Cell injury
•Download as PPT, PDF•
6 likes•544 views
This document discusses cell injury and homeostasis. It defines cell injury as occurring when adaptive responses are exceeded or the cell is exposed to an injurious stimulus. There are two types of cell injury: reversible and irreversible. Free radicals can cause cell injury by reacting with lipids, DNA and proteins. Free radicals are generated through normal metabolic processes, radiation exposure, and chemical metabolism, and can be neutralized by antioxidants. Increased calcium levels and decreased ATP can also occur during cell injury.
Report
Share
Report
Share
Recommended
Cell injury
This document discusses cell injury and cell death. It defines cell injury as a change in cell structure, metabolism or function that impairs its vital activity. Causes of cell injury include internal stresses like metabolic imbalances and external stresses such as physical agents, toxins, and chemicals. Cell injury can be reversible or irreversible and lead to cell death through mechanisms like necrosis, autolysis, or apoptosis. Signs of cell injury include morphological changes, functional impairments, and metabolic derangements. Specific types of cell injury discussed include fatty change, pigmentation, calcification, amyloidosis, and various forms of necrosis.
Pathogenesis of Cell Injury
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.
Cell injury, adaptation, and death fix
This document summarizes key concepts relating to cell injury, adaptation, and death. It discusses how cells respond to stress through reversible or irreversible injury, adaptation, or death. It also describes various types of cellular adaptation like hypertrophy, hyperplasia, atrophy, and metaplasia that cells undergo in response to stress. Additionally, it covers the mechanisms and morphological changes associated with different types of cell injury like necrosis and 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.
Pathophysiology cell injury
Cell injury and its pathophysiology
Apoptosis, Necrosis, Cellular adaptations, Cell morphology
Cell injury types, etiology
Cell injury & Cell death
This document provides an overview of cellular adaptation and injury. It defines four types of cellular adaptation - atrophy, hypertrophy, hyperplasia, and metaplasia. It also lists common causes of cell injury and describes the differences between reversible and irreversible injury. Specific changes that characterize necrosis and apoptosis are discussed. Examples of cellular adaptations and morphologies of reversible and irreversible injury are provided.
Intracellular and Extracellular accumulation
The document discusses intracellular and extracellular accumulation in various organs. It describes cases of glycogen accumulation seen as vacuolation in hepatocyte cytoplasm on H&E staining of the liver. Kidney samples show intracellular hyaline droplets and extracellular hyaline occupying renal tubules. Amyloidosis is seen in the pancreas, kidney, lymph node, duodenum and heart, appearing as extracellular deposition of amorphous eosinophilic material that stains pink with Congo Red.
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injury
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injuryGovernment Medical College
Irreversible cell injury can occur through necrosis or apoptosis. Necrosis is unprogrammed cell death due to intracellular protein denaturation and lysosomal enzyme digestion, resulting in cell membrane rupture and content leakage. Apoptosis is genetically programmed cell death where cells activate enzymes to degrade their own DNA and proteins. Key differences are that apoptotic cells shrink while necrotic cells swell, and apoptotic cells remain intact while necrotic cells lyse. Free radicals can also cause cell injury by attacking cell components and structures like membranes, proteins, and DNA, resulting in lipid peroxidation, protein damage, and DNA lesions.Recommended
Cell injury
This document discusses cell injury and cell death. It defines cell injury as a change in cell structure, metabolism or function that impairs its vital activity. Causes of cell injury include internal stresses like metabolic imbalances and external stresses such as physical agents, toxins, and chemicals. Cell injury can be reversible or irreversible and lead to cell death through mechanisms like necrosis, autolysis, or apoptosis. Signs of cell injury include morphological changes, functional impairments, and metabolic derangements. Specific types of cell injury discussed include fatty change, pigmentation, calcification, amyloidosis, and various forms of necrosis.
Pathogenesis of Cell Injury
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.
Cell injury, adaptation, and death fix
This document summarizes key concepts relating to cell injury, adaptation, and death. It discusses how cells respond to stress through reversible or irreversible injury, adaptation, or death. It also describes various types of cellular adaptation like hypertrophy, hyperplasia, atrophy, and metaplasia that cells undergo in response to stress. Additionally, it covers the mechanisms and morphological changes associated with different types of cell injury like necrosis and 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.
Pathophysiology cell injury
Cell injury and its pathophysiology
Apoptosis, Necrosis, Cellular adaptations, Cell morphology
Cell injury types, etiology
Cell injury & Cell death
This document provides an overview of cellular adaptation and injury. It defines four types of cellular adaptation - atrophy, hypertrophy, hyperplasia, and metaplasia. It also lists common causes of cell injury and describes the differences between reversible and irreversible injury. Specific changes that characterize necrosis and apoptosis are discussed. Examples of cellular adaptations and morphologies of reversible and irreversible injury are provided.
Intracellular and Extracellular accumulation
The document discusses intracellular and extracellular accumulation in various organs. It describes cases of glycogen accumulation seen as vacuolation in hepatocyte cytoplasm on H&E staining of the liver. Kidney samples show intracellular hyaline droplets and extracellular hyaline occupying renal tubules. Amyloidosis is seen in the pancreas, kidney, lymph node, duodenum and heart, appearing as extracellular deposition of amorphous eosinophilic material that stains pink with Congo Red.
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injury
irreversible cell injury, necrosis, apoptosis, free radicles, reperfusion injuryGovernment Medical College
Irreversible cell injury can occur through necrosis or apoptosis. Necrosis is unprogrammed cell death due to intracellular protein denaturation and lysosomal enzyme digestion, resulting in cell membrane rupture and content leakage. Apoptosis is genetically programmed cell death where cells activate enzymes to degrade their own DNA and proteins. Key differences are that apoptotic cells shrink while necrotic cells swell, and apoptotic cells remain intact while necrotic cells lyse. Free radicals can also cause cell injury by attacking cell components and structures like membranes, proteins, and DNA, resulting in lipid peroxidation, protein damage, and DNA lesions.Cell injury
cell injury definition, stages, events, mechanisms, Types, etiology, necrosis, apoptosis, morphological changes due to cell injury, atrophy,hypertrophy, calcification etc
Hemolytic anemia and post hemorrhagic syndrome
Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can replace them, leading to anemia. It can be caused by intrinsic issues with red blood cells themselves or extrinsic factors like infections, medications, autoimmune disorders, or enlarged organs destroying healthy cells. Symptoms include paleness, fatigue, fever, and abdominal pain. Diagnosis involves blood tests measuring red blood cell counts and liver function. Treatment options depend on the underlying cause but may include blood transfusions, immunosuppressants, corticosteroids, or spleen removal. Posthemorrhagic anemia develops after acute blood loss and is treated by addressing the cause of bleeding with fluids, transfusions, or surgery along
Cell injury – cell injury and cell death
Most forms of disease begin with cell injury and loss of function. Cell injury is defined as stresses that disrupt a cell's internal and external environment. The response to injury depends on the cell/tissue type, extent, and type of injury.
Cells are classified by proliferative potential as labile, stable, or permanent. Labile cells continuously divide with a short lifespan in skin and gastrointestinal epithelia. Stable cells undergo limited postnatal division and can regenerate injured tissues like liver and kidney. Permanent cells cannot divide postnatally, like neurons, and cannot regenerate once destroyed. Prolonged hypoxia can lead to irreversible cell injury characterized by mitochondrial and membrane damage, ultimately resulting in cell death
General pathology lecture 4 cellular adaptation
Cellular adaptations can occur through hyperplasia, hypertrophy, atrophy, or metaplasia in response to stress or changes in workload or stimulation. Hyperplasia involves an increased number of cells through cell proliferation. Hypertrophy involves cellular enlargement without an increase in cell number. Atrophy is a decrease in cell size. Metaplasia is the replacement of one adult cell type with another. Examples provided include uterine hyperplasia during pregnancy, cardiac hypertrophy in hypertension, muscle fiber atrophy after injury or disuse, and squamous metaplasia in the lungs of smokers. Dysplasia refers to alterations in cell size, shape, and organization and is a pre-cancerous condition.
