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Reversible Cell Injury, Mechanism and Morphology

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  REVERSIBLE CELL INJURY, MECHANISM AND MORPHOLOGY REVERSIBLE CELL INJURY: If the ischaemia or hypoxia is of short duration, the effects may be reversible on rapid restoration of circulation e.g. in coronary artery occlusion, myocardial contractility, metabolism and ultra structure are reversed if the circulation is quickly restored. Th e sequential biochemical and ultra structural changes in reversible cell injury are as under: 1. Decreased generation of cellular ATP : Damage by ischaemia from interruption versus hypoxia from other causes. All living cells require continuous supply of oxygen to produce ATP which is essentially required for a variety of cellular functions (e.g. membrane trans port, protein synthesis, lipid synthesis and phospholipid metabolism). ATP in human cell is derived from 2 sources: a) Firstly, by aerobic respiration or oxidative phosphorylation (which requires oxygen) in the mitochondria. b) Secondly, cells may subsequently switch over to anaerobic glycolytic

CELL INJURY AND CAUSES

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  CELL INJURY Cell injury is defined as the effect of a variety of stresses due to etiologic agents a cell encounters resulting in changes in its internal and external environment. In general, cells of the body have inbuilt mechanism to deal with changes in environment to an extent.  The cellular response to stress may vary and depends upon following two variables:  i) Host factors i.e. the type of cell and tissue involved.  ii) Factors pertaining to injurious agent i.e. extent and type of cell injury. CAUSES OF CELL INJURY A. Genetic Causes Genetic abnormalities may result in a defect as severe as the congenital malformations associated with Down syndrome, caused by a chromosomal anomaly, or as subtle as the decreased life span of red blood cells caused by a single amino acid substitution in hemoglobin in sickle cell anemia. Genetic defects may cause cell injury because of deficiency of functional proteins, such as enzyme defects in inborn errors of metabolism, or accumulation of d