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There are some muscle fibers here that show atrophy. The number of
cells is the same as before the atrophy occurred, but the size of some
fibers is reduced. This is a response to injury by "downsizing" to
conserve the cell. In this case, innervation of the small fibers in the
center was lost. This is a trichrome stain.

The testis at the right has undergone atrophy and is much smaller than
the normal testis at the left.

Patricia Ann O. Detabali

This is cerebral atrophy in a patient with Alzheimer disease. The gyri

are narrowed and the intervening sulci widened, particularly
pronounced toward the frontal lobe region

Here is the centrilobular portion of liver next to a central vein. The cells
have reduced in size or been lost from hypoxia. The pale brown-yellow
pigment is lipochrome that has accumulated as the atrophic and dying
cells undergo autophagocytosis.

Pathology Practical Exam 1st shift

This is cardiac hypertrophy involving the left ventricle. The number of

myocardial fibers does not increase, but their size can increase in
response to an increased workload, leading to the marked thickening
of the left ventricle in this patient with systemic hypertension . Any
increase in tissue size is not necessarily neoplasia. Here is an example of left
ventricular cardiac hypertrophy in which there has been an increase in the size of the
myocardial fibers in response to an increased pressure load from hypertension. With
hypertrophy, the cells increase in size, but the cells do not increase in number. Except
for being larger, the cells are normal in appearance.
Alterations in cell growth can be physiologic (normal responses to stimuli) or
pathologic. These alterations of cell growth are potentially reversible and include:

Hypertrophy: an increase in cell size. Increase in skeletal muscle fiber size

is a physiologic response to exercise, but the cardiac hypertrophy shown
above is a pathologic response to abnormally elevated blood pressure.

Hyperplasia: an increase in the number of cells. Postpartum breast lobules

undergo hyperplasia for lactation, but endometrial hyperplasia in a
postmenopausal woman is abnormal.

Patricia Ann O. Detabali

The prominent folds of endometrium in this uterus opened to reveal

the endometrial cavity are an example of hyperplasia. Cells forming
both the endometrial glands and the stroma have increased in number.
As a result, the size of the endometrium has increased. This increase is
physiologic with a normal menstrual cycle. The large fronds of
endometrium seen in this uterus opened to reveal the endometrial cavity are a result
of hyperplasia. This resulted from increased estrogen. With hyperplasia, there is an
increase in cell numbers to produce an increase in tissue size. However, the cells are
normal in appearance. Sometimes hyperplasias can be "atypical" and the cells not
completely normal. Such conditions can be premalignant.

Pathology Practical Exam 1st shift

epithelium. This is farther down the road toward neoplasia, but

dysplasia is still a potentially reversible process.

Metaplasia of the normal esophageal squamous mucosa has occurred

here, with the appearance of gastric type columnar mucosa.

When there is marked cellular injury, there is cell death. This

microscopic appearance of myocardium is a mess because so many
cells have died that the tissue is not recognizable. Many nuclei have
become pyknotic (shrunken and dark) and have then undergone
karorrhexis (fragmentation) and karyolysis (dissolution). The
cytoplasm and cell borders are not recognizable

This is dysplasia. The normal cervical squamous epithelium has

become transformed to a more disorderly growth pattern, or dysplastic

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

Here is myocardium in which the cells are dying. The nuclei of the
myocardial fibers are being lost. The cytoplasm is losing its structure,
because no well-defined cross-striations are seen.

This is liquefactive necrosis in the brain in a patient who suffered a

"stroke" with focal loss of blood supply to a portion of cerebrum. This
type of infarction is marked by loss of neurons and neuroglial cells and
the formation of a clear space at the center left.

The liver shows a small abscess here filled with many neutrophils. This
abscess is an example of localized liquefactive necrosis.

At high magnification, liquefactive necrosis of the brain demonstrates

many macrophages at the right which are cleaning up the necrotic

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

cellular debris. The job description of a macrophage includes janitorial

services such as this, particularly when there is lipid.

As this infarct in the brain is organizing and being resolved, the

liquefactive necrosis leads to resolution with cystic spaces.

Grossly, the cerebral infarction at the upper left here demonstrates

liquefactive necrosis. Eventually, the removal of the dead tissue leaves
behind a cavity.
This is more extensive caseous necrosis, with confluent cheesy tan
granulomas in the upper portion of this lung in a patient with
tuberculosis. The tissue destruction is so extensive that there are
areas of cavitation (cystic spaces) being formed as the necrotic (mainly
liquefied) debris drains out via the bronchi.

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

Acute inflammation is marked by an increase in inflammatory cells. Perhaps the

simplest indicator of acute inflammation is an increase in the white blood cell
count in the peripheal blood, here marked by an increase in segmented
neutrophils (PMN's).

Intracellular accumulations of a variety of materials can occur in

response to cellular injury. Here is fatty metamorphosis (fatty change)
of the liver in which deranged lipoprotein transport from injury (most
often alcoholism) leads to accumulation of lipid in the cytoplasm of
hepatocytes.
Seen here is vasodilation with exudation that has led to an outpouring of
fluid with fibrin into the alveolar spaces, along with PMN's. The series of
events in the process of inflammation are:
1. Vasodilation: leads to greater blood flow to the area of
inflammation, resulting in redness and heat.