Cell injury pathophysiology
Pathology is the scientific study of disease through examination of tissues and cells. Key terms include:
- Pathology examines structural and functional changes in disease (pathophysiology examines disordered function).
- Disease is a condition causing discomfort, while illness is one's reaction to disease through symptoms and signs.
- Syndromes describe combinations of symptoms from altered physiology. Important tissues include lesions in patients and pathologic changes seen macroscopically and microscopically. Etiology examines causal factors and pathogenesis examines how lesions are produced.
Cell injury, adaptations and death
1. Cells actively control their environment and internal conditions through homeostasis, but can undergo adaptation or injury in response to stresses.
2. If injury is too severe, it leads to irreversible injury and cell death. Common causes of cell injury include hypoxia, chemicals, physical agents, infections, and genetics.
3. In response to injury, cells exhibit general biochemical mechanisms like ATP depletion, mitochondrial damage, calcium imbalance, and free radical generation, which can damage cells through lipid peroxidation, DNA fragmentation, and protein crosslinking if not neutralized.
Cell injury. intracellular extracellular accumulation
Cell injury and alterations can occur through various causes and result in reversible or irreversible changes to cells. Reversible cell injury may allow the cell to return to normal, while irreversible injury leads to cell death through necrosis or apoptosis. Specific patterns of acute cell injury include cellular swelling and fatty change. Long-term or persistent stimuli can also result in subcellular alterations and intracellular accumulations of substances such as lipids, proteins, pigments, and more. Extracellular accumulations may involve changes to collagen, elastic fibers, proteoglycans, and basement membranes in connective tissue.
Irreversible cell injury
The molecular mechanisms connecting cell injury to cell death are complex and not fully understood. There are many potential causes of cell injury that may or may not be fatal, and the "point of no return" where damage becomes irreversible is still unclear. Additionally, cells can die through different pathways, making the definition of irreversible injury difficult. Cell injury can result in either reversible or irreversible cell death through mechanisms like apoptosis, the body's normal programmed cell death process, or necrosis, pathological cell death resulting in inflammation.
Cell injury, adaptation and apoptosis
Cell injury and death can occur through various mechanisms including hypoxia, physical or chemical insults, and microbial or immunological agents. The cellular response to injury depends on the cell type, extent, and type of injury. Initial responses include cellular adaptation, subcellular changes, or intracellular accumulations. Injury may result in reversible or irreversible cell damage and cell death. Irreversible injury is characterized by mitochondrial dysfunction and membrane damage, leading to necrosis or apoptosis. Different patterns of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Cell Injury and Cell Death
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
Cellular adaptation
Cells can adapt to changes in their environment through various processes including hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Hyperplasia is an increase in cell number, hypertrophy is an increase in cell size, and atrophy is a decrease in cell size or number. Metaplasia is a reversible change where one adult cell type replaces another. Dysplasia involves disordered cellular development and proliferation with cytological abnormalities. These adaptations allow cells to survive stresses and ensure tissue homeostasis.
Cellular pathology
This document summarizes cellular pathology by discussing normal cell structure and function, as well as how cells adapt, become injured, and die in response to stress or disease. It states that understanding normal cells is crucial to appreciating abnormalities and outlines the basic organelles shared by most cells, including the plasma membrane, nucleus, mitochondria, endoplasmic reticulum, ribosomes, Golgi apparatus, lysosomes, and peroxisomes. It then defines homeostasis, cellular adaptation, reversible and irreversible cell injury, and the types of cell death including necrosis and apoptosis.
Cell injury: CELL ADAPTATIONS
This document discusses various cellular adaptations and injury. It defines atrophy, hypertrophy, hyperplasia, and metaplasia. Atrophy is a decrease in cell size and number. Hypertrophy is an increase in cell size. Hyperplasia is an increase in cell number. Metaplasia is the replacement of one cell type with another. Examples of each type of adaptation are given, including how squamous cell metaplasia in smokers replaces normal trachea and bronchial cells, and how warts represent skin hyperplasia.
General pathology lecture 2 intracellular accumulations
This document discusses different types of intracellular accumulations, including exogenous and endogenous accumulations. Exogenous accumulations result from inhaled or ingested materials depositing in cells, such as coal dust (anthracosis) or asbestos fibers. Endogenous accumulations occur due to the body's normal metabolic processes or errors in metabolism, including lipofuchsin, bile pigments, melanin, hemosiderin, and amyloid deposits. The document provides examples of different accumulations seen in tissues under the microscope.
Mechanisms of cell injury
Cellular injury occurs when stress exceeds a cell's ability to adapt and can be caused by factors like oxygen deprivation, toxins, infections, or genetic mutations. The main mechanisms of cellular injury include ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of reactive oxygen species, defects in membrane permeability, and damage to DNA and proteins. Without adequate response to injury, irreversible damage occurs through mechanisms like lipid peroxidation, DNA fragmentation, and protein cross-linking, ultimately leading to cell necrosis.
Cell injury: causes, pathogenesis, Morphology of reversible cell injury
The document discusses cell injury and its mechanisms. It describes how cells can become injured through various stressors like hypoxia, physical/chemical agents, infections, etc. This causes damage to key cellular components like membranes, respiration, and DNA. The injury can be reversible through mild changes like hydropic swelling, or progress to irreversible necrosis or apoptosis if the cell cannot adapt. Free radicals are also discussed as a mediator of injury through lipid peroxidation, protein/DNA oxidation, and cytoskeletal damage. Examples of reversible changes include hydropic swelling seen as cloudy vacuoles, while irreversible injury leads to cell death.
Pathological anatomy intro
Pathology is the scientific study of disease through examination of organs, tissues, bodily fluids, and sometimes whole bodies. It involves studying the structural and functional changes caused by disease. Pathologists examine samples through various methods including gross examination, histopathology, immunohistochemistry, and electron microscopy to diagnose disease and understand disease processes and causes. The main subdivisions of pathology are anatomical pathology, clinical pathology, forensic pathology, and neuropathology.
Cell injury etiology and pathogenesis
This document discusses etiology and pathogenesis of cell injury. It defines cell injury as changes in a cell's internal and external environment due to various stresses from etiological agents. The cellular response depends on host factors like cell type and extent of injury. Injury can result in reversible or irreversible cell injury depending on factors like agent type/duration and cell adaptability. Common causes of cell injury include hypoxia, ischemia, toxins, microbes, nutrition imbalances, and aging. Ischemia and hypoxia are the most frequent causes of cell injury in humans. Reversible injury involves ATP depletion and membrane changes, while irreversible injury brings further damage including to mitochondria and nuclei, leading to cell death.
Hematology
The document discusses general hematology and various blood disorders. It covers red blood cell disorders like anemia, bone marrow failure syndromes, and red blood cell membrane defects. It also discusses bleeding disorders, platelet disorders, coagulation defects, and leukemia. Key points about various conditions like iron deficiency anemia, thalassemia, sickle cell disease, immune hemolytic anemia, and vitamin deficiencies are summarized. Screening tests for evaluation of hemostatic abnormalities are also mentioned.
