The document discusses cell injury and its causes, pathogenesis, and morphology. It defines cell injury as stress encountered by cells due to changes in their internal or external environment. Cell injury can be caused genetically or acquired through various external factors like hypoxia, physical or chemical agents, microbes, immunological reactions, nutritional imbalances, aging, and psychological stress. The pathogenesis of cell injury depends on the type of cell, extent of injury, and underlying biochemical processes. Reversible cell injury causes changes like hydropic swelling, fatty changes, and hyaline changes. Irreversible injury leads to autolysis, necrosis, apoptosis, or gangrene.
La lesión celular puede ser reversible o irreversible dependiendo de la intensidad y duración del estímulo dañino. La lesión reversible incluye cambios funcionales y morfológicos como hinchazón celular, mientras que la lesión irreversible conduce a la muerte celular. La lesión celular puede ser causada por privación de oxígeno, agentes físicos, químicos, infecciosos o trastornos genéticos e involucra mecanismos como depleción de ATP, aumento de calcio intracelular y estr
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
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.
dear students,, myself dr manish tiwari tutor department of microbiology at saraswati medical college unnao lucknow if any query regarding this ppt olease contact me my whatsaap no 8979352824.
Amyloidosis refers to conditions where normally soluble proteins become insoluble and deposit in tissues, disrupting their normal function. There are two main types - systemic, which affects multiple organs, and localized, which affects a single organ. Amyloidosis can be primary, arising from a disease affecting immune cells, or secondary, occurring due to another chronic inflammatory condition. The pathogenesis involves misfolding of protein fragments that are not dissolved during proteolysis, causing them to aggregate into oligomers and amyloid fibrils within tissues like the liver and kidneys. In the liver, amyloid deposits may cause hepatomegaly and rupture, while in the kidneys it causes vascular narrowing and glomerular deposition leading to ischemia.
This document provides an overview of pathology, including its definition and branches. Pathology is defined as the study and diagnosis of disease through examination of organs, tissues, bodily fluids, and whole bodies. The main branches of pathology discussed are general pathology, anatomical pathology, cytopathology, surgical pathology, forensic pathology, and clinical/laboratory pathology. The document also covers topics such as roots/suffixes/prefixes, cellular adaptation/injury, reversible vs. irreversible injury, necrosis, and apoptosis.
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.
La lesión celular puede ser reversible o irreversible dependiendo de la intensidad y duración del estímulo dañino. La lesión reversible incluye cambios funcionales y morfológicos como hinchazón celular, mientras que la lesión irreversible conduce a la muerte celular. La lesión celular puede ser causada por privación de oxígeno, agentes físicos, químicos, infecciosos o trastornos genéticos e involucra mecanismos como depleción de ATP, aumento de calcio intracelular y estr
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
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.
dear students,, myself dr manish tiwari tutor department of microbiology at saraswati medical college unnao lucknow if any query regarding this ppt olease contact me my whatsaap no 8979352824.
Amyloidosis refers to conditions where normally soluble proteins become insoluble and deposit in tissues, disrupting their normal function. There are two main types - systemic, which affects multiple organs, and localized, which affects a single organ. Amyloidosis can be primary, arising from a disease affecting immune cells, or secondary, occurring due to another chronic inflammatory condition. The pathogenesis involves misfolding of protein fragments that are not dissolved during proteolysis, causing them to aggregate into oligomers and amyloid fibrils within tissues like the liver and kidneys. In the liver, amyloid deposits may cause hepatomegaly and rupture, while in the kidneys it causes vascular narrowing and glomerular deposition leading to ischemia.
This document provides an overview of pathology, including its definition and branches. Pathology is defined as the study and diagnosis of disease through examination of organs, tissues, bodily fluids, and whole bodies. The main branches of pathology discussed are general pathology, anatomical pathology, cytopathology, surgical pathology, forensic pathology, and clinical/laboratory pathology. The document also covers topics such as roots/suffixes/prefixes, cellular adaptation/injury, reversible vs. irreversible injury, necrosis, and apoptosis.
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.
This document discusses chronic inflammation. It defines chronic inflammation as a prolonged process where tissue destruction and inflammation occur simultaneously. Chronic inflammation can result from acute inflammation becoming chronic, recurrent acute inflammation, or starting as a chronic process. It is characterized by mononuclear cell infiltration, tissue destruction, and proliferative changes. The main cell types involved are macrophages, lymphocytes, plasma cells, and sometimes giant cells. Chronic inflammation can lead to risks like cardiovascular disease and cancer if left unchecked.
Free radicals are highly reactive chemical entities with unpaired electrons that can be toxic under some conditions. There are several types of free radicals including oxygen, sulfur, carbon, and nitrogen centered radicals. Free radicals are formed by either losing or gaining a single electron from a non-radical species and play a role in oxidative stress through reactions like the Fenton reaction.