Patricia Ann O. Detabali

2.

Vascular permeability: endothelial cells become "leaky" from either

direct endothelial cell injury or via chemical mediators.

3.

Exudation: fluid, proteins, red blood cells, and white blood cells
escape from the intravascular space as a result of increased
osmotic pressure extravascularly and increased hydrostatic
pressure intravascularly

Pathology Practical Exam 1st shift

4.

Vascular stasis: slowing of the blood in the bloodstream with

vasodilation and fluid exudation to allow chemical mediators and
inflammatory cells to collect and respond to the stimulus.

Here is an example of the fibrin mesh in fluid with PMN's that has
formed in the area of acute inflammation. It is this fluid collection that
produces the "tumor" or swelling aspect of acute inflammation.

As in the preceding diagram, here PMN's that are marginated along the
dilated venule wall (arrow) are squeezing through the basement
membrane (the process of diapedesis) and spilling out into
extravascular space.

Microscopically, the extensive neutrophilic exudate of an acute

abscessing pneumonia is seen here. Normal tissues are destroyed in
the region of the abscess.

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

infiltrate of chronic inflammation consists mainly of mononuclear cells

("round cells"): lymphocytes, plasma cells, and macrophages.

One consequence of acute inflammation is ulceration. This occurs on

epithelial surfaces. Here the gastric mucosa has been lost, or
ulcerated. A larger ulcer and several adjacent smaller ones with
surrounding erythema appear at the left of center.
At high magnification, granulation tissue has capillaries, fibroblasts,
and a variable amount of inflammatory cells (mostly mononuclear, but
with the possibility of some PMN's still being present).

Chronic inflammation is more difficult to understand, because it is so

variable. Seen here is chronic endometritis with lymphocytes as well
as plasma cells in the endometrial stroma. In general, the inflammatory

Patricia Ann O. Detabali

The focal nature of granulomatous inflammation is demonstrated in

this microscopic section of lung in which there are scattered
granulomas in the parenchyma. This is why the chest radiograph with

Pathology Practical Exam 1st shift

tuberculosis or other granulomatous diseases is often described as

"reticulonodular". A biopsy could miss such lesions from sampling
error, too.

Here are two pulmonary granulomas. Granulomatous inflammation

typically consists of mixtures of cells including epithelioid
macrophages, giant cells, lymphocytes, plasma cells, and fibroblasts.
There may even be some neutrophils.

Patricia Ann O. Detabali

Granulomatous inflammation occurs in response to some agents

which persist for a long time and require a more orchestrated immune
response to fight them. The granuloma seen here demonstrates the
typical rounded and focal nature of this type of inflammation. A couple
of spherules of C. immitis are present in the giant cell in the center.

Giant cells are a "committee" of epithelioid macrophages. Seen here

are two Langhans type giant cells in which the nuclei are lined up
around the periphery of the cell. Additional pink epithelioid
macrophages compose most of the rest of the granuloma.

Pathology Practical Exam 1st shift

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These are epithelioid cells around the center of a granuloma. They get
their name from the fact that they have lots of pink cytoplasm similar to
squamous epithelial cells. Their nuclei tend to be long and stringy.

This is a caseating granuloma. Epithelioid cells surround a central area

of necrosis that appears irregular, amorphous, and pink. Grossly, areas
of caseation appear cheese-like.

Patricia Ann O. Detabali

Granulomas caused by tuberculosis and by pathogenic fungi such as

Histoplasma capsulatum or Cryptococcus neoformans are often
caseating. Here, the area of caseation is seen at the upper right.

This young woman has a malar rash (the so-called "butterfly" rash
because of the shape across the cheeks). Such a rash suggests lupus.
Discoid lupus erythematosus (DLE) involves mainly just the skin and
is, therefore, relatively benign compared to systemic lupus
erythematosus (SLE). In either case, sunlight exposure accentuates
this erythematous rash ("photosensitivity"). A small number (5 to 10%)

Pathology Practical Exam 1st shift

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of DLE patients go on to develop SLE (usually the DLE patients with a

positive ANA).

Histologically, the skin of a patient with SLE may demonstrate a

vasculitis and dermal chronic inflammatory infiltrates, as seen here.
Vasculitis with autoimmune disease (often related to deposition of
antigen-antibody complexes) can occur in many different organs and
can lead to the often confusing signs and symptoms of patients with
rheumatic diseases.

Patricia Ann O. Detabali

Here is a more severe inflammatory skin infiltrate in the upper dermis

of a patient with SLE in which the basal layer of epidermis is
undergoing vacuolization and dissolution, and there is purpura with
RBCs extravasated into the upper dermis (which are the reasons for
the rash).