Cell adaptations, Cell injury, Necrosis, Apoptosis - Pathology - Nursing
Cellular adaptations are reversible changes that allow cells to survive in abnormal environments, such as hypertrophy, hyperplasia, atrophy, and metaplasia. Cell injury can be reversible or irreversible. Reversible injury includes hydropic change and fatty change. Irreversible injury is cell death by necrosis or apoptosis. Necrosis is unprogrammed cell death from severe injury and involves cell contents leaking out. Apoptosis is programmed cell death that occurs normally or in response to cell damage.
Cell injury
Prepared by M.D., PhD, Marta R. Gerasymchuk
Department of Pathophysiology
Ivano-Frankivsk National Medical University
Cell injury, cell death & adaptations by Dr Nadeem (RMC)
This document provides an overview of cellular responses to stress and injury, including cellular adaptations and cell death. It discusses how cells attempt to maintain homeostasis in response to stress through adaptations like hypertrophy (increase in cell size), hyperplasia (increase in cell number), atrophy, and metaplasia. If the stress becomes too severe or persistent, it can lead to reversible or irreversible cell injury, ultimately resulting in cell death through necrosis or apoptosis. Examples of cellular adaptations like cardiac muscle hypertrophy and smooth muscle hypertrophy in response to mechanical stresses are also provided.
More Related Content
What's hot
Cell injury
cell injury definition, stages, events, mechanisms, Types, etiology, necrosis, apoptosis, morphological changes due to cell injury, atrophy,hypertrophy, calcification etc
Hemolytic anemia and post hemorrhagic syndrome
Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can replace them, leading to anemia. It can be caused by intrinsic issues with red blood cells themselves or extrinsic factors like infections, medications, autoimmune disorders, or enlarged organs destroying healthy cells. Symptoms include paleness, fatigue, fever, and abdominal pain. Diagnosis involves blood tests measuring red blood cell counts and liver function. Treatment options depend on the underlying cause but may include blood transfusions, immunosuppressants, corticosteroids, or spleen removal. Posthemorrhagic anemia develops after acute blood loss and is treated by addressing the cause of bleeding with fluids, transfusions, or surgery along
Cell injury – cell injury and cell death
Most forms of disease begin with cell injury and loss of function. Cell injury is defined as stresses that disrupt a cell's internal and external environment. The response to injury depends on the cell/tissue type, extent, and type of injury.
Cells are classified by proliferative potential as labile, stable, or permanent. Labile cells continuously divide with a short lifespan in skin and gastrointestinal epithelia. Stable cells undergo limited postnatal division and can regenerate injured tissues like liver and kidney. Permanent cells cannot divide postnatally, like neurons, and cannot regenerate once destroyed. Prolonged hypoxia can lead to irreversible cell injury characterized by mitochondrial and membrane damage, ultimately resulting in cell death
General pathology lecture 4 cellular adaptation
Cellular adaptations can occur through hyperplasia, hypertrophy, atrophy, or metaplasia in response to stress or changes in workload or stimulation. Hyperplasia involves an increased number of cells through cell proliferation. Hypertrophy involves cellular enlargement without an increase in cell number. Atrophy is a decrease in cell size. Metaplasia is the replacement of one adult cell type with another. Examples provided include uterine hyperplasia during pregnancy, cardiac hypertrophy in hypertension, muscle fiber atrophy after injury or disuse, and squamous metaplasia in the lungs of smokers. Dysplasia refers to alterations in cell size, shape, and organization and is a pre-cancerous condition.
Cell injury pathophysiology
Pathology is the scientific study of disease through examination of tissues and cells. Key terms include:
- Pathology examines structural and functional changes in disease (pathophysiology examines disordered function).
- Disease is a condition causing discomfort, while illness is one's reaction to disease through symptoms and signs.
- Syndromes describe combinations of symptoms from altered physiology. Important tissues include lesions in patients and pathologic changes seen macroscopically and microscopically. Etiology examines causal factors and pathogenesis examines how lesions are produced.
Cell injury, adaptations and death
1. Cells actively control their environment and internal conditions through homeostasis, but can undergo adaptation or injury in response to stresses.
2. If injury is too severe, it leads to irreversible injury and cell death. Common causes of cell injury include hypoxia, chemicals, physical agents, infections, and genetics.
3. In response to injury, cells exhibit general biochemical mechanisms like ATP depletion, mitochondrial damage, calcium imbalance, and free radical generation, which can damage cells through lipid peroxidation, DNA fragmentation, and protein crosslinking if not neutralized.
Cell injury. intracellular extracellular accumulation
Cell injury and alterations can occur through various causes and result in reversible or irreversible changes to cells. Reversible cell injury may allow the cell to return to normal, while irreversible injury leads to cell death through necrosis or apoptosis. Specific patterns of acute cell injury include cellular swelling and fatty change. Long-term or persistent stimuli can also result in subcellular alterations and intracellular accumulations of substances such as lipids, proteins, pigments, and more. Extracellular accumulations may involve changes to collagen, elastic fibers, proteoglycans, and basement membranes in connective tissue.
Irreversible cell injury
The molecular mechanisms connecting cell injury to cell death are complex and not fully understood. There are many potential causes of cell injury that may or may not be fatal, and the "point of no return" where damage becomes irreversible is still unclear. Additionally, cells can die through different pathways, making the definition of irreversible injury difficult. Cell injury can result in either reversible or irreversible cell death through mechanisms like apoptosis, the body's normal programmed cell death process, or necrosis, pathological cell death resulting in inflammation.
Cell injury, adaptation and apoptosis
Cell injury and death can occur through various mechanisms including hypoxia, physical or chemical insults, and microbial or immunological agents. The cellular response to injury depends on the cell type, extent, and type of injury. Initial responses include cellular adaptation, subcellular changes, or intracellular accumulations. Injury may result in reversible or irreversible cell damage and cell death. Irreversible injury is characterized by mitochondrial dysfunction and membrane damage, leading to necrosis or apoptosis. Different patterns of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Cell Injury and Cell Death
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
Cellular adaptation
Cells can adapt to changes in their environment through various processes including hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Hyperplasia is an increase in cell number, hypertrophy is an increase in cell size, and atrophy is a decrease in cell size or number. Metaplasia is a reversible change where one adult cell type replaces another. Dysplasia involves disordered cellular development and proliferation with cytological abnormalities. These adaptations allow cells to survive stresses and ensure tissue homeostasis.
Cellular pathology
This document summarizes cellular pathology by discussing normal cell structure and function, as well as how cells adapt, become injured, and die in response to stress or disease. It states that understanding normal cells is crucial to appreciating abnormalities and outlines the basic organelles shared by most cells, including the plasma membrane, nucleus, mitochondria, endoplasmic reticulum, ribosomes, Golgi apparatus, lysosomes, and peroxisomes. It then defines homeostasis, cellular adaptation, reversible and irreversible cell injury, and the types of cell death including necrosis and apoptosis.
Cell injury: CELL ADAPTATIONS
This document discusses various cellular adaptations and injury. It defines atrophy, hypertrophy, hyperplasia, and metaplasia. Atrophy is a decrease in cell size and number. Hypertrophy is an increase in cell size. Hyperplasia is an increase in cell number. Metaplasia is the replacement of one cell type with another. Examples of each type of adaptation are given, including how squamous cell metaplasia in smokers replaces normal trachea and bronchial cells, and how warts represent skin hyperplasia.
General pathology lecture 2 intracellular accumulations
This document discusses different types of intracellular accumulations, including exogenous and endogenous accumulations. Exogenous accumulations result from inhaled or ingested materials depositing in cells, such as coal dust (anthracosis) or asbestos fibers. Endogenous accumulations occur due to the body's normal metabolic processes or errors in metabolism, including lipofuchsin, bile pigments, melanin, hemosiderin, and amyloid deposits. The document provides examples of different accumulations seen in tissues under the microscope.