This document summarizes different types of cell death including apoptosis and necrosis. It describes the morphology and causes of apoptosis and discusses examples of apoptosis occurring in physiological and pathological situations. It also discusses various mechanisms of intracellular accumulations including lipids, proteins, glycogen, and pigments. Finally, it outlines the morphology and patterns of cell injury and necrosis.
Necrosis is a form of cell death where the cell membrane breaks down and cellular contents leak out. It can be focal, affecting a small area, or diffuse, affecting a large area. Necrosis is caused by factors like toxins, infections, circulatory issues, or physical injuries. The dead cells may undergo coagulative necrosis, where structures remain intact, or liquefactive necrosis, where enzymes break down the cells. Other types include caseous, fat, and fibroid necrosis.
Este documento describe el proceso inflamatorio agudo en tres fases: 1) Iniciación, que incluye vasoconstricción, vasodilatación e incremento de la permeabilidad vascular; 2) Amplificación, que implica la acción de mediadores químicos que atraen más leucocitos al área lesionada; y 3) Terminación, que requiere sustancias químicas para detener el proceso inflamatorio. También explica los roles de los leucocitos, mediadores químicos y exudado en la respuesta inflamatoria.
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
Cellular injury can be reversible or irreversible, leading to cell death through necrosis or apoptosis. Reversible injury involves cellular swelling and changes that can be repaired, while irreversible injury destroys cell structures and function. ATP depletion disrupts sodium and calcium pumps, causing cellular swelling and damage from lysosomal enzymes and reactive oxygen species, leading to necrosis. Apoptosis is a genetically programmed form of cell death where caspases activate an intracellular death pathway, condensing and fragmenting the nucleus while keeping the plasma membrane intact.
Cell injury, death, inflammation and repair involves complex biological processes in the body. Acute inflammation is characterized by increased blood flow, swelling, heat and pain as the body responds to injury. This involves vascular changes that allow fluid and immune cells to enter injured tissues. Chronic inflammation is a prolonged response involving lymphocytes and macrophages that can lead to tissue destruction and fibrosis. The body aims to resolve acute inflammation and repair damage, but chronic inflammation can persist long-term from infections, toxins or autoimmune conditions.
Cell injury occurs when cells are exposed to injurious agents and can be reversible or irreversible depending on the severity and persistence of the stimulus. There are two main types of cell death: necrosis, which is unregulated cell lysis causing inflammation, and apoptosis, which is a regulated and programmed form of cell death. Early changes in cell injury are reversible but persistent injury leads to irreversible changes and ultimately cell death through necrosis or apoptosis.
Cell injury occurs when homeostasis is disturbed and the limits of adaptive responses are exceeded. There are two main types of cell injury: reversible and irreversible. Reversible injury involves functional and morphological changes that can be reversed if the damaging stimulus is removed, such as reduced ATP and cellular swelling. Irreversible injury cannot be recovered from and leads to cell death, either through necrosis or apoptosis. Common causes of cell injury include oxygen deprivation, physical agents, chemical agents, infectious agents, immunological reactions, genetic defects, and nutritional imbalances. The initial manifestation of most injuries is cellular swelling. Mechanisms of injury involve ATP depletion, mitochondrial damage, calcium influx, reactive oxygen species accumulation, and increased membrane permeability, typically culminating in necrosis or
Cell injury – cell injury and cell deathaanchal puri
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
CELL INJURY,ADAPTATION AND DEATH-2.1.pptxPharmTecM
This document discusses cell injury, adaptation, and death. It begins by introducing cells as the basic units that make up tissues and organs. There are two main types of cells: epithelial and mesenchymal. Diseases occur due to abnormalities at the cellular level. Cell injury can be caused by various stresses and etiologic agents, and cells can respond through adaptation or death. Causes of cell injury include genetic, hypoxic, physical, chemical, microbial, immunologic, nutritional, and iatrogenic factors. Reversible cell injury involves changes like decreased ATP and membrane damage that can be reversed, while irreversible injury leads to cell death through mechanisms like calcium influx and DNA damage. Necrosis, autolysis, and
This document discusses reversible cell injury. It describes the adaptive responses cells undergo to stress initially, including hypertrophy, hyperplasia and metaplasia. If the stress persists and exceeds the cell's adaptive capabilities, reversible cell injury occurs, marked by membrane and nuclear alterations. Various causes of cell injury are listed. The main morphological alterations seen in reversible cell injury are cellular swelling, fatty change, and other changes like plasma membrane distortions and mitochondrial swelling. If the stressor persists further, irreversible cell injury and necrosis result.
