Mechanism of cell injury Pathophysiology

Mechanism of cell injury Pathophysiology

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  Mechanism of cellinjury Done by ABSHA BASHEER Asst. Professor Department of pharmacology KMCT College of Pharmaceutical Sciences
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  INTRODUCTION • The cellularresponse to injurious stimuli depends on the type of injury, its duration, and its severity • low doses of toxins or a brief duration of ischemia  REVERSIBLE CELL INJURY • larger toxin doses or longer ischemic intervals IRREVERSIBLE CELL INJURY • Cell injury results from functional and biochemical abnormalities in one or more of several essential cellular components
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  • important targetsof injurious stimuli are 1. Mitochondria 2. Cell membranes 3. protein synthesis 4. the cytoskeleton 5. The genetic apparatus of the cell
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  1. Damage tomitochondria
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  2. Cell membranedamage
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  3. Damage toribosome Continued hypoxia Detachment of ribosome from rough endoplasmic reticulum Polysomes are degraded into monosomes Reduction in protein synthesis If hypoxia persists, it will lead to increased membrane permeability and finally cell death
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  4. Nuclear damage
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  5. Depletion ofATP
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  6. Influx ofcalcium
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  7. Accumulation ofoxygen free radicals
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  SUMMERY • Damage tomitochondria leads to the formation of mitochondrial permeability transition pore and leakage of cytochrome c. Continuous exposure ti ischemia leads to cell death • Loss of membrane permeability leads to membrane damage • Continued hypoxia will leads to the reduction of protein synthesis by damaging the ribosomes
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  • Decreased ATPlevel in cell leads to the activation of anaerobic glycolysis, resulting in the decreased pH and chromatin condensation • Ischemia cause increased Ca2+ influx in cells. This activate cell membrane damaging enzymes • Radiation, inflammation and chemicals cause liberation of free radicals causing oxidative stress, leads to cell membrane damage and injury
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