Mechanisms of cell injury
Cellular injury occurs when stress exceeds a cell's ability to adapt and can be caused by factors like oxygen deprivation, toxins, infections, or genetic mutations. The main mechanisms of cellular injury include ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of reactive oxygen species, defects in membrane permeability, and damage to DNA and proteins. Without adequate response to injury, irreversible damage occurs through mechanisms like lipid peroxidation, DNA fragmentation, and protein cross-linking, ultimately leading to cell necrosis.
Cell injury: causes, pathogenesis, Morphology of reversible cell injury
The document discusses cell injury and its mechanisms. It describes how cells can become injured through various stressors like hypoxia, physical/chemical agents, infections, etc. This causes damage to key cellular components like membranes, respiration, and DNA. The injury can be reversible through mild changes like hydropic swelling, or progress to irreversible necrosis or apoptosis if the cell cannot adapt. Free radicals are also discussed as a mediator of injury through lipid peroxidation, protein/DNA oxidation, and cytoskeletal damage. Examples of reversible changes include hydropic swelling seen as cloudy vacuoles, while irreversible injury leads to cell death.
Pathological anatomy intro
Pathology is the scientific study of disease through examination of organs, tissues, bodily fluids, and sometimes whole bodies. It involves studying the structural and functional changes caused by disease. Pathologists examine samples through various methods including gross examination, histopathology, immunohistochemistry, and electron microscopy to diagnose disease and understand disease processes and causes. The main subdivisions of pathology are anatomical pathology, clinical pathology, forensic pathology, and neuropathology.
Cell injury etiology and pathogenesis
This document discusses etiology and pathogenesis of cell injury. It defines cell injury as changes in a cell's internal and external environment due to various stresses from etiological agents. The cellular response depends on host factors like cell type and extent of injury. Injury can result in reversible or irreversible cell injury depending on factors like agent type/duration and cell adaptability. Common causes of cell injury include hypoxia, ischemia, toxins, microbes, nutrition imbalances, and aging. Ischemia and hypoxia are the most frequent causes of cell injury in humans. Reversible injury involves ATP depletion and membrane changes, while irreversible injury brings further damage including to mitochondria and nuclei, leading to cell death.
Hematology
The document discusses general hematology and various blood disorders. It covers red blood cell disorders like anemia, bone marrow failure syndromes, and red blood cell membrane defects. It also discusses bleeding disorders, platelet disorders, coagulation defects, and leukemia. Key points about various conditions like iron deficiency anemia, thalassemia, sickle cell disease, immune hemolytic anemia, and vitamin deficiencies are summarized. Screening tests for evaluation of hemostatic abnormalities are also mentioned.
Cell adaptations, Cell injury, Necrosis, Apoptosis - Pathology - Nursing
Cellular adaptations are reversible changes that allow cells to survive in abnormal environments, such as hypertrophy, hyperplasia, atrophy, and metaplasia. Cell injury can be reversible or irreversible. Reversible injury includes hydropic change and fatty change. Irreversible injury is cell death by necrosis or apoptosis. Necrosis is unprogrammed cell death from severe injury and involves cell contents leaking out. Apoptosis is programmed cell death that occurs normally or in response to cell damage.
What's hot (20)
Cell injury. intracellular extracellular accumulation
Cell injury. intracellular extracellular accumulation
General pathology lecture 2 intracellular accumulations
General pathology lecture 2 intracellular accumulations
Cell injury: causes, pathogenesis, Morphology of reversible cell injury
Cell injury: causes, pathogenesis, Morphology of reversible cell injury
Cell adaptations, Cell injury, Necrosis, Apoptosis - Pathology - Nursing
Cell adaptations, Cell injury, Necrosis, Apoptosis - Pathology - Nursing
Viewers also liked
Cell injury
Prepared by M.D., PhD, Marta R. Gerasymchuk
Department of Pathophysiology
Ivano-Frankivsk National Medical University
Cell injury, cell death & adaptations by Dr Nadeem (RMC)
This document provides an overview of cellular responses to stress and injury, including cellular adaptations and cell death. It discusses how cells attempt to maintain homeostasis in response to stress through adaptations like hypertrophy (increase in cell size), hyperplasia (increase in cell number), atrophy, and metaplasia. If the stress becomes too severe or persistent, it can lead to reversible or irreversible cell injury, ultimately resulting in cell death through necrosis or apoptosis. Examples of cellular adaptations like cardiac muscle hypertrophy and smooth muscle hypertrophy in response to mechanical stresses are also provided.
cell injury
This document discusses cellular injury and cell death. It begins by introducing the hierarchical structure of the human body from cells to organs to systems. It then describes the different types of tissues and cellular adaptations and injuries. The main types of cellular injury discussed are reversible and irreversible injuries. Reversible injuries include changes like swelling while irreversible injuries involve cell death through necrosis or apoptosis. The document closes by defining different patterns of necrosis like coagulation, liquefactive, and caseous necrosis.
Cell Injury Patho
The document summarizes cell injury, adaptation, and death. It discusses various types of cell death including necrosis, apoptosis, necrapoptosis, and anoikis. Causes of cell injury include internal stresses and external factors. Cells can respond to injury through recovery, adaptation mechanisms like atrophy, hypertrophy, hyperplasia, metaplasia, and storage, or death. Adaptation responses aim to restore homeostasis. The stages of cell injury and mechanisms of apoptosis and necrosis are described in detail.
General pathology lecture 1 introduction & cell injury
This document provides an overview of pathology and cell injury. It begins with definitions of pathology and discusses its focus on etiology, pathogenesis, morphology, and manifestations of disease. It then covers cell injury, describing the process from normal cell to reversible and irreversible injury. Specific types of cell injury are outlined like cloudy swelling, fatty change, and hyaline degeneration. The document concludes with examples of intracellular accumulations seen in various disease states.
Pathophysiology ch 01 introduction, cell injury, adaptaion, death v2
This document provides an introduction to pathophysiology and cellular changes. It discusses the following key points:
1. Pathophysiology involves studying the functional and physiological changes that occur in the body due to disease. This builds on knowledge of normal human anatomy and physiology.
2. Common cellular adaptations to injury include atrophy, hypertrophy, hyperplasia, and metaplasia. Prolonged or severe stress can lead to irreversible cell injury or death through necrosis or apoptosis.
3. The most common cause of cell damage is ischemia or lack of oxygen. This interferes with energy production and cell function, ultimately leading to cell swelling, rupture, and death. Necrosis can take different
Cell injury, adaptation, and death fix
Cell injury, adaptation, and death can occur through various stimuli and stresses. Cells may undergo reversible or irreversible changes. Reversible changes include cellular adaptation through hypertrophy, hyperplasia, and metaplasia to stressors. Irreversible changes result in cellular atrophy and eventually cell death through necrosis or apoptosis. The morphology of reversible injury includes cellular swelling, fatty change, and changes to organelles. Necrosis is the degradative process of cell death where cellular contents are digested by enzymes.
Cell injury
This is the topic related to basic pathology
In this power point you will get a clear information about the cell and types of cells & what factors will cause damage to cell
Cell injury 2
1. The document describes the morphological changes that occur in cells undergoing reversible injury, irreversible injury, necrosis, and apoptosis as observed by light and electron microscopy.
2. Key differences are noted between necrosis, which involves the uncontrolled digestion of cells and release of cellular contents, versus apoptosis, which is a tightly regulated form of programmed cell death where cells break into fragments that are phagocytosed without inflammation.
