Cell Injury 17 Lecture4

INTRODUCTION TO
PATHOLOGY/ cell injury

Dr Heyam Awad
MD, FRCPATH, Jordanian Board
LECTURE 4
Morphology of cell
injury
• The first effect of all injuries is on the biochemical and
molecular level
• Functional derangement happens next
• Ultrastructural changes seen by electron microscopy follow
• Then light microscopic changes occur
• The last visible change is at the gross; macroscopic level.
exampl
e
• In heart attack= myocardial infarction ,first change is at the molecular
level: so cardiac enzymes increase in the blood. Example troponin
• Then cardiac muscle becomes non contractile (loss of function). This
happens within 1-2 minutes of ischemia… note that loss of function
doesn't mean cell death
• Cells die within 20-20 minutes of ischemia
• It takes 2-3 hours to see any EM changes
• Light microscopic changes need 6-12 hours to be noted
• Macroscopic changes are the last to be seen; within 12-24 hours
Myocardial infarction: Microscopic changes
need time to develop
Macroscopic changes due to cell injury
are the last to be recognized
Morphology of reversible cell
injury
• The main two morphologic changes in reversible cell injury are:
• 1. cellular swelling
• 2. fatty change
swellin
g
• Results from failure of the sodium potassium pump due to ATP
depletion
• It is the first manifestation of all forms of injury
• It is reversible
• The organ affected will have increased weight
• Microscopy shows small clear vacuoles within the cytoplasm this is
called hydropic change or vacular degeneration
• The organelles within the cells are also swollen
Fatty
change
• Occurs mainly in hypoxic injury and in toxic and metabolic
injury.
• Microscopy: lipid vacuoles in the cytoplasm
• Seen mainly in cells that participate in fat metabolism like
hepatocytes and myocardial cells
• It is reversible.
Fatty change: the white vacuoles are
lipid
Electron microscopic changes in reversible
injury
• Plasma membrane blebbing
• Mitochondrial swelling with appearance of amorphous densities
• Dilation of endoplasmic reticulum with detachment of ribosomes and
dissociation with polysomes
• Nuclear changes with clumping of chromatin.. This happens due to
changes in pH and can be reversible.
• Formation of phospholipid aggregates called myelin figures which are
derived from damaged cellular membranes
Necrosi
s
• Necrosis is the type of cell death that is associated with loss of cell
membrane integrity and leakage of cellular contents causing
dissolution of cells.
• The dissolution occurs due to enzymatic action.
• Leakage of cellular content causes inflammation which aims at getting
rid f the dead necrotic tissue
NECROS
IS
It is caused by:
• Denaturation of intracellular proteins.
• Digestion of cells by lysosomal enzymes of dying cells ( autolysis) and
leukocytes (heterolysis).
Protein denaturation: a change in protein
structure caused by changes in pH,
temperature ..
denaturation
Morphology of
necrosis
• There are cytoplasmic and nuclear changes.
• Cytoplasmic changes: increased eosinophilia (pink staining from the
eosin dye).
• Increased eosinophilia is due to 1. increased binding of eosin to
dentures proteins and 2. to loss of basophilia (decreases hematoxylin
binding to RNA, because RNA in the cytoplasm decreases.
• Due to these changes cells appear homogenous and glassy
• Myelin figures can be a nidus for calcium deposition and calcifications
might occur.
Nuclear changes in
necrosis one of three
patterns
1.karyolysis: decreased chromatin basophilia secondary to
deoxyribonuclease (DNAase) activity.
2.pyknosis: nuclear shrinkage and increased basophilia (DNA
condenses into a solid shrunken mass.
3. karyorrhexis, fragmentation then disappearance of
nucleus.
EM
changes
1)Discontinuities in plasma and organelle
membranes.
2)Marked dilation of mitochondria and large amorphous densities.
3)Disruption of lysosomes.
4) Intracytoplasmic myelin figures
Myelin
figures
• Myelin figures: aggregates of damaged cell membranes
(phospholipids).
Fate of Myelin figures:

• phagocytosed by other cells
• or further degraded into fatty acids and calcify
Patterns of
necrosis
• Denaturation of protein predominates…. Coagulative necrosis.
• Enzymatic digestion predominates… liquefactive necrosis.
• Special circumstances: caseous necrosis and fat necrosis.

Coagulative
necrosis
• preserved architecture of dead tissue .
• Denaturation of structural proteins and enzymes… so no cellular
proteolysis.
• Eosiniphilic anucleated cells
• Cells are removed by inflammatory cells.
• Ischemia in all solid organs except the brain may lead to coagulative
necrosis.
Coagulative
necrosis
Liquifactive
necrosis
• digestion of the dead cells resulting into a liquid jelly-like mass.
• In focal bacterial or fungal infections and in hypoxic death in central
nervous system.
Caseous
necrosis
• White cheese like friable necrosis.
• Prototype: Tuberculosis
• Typical finding is granuloma :Collection of fragmented or lysed cells
with amorphous granular eosinophilic debris surrounded by
macrophages.
Caseous
necrosis
Fat
necrosis
• used as a clinical terms and not a specific type.
• Necrosis of fat.
• Typical example: pancreatic enzymes (lipases) release in acute
pancreatitis.
Fate of necrotic
tissue
• Phagocytosis.
• Replacement by scar.
• Regeneration.
• Calcification.

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Cell Injury 17 Lecture4

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INTRODUCTION TO

PATHOLOGY/ cell injury

Fate of Myelin figures:

• Special circumstances: caseous necrosis and fat necrosis.

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