cellular injury
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Introduction
General mechanisms of cell injury:
Pathology
- reactive oxygen metabolites
- loss of calcium homeostasis
- activation of Ca+2-dependent proteases
- activation of Ca+2-dependent phospholipases
- activation of Ca+2-dependent ATPases
- activation of Ca+2-dependent endonucleases
- ATP depletion
- defects in membrane permeability
- genetic aberrations
Sequence of events (hypoxic & ischemic cellular injury):
- compromise of mitochondrial oxidative phosphorylation
- decreased cellular ATP
- failure of plasma-membrane Na+/K+ ATPase
- increased glycolysis
- diminished glycogen stores
- accumulation of lactic acid
- increased inorganic phosphate
- decreased creatine phosphate stores
- decreased cellular ATP
- cellular edema
- dilation of the endoplasmic reticulum
- loss of cellular polarity
- ribosomal disruption
- detachment of ribosomes from endoplasmic reticulum
- dissociation of polysomes into monosomes
- formation of blebs
- loss of microvillae
- mitochondrial swelling
- injury to lysosomal membranes.
The duration of ischemia require to produce irreversible cell injury varies with tissue:
- hepatocyte: 1-2 hours
- neuron: 3-5 minutes
Morphologic changes:
- light microscopy
- cellular swelling
- fatty change
- electron microscopy
- plasma membrane alterations
- blebbing
- distortion of microvilli
- formation of myelin figures
- loosening of intercellular attachments
- alterations in the cytoskeleton
- mitochondrial changes
- swelling
- rarefaction
- appearance of small amorphous phospholipid-rich amorphous densities
- ribosomal disruption
- dilation of the endoplasmic reticulum
- detachment of ribosomes from endoplasmic reticulum
- dissociation of polysomes into monosomes
- plasma membrane alterations
- nucleolar alterations
More general terms
More specific terms
References
- ↑ Cotran et al Robbins Pathologic Basis of Disease, 5th ed. W.B. Saunders Co, Philadelphia, PA 1994 pg 4-9