3. Examples are provided of physiological apoptosis during development and tissue remodeling, as well as pathological apoptosis resulting from DNA damage, misfolded proteins, viral infections, and organ atrophy.
2. cell injury etiology- mdzah- sp sinhasan
This document discusses cellular injury and adaptation. It notes that cells exist in a state of homeostasis but can become injured by various stressors like hypoxia or toxins. Injuries can be reversible or irreversible. Initial injuries disrupt ATP production and increase intracellular calcium levels, activating damaging enzymes. This can lead to further damage of mitochondria and lysosomes as well as increased reactive oxygen species. Depending on the severity and duration of injury, cells may undergo apoptosis, necrosis, or adaptational changes in an attempt to survive.
The hallucinogenic
The document discusses several hallucinogenic plants and fungi, including:
- Amanita muscaria mushroom, which can cause temporary paralysis in insects.
- Peyote cactus, which has been used for thousands of years in spiritual rituals by indigenous groups in North America.
- Ayahuasca vine, from which a ceremonial drink is prepared using vines and leaves from plants in the Amazon region.
- Datura and Brugmancia, which are shrubs or small trees up to 11 meters tall with serrated leaves.
- The hallucinogenic effects of these plants depend on factors like a person's characteristics, health, experience with the drug, as well as the plant
Cns stimulants drugs (1)
The document discusses central nervous system (CNS) stimulants. It defines stimulants as substances that increase behavioral activity when administered. CNS stimulants can elevate mood, increase motor activity and alertness, and decrease need for sleep. The mechanisms of action of stimulants include blocking neurotransmitter reuptake, promoting neurotransmitter release, and blocking metabolism or antagonizing inhibitory neurotransmitters. Specific stimulants discussed include amphetamine, picrotoxin, and strychnine, along with their mechanisms and effects on mice.
Cell injury
This document discusses various types of cell injury and cellular adaptations. It defines cell injury as stress encountered by cells due to changes in their internal or external environment. Virchow's cellular theory of disease proposed that diseases occur due to abnormalities at the cellular level. The document then discusses various genetic and acquired causes of cell injury, including physical, chemical, microbial, immunological, nutritional, aging, and iatrogenic factors. It also describes different types of cellular responses to stress like hypoxia, as well as cellular adaptations such as hyperplasia, hypertrophy, atrophy, metaplasia, and dysplasia. Finally, it discusses reversible cell injuries including edema, fatty change, hyaline change, amyloidosis, mu
Hallucinogens Helth Ed Project
Hallucinogens are drugs that cause hallucinations by disrupting the interaction of nerve cells and the neurotransmitter serotonin in the brain. Under their influence, people see images and hear sounds that do not exist in reality. Some hallucinogens also produce rapid and intense emotional swings. Common hallucinogens include mushrooms, LSD, and PCP. They alter a person's perception of reality and may cause hallucinations or other sensory distortions. Repeated use leads to cross-tolerance, meaning a higher tolerance develops with more frequent use over shorter periods of time.
Cell injury, apotosis and necrosis(1)
Cell injury, apoptosis and necrosis are described. Cell injury results from disruption of cellular components maintaining viability and can be reversible, lead to adaptation, or cell death. Necrosis is accidental cell death resulting from external factors like ischemia, toxins or radiation. It is characterized by cellular swelling, membrane rupture and nuclear changes like karyorrhexis. Apoptosis is programmed cell death important in development and homeostasis, involving nuclear condensation and fragmentation followed by phagocytosis without inflammation. Different types of necrosis include coagulative, liquefactive, caseous and gangrenous necrosis.
Cell injury 1
There are two main patterns of cell death: necrosis and apoptosis. Necrosis is characterized by cell swelling and membrane rupture, releasing cellular contents. Apoptosis involves cell shrinkage and intact membranes, with nuclear fragmentation. Cell injury can result from hypoxia, depletion of ATP, calcium influx, oxidative stress, and free radical damage. Specific mechanisms include impaired sodium/potassium pumping and protein synthesis, mitochondrial damage, and lipid peroxidation. This leads to loss of organelles and cellular digestion.
Evaluation of CNS Stimulants
This document discusses the central nervous system (CNS) and methods for evaluating CNS stimulants. It defines the CNS as the brain and spinal cord, describes CNS parts and functions. It then lists several classes and examples of CNS stimulants, and provides details on 10 methods for evaluating CNS stimulants in animals, including tests measuring locomotor activity, motor coordination, and duration of anesthesia.
Free radicals & antioxidants
Free radicals are highly reactive molecules that are produced during normal cellular processes and can cause oxidative damage. Antioxidants help prevent this damage by neutralizing free radicals. Common sources of free radicals include mitochondria, inflammation, pollution, and radiation. Free radicals can damage cells by oxidizing lipids, proteins, and DNA, and are implicated in many diseases including cancer, atherosclerosis, and neurological conditions. Antioxidants help reduce oxidative stress and may protect against disease.
Cell Injury And Death Lecture I
The document provides an overview of pathology, which is the study of disease and structural and functional abnormalities that cause disease. It discusses various types of cell injuries including hypoxia, which is the most common cause of cell injury and death. It then describes different types of tissue changes that can occur during disease such as atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, and intracellular storage. It also discusses various types of cell death including necrosis, apoptosis, and gangrene.
Viewers also liked (20)
Cell injury, cell death & adaptations by Dr Nadeem (RMC)
Cell injury, cell death & adaptations by Dr Nadeem (RMC)
General pathology lecture 1 introduction & cell injury
General pathology lecture 1 introduction & cell injury
Pathophysiology ch 01 introduction, cell injury, adaptaion, death v2
Pathophysiology ch 01 introduction, cell injury, adaptaion, death v2
Similar to Cell injury
Cell Injury 1 pptx.pptx
This document discusses human pathology and cell injury. It defines pathology as the study of disease and notes that modern pathology studies cellular abnormalities. It explains that cell injury occurs through a limited set of basic biochemical processes, including plasma membrane damage, mitochondrial damage, ATP depletion, and nucleic acid damage. The document outlines various causes of cell injury like metabolic, chemical, free radical, immune, infectious, genetic, physical and iatrogenic insults. It describes different cellular responses to injury including recovery, cell death mechanisms like apoptosis, autophagy and necrosis, and subcellular changes or intracellular accumulations. The mechanisms of free radical generation and the role of reactive oxygen species in cell injury are explained. Methods of free radical removal like antioxidants
Free Radical Injury by prof dr naseer ppt
Free radicals are unstable chemical species with unpaired electrons that can damage cells. They are normally produced during respiration but are neutralized by cellular defenses. Oxidative stress occurs when free radical production overwhelms these defenses, potentially leading to conditions like aging, cancer, and neurodegenerative diseases. Cells contain antioxidant molecules and enzymes like catalase and superoxide dismutase that break down free radicals into less reactive species and prevent cellular injury. However, toxins, radiation, and other stresses can produce excessive free radicals that evade these protective systems, damaging lipids, proteins, DNA and potentially causing toxicity, inflammation, and cell death.
5d9fc831490924cbf1c6daa3a4f26d9d_cellinjury_2003.pdf
This document provides an overview of cell injury, adaptation, and death. It discusses how cells maintain homeostasis but can undergo injury from various stressors like hypoxia, chemicals, physical trauma, infections, etc. If the injury is too severe, the cells die. The mechanisms of injury involve loss of energy, mitochondrial damage, loss of calcium homeostasis, defects in membrane permeability, and generation of reactive oxygen species. Cells can adapt to injury through atrophy, hypertrophy, hyperplasia, or metaplasia. Reperfusion after ischemia can paradoxically cause more damage through calcium overload and free radical production.
