CELL INJURY

CAUSES OF CELL INJURY

• Oxygen deprivation
• Physical agents
• Chemical agents and drugs
• Infectious agents
• Immunological reactions
• Genetic derangements
• Nutritional imbalance
MORPHOLOGICAL ALTERATIONS
CHANGES IN REVERSIBLE CELL INJURY
NECROSIS VS APOPTOSIS
NECROSIS A P O P TO S IS

• Cell swelling • Cell shrinkage

• Pyklnosis karyorrhesis karyolysis • Fragmentation to nucleosomes size
fragments
• Plasma membrane disrupted • Intact plasma membrane
• Enzymatic digestion of cellular contents • Cellular contents intact
• Adjacent inflammation • No inflammation
• Pathological • Pathological or physiological
MICROSCOPY
NORMAL RENAL TUBULAR CELLS

• Epithelial cells stain cytoplasm pink and

nucleic acid purple basophilic
• Ciliated apical surface
• No infiltration in interstitium
• No congestion
EARLY (REVERSIBLE) INJURY
NECROSIS (IRREVERSIBLE) OF RT CELLS

• Loss of nuceli
• Fragmentation of cells
• Leakage of cellular content
 PATTERNS OF NECROSIS

• Coagulative necrosis
• Liquefactive necrosis
• Caseous necrosis
• Fat necrosis
• Fibrinoid necrosis
• Gangrenous necrosis
COAGULATIVE NECROSIS

• Due to obstruction of blood supply

• Denaturation of structural proteins and
enzymes
• Architecture of dead tissue is maintained
• Eosinophilic anucleated cells
• Necrotic cells are removed by
phagocytosis
LIQUEFACTIVE NECROSIS

• Seen in bacterial and fungal infections

• Digestion of dead cells
• Architecture not preserved
• Tissue transforms into liquid viscous
material
• Creamy yellow material – pus
• Hypoxic cell death in brain
CASEOUS NECROSIS

• In tuberculosis infection
• Cheese like appearance
• Friable white appearance of necrotic tissue
MICROSCOPY

• Eosinophilic pink granular necrotic

material
• Giant cells
• Macrophages
• Lymphocytes and
• Polymorphs
FAT NECROSIS

• Focal areas of fat destruction

• Most commonly in pancreas and breast
• Mechanism – pancreatic injury

release of pancreatic lipases

splitting of triglycerides

combines with calcium

MICROSCOPY
FIBRINOID NECROSIS

• Seen in immune reactions

• Involves blood vesels
• Mechanism – antigen antibody deposition
• Fibrin + Immune complex – pink
amorphous appearance k/a fibrinoid
• M/C in immune medicated vasculitis
 MECHANISM OF CELL INJURY

• Depletion of ATP
• Mitochondrial damage
• Influx of calcium and loss of calcium homeostasis
• Accumulation of oxygen derived free radicles
• Defect in membrane permeability
• Damage of DNA and proteins
DEPLETION OF ATP
 MITOCHONDRIAL DAMAGE

• Critical in cell injury and cell death

• Sensitive to injurious stimuli like
1. Increase in calcium
2. Reactive oxygen species
3. Toxins
4. Hypoxia
• Mutation due to inherent diseases
• Consequences of mitochondrial damage

1. Formation of high conductance channels k/a mitochondrial permeability transition pores

2. Abnormal oxidative phosphorylation
3. Activation of apoptosis
LOSS OF CALCIUM HAEMOSTASTS
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