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Cell Injury & Cell Death

The document discusses cell injury and death, focusing on necrosis and apoptosis. It details various types of necrosis, including coagulative, liquefactive, fat, and fibrinoid necrosis, along with their morphological characteristics and underlying mechanisms. Additionally, it highlights the differences between apoptosis and necrosis, emphasizing the programmed nature of apoptosis compared to the inflammatory response associated with necrosis.

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8 views13 pages

Cell Injury & Cell Death

The document discusses cell injury and death, focusing on necrosis and apoptosis. It details various types of necrosis, including coagulative, liquefactive, fat, and fibrinoid necrosis, along with their morphological characteristics and underlying mechanisms. Additionally, it highlights the differences between apoptosis and necrosis, emphasizing the programmed nature of apoptosis compared to the inflammatory response associated with necrosis.

Uploaded by

jayb.seraph
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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CELL INJURY & CELL DEATH

ROY OLUNGA – MASTERMIND ACADEMIC CONSULTANCY


OBJECTIVES

 CELL DEATH: Apoptosis, necrosis, autophagy


 Adaptive changes in cell injury
 Mechanisms of cell death
1. NECROSIS

• cellular membranes fall apart during cell injury, cellular enzymes leak out and
ultimately digest the cell, and there is an accompanying inflammatory reaction.
• MORPHOLOGY
• Cytoplasmic changes: Have a glassy, homogeneous appearance, mostly due to
the loss of glycogen particles. Vacuolated and appears “moth eaten” cytoplasm
• Discontinuities in the plasma and organelle membranes.
• Marked dilation of mitochondria associated with large amorphous
intramitrochondrial densities, disruption of lysosomes, and intracytoplasmic
myelin figures
NUCLEAR CHANGES

• Pyknosis is characterized by nuclear


shrinkage and increased basophilia;
the DNA condenses into a dark,
shrunken mass.
• karyorrhexis – Fragmentation of the
nucleus
• Karyolysis - which the basophilia
fades due to digestion of
deoxyribonucleic acid (DNA) by
DNase. In 1 to 2 days, the nucleus in
a dead cell may undergo complete
dissolution.
MORPHOLOGIC PATTERNS OF TISSUE NECROSIS

• Caseous necrosis: Most often in foci of tuberculous


infection. Caseous means “cheese-like,” referring to
the friable yellow-white appearance of the area of
necrosis.
• Unlike coagulative necrosis, the tissue architecture is
obliterated and cellular outlines cannot be
discerned. Caseous necrosis is often surrounded by a
collection of macro phages and other inflammatory
cells; this appearance is characteristic of a nodular
inflammatory lesion called a granuloma.
COAGULATIVE NECROSIS

• The underlying tissue architecture is preserved


for at least several days after the injury.
• Injury denatures not only structural proteins but
also enzymes, limiting the proteolysis of the
dead cells; as a result, eosinophilic, anucleate
cells may persist for days or weeks.
• Coagulative necrosis is characteristic of infarcts
(areas of necrosis caused by ischemia) in all
solid organs except the brain.
LIQUEFACTIVE NECROSIS/COLLIQUATIVE
NECROSIS
• Seen at sites of bacterial or, occasionally, fungal
infections, because microbes stimulate the
accumulation of infllammatory cells and the
enzymes of leukocytes digest (“liquefy”) the tissue.
• The dead cells are completely digested,
transforming the tissue into a viscous liquid that is
eventually removed by phagocytes.
• The material is frequently creamy yellow and is
called pus. A localized collection of pus is called an
abscess.
FAT NECROSIS

• Focal areas of fat destruction, which can


be due to abdominal trauma or acute
pancreatitis in which enzymes leak out of
damaged pancreatic acinar cells and
ducts and digest peritoneal fat cells and
their contents, including stored
triglycerides. The released fatty acids
combine with calcium to produce grossly
identifiable chalky white lesions
FIBRINOID NECROSIS

• Seen in immune reactions in which


complexes of antigens and
antibodies are deposited in the walls
of blood vessels, and in severe
hypertension.
• Deposited immune complexes and
plasma proteins that have leaked
into the walls of injured vessels
produce a bright pink, amorphous
appearance on H&E preparations
called fibrinoid (fibrin-like).
APOPTOSIS

• Programmed cell
death
• Physiologic
apoptosis.
• Pathologic
apoptosis
PHYSIOLOGIC AND PATHOLOGIC CONDITIONS ASSOCIATED
WITH APOPTOSIS
DIFFERENCES BETWEEN APOPTOSIS AND NECROSIS

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