This document discusses cell death and necrosis. It begins by introducing cell injury and defining it as stresses that cells encounter internally and externally. There are two main types of cell death - necrosis and apoptosis. Necrosis is the irreversible cell injury and death that occurs when damage becomes too severe for the cell to recover. Apoptosis is programmed cell death that is important for normal physiology. The document further explores the mechanisms, morphology, and types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. It also discusses the mechanisms, initiators, regulators and roles of apoptosis. Gangrene is defined as a condition caused by critically insufficient blood supply that results in cell death.
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.
This report, prepared by the student at the College of Dentistry, Hassan Atheed , in the third phase discusses scientific topics, but it maybe did not be 100% complete.
Cell injury (cell death): it is the variable changes in morphological and functional properties of cell occurs due to internal or external causes (ex. Chemical, physical, infectious and genetic agents), that obligate cell to respond for preserving normal hemostasis (adaptation) or death (necrosis) when the injury factors sever cell unable to adept, cell may also killed by another pathway even when it have the ability to adept for saving other cells and tissue by programed cell death (apoptosis).
حسن عضيد
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.
Morphology of cell injury and Intracellular accumulationspptxvaishaliwasnik
MORPHOLOGY OF REVERSIBLE CELL INJURY
Common examples of morphologic forms of reversible cell injury are as under:
Hydropic change
2. Hyaline change
3. Mucoid change
4. Fatty change (discussed under intracellular accumulations)
1. HYDROPIC CHANGE
Hydropic change means accumulation of water within the cytoplasm of the cell.
Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation).
Hydropic swelling is an entirely reversible change upon removal of the injurious agent.
ETIOLOGY
This is the commonest and earliest form of cell
injury from almost all causes.
The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc.
PATHOGENESIS
Cloudy swelling results from impaired
regulation of sodium and potassium at the level of cell membrane.
This results in intracellular accumulation of sodium and escape of potassium.
This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic
2. HYALINE CHANGE
The word ‘hyaline’ or ‘hyalin’ means glassy (hyalos = glass).
Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance.
Though fibrin and amyloid have hyaline appearance, they have distinctive features and
staining reactions and can be distinguished from non-specific hyaline material.
Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular.
INTRACELLULAR HYALINE
Intracellular hyaline is mainly seen in epithelial cells.
1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria.
2. Hyaline degeneration of rectus abdominalis muscle called Zenker’s degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline.
3. Mallory’s hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury.
4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections.
5. Russell’s bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell
EXTRACELLULAR HYALINE
Extracellular hyaline commonly termed hyalinisation is seen in connective tissues.
1. Hyaline degeneration in leiomyomas of the uterus.
2. Hyalinised old scar of fi brocollagenous tissues.
3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus.
4. Hyalinised glomeruli in chronic glomerulonephritis.
5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the
lung.
This document discusses chronic inflammation. It defines chronic inflammation as a prolonged process where tissue destruction and inflammation occur simultaneously. Chronic inflammation can result from acute inflammation becoming chronic, recurrent acute inflammation, or starting as a chronic process. It is characterized by mononuclear cell infiltration, tissue destruction, and proliferative changes. The main cell types involved are macrophages, lymphocytes, plasma cells, and sometimes giant cells. Chronic inflammation can lead to risks like cardiovascular disease and cancer if left unchecked.
Free radicals are highly reactive chemical entities with unpaired electrons that can be toxic under some conditions. There are several types of free radicals including oxygen, sulfur, carbon, and nitrogen centered radicals. Free radicals are formed by either losing or gaining a single electron from a non-radical species and play a role in oxidative stress through reactions like the Fenton reaction.
This document summarizes different types of cell death including apoptosis and necrosis. It describes the morphology and causes of apoptosis and discusses examples of apoptosis occurring in physiological and pathological situations. It also discusses various mechanisms of intracellular accumulations including lipids, proteins, glycogen, and pigments. Finally, it outlines the morphology and patterns of cell injury and necrosis.
Necrosis is a form of cell death where the cell membrane breaks down and cellular contents leak out. It can be focal, affecting a small area, or diffuse, affecting a large area. Necrosis is caused by factors like toxins, infections, circulatory issues, or physical injuries. The dead cells may undergo coagulative necrosis, where structures remain intact, or liquefactive necrosis, where enzymes break down the cells. Other types include caseous, fat, and fibroid necrosis.
Este documento describe el proceso inflamatorio agudo en tres fases: 1) Iniciación, que incluye vasoconstricción, vasodilatación e incremento de la permeabilidad vascular; 2) Amplificación, que implica la acción de mediadores químicos que atraen más leucocitos al área lesionada; y 3) Terminación, que requiere sustancias químicas para detener el proceso inflamatorio. También explica los roles de los leucocitos, mediadores químicos y exudado en la respuesta inflamatoria.
Cellular Adaptation
as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis.
Injury - altered homeostasis
if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs.
Reversible Cell Injury
removal of stress results in complete restoration of structural & functional integrity.
b) Irreversible Cell Injury / Cell Death
if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death.