If immunofluorescence microscopy using an antibody to complement

or immunoglobulin is performed, then one can see the brightly
fluorescing band along the dermal epidermal junction that indicates
immune complex deposits are present. A variety of immunoglobulins
can be present, usually IgG, and the immune complexes trigger the
"classic" complement cascade so that components such as C3 are
present.

Pathology Practical Exam 1st shift

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This biopsy of the lower esophagus in a patient with chronic

gastroesophageal reflux disease (GERD) shows columnar metaplasia
(Barrett's esophagus), and the goblet cells are typical of an intestinal
type of epithelium. Squamous epithelium typical of the normal
esophagus appears at the right.

This is a neoplasm. Neoplasia is uncontrolled new growth. Neoplastic

cells are no longer under complete physiologic control. Note the mass
of abnormal tissue on the surface of this cervix. The term "tumor" is
often used synonymously with neoplasm, but a "tumor" can mean any
mass effect, whether it is inflammatory, hemodynamic, or neoplastic in
origin. Once a neoplasm has started, it is not reversible.

Patricia Ann O. Detabali

The schwannoma is seen microscopically to be composed of spindle

cells (like most neoplasms of mesenchymal origin), but the cells are
fairly uniform and there is plenty of pink cytoplasm.

The concept of differentiation is demonstrated by this small adenomatous polyp

(tubular adenoma) of the colon. Note the difference in staining quality between
the epithelial cells of the adenoma at the top and the normal glandular
epithelium of the colonic mucosa below.

Pathology Practical Exam 1st shift

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anomalies, as well as detail size and gestational age. The anomaly

seen in this photograph, a large bilateral cleft lip, is not so subtle, but
some anomalies are. Call a clinical geneticist for consultation. The
presence of one anomaly suggests that additional anomalies may be
present, including internal anomalies such as congenital cardiac
defects that may be life-threatening.

Here is a ventral abdominal wall defect. This defect involves the region
of the umbilical cord, so this is an omphalocele. Note that there is a
thin membrane covering the herniated abdominal contents (loops of
bowel can be seen under the membrane). This defect would have to be
repaired over a period of time. Since the bowel has mainly developed
outside of the abdominal cavity, it is malrotated and the cavity is not
properly formed (too small).

The yellow staining in the brain of a neonate is known as kernicterus. There is a

coronal section of medulla on the left and cerebral hemisphere on the right
demonstrating kernicterus in deep grey matter of hemisphere and brain stem.
Increased unconjugated bilirubin, which accounts for the kernicterus, is toxic to
the brain tissue. Kernicterus is more likely to occur with prematurity, low birth
weight, and increased bilirubin levels.

Examination of a stillborn fetus or neonate should consist of a careful

and detailed physical examination. You must note the presence of any

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

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NEC at the right shows hemorrhagic necrosis, beginning in the mucosa and
extending to involve the muscular wall, with the potential for perforation.

A complication of prematurity and low birth weight is neonatal

necrotizing enterocolitis (NEC) in which ischemia results in focal to
confluent areas of bowel necrosis, most often in the terminal ileum.
Seen at autopsy here is a dark red appearance to the small intestine of
a premature neonate

This is hyaline membrane disease due to prematurity and lack of surfactant

production from type II pneumonocytes within the immature lung. Note the thick
pink membranes lining the alveolar spaces.

The clinical manifestations of neonatal necrotizing enterocolitis (NEC) in

premature neonates include abdominal distension, ileus, and bloody stool at
several days of age. Compared to normal bowel at the left, bowel involved by

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

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This is anencephaly. This condition occurs when there is failure of formation of

the fetal cranial vault. The brain cannot form properly when exposed to amniotic
fluid. Note that this fetus died in utero--there are signs of maceration, with skin
slippage and reddening.

\
Wilms tumor microscopically resembles the primitive nephrogenic
zone of the fetal kidney, with primitive glomeruloid structures and a
cellular stroma. Wilms tumor is associated with mutations involving
the WT1 tumor suppressor gene on chromosome 11. This neoplasm is
very treatable with an excellent prognosis and >80% cure rate overall.

This lobulated tan-white mass involving the kidney of a child is a Wilms tumor. It
manifests most often as an abdominal mass. Over 90% of Wilms tumors are
diagnosed during the first 6 years of life. About a fourth of cases are associated
with hypertension.

Patricia Ann O. Detabali

Pathology Practical Exam 1st shift

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In this case, the diaphragmatic dome is missing on the left, allowing

herniation of the abdominal contents into the chest cavity. The metal
probe in the photograph is behind the left lung, which has been
displaced by the stomach. Below the stomach is a dark spleen (at the
white arrow). The white arrow overlies the left lobe of liver which is
extending upward.

Patricia Ann O. Detabali

Agenesis refers to the absence of formation of a body part in

embryogenesis. Here the kidneys are absent from the retroperitoneum,
and this renal agenesis will result in oligohydramnios, because
amniotic fluid is mainly derived from fetal urine. The oligohydramnios
leads to deformations such as a constricted chest, diminished lung
development, and pulmonary hypoplasia.

Pathology Practical Exam 1st shift