Free Radical Injury from ROBIN ( prof dr naseer lecture)
Free radicals are unstable chemical species that can damage cells. They are normally produced during cellular metabolism but can increase during oxidative stress, leading to cell injury. Free radicals react with proteins, lipids, carbohydrates and nucleic acids, causing damage through lipid peroxidation, protein oxidation and DNA lesions. Cells have antioxidant defenses and scavenging systems like catalase, superoxide dismutase and glutathione peroxidase to remove free radicals, but excessive free radicals overwhelm these systems and cause pathological effects that contribute to conditions like cancer, aging and neurodegenerative diseases.
Theories of Aging
Oxidative stress occurs due to an accumulation of reactive oxygen species (ROS) generated during normal metabolism. ROS can damage cells by reacting with and modifying proteins, lipids, DNA, and other molecules. Theories of aging propose that oxidative stress and the resulting damage contributed to aging over time. While cells have antioxidant defenses against ROS, these defenses decline with age. Emerging evidence suggests oxidative stress plays a role in aging and age-related diseases such as Alzheimer's disease.
Free radicals
Free radicals are unstable molecules that contain unpaired electrons. This instability causes free radicals to be highly reactive and seek to pair their unpaired electrons by interacting with other molecules. This reactivity can damage cells and lead to diseases. Specifically:
- Free radicals become more stable by taking electrons from other atoms, which can cause cellular damage and diseases or signs of aging over time.
- Common diseases associated with free radicals include atherosclerosis, heart disease, arthritis, stroke, respiratory diseases, Parkinson's and Alzheimer's disease.
- Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species/reactive nitrogen species like free radicals and a body's antioxidant defenses. This stress can damage biom
Reactive oxygen species
1. Reactive oxygen species (ROS) are generated through normal metabolic processes and can cause cell damage. Antioxidants help prevent this damage by neutralizing free radicals.
2. The document discusses various sources of ROS like mitochondria and inflammation, examples of ROS like superoxide and hydroxyl radicals, and the cell damage they can cause.
3. It also outlines the body's natural antioxidant protection systems including enzymes like superoxide dismutase and catalase, as well as dietary and plant-derived antioxidants. When antioxidant levels are insufficient to deal with ROS, oxidative stress can lead to diseases.
Free radicals and antioxidants
definition, properties, types of free radical, neurodegenerative disorder, cardiovascular disease, and cancer due to free radicals, importance of antioxidants and their role.
Oxidative stress
ITS DESCRIBE THE ROLE OF OXIDATIVE STRESS IN ALZHEIMER'S DISEASE AND PROCEDURE FOR MEASUREMENT OF OXIDATIVE PARAMETERS.
Overview of Cell Injury and Cell Death.pptx
This document discusses mechanisms of cell injury. It states that cell injury results from damage to key cellular components like mitochondria, cell membranes, and DNA by various biochemical mechanisms. The type and severity of injury depends on factors like the injurious stimulus, its duration and nature. Common causes of injury include mitochondrial damage, calcium influx, oxidative stress from reactive oxygen species, and defects in membrane permeability. Prolonged injuries can exceed a cell's repair capabilities and lead to necrosis. The document provides detailed explanations of these injury mechanisms.
pathology 2.pptx
This document provides an overview of cell injury, adaptation, and death from a pathology perspective. It defines pathology and discusses homeostasis, the types and mechanisms of cell injury including hypoxia, chemicals, infections, and genetics. It describes cellular adaptations like atrophy, hypertrophy, hyperplasia, and metaplasia that cells undergo in response to injury. It also discusses the types of cell death including necrosis, apoptosis, and gangrene.
ROS and redox regulation
The document discusses oxidative stress and redox regulation. It defines oxidative stress as an imbalance between reactive oxygen species and antioxidants in cells. Reactive oxygen species are formed through normal metabolism but also during environmental stress. They can damage biomolecules and lead to diseases. Antioxidants help neutralize reactive oxygen species and may help prevent certain diseases. Redox regulation involves electron transfer processes like oxidation, which is the loss of electrons, and reduction, which is the gain of electrons. An example of redox regulation is the mitogen-activated protein kinase pathway, which is involved in cell survival signaling and can be activated under oxidative stress conditions through redox modification.
Free radicals
Free radicals are unstable molecules that can damage cells. This document discusses free radicals, how they are produced in the body, and how they damage lipids, proteins, and DNA through oxidation. It also describes biomarkers that are used to measure free radical damage, such as markers of lipid peroxidation (MDA, HNE), protein oxidation (protein carbonyls), and DNA oxidation (8-OHdG). Antioxidants in the body help neutralize free radicals and prevent oxidative damage.
Oxidative stress and Alzheimer's disease
Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them. ROS play a role in many chronic diseases including Alzheimer's disease (AD). The document discusses the sources and reactivity of oxygen free radicals like superoxide, hydrogen peroxide, and hydroxyl radicals that are generated in cells. It also describes how cells protect themselves against oxidants through enzymatic antioxidants like superoxide dismutase, catalase, and glutathione peroxidase. The document then focuses on AD, stating that oxidative stress is thought to play a central role in its pathogenesis by leading to neuronal dysfunction and cell death. Elevated peripheral markers of oxidative stress in AD
Free radicals in human diseases and the role
Free radicals reactive oxygen species and reactive nitrogen species are generated by our body by various endogenous systems, exposure to different physiochemical conditions or pathological states. A balance between free radicals and antioxidants is necessary for proper physiological function. If free radicals overwhelm the body's ability to regulate them, a condition known as oxidative stress ensues. Free radicals thus adversely alter lipids, proteins, and DNA and trigger a number of human diseases. Free radicals are a main cause of cardiovascular diseases, cancer, aging and immune defense disorders. Foods like berries and carrot protect us against free radicals.
Free radicals and reactive oxygen species
Free radicals are highly reactive molecules with unpaired electrons that persist for very short durations. They react with other molecules by donating or abstracting electrons to achieve stability. Common types of free radicals include superoxide, hydrogen peroxide, and hydroxyl radicals. Antioxidants help scavenge free radicals and delay or inhibit oxidation, with one antioxidant typically reacting with one free radical. Enzymatic antioxidants include superoxide dismutase and catalase, while nutrient antioxidants include beta-carotene and vitamin E. Reactive oxygen species are oxygen metabolites produced from one-electron reductions of oxygen that can damage DNA, proteins, and lipids, potentially leading to diseases like cancer, diabetes, and age-related illnesses.
Pathogenesis of cell injury
1. The presentation discusses the pathogenesis of cell injury, outlining factors like the type, duration, and severity of injurious stimuli and the target cell's adaptability.
2. Common mechanisms of cell injury are discussed, including ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects.
3. Specific causes of injury like ischemia and hypoxia can lead to ATP loss, pH changes, impaired sodium pumping, and decreased protein synthesis, ultimately causing reversible or irreversible cell injury.
cell injury...VAN.ppt
This document discusses cell injury and cell death. It defines four types of cellular adaptation - atrophy, hypertrophy, hyperplasia, and metaplasia. It also lists common causes of cell injury like oxygen deprivation, physical/chemical/infectious agents, and genetic defects. The document explains the differences between reversible and irreversible cell injury, and necrosis versus apoptosis. It describes patterns of necrosis in tissues/organs like coagulative, liquefactive, caseous, fat, and gangrenous necrosis. The document concludes by discussing apoptosis as a programmed form of cell death.
Free redical vs antioxident
1. Free radicals are unstable molecules that react quickly to gain stability by capturing electrons from other compounds, causing damage. Common types include superoxide and hydroxyl radicals.
