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Mechanisms of Cell Injury
Mechanisms of Cell Injury
Concluding points
The identification of factors that determine when reversible injury becomes irreversible and progresses to cell death would be very useful so we may be able to identify strategies to prevent permanent consequences of cell injury. Leakage of intracellular proteins into blood through damaged membranes provides a means of detecting tissue damage. CK & troponin in MI and ALT,
Chemical injury
Major problem. Drugs. Liver as a major site of drug metabolism is a target for drug toxicity. Mechanisms: Directly by combining with critical molecular component. Example mercuric chloride poisoning bind to the sulfhydryl groups of cell membrane proteins causing increased permeability. More in GIT
Chemical injury
Cyanide poisons mitochondrial cytochrome oxidase and inhibits oxidative phosphorelation Most chemicals are not biologically active and need to be converted into active forms (toxic metabolites) which usually takes place in liver ( cytochrome P-450 mixed-function oxidases). Free radical formation and lipid peroxidation. CCl4 is converted to CCl3 which causes lipid
Chemical injury
Acetaminophen (paracetamol) converted to to toxic products in liver leading to injury.
Apoptosis
Pathway of cell death induced by a suicide program in which activation of degrading enzymes takes place. Apoptotic cells break up into fragments called apoptotic bodies which contain portions of the cytoplasm and nucleus. Become targets for phagocytosis before their contents leak out and so there would be no inflammatory reaction.
Apoptosis
Occurs normally during development and adulthood and in pathologic conditions. Physiologic situations: Embryogenesis, involution of hormone-dependent tissues upon hormone withdrawal, cell loss in proliferating cell populations and death of host cells after serving their usful function.
Apoptosis
Pathologic situations: (no host reaction) DNA damage, accumulation of misfolded proteins (Excessive accumulation of these proteins in the ER called ER stress), certain infections (viral ones), pathologic atrophy in parenchymal organs after duct obstruction (pancreas, parotid and kidney)