2 main morphologic patterns: necrosis & apoptosis.
Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptations are responses of cells to normal stimulation by hormones or endogenous chemical mediators
Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy refers to an increase in the size of cells, that results in an increase in the size of the affected organ
The hypertrophied organ has no new cells, just larger cells.
Types:
a) physiologic b) pathologic
Causes:
a) increased functional demand b) hormonal stimulation
Cellular injury can be reversible or irreversible, leading to cell death through necrosis or apoptosis. Reversible injury involves cellular swelling and changes that can be repaired, while irreversible injury destroys cell structures and function. ATP depletion disrupts sodium and calcium pumps, causing cellular swelling and damage from lysosomal enzymes and reactive oxygen species, leading to necrosis. Apoptosis is a genetically programmed form of cell death where caspases activate an intracellular death pathway, condensing and fragmenting the nucleus while keeping the plasma membrane intact.
Cell injury, death, inflammation and repair involves complex biological processes in the body. Acute inflammation is characterized by increased blood flow, swelling, heat and pain as the body responds to injury. This involves vascular changes that allow fluid and immune cells to enter injured tissues. Chronic inflammation is a prolonged response involving lymphocytes and macrophages that can lead to tissue destruction and fibrosis. The body aims to resolve acute inflammation and repair damage, but chronic inflammation can persist long-term from infections, toxins or autoimmune conditions.
Cell injury occurs when cells are exposed to injurious agents and can be reversible or irreversible depending on the severity and persistence of the stimulus. There are two main types of cell death: necrosis, which is unregulated cell lysis causing inflammation, and apoptosis, which is a regulated and programmed form of cell death. Early changes in cell injury are reversible but persistent injury leads to irreversible changes and ultimately cell death through necrosis or apoptosis.
Cell injury occurs when homeostasis is disturbed and the limits of adaptive responses are exceeded. There are two main types of cell injury: reversible and irreversible. Reversible injury involves functional and morphological changes that can be reversed if the damaging stimulus is removed, such as reduced ATP and cellular swelling. Irreversible injury cannot be recovered from and leads to cell death, either through necrosis or apoptosis. Common causes of cell injury include oxygen deprivation, physical agents, chemical agents, infectious agents, immunological reactions, genetic defects, and nutritional imbalances. The initial manifestation of most injuries is cellular swelling. Mechanisms of injury involve ATP depletion, mitochondrial damage, calcium influx, reactive oxygen species accumulation, and increased membrane permeability, typically culminating in necrosis or
Cell injury – cell injury and cell deathaanchal puri
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
CELL INJURY,ADAPTATION AND DEATH-2.1.pptxPharmTecM
This document discusses cell injury, adaptation, and death. It begins by introducing cells as the basic units that make up tissues and organs. There are two main types of cells: epithelial and mesenchymal. Diseases occur due to abnormalities at the cellular level. Cell injury can be caused by various stresses and etiologic agents, and cells can respond through adaptation or death. Causes of cell injury include genetic, hypoxic, physical, chemical, microbial, immunologic, nutritional, and iatrogenic factors. Reversible cell injury involves changes like decreased ATP and membrane damage that can be reversed, while irreversible injury leads to cell death through mechanisms like calcium influx and DNA damage. Necrosis, autolysis, and
This document discusses reversible cell injury. It describes the adaptive responses cells undergo to stress initially, including hypertrophy, hyperplasia and metaplasia. If the stress persists and exceeds the cell's adaptive capabilities, reversible cell injury occurs, marked by membrane and nuclear alterations. Various causes of cell injury are listed. The main morphological alterations seen in reversible cell injury are cellular swelling, fatty change, and other changes like plasma membrane distortions and mitochondrial swelling. If the stressor persists further, irreversible cell injury and necrosis result.
This document discusses cell death and necrosis. It begins by introducing cell injury and defining it as stresses that cells encounter internally and externally. There are two main types of cell death - necrosis and apoptosis. Necrosis is the irreversible cell injury and death that occurs when damage becomes too severe for the cell to recover. Apoptosis is programmed cell death that is important for normal physiology. The document further explores the mechanisms, morphology, and types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. It also discusses the mechanisms, initiators, regulators and roles of apoptosis. Gangrene is defined as a condition caused by critically insufficient blood supply that results in cell death.
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.
This report, prepared by the student at the College of Dentistry, Hassan Atheed , in the third phase discusses scientific topics, but it maybe did not be 100% complete.
Cell injury (cell death): it is the variable changes in morphological and functional properties of cell occurs due to internal or external causes (ex. Chemical, physical, infectious and genetic agents), that obligate cell to respond for preserving normal hemostasis (adaptation) or death (necrosis) when the injury factors sever cell unable to adept, cell may also killed by another pathway even when it have the ability to adept for saving other cells and tissue by programed cell death (apoptosis).
حسن عضيد
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.