2. Free radicals are generated as a normal product of oxygen metabolism in cells and can also come from environmental exposures like pollution, smoking, and radiation. They cause oxidative damage to biomolecules like lipids, proteins, DNA and carbohydrates.
3. This damage is implicated in diseases such as cancer, heart disease, and neurological disorders. Antioxidants help counter the damaging effects of free radicals by reacting with and neutralizing them.
Pathogenesis of cell injury By Rohit Kumar Trivedi
Pathogenesis of Cell Injury
Pathophysiology Google Classroom Code: vbwvno4
Google Classrom Link: https://classroom.google.com/c/MzM1NjcyOTIxMjgy?cjc=vbwvno4
FACEBOOK: https://www.facebook.com/rohitkrtrivedi
INSTAGRAM: https://www.instagram.com/rohit_kumar_trivedi
SLIDESHARE: https://www.slideshare.net/Rohittrivedi321
#RohitKumarTrivedi
Pathophysiology B Pharm 2nd Semester
CONTENTS:
1. Mitochondrial damage
2. Cell membrane damage
3. Ribosome damage
4. Nuclear damage
Similar to Cell injury (20)
5d9fc831490924cbf1c6daa3a4f26d9d_cellinjury_2003.pdf
5d9fc831490924cbf1c6daa3a4f26d9d_cellinjury_2003.pdf
Free Radical Injury from ROBIN ( prof dr naseer lecture)
Free Radical Injury from ROBIN ( prof dr naseer lecture)
Pathogenesis of cell injury By Rohit Kumar Trivedi
Pathogenesis of cell injury By Rohit Kumar Trivedi
Recently uploaded
ESA/ACT Science Coffee: Diego Blas - Gravitational wave detection with orbita...
ESA/ACT Science Coffee: Diego Blas - Gravitational wave detection with orbita...Advanced-Concepts-Team
Presentation in the Science Coffee of the Advanced Concepts Team of the European Space Agency on the 07.06.2024.
Speaker: Diego Blas (IFAE/ICREA)
Title: Gravitational wave detection with orbital motion of Moon and artificial
Abstract:
In this talk I will describe some recent ideas to find gravitational waves from supermassive black holes or of primordial origin by studying their secular effect on the orbital motion of the Moon or satellites that are laser ranged.THEMATIC APPERCEPTION TEST(TAT) cognitive abilities, creativity, and critic...
THEMATIC APPERCEPTION TEST(TAT) cognitive abilities, creativity, and critic...Abdul Wali Khan University Mardan,kP,Pakistan
hematic appreciation test is a psychological assessment tool used to measure an individual's appreciation and understanding of specific themes or topics. This test helps to evaluate an individual's ability to connect different ideas and concepts within a given theme, as well as their overall comprehension and interpretation skills. The results of the test can provide valuable insights into an individual's cognitive abilities, creativity, and critical thinking skillsImmersive Learning That Works: Research Grounding and Paths Forward
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
Sharlene Leurig - Enabling Onsite Water Use with Net Zero Water
Sharlene Leurig - Enabling Onsite Water Use with Net Zero WaterTexas Alliance of Groundwater Districts
Presented at June 6-7 Texas Alliance of Groundwater Districts Business MeetingThe cost of acquiring information by natural selection
This is a short talk that I gave at the Banff International Research Station workshop on Modeling and Theory in Population Biology. The idea is to try to understand how the burden of natural selection relates to the amount of information that selection puts into the genome.
It's based on the first part of this research paper:
The cost of information acquisition by natural selection
Ryan Seamus McGee, Olivia Kosterlitz, Artem Kaznatcheev, Benjamin Kerr, Carl T. Bergstrom
bioRxiv 2022.07.02.498577; doi: https://doi.org/10.1101/2022.07.02.498577
11.1 Role of physical biological in deterioration of grains.pdf
Storagedeteriorationisanyformoflossinquantityandqualityofbio-materials.
Themajorcausesofdeteriorationinstorage
•Physical
•Biological
•Mechanical
•Chemical
Storageonlypreservesquality.Itneverimprovesquality.
Itisadvisabletostartstoragewithqualityfoodproduct.Productwithinitialpoorqualityquicklydepreciates
Authoring a personal GPT for your research and practice: How we created the Q...
Thematic analysis in qualitative research is a time-consuming and systematic task, typically done using teams. Team members must ground their activities on common understandings of the major concepts underlying the thematic analysis, and define criteria for its development. However, conceptual misunderstandings, equivocations, and lack of adherence to criteria are challenges to the quality and speed of this process. Given the distributed and uncertain nature of this process, we wondered if the tasks in thematic analysis could be supported by readily available artificial intelligence chatbots. Our early efforts point to potential benefits: not just saving time in the coding process but better adherence to criteria and grounding, by increasing triangulation between humans and artificial intelligence. This tutorial will provide a description and demonstration of the process we followed, as two academic researchers, to develop a custom ChatGPT to assist with qualitative coding in the thematic data analysis process of immersive learning accounts in a survey of the academic literature: QUAL-E Immersive Learning Thematic Analysis Helper. In the hands-on time, participants will try out QUAL-E and develop their ideas for their own qualitative coding ChatGPT. Participants that have the paid ChatGPT Plus subscription can create a draft of their assistants. The organizers will provide course materials and slide deck that participants will be able to utilize to continue development of their custom GPT. The paid subscription to ChatGPT Plus is not required to participate in this workshop, just for trying out personal GPTs during it.
Compexometric titration/Chelatorphy titration/chelating titration
Classification
Metal ion ion indicators
Masking and demasking reagents
Estimation of Magnisium sulphate
Calcium gluconate
Complexometric Titration/ chelatometry titration/chelating titration, introduction, Types-
1.Direct Titration
2.Back Titration
3.Replacement Titration
4.Indirect Titration
Masking agent, Demasking agents
formation of complex
comparition between masking and demasking agents,
Indicators/Metal ion indicators/ Metallochromic indicators/pM indicators,
Visual Technique,PM indicators (metallochromic), Indicators of pH, Redox Indicators
Instrumental Techniques-Photometry
Potentiometry
Miscellaneous methods.
Complex titration with EDTA.
Katherine Romanak - Geologic CO2 Storage.pdf
Presented at June 6-7 Texas Alliance of Groundwater Districts Business Meeting
Micronuclei test.M.sc.zoology.fisheries.
Current Ms word generated power point presentation covers major details about the micronuclei test. It's significance and assays to conduct it. It is used to detect the micronuclei formation inside the cells of nearly every multicellular organism. It's formation takes place during chromosomal sepration at metaphase.
ESR spectroscopy in liquid food and beverages.pptx
With increasing population, people need to rely on packaged food stuffs. Packaging of food materials requires the preservation of food. There are various methods for the treatment of food to preserve them and irradiation treatment of food is one of them. It is the most common and the most harmless method for the food preservation as it does not alter the necessary micronutrients of food materials. Although irradiated food doesn’t cause any harm to the human health but still the quality assessment of food is required to provide consumers with necessary information about the food. ESR spectroscopy is the most sophisticated way to investigate the quality of the food and the free radicals induced during the processing of the food. ESR spin trapping technique is useful for the detection of highly unstable radicals in the food. The antioxidant capability of liquid food and beverages in mainly performed by spin trapping technique.
