Irreversible cell injury

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Information about Irreversible cell injury

Published on August 8, 2011

Author: suraj_mindgamer

Source: slideshare.net

IRREVERSIBLECELL INJURY

The molecular mechanisms connecting most forms of cell injury to ultimate cell death have proved elusive, for several reasons.

First, there are clearly many ways to injure a cell, not all of them invariably fatal.

Second, the numerous macromolecules, enzymes, and organelles within the cell are so closely interdependent that it is difficult to distinguish a primary injury from secondary (and not necessarily relevant) ripple effects.

Third, the "point of no return," at which irreversible damage has occurred, is still largely undetermined; thus, we have no precise cut-off point to establish cause and effect.

Finally, there is probably no single common final pathway by which cells die. It is, therefore, difficult to define the stage beyond which the cell is irretrievably doomed to destruction.

Classes of Cell Injury Reversible If stressor removed, and If cell damage mild: cells survive Irreversible --> cell death. Types: Apoptosis: normal (leaves falling) as in menses, aging PROGRAMMED Necrosis: patho-logical... Autolysis: after death of entire organism (dissolution of dead cells by its own digestive enzymes)

PROBABLE CAUSES The first is the inability to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATPgeneration) even after resolution of the original injury. The second is the development of profound disturbances in membrane function.

NECROSIS

NECROSIS DEFINITION: Death of a group of contiguous cells within a living tissue or organ Affect both nucleus and cytoplasm Unregulated cell death with inflammation

Morphological changesDURING NECROSIS CytoplasmicNuclearCytoplasmic changes : Cytoplasmiceosinophilia due to loss of normal basophilia& increased binding of eosin to denaturated proteins (Granular or homogenous glassy)  Nuclear changes: Pyknosis: shrinkage-increased staining with haematoxylin Karyorrhexis: fragmentation Karyolysis: total disappearance

Cytoplasmic

Nuclear

TYPES: NECROSIS Coagulative Liquefactive Caseation Fat

COAGULATIVE NECROSIS In: infarcts of kidney, heart, spleen Gross: pale , yellow, opaque, firm Mic.: All cellular details are lost but general architecture of the tissue is preserved Surrounding tissue----acute inflammation Ex: Infarction - heart  Infarction - kidney        

LIQUEFACTIVE NECROSIS In: centers of pyogenic abscess amoebiasis infarcts of C.N.S. Necrotic tissue---completely liquified---turbid fluid----absorbed----space Ex: Brain - infarction  Amoebiasis ---liver 

CASEATION NECROSIS In: Tuberculosis Necrotic tissue is partially liquefied---cheesy material (caseation) Mic: Both cellular details & general architecture of dead tissue are lost---structurelesseosinophilic material

FAT NECROSIS Traumatic: in female breast Enzymatic: in acute hemorrhagic pancreatitis Gross: opaque & white fat cells appear cloudy, surrounded by chronic inflammatory cells, histiocytes, foreign body giant cells      

APOPTOSIS

APOPTOSIS   (programmed cell death)  Definition:death of individual cells surrounded by viable cells when a cell dies through activation of an internally suicide program It is an active process—energy dependent Does not elicit inflammatory response May be physiologic or pathologic

APOPTOSIS CAUSES PHYSIOLOGIC During embryogenesis e.g. removal of interdigital webs during embryonic development of toes and fingers Hormone-dependent e.g. endometrial cellloss in menstruation PATHOLOGIC Irradiated tissues Cell death induced by cytotoxic T-lymphocytes Viral infections e.g. viral hepatitis Cell death in tumours

Differences between necrosis and apoptosis Necrosis Death of groups of cells A passive process—not energy-dependent Elicits inflammatory response Always pathologic Apoptosis Death of individual cells Active process—energy-dependent Does not elicit inflammatory response May be pathologic or physiologic

FATNECROSIS

FATTY CHANGE  Definition: -abnormal accumulation of triglycerides within parenchymal cells Sites: Liver (the most common) Others, heart, kidney,-- Pathogenesis:  Excessive accumulation of triglycerides within the liver may result from defects in any one of the events in the sequence from fatty acid entry to lipoprotein exit

FATTY CHANGE CAUSES Congestive heart failure Diabetes mellitus Severe anaemia Ischaemia Septicaemia Poisons malnutrition

FATTY CHANGE EFFECTS In all organs, fatty change appears as clear vacuoles within parenchymal cells Due to fat solvents used in paraffin embedding To identify fat, frozen tissue sections are stained with Sudan IV or Oil Red-O---orange-red colour When mild - - - no effects on cell function Severe - - - - - -impair cell function

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