Morphology of cell injury and Intracellular accumulationspptxvaishaliwasnik
MORPHOLOGY OF REVERSIBLE CELL INJURY
Common examples of morphologic forms of reversible cell injury are as under:
Hydropic change
2. Hyaline change
3. Mucoid change
4. Fatty change (discussed under intracellular accumulations)
1. HYDROPIC CHANGE
Hydropic change means accumulation of water within the cytoplasm of the cell.
Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation).
Hydropic swelling is an entirely reversible change upon removal of the injurious agent.
ETIOLOGY
This is the commonest and earliest form of cell
injury from almost all causes.
The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc.
PATHOGENESIS
Cloudy swelling results from impaired
regulation of sodium and potassium at the level of cell membrane.
This results in intracellular accumulation of sodium and escape of potassium.
This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic
2. HYALINE CHANGE
The word ‘hyaline’ or ‘hyalin’ means glassy (hyalos = glass).
Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance.
Though fibrin and amyloid have hyaline appearance, they have distinctive features and
staining reactions and can be distinguished from non-specific hyaline material.
Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular.
INTRACELLULAR HYALINE
Intracellular hyaline is mainly seen in epithelial cells.
1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria.
2. Hyaline degeneration of rectus abdominalis muscle called Zenker’s degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline.
3. Mallory’s hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury.
4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections.
5. Russell’s bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell
EXTRACELLULAR HYALINE
Extracellular hyaline commonly termed hyalinisation is seen in connective tissues.
1. Hyaline degeneration in leiomyomas of the uterus.
2. Hyalinised old scar of fi brocollagenous tissues.
3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus.
4. Hyalinised glomeruli in chronic glomerulonephritis.
5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the
lung.
Degeneration, necrosis, and pathological pigmentationBruno Mmassy
This document provides an overview of degeneration, necrosis, and pathological pigmentation. It defines degeneration as the deterioration of live cells following injury. Various types of cell injuries are classified, including physical, chemical, biological, nutritional, and genetic injuries. The document also describes different types of degenerative changes based on the accumulation of water, carbohydrates, proteins, and lipids inside and outside cells. Examples of each type are given.
The document discusses cell injury and its causes. It defines cell injury as damage to cells from changes in their internal or external environment. There are two main types of causes of cell injury - genetic and acquired. Acquired causes are more common and include hypoxia/ischemia, physical agents, chemicals/drugs, microbes, immunological factors, nutritional imbalances, aging, and psychological stress. The severity and reversibility of cell injury depends on factors like the injurious agent, duration of exposure, cell type, and underlying intracellular changes. Reversible cell injury from short-term hypoxia/ischemia involves decreased ATP production, lactic acidosis, and damage to membrane pumps causing swelling.
This is the brief overview on the topic CELL INJURY. After reading this you will get to know about adaptations, types, etiology, pathogenesis of cell injury.
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.
cell injury and necrosis mechanism Pathology.pptssuser7ec6af
Cell death
Cell Injury - Types, Pathogenesis , Mechanism, Factors, Reversible & Irreversible
Cell injury: Sequence of events that occurs when stresses exceed ability of cells to adapt. Responses are initially reversible, but may progress to irreversible injury and cell death. Cell death: Results when continuing injury becomes irreversible, at which time the cell cannot recover.
1. Cell injury refers to changes in a cell's internal and external environment due to stresses like lack of oxygen, toxins, or infections.
2. Causes of cell injury include hypoxia, physical and chemical agents, microbes, immunological reactions, nutritional imbalances, and genetic factors.
3. Cellular responses to injury include reversible changes like fatty change and swelling, or irreversible cell death through necrosis or apoptosis. Adaptive changes like hypertrophy and hyperplasia can also occur.
This document discusses different methods for delivering fluorides, including topical and systemic methods. It focuses on topical fluoride delivery methods which are applied directly to teeth. Topical fluorides can be divided into professionally applied and self-applied products. Professionally applied products contain higher fluoride concentrations and include neutral sodium fluoride, acidulated phosphate fluoride, and stannous fluoride solutions, gels, pastes, and varnishes. Application techniques for professionals include the paint on and tray methods. Stannous fluoride and sodium fluoride are discussed in more detail regarding their preparation, mechanisms of action, advantages, and application procedures. Repeated topical fluoride treatments over time help strengthen tooth enamel and reduce the risk of dental caries.
Megaloblastic anaemia . And all anout anaemia, pernicious anaemia,GaurishChandraRathau
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This document discusses megaloblastic anemia, which is caused by deficiencies in vitamin B12 or folic acid. It describes the history and discoveries regarding B12 and folic acid, including their roles in DNA synthesis and hematopoiesis. The document covers absorption, transport, functions and deficiencies of B12 and folic acid, as well as their treatment and uses. It also briefly discusses erythropoietin and drugs used to treat neutropenia.
