Irreversible cell injury by jayashri
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Irreversible cell injury occurs when ischemia persists and damages the structure and functions of the cell beyond repair. This involves 5 steps: 1) calcium influx damages mitochondria, 2) activated phospholipases damage membranes, 3) intracellular proteases damage cytoskeletons, 4) activated endonucleases damage nuclei, and 5) lysosomal enzymes cause cell death and phagocytosis. The changes that characterize irreversible injury include morphological changes to mitochondria and nuclei, degradation of cell membranes and cytoskeletons, and the leakage of hydrolytic enzymes from lysosomes, indicating irreparable cell damage and death.
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Cell injury can be reversible or irreversible. Reversible injury is caused by decreased ATP and acidosis within cells. Irreversible injury occurs when mitochondrial and cell membrane dysfunction cannot be reversed, leading to calcium influx, membrane damage, and cell death. Free radicals generated during ischemia-reperfusion can also cause irreversible injury through lipid peroxidation, protein and DNA oxidation, and cytoskeletal damage. Stress proteins help cells cope with injury by moving molecules within the cell.
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Irreversible cellular injury can occur through two main types of cell death: necrosis and apoptosis. Necrosis is premature, unprogrammed cell death that is always pathological, occurring due to external factors like ischemia, toxins, or infections. It is characterized by loss of membrane integrity and inflammatory changes. Apoptosis is a normal, programmed form of cell death important for development, hormone regulation, and removing damaged cells. It occurs through an active enzymatic process and does not cause inflammation. Both pathways ultimately lead to cellular demise but differ significantly in their mechanisms and morphological appearance.
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Irreversible cellular injury can occur through two main types of cell death: necrosis and apoptosis. Necrosis is premature, unprogrammed cell death that is always pathological, occurring due to external factors like ischemia, toxins, or infections. It is characterized by loss of membrane integrity and inflammatory changes. Apoptosis is a normal, programmed form of cell death important for development, hormone regulation, and removing damaged cells. It occurs through an active enzymatic process and does not cause inflammation. Both pathways ultimately lead to cellular demise but differ significantly in their mechanisms and morphological appearance.
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Cells can become rapidly nonfunctional after injury, though the damage may be reversible. Prolonged injury can lead to irreversible damage and cell death. Under the microscope, reversible injury shows cellular swelling and fatty change, while necrosis appears glassy and homogeneous as proteins and RNA denature. Necrotic cells release enzymes and can be detected in blood earlier than microscopic changes appear.
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The document discusses the pathogenesis of cell injury, including causes like hypoxia, toxins, and radiation. It explains the mechanisms of cell injury such as depletion of ATP, mitochondrial damage, calcium influx, and reactive oxygen species accumulation. The stages of cellular response are described, from reversible injury involving swelling and metabolic changes, to irreversible injury of necrosis and apoptosis involving membrane damage and DNA degradation.
cellular adaptation and response to injury
1. Cells have the ability to adapt and respond to injury through processes like hypertrophy, hyperplasia, atrophy, and metaplasia. However, if the injury is too severe, it can lead to cell death through either necrosis or apoptosis.
2. Necrosis is unprogrammed cell death that results in cell contents leaking out. Apoptosis is programmed cell death where the cell activates enzymes to degrade its own DNA and proteins in a controlled manner.
3. Oxidative stress from free radicals and mitochondrial damage are key mechanisms that can lead to cell injury. If the injury is not reversible, it triggers signaling pathways to initiate necrosis or apoptosis.
Cell injury
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
Cell injury
cell injury definition, stages, events, mechanisms, Types, etiology, necrosis, apoptosis, morphological changes due to cell injury, atrophy,hypertrophy, calcification etc
Necrosis
This document discusses different types of cell death, specifically necrosis. It defines necrosis as cell death and describes some key features. It then discusses different types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. For each type, it provides the mechanisms, characteristic features, and examples to illustrate the histological appearance of different forms of necrosis.
Cellular and tissue response to injury By Dr. Tareni Das.pdf
Cellular and tissue response to injury, cell injury, reversible injury, irreversible injury, necrosis, apoptosis, intracellular accumulation etc.
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Irreversible cell injury by jayashri
- 1. Irreversible cell injury By jayashri
- 2. Persistence of ischemialeads to irreversiblecell injury,and that totallydamagethe structure and functions of cell. • Essential phenomenon to distinguish irreversible cell injury from Reversible cell injury. • Inability of the cell to reverse the mitochondrial function on reperfusion or reoxygenation. • Disturbance in the cell membrane function. • Reduction in ATP, Ph ,leakage of lysosomal enzymes.
- 3. Pathological changes in irreversible cell injury there are 5 steps:- 1) Calcium influx—mitochondrial damage 2) Activated phospholipases---membrane damage 3) Intracellular proteases----cytoskeletal damage 4) Activated endonucleases---nuclear damage 5) Lysosomal enzymes---cell death and phagocytosis
- 4. Changes in irci • Calciuminflux:-mitochondrial damage • Hypoxia continues • Large cytosolic calcium influx occurs after reperfusion of injured cell. • Excess calcium into mitochondria • Disable the function • Morphological changes is formation of vacuoles • deposition of calcium
- 5. Activated phospholipases:-membrane damage • increased cytosolic influx of calcium • Activates endogeneous phospholipases • Degrade the membrane phospholipid • There is also decreased replacement synthesis of membrane phospholipids due to ATP ATPase enzyme also cause decreased ATP.
- 7. Intracellular proteases • Normal cytoskeletal of the cell microfilaments , microtubules anchors cell membrane damaged by degradation of activated intracellular proteases.
- 8. Activated endonucleases:-nuclear damage • Nucleoproteins are damaged by lysosomal proteases and endonucleases. • 3 forms:- • Pyknosis:-condensation and clumping of nucleus becomes dark basophilic. • Karyorrhexis:-nuclear fragmentation into small bits dispersed in cyto • Karyolysis:- dissolution of nucleus.
- 10. Lysosomal hydrolytic enzymes • Lysosomal membrane damage leads to escape of enzymes which is activated due to lack of oxygen. • Enzyme activation leads to cell death • Death cells are replaced by myelin fibres and form calcium soaps. • Liberated enzymes leak into serum used as clinical parameters. • Hydrolytic enzymes are, hydrolase,RNAase,DNAase,protease,glycosidase etc.
- 11. Enzyme markers of cell death • AST,SGOT • ALT,SGPT • Creatinine kinase • lipase • Amylase • LDH • Cardiac troponin • Viral hepatitis,M.I,liver disease • More specific for liver cell damage,and viral hepatitis. • Acute M.I,skeletal muscle injury • Acute hepatitis • Acute hepatitis,siadentitis • Acute M.I,skeletal muscle injury • For acute M.I