在线办理(salfor毕业证书)索尔福德大学毕业证毕业完成信一模一样
学校原件一模一样【微信：741003700 】《(salfor毕业证书)索尔福德大学毕业证》【微信：741003700 】学位证，留信认证（真实可查，永久存档）原件一模一样纸张工艺/offer、雅思、外壳等材料/诚信可靠,可直接看成品样本，帮您解决无法毕业带来的各种难题！外壳，原版制作，诚信可靠，可直接看成品样本。行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备。十五年致力于帮助留学生解决难题，包您满意。
本公司拥有海外各大学样板无数，能完美还原。
1:1完美还原海外各大学毕业材料上的工艺：水印，阴影底纹，钢印LOGO烫金烫银，LOGO烫金烫银复合重叠。文字图案浮雕、激光镭射、紫外荧光、温感、复印防伪等防伪工艺。材料咨询办理、认证咨询办理请加学历顾问Q/微741003700
【主营项目】
一.毕业证【q微741003700】成绩单、使馆认证、教育部认证、雅思托福成绩单、学生卡等！
二.真实使馆公证(即留学回国人员证明,不成功不收费)
三.真实教育部学历学位认证（教育部存档！教育部留服网站永久可查）
四.办理各国各大学文凭(一对一专业服务,可全程监控跟踪进度)
如果您处于以下几种情况：
◇在校期间，因各种原因未能顺利毕业……拿不到官方毕业证【q/微741003700】
◇面对父母的压力，希望尽快拿到；
◇不清楚认证流程以及材料该如何准备；
◇回国时间很长，忘记办理；
◇回国马上就要找工作，办给用人单位看；
◇企事业单位必须要求办理的
◇需要报考公务员、购买免税车、落转户口
◇申请留学生创业基金
留信网认证的作用:
1:该专业认证可证明留学生真实身份
2:同时对留学生所学专业登记给予评定
3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
The debris of the ‘last major merger’ is dynamically young
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...
Current descriptions of immersive learning cases are often difficult or impossible to compare. This is due to a myriad of different options on what details to include, which aspects are relevant, and on the descriptive approaches employed. Also, these aspects often combine very specific details with more general guidelines or indicate intents and rationales without clarifying their implementation. In this paper we provide a method to describe immersive learning cases that is structured to enable comparisons, yet flexible enough to allow researchers and practitioners to decide which aspects to include. This method leverages a taxonomy that classifies educational aspects at three levels (uses, practices, and strategies) and then utilizes two frameworks, the Immersive Learning Brain and the Immersion Cube, to enable a structured description and interpretation of immersive learning cases. The method is then demonstrated on a published immersive learning case on training for wind turbine maintenance using virtual reality. Applying the method results in a structured artifact, the Immersive Learning Case Sheet, that tags the case with its proximal uses, practices, and strategies, and refines the free text case description to ensure that matching details are included. This contribution is thus a case description method in support of future comparative research of immersive learning cases. We then discuss how the resulting description and interpretation can be leveraged to change immersion learning cases, by enriching them (considering low-effort changes or additions) or innovating (exploring more challenging avenues of transformation). The method holds significant promise to support better-grounded research in immersive learning.
20240520 Planning a Circuit Simulator in JavaScript.pptx
Evaporation step counter work. I have done a physical experiment.
(Work in progress.)
Recently uploaded (20)
ESA/ACT Science Coffee: Diego Blas - Gravitational wave detection with orbita...
ESA/ACT Science Coffee: Diego Blas - Gravitational wave detection with orbita...
GBSN - Biochemistry (Unit 6) Chemistry of Proteins
GBSN - Biochemistry (Unit 6) Chemistry of Proteins
THEMATIC APPERCEPTION TEST(TAT) cognitive abilities, creativity, and critic...
THEMATIC APPERCEPTION TEST(TAT) cognitive abilities, creativity, and critic...
Immersive Learning That Works: Research Grounding and Paths Forward
Immersive Learning That Works: Research Grounding and Paths Forward
Sharlene Leurig - Enabling Onsite Water Use with Net Zero Water
Sharlene Leurig - Enabling Onsite Water Use with Net Zero Water
The cost of acquiring information by natural selection
The cost of acquiring information by natural selection
11.1 Role of physical biological in deterioration of grains.pdf
11.1 Role of physical biological in deterioration of grains.pdf
Authoring a personal GPT for your research and practice: How we created the Q...
Authoring a personal GPT for your research and practice: How we created the Q...
Compexometric titration/Chelatorphy titration/chelating titration
Compexometric titration/Chelatorphy titration/chelating titration
ESR spectroscopy in liquid food and beverages.pptx
ESR spectroscopy in liquid food and beverages.pptx
The debris of the ‘last major merger’ is dynamically young
The debris of the ‘last major merger’ is dynamically young
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...
20240520 Planning a Circuit Simulator in JavaScript.pptx
20240520 Planning a Circuit Simulator in JavaScript.pptx
Cell injury
- 1. CELL INJURY
- 2. HOMEOSTASIS Def Mechanism Narrow range of function and structure by Its genetic programs of metabolism Differentiation and specialization by Constraints of neighboring cells The availability of metabolic substrates
- 3. ADAPTATIONS A condition during which new but altered steady states are achieved, preserving the viability of the cell and modulating its function as it responds to such stimuli. The adaptive response may consist Hyperplasia Hypertrophy Atrophy
- 5. CELL INJURY Dif: If the limits of adaptive response to a stimulus are exceeded or in certain instances when the cell is exposed to an injurious agent or stress, a sequence of events follows that is loosely termed cell injury. Types: 1. Reversible cell injury 2. Irreversible cell injury
- 6. GENERAL CONSIDERATIONS Morphology becomes apparent late in cell injury, changes in physiology early Reaction of cell to injury depends on type of injury, duration and severity Reaction of cell to injury also depends on the type, state & adaptability of the cell
- 7. CAUSES Reduced oxygen -Ischemia, Infarction Physical agents Chemicals Toxins Biological agents -Viruses, Bacteria etc. Immune reaction -Hypersensitivity Nutritional deficiencies Genetic abnormality -Sickle, Hemophilia
- 9. FREE RADICALS Free radicals are chemical species with a single unpaired electron in an outer orbital Free radicals are chemically unstable and therefore readily react with other molecules, resulting in chemical damage Free radicals initiate autocatalytic reactions; molecules that react with free radicals are in turn converted to free radicals
- 11. INTRACELLULAR SOURCES OF FREE RADICALS Normal redox reactions generate free radicals Nitric oxide (NO) can act as a free radical Ionizing radiation (UV, X-rays) can hydrolyze water into hydroxyl (OH) and hydrogen (H) free radicals Metabolism of exogenous chemicals such as CCl4 can generate free radicals Fenton Reaction: Transition metals such as copper and iron also accept or donate free electrons during certain intracellular reactions and thereby catalyze free-radical formation (Fe2+ + H2O2 → Fe3+ + OH• + O).
- 12. NEUTRALIZATION OF FREE RADICALS Spontaneous decay Superoxide dismutase(SOD) 2O2+ 2H →O2+ H2O2 Glutathione (GSH): 2OH+ 2GSH →2H2O + GSSG Catalase: 2H2O2→O2+ H2O 5.Endogenous and exogenous antioxidants (Vitamins E, A, C and β-carotene)
- 13. FREE RADICAL-INDUCED INJURY If not adequately neutralized, free radicals can damage cells by three basic mechanisms: 1. Lipid Peroxidation of membranes: double bonds in polyunsaturated membrane lipids are vulnerable to attack by oxygen free radicals 2. DNA fragmentation: Free radicals react with thymine in nuclear and mitochondrial DNA to produce single strand breaks 3. Protein cross-linking: Free radicals promote sulfhydryl-mediated protein cross-linking, resulting in increased degradation or loss of activity
- 14. ROLE OF CA+ IN CELL INJURY
- 19. MEMBRANE DAMAGE
- 23. DECREASED INTRACELLULAR ATP DURING CELL INJURY.