of Candida
Aspergillus infection

Invasive aspergillosis of the lung in a bone marrow

transplant patient
 MICROSCOPIC VIEW OF
ASPERGILLUS INFECTION

Gomori methenamine-silver (GMS) stain shows

septate hyphae with acute-angle branching,
consistent with Aspergillus.
TRICHINELLA SPIRALIS

Multiple coiled Trichinella spiralis larvae

within skeletal muscle cells.
 elephantiasis

Massive edema and elephantiasis

caused by filariasis of the leg.
Enterobius vermicularis
Hyaline arteriolosclerosis

Vascular pathology in hypertension. A, Hyaline

arteriolosclerosis. The arteriolar wall is thickened
with increased protein deposition (hyalinized), and
the lumen is markedly narrowed. B
 Hyperplastic
arteriolosclerosis

Hyperplastic arteriolosclerosis (onion-

skinning) causing luminal obliteration
 FATTY STREAKS

Fatty streak, a collection of foamy macrophages in the

intima. A, Aorta with fatty streaks (arrows), associated
largely with the ostia of branch vessels.
Microscopic section of
fatty streak

Photomicrograph of fatty streak in an

experimental hypercholesterolemic rabbit,
demonstrating intimal, macrophage-derived foam
cells
 Abdominal aortic aneurysm
Abdominal aortic aneurysm. A,
External view, gross photograph
of a large aortic aneurysm that
ruptured (rupture site is indicated
by the arrow). B, Opened view,
with the location of the rupture
tract indicated by a probe. The
wall of the aneurysm is
exceedingly thin, and the lumen
is filled by a large quantity of
layered but largely unorganized
thrombus
 Polyarteritis nodosa

Polyarteritis nodosa. There is segmental fibrinoid

necrosis and thrombotic occlusion of the lumen of
this small artery. Note that part of the vessel wall at
the upper right (arrow) is uninvolved.
Blood vessel tumor

Histology of juvenile capillary hemangioma.

cavernous hemangioma

Histology of cavernous hemangioma

 ANGIOSACROMA

Moderately differentiated angiosarcoma

with dense clumps of atypical cells
lining distinct vascular lumens.
VENTRICULAR HYPERTROPHY

Left ventricular hypertrophy with and without dilation,

viewed in transverse heart sections. Compared with a
normal heart (center), the pressure-hypertrophied hearts
(left ) have increased mass and a thick left ventricular wall,
while the hypertrophied, dilated heart (right) has increased
mass and a normal wall thickness. C, Normal myocardium.
 MICROSCOPIC APPEARANCE OF
THE NORMAL HEART AND THE
HYPERTROPHIC

C, Normal myocardium. D, Hypertrophied myocardium (panels C

and D are photomicrographs at the same magnification). Note the
increases in both cell size and nuclear size in the hypertrophied
myocytes.
CALCIFIC VALVULAR
DEGENERATION
Calcific valvular degeneration. A, Calcific aortic
stenosis of a previously normal valve (viewed from
aortic aspect). Nodular masses of calcium are
heaped up within the sinuses of Valsalva (arrow).
Note that the commissures are not fused, as in
postrheumatic aortic valve stenosis (see Fig. 12-
27E ). B, Calcific aortic stenosis of a congenitally
bicuspid valve. One cusp has a partial fusion at its
center, called a raphe (arrow). C and D, Mitral
annular calcification, with calcific nodules at the
base (attachment margin) of the anterior mitral
leaflet (arrows). C, Left atrial view. D, Cut section of
myocardium.
Infective endocarditis
The more virulent bacteria
causing the acute bacterial
form of infective endocarditis
can lead to serious valvular
destruction, as shown here
involving the aortic valve.
Irregular reddish tan
vegetations overlie valve
cusps that are being
destroyed by the action of
the proliferating bacteria.
Portions of the vegetation
can break off and
become septic emboli that
travel to other organs,
leading to foci of infarction
or infection.
 Infective endocarditis,
microscopic
The valve leaflet in the left panel has
friable vegetations composed of fibrin
and platelets (pink) mixed with
inflammatory cells and bacterial
colonies (blue). The friability explains
how portions of the vegetation can
break off and embolize. In the right
panel a septic embolus fills the lumen
of a small artery showing inflammation
and necrosis. Left-sided endocarditis
can be complicated by embolization to
the systemic circulation,
whereas right-sided embolization
affects the lungs. Cardiac valves are
relatively avascular, so high-dose,
prolonged antibiotic therapy is needed
to eradicate the infection.
 Acute myocardial infarct

Acute myocardial infarct, predominantly

of the posterolateral left ventricle,
demonstrated histochemically by a lack
of staining by triphenyltetrazolium
chloride in areas of necrosis (arrow).
The staining defect is due to the lactate
dehydrogenase leakage that follows cell
death. Note the myocardial hemorrhage
at one edge of the infarct that was
associated with cardiac rupture, and the
anterior scar (arrowhead), indicative of
old infarct.Specimen is oriented with
the posterior wall at the top.
Dilated cardiomyopathy

Four-chamber dilatation and hypertrophy are evident.

There is a mural thrombus (arrow) at the apex of the left
ventricle (on the right in this apical four-chamber view).
The coronary arteries were patent.
 Microscopic view of
cardiomyopathy

Histologic section demonstrating variable

myocyte hypertrophy and interstitial fibrosis
(collagen is highlighted as blue in this Masson
trichrome stain).
 Hypertrophic cardiomyopathy
with
asymmetric septal hypertrophy.

The septal muscle bulges into the left

ventricular outflow tract, and the left
atrium is enlarged. The anterior mitral
leaflet has been reflected away from the
septum to reveal a fibrous endocardial
plaque
Microscopic section of
hypertrophic cardio
myopathy

Histologic appearance demonstrating myocyte

disarray, extreme hypertrophy, and exaggerated
myocyte branching, as well as the characteristic
interstitial fibrosis (collagen is blue in this Masson
trichrome stain).
Atrial septal defect
Ventricular septal defect
Teratology of fallot
Transposition of the great
arteries.
Thrombus arteriosus
Coarctation of the aorta
Pulmonary stenosis