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Cell Injury, Cell Death, and
Adaptations
Cell adaptation
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Hypertrophy Vs. Hyperplasia
• B, Small spindle-shaped uterine smooth muscle cells from a normal
uterus. Compare this with (C) large, plump hypertrophied smooth
muscle cells from a gravid uterus.
Physiologic hypertrophy of the uterus during pregnancy. A, Gross
appearance of a normal uterus (right) and a gravid uterus (left)
• 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.
• Here is one of the nodules of hyperplastic prostate, with many glands along
with some intervening stroma. The cells making up the glands are normal in
appearance, but there are just too many of them.
• Nodular Prostatic Hyperplasia
• 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.
Atrophy
• The testis at the right has undergone atrophy and is much
smaller than the normal testis at the left.
• This is cerebral atrophy in a patient with Alzheimer disease. The gyri
are narrowed and the intervening sulci widened.
Metaplasia
• Metaplasia of normal columnar (left) to squamous epithelium (right)
in a bronchus, shown (A) schematically and (B) histologically.
•
Metaplasia of laryngeal respiratory epithelium has occurred here in a
smoker. The chronic irritation has led to an exchanging of one type of
epithelium (the normal respiratory epithelium at the right) for another (the
more resilient squamous epithelium at the left).
• Metaplasia of the normal esophageal squamous mucosa has
occurred here, with the appearance of gastric type columnar
mucosa.
Cell Death
Necrosis Vs. Apoptosis
• 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.
• 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.
• In this example, liver cells are dying individually (arrows) from injury
by viral hepatitis. The cells are pink and without nuclei.
• In this fetal thymus there is involution of thymic lymphocytes by the
mechanism of apoptosis. Individual cells fragment and are
consumed by phagocytes to give the appearance of clear spaces
filled with cellular debris.
Patterns of Tissue Necrosis
Coagulative Necrosis
• Two large infarctions (areas of coagulative necrosis) are seen in this
sectioned spleen. Since the etiology of coagulative necrosis is usually
vascular with loss of blood supply, the infarct occurs in a vascular
distribution. Thus, infarcts are often wedge-shaped with a base on the organ
capsule.
• This is an example of coagulative necrosis. This is the typical pattern with
ischemia and infarction (loss of blood supply and resultant tissue anoxia).
Here, there is a wedge-shaped pale area of coagulative necrosis (infarction) in
the renal cortex of the kidney.
• Microscopically, the renal cortex has undergone anoxic injury at the left so
that the cells appear pale and ghost-like. There is a hemorrhagic zone in the
middle where the cells are dying or have not quite died, and then normal
renal parenchyma at the far right. This is an example of coagulative
necrosis.
• The contrast between normal adrenal cortex and the small pale infarct is
good. The area just under the capsule is spared because of blood supply
from capsular arterial branches. It illustrates the shape and appearance of an
ischemic (pale) infarct well.
Liquefactive Necrosis
• The liver shows a small abscess here filled with many neutrophils. This
abscess is an example of localized liquefactive necrosis.
• 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.
• At high magnification, liquefactive necrosis of the brain
demonstrates many macrophages at the right which are
cleaning up the necrotic cellular debris.
• Grossly, the cerebral infarction at the upper left here
demonstrates liquefactive necrosis. Eventually, the removal of
the dead tissue leaves behind a cavity.
Fat Necrosis
• This is fat necrosis of the pancreas. Appear grossly as the soft, chalky white areas
seen here on the cut surfaces.
•
Microscopically, fat necrosis adjacent to pancreas is seen here. There are some
remaining steatocytes at the left which are not necrotic. The necrotic fat cells at the
right have vague cellular outlines, have lost their peripheral nuclei, and their
cytoplasm has become a pink amorphous mass of necrotic material.
Caseous Necrosis
• This is the gross
appearance of
caseous necrosis in a
hilar lymph node
infected with
tuberculosis. The
node has a cheesy tan
to white appearance.
• This is more
extensive
caseous
necrosis, with
confluent cheesy
tan granulomas
in the upper
portion of this
lung in a patient
with
tuberculosis.
• Microscopically, caseous necrosis is characterized by acellular
areas, as the tissue architecture is completely lost (at the upper
right), surrounded by a granulomatous inflammatory process.
Gangrenous Necrosis
• This is gangrene of the lower extremity. In this case the term "wet"
gangrene is more applicable because of the liquefactive component from
superimposed infection in addition to the coagulative necrosis from loss of
blood supply. This patient had diabetes mellitus.
• Gangrenous necrosis involves the tissues of a body part. The
inflammation seen here is extending beneath the skin of a toe to
involve soft tissue (fat and connective tissue) and bone.
Intracellular Accumulations
• Here is fatty change of the liver due to accumulation of lipid in the
cytoplasm of hepatocytes.
• Here are Mallory bodies (the red globular material) composed of
cytoskeletal filaments in liver cells chronically damaged from
alcoholism. These are a type of "intermediate" filament between the
size of actin (thin) and myosin (thick). (proteins accumulation)
• Here are neurofibrillary tangles in neurons of a patient with
Alzheimer's disease. The cytoskeletal filaments are grouped together
in the elongated tangles.
• The yellow-brown granular pigment seen in the hepatocytes here is
(lipofuscin) which accumulates over time in cells (particularly liver
and heart) as a result of "wear and tear" with aging.
• The brown coarsely granular material in macrophages in this
alveolus is hemosiderin that has accumulated as a result of the
breakdown of RBC's and release of the iron in heme. The
macrophages clear up this debris, which is eventually recycled.
• Here is anthracotic pigment in macrophages in a hilar lymph node.
Anthracosis is nothing more than accumulation of carbon pigment
from breathing dirty air. Smokers have the most pronounced
anthracosis.
• The black streaks seen
between lobules of lung
beneath the pleural
surface are due to
accumulation of
anthracotic pigment. This
anthracosis of the lung is
not harmful and comes
from the carbonaceous
material breathed in from
dirty air typical of
industrialized regions of
the planet. Persons who
smoke would have even
more of this pigment.
Pathologic Calcification
• This is dystrophic calcification in the wall of the stomach. At the far
left is an artery with calcification in its wall. There are also irregular
bluish-purple deposits of calcium in the submucosa.
• Calcification of the aortic valve. A view looking down onto the
unopened aortic valve in a heart with calcific aortic stenosis. The
semilunar cusps are thickened and fibrotic. Behind each cusp are
large, irregular masses of dystrophic calcification that will prevent
normal opening of the cusps.
• Here is so-called "metastatic calcification" in the lung of a patient
with a very high serum calcium level (hypercalcemia).
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