This document provides an overview of the Russel's Periodontal Index and the CPITN (Community Periodontal Index of Treatment Needs). It discusses the scope, procedure, scoring criteria, and calculation methods for both indices. The Russel's Periodontal Index was developed in 1956 to estimate the prevalence and severity of periodontal disease on a scale of 0-8. The CPITN was developed in 1982 by the WHO and FDI to survey and evaluate periodontal treatment needs, examining six index teeth in each sextant and assigning codes from 0-4 based on probing depth and other factors. The document reviews the advantages, limitations, and modifications of these two common indices used in epidemiological studies of periodontal health.
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The document discusses the role and importance of adhesive dentistry. It describes the different generations of dentine bonding agents from the early phosphoric acid-based systems to newer self-etch adhesives. Key challenges in dentine adhesion are the structural differences between enamel and dentine such as dentine's high water content and presence of a smear layer. Conditioning with acid or chelators is needed to remove the smear layer and expose collagen fibers for bonding to occur. Current adhesive systems are classified as etch-and-rinse or self-etch and involve either two or three step application processes.
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This document summarizes the key properties and characteristics of different elastomeric impression materials, including polysulfide, condensation silicone, addition silicone, and polyether elastomers. It describes the composition, setting reactions, available consistencies, and mechanical properties of each material. Properties like viscosity, working and setting times, dimensional stability, hardness, tear strength, and detail reproduction are compared between the different elastomers. The document also discusses techniques for mixing and using impression materials, as well as their wettability and hydrophilicity.
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"Learn about all the ways Walmart supports nonprofit organizations.
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The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
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Answers about how you can do more with Walmart!"
1. DEFINATION
NORMAL CELL
ETIOLOGY OF CELL INJURY
PATHOGENESIS OF CELL INJURY
MORPHOLOGY OF CELL INJURY
2. Cells are the basic units of tissues, which form organs and systems in the
human body.
Cell injury is defined as a variety of stresses a cell encounters as a result of
changes in its internal and external environment.
The cellular response to stress may vary and depends upon the following
variables:
i) The type of cell and tissue involved.
ii) Extent and type of cell injury.
3.
4. The cells may be broadly injured by two major ways:
A. By genetic causes
B. By acquired causes
GENETIC CAUSES:-
1. Development defect: error on morphogenesis
2. Cytogenetic defect: chromosomal abnormalities
5. ACQUIRED CAUSES:-
1. Hypoxia and ischemia(Deficiency of oxygen)
2. Physical agents
3. Chemical agents and drugs
4. Microbial agents
5. Immunologic agents
6. Nutritional derangements
7. Aging
8. Psychogenic diseases
6. 1. HYPOXIA AND ISCHAEMIA
Cells of different tissues essentially require oxygen to
generate energy and perform metabolic functions.
Hypoxia is the most common cause of cell injury.
Hypoxia may result from the following:
1. Cell injury is by reduced supply of blood to cells due
to interruption.
2. Disorders of oxygen-carrying RBCs (e.g. anaemia,
carbon monoxide poisoning), heart diseases, lung
diseases and increased demand of tissues.
7. 2. PHYSICAL AGENTS
Physical agents in causation of disease are as under:
1. Mechanical trauma (e.g. road accidents)
2. Thermal trauma (e.g. by heat and cold)
3. Electricity
4. Radiation (e.g. ultraviolet and ionising)
5. Rapid changes in atmospheric pressure.
8. 3. CHEMICALS AND DRUGS
An ever increasing list of chemical agents and drugs may
cause cell injury
1. chemical poisons such as cyanide, arsenic, mercury
2. strong acids and alkalis
3. environmental pollutants
4. insecticides and pesticides
5. oxygen at high concentrations
6. hypertonic glucose and salt
7. social agents such as alcohol and narcotic drugs
8. therapeutic administration of drugs
9. 4. MICROBIAL AGENTS
Injuries by microbes include infections caused by
1. Bacteria,
2. Rickettsiae
3. Viruses
4. Fungi
5. Protozoa
6. Metazoa
7. Parasites
10. 5. IMMUNOLOGIC AGENTS
It protects the host against various injurious agents but
it may also turn lethal and cause cell injury e.g.
1. Hypersensitivity reactions
2. Anaphylactic reactions
3. Autoimmune diseases.
11. 6. NUTRITIONAL DERANGEMENTS
A deficiency of nutrients may result in nutritional
imbalances.
1. Deficiency of nutrients (e.g. Starvation)
2. Protein calorie (e.g. Marasmus, Kwashiorkor)
3. Minerals (e.g. Anaemia)
4. Nutritional excess is a problem of affluent societies
resulting in obesity, atherosclerosis, heart disease
and hypertension.
12. 7. AGING
Cellular aging leads to impaired ability of the cells to
undergo replication and repair, and ultimately lead to
cell death culminating in death of the individual.
8. PSYCHOGENIC DISEASES
Diseases due to mental stress, strain, anxiety, overwork
and frustration e.g. depression, schizophrenia.
13. The underlying alterations in biochemical systems of
cells for reversible and irreversible cell injury by
various agents is complex and varied.
The following principles apply in pathogenesis of most
forms of cell injury by various agents:
1. Type, duration and severity of injurious agent
2. Type, status and adaptability of target cell
3. Underlying intracellular phenomena
4. Morphologic consequences
15. Ischaemia and hypoxia are the most common forms of cell injury.
Although underlying intracellular mechanisms and ultrastructural
changes involved in reversible and irreversible cell injury by
hypoxia and ischaemia.
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 ultrastructure
are reversed if the circulation is quickly restored. The sequential
biochemical and ultrastructural changes in reversible cell injury
are as under
1. Decreased generation of cellular ATP: Damage by ischaemia
versus hypoxia from other causes
2. Intracellular lactic acidosis: Nuclear clumping.
3. Damage to plasma membrane pumps: Hydropic swelling and
other membrane changes.
4. Reduced protein synthesis: Dispersed ribosomes.
16. IRREVERSIBLE CELL INJURY
Persistence of ischaemia or hypoxia results in irreversible damage to
the structure and function of the cell (cell death). The stage at which
this point of no return or irreversibility is reached from reversible cell
injury is unclear but the sequence of events is a continuation of
reversibly injured cell.
Two essential phenomena always distinguish irreversible from
reversible cell injury
1. Inability of the cell to reverse mitochondrial dysfunction on
reperfusion or reoxygenation.
2. Disturbance in cell membrane function in general, and in plasma
membrane in particular.
These biochemical changes have effects on the ultrastructural
components of the cell
1. Calcium influx: Mitochondrial damage
2. Activated phospholipases: Membrane damage
3. Intracellular proteases: Cytoskeletal damage
4. Activated endonucleases: Nuclear damage
5. Lysosomal hydrolytic enzymes: Lysosomal damage, cell death
and phagocytosis.
17.
18. The molecular and biochemical mechanisms of various forms of cell
injury, we now turn to light microscopic morphologic changes of
reversible and irreversible cell injury.
Reversible cell injury Irreversible cell injury
HYDROPIC CHANGES AUTOLYSIS
HYALINE CHANGES NECROSIS
MUCOID CHANGES APOPTOSIS
FATTY CHANGES GANGRENE
19. MORPHOLOGY OF REVERSIBLE
CELL INJURY
• The term degeneration has been used to denote
morphology of reversible cell injury.
• Following morphologic forms of reversible cell injury are
included under this heading:
1. Hydropic change
2. Fatty change
3. Hyaline change
4. Mucoid change
20. HYDROPIC CHANGES
• It means accumulation of water within the cytoplasm of
the cell.
ETIOLOGY:- The common causes include acute and sub
acute cell injury from various etiologic agents such as
bacterial toxins, chemicals, poisons, burns, high fever,
saline etc.
PATHOGENESIS:- Cloudy swelling results from impaired
regulation of sodium and potassium at the level of cell
membrane. This results in intracellular accumulation of
sodium and escape of potassium. This, in turn, leads to
rapid flow of water into the cell to maintain iso-osmotic
conditions and hence cellular swelling occurs. Hydropic
swelling is an entirely reversible change upon removal of
the injurious agent.
21. HYALINE CHANGES
Hyaline is a descriptive histologic term for glassy, homogeneous,
eosinophilic appearance of material in haematoxylin and eosin-
stained sections.
It may be intracellular or extracellular
INTRACELLULAR HYALINE:- It is mainly seen in epithelial cells.
A few examples are as follows:
1. Hyaline droplets in the proximal tubular epithelial cells in cases of
excessive reabsorption of plasma proteins.
2. Hyaline degeneration of rectus abdominalis muscle called
Zenker’s degeneration, occurring in typhoid fever..
3. Mallory’s hyaline represents aggregates of intermediate filaments
in the hepatocytes in alcoholic liver cell injury.
4. Nuclear hyaline inclusions seen in some viral infections.
5. Russell’s bodies representing excessive immunoglobulinsnin the
rough endoplasmic reticulum of the plasma cells
22. EXTRACELLULAR HYALINE:- It is seen in connective
tissues. A few examples of extracellular hyaline change
are as under:
1. Hyaline degeneration in leiomyomas of the uterus
2. Hyalinised old scar of fibrocollagenous tissues.
3. Hyaline arteriolosclerosis in renal vessels in
hypertension and diabetes mellitus.
4. Hyalinised glomeruli in chronic glomerulonephritis.
5. Corpora amylacea are rounded masses of concentric
hyaline laminae seen in the prostate in the elderly, in
the brain and in the spinal cord in old age, and in old
infarcts of the lung.
23. MUCOID CHANGES
Mucus secreted by mucous glands is a combination of
proteins complexed with mucopolysaccharides
Mucin, a glycoprotein,
Mucin is normally produced by epithelial cells of
mucous membranes and mucous glands, as well as by
some connective tissues like in the umbilical cord.
Both types of mucin are stained by alcian blue.
Epithelial mucin stains positively with periodic acid-
Schiff (PAS), while connective tissue mucin is PAS
negative but is stained positively with colloidal iron.
24. EPITHELIAL MUCIN.:-Following are some examples of functional
excess of epithelial mucin:
1. Catarrhal inflammation of mucous membrane (e.g. of
respiratory tract, alimentary tract, uterus).
2. Obstruction of duct leading to mucocele in the oral cavity and
gallbladder.
3. Cystic fibrosis of the pancreas.
4. Mucin-secreting tumour.
CONNECTIVE TISSUE MUCIN:- A few examples of disturbances of
connective tissue mucin are as under:
1. Mucoid degeneration in some tumours e.g. myxomas, neurofibromas,
fibroadenoma, soft tissue sarcomas etc
2. Dissecting aneurysm of the aorta due to Erdheim’s medial degeneration
and Marfan’s syndrome.
3. Myxomatous change in the dermis in myxoedema.
4. Myxoid change in the synovium in ganglion on the wrist.
25. FATTY CHANGES
It is the intracellular accumulation of neutral fat
within parenchymal cells.
It includes the older, now abandoned, terms of fatty
degeneration and fatty infiltration because fatty
change neither necessarily involves degeneration nor
infiltration.
It is especially common in the liver but may occur in
other non-fatty tissues like the heart, skeletal muscle,
kidneys and other organ.
26. Fatty Liver
Liver is the commonest site for accumulation of fat because it plays central role in fat
metabolism.
ETIOLOGY:- Fatty change in the liver may result from one of the two types of causes:
1. Conditions with excess fat: exceeding the capacity of the liver to metabolise it.
i) Obesity
ii) Diabetes mellitus
iii) Congenital hyperlipidaemia
2. Liver cell damage: when fat cannot be metabolised in it
i) Alcoholic liver disease
ii) Starvation
iii) Protein calorie malnutrition
iv) Chronic illnesses (e.g. tuberculosis)
v) Acute fatty liver in late pregnancy
vi) Hypoxia (e.g. anaemia, cardiac failure)
vii) Hepatotoxins (e.g. carbon tetrachloride etc.)
viii) Drug-induced liver cell injury (e.g. methotrexate, steroids, CCl4, etc)
ix) Reye’s syndrome
27. PATHOGENESIS:- Mechanism
of fatty liver depends upon the
stage at which the etiologic
agent acts in the normal fat
transport and metabolism.
Hence, pathogenesis of fatty
liver is best understood in the
light of normal fat metabolism
in the liver .
Lipids as free acids enter the
liver cell from either of the
following 2 sources
1. From diet as chylomicrons
2. From adipose tissue as free
fatty acids.
28. In fatty liver, intracellular accumulation of triglycerides
can occur due to defect at one or more of the following 6 steps in
the normal fat metabolism shown in
1. Increased entry of free fatty acids into the liver.
2. Increased synthesis of fatty acids by the liver.
3. Decreased conversion of fatty acids into ketone bodies resulting
in increased esterification of fatty acids to triglycerides.
4. Increased α-glycerophosphate causing increased esterification of
fatty acids to triglycerides.
5. Decreased synthesis of ‘lipid acceptor protein’ resulting in
decreased formation of lipoprotein from triglycerides.
6. Block in the excretion of lipoprotein from the liver into plasma.
29. MORPHOLOGY OF IRREVERSIBLE
CELL INJURY (CELL DEATH)
Cell death is a state of irreversible injury.
It may occur in the living body as a local change (i.e.
autolysis, necrosis and apoptosis) and the changes that
follow it (i.e. gangrene and pathologic calcification), or
result in end of the life.
processes involved in cell death are described below.
1. AUTOLYSIS
2. NECROSIS
3. APOPTOSIS
4. GANGRENE
30. AUTOLYSIS
Autolysis (i.e. self-digestion) is disintegration of the cell by
its own hydrolytic enzymes liberated from lysosomes.
It can occur in the living body when it is surrounded by
inflammatory reaction but the term is generally used for
postmortem change in which there is complete absence of
surrounding inflammatory response.
It is rapid in some tissues rich in hydrolytic enzymes such
as in the pancreas, and gastric mucosa; intermediate in
tissues like the heart, liver and kidney; and slow in fibrous
tissue.
Morphologically, it is identified by homogeneous and
eosinophilic cytoplasm with loss of cellular details and
remains of cell as debris.
31. NECROSIS
It is defined as