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Cellular injury and
The normal cell is said to in homeostatic
(steady) state, that is able to handle normal
.physiological demands
If the normal cell is exposed to some excessive
physiological stresses or some pathological
stimuli may lead to cellular adaptation which
.is a new but altered steady state
.Example : atrophy hypertrophy , metaplasia
If the limits of adaptive capability are
exceeded cell injury will occur
So in response to injury the cell may :

 Adapt
 Reversible injury
 Irreversible injury
 Or cell death occur either by
 Or apoptosis.
The type of injury
:depends on
 Its nature
 Its severity

 Duration of injury

 Type of cell injured

its adaptability-
its metabolic demands-
.its nutritional &hormonal state-
:Causes of cell injury
1- Hypoxia ( reduced O2 supply):
As in respiratory diseases,
anaemia , cardiovascular
2- Physical agents:
As mechanical trauma , excessive
heat or cold, radiation, electric
:Chemical agents & drugs- 3
As alcohol, some drugs,
insecticides, or industrial ,or
.occupational hazards
:Biological agents- 4
As viruses, bacteria, parasites,
:Immunologic reactions- 5
.As hypersensitivity reactions
:Genetic derangement- 6
As inborn errors of metabolism,
congenital anomalies
:Nutritional imbalances- 7
Either by deficiency( as protein or
vitamins) Or by excess( obesity,
:Aging- 8
Which cause progressive loss of
function, lead to cell
.senescence& death
General mechanisms of cell
Four intracellular systems are targets to be
affected by the injurious agents:
1-Cell membrane integrity.
By affecting sodium potassium pump.
2-Aerobic respiration (ATP energy stores)
through affecting mitochondria
3-Enzymes& protein synthesis
through affecting ribosome & endoplasmic
4 -Genetic apparatus integrity.
Through affecting the nucleus..
Morphology of acute cell
1-reversible injury:

:a- Cloudy swelling

.It is the mildest form of injury-
It is due to disturbance of active transport of water-
.outside the cell , and mitochondrial damage
.Grossly: The organ appears paler, & heavier-
Microscopically: swollen cells, with granular-
:b- Hydropic degeneration
It is an advanced state of cloudy swelling , with -
continuous accumulation of water inside the cell ,so
the cytoplasm appears as if it contains clear

:c- Fatty change

It is the abnormal accumulation of fat in -
parenchymatous organs(eg. Liver, heart,
(. muscles
It may be due to: starvation ,toxins, D.M ,or -
Grossly: the organ appears larger ,heavier, -
.yellowish, soft, and greasy
Microscopically: foamy cells , with vacuoles in -
cytoplasm , then their coalesce to form larger
spaces pushing the nucleus to the periphery of the
:Irreversible cell injury- 2
 Where severe mitochondrial damage,
depletion of ATP stores, severe damage
of plasma membrane occur.
 Then denaturation of proteins ,and
enzymatic digestion of organelles will
 Ending in cell death either by necrosis
or apoptosis.
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
:Types of necrosis

 - Coagulative necrosis
 - Liquefactive necrosis
 - Caseous necrosis
 - Fat 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.
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. This is an odd place
for an infarct, but it illustrates the shape and appearance of an ischemic (pale) infarct well.
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 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 cellular debris. The job description of a macrophage
includes janitorial services such as this, particularly when there is lipid.
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 the gross appearance of caseous necrosis in a hilar lymph node infected with tuberculosis.
The node has a cheesy tan to white appearance. Caseous necrosis is really just a combination of
coagulative and liquefactive necrosis that is most characteristic of granulomatous inflammation.
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
This is fat necrosis of the pancreas. Cellular injury to the pancreatic acini leads to release of powerful
enzymes which damage fat by the production of soaps, and these appear grossly as the soft, chalky
white areas seen here on the cut surfaces.
 - Grossly : it appears few hours later ,
as an opaque pale area (or liquefied)
 - Microscopically : increased
eosinophilia , disappearance of cell
boundaries (outlines are indistinct) ,
the nuclei either show pyknosis,
karyolysis, or karyohexis.
 Later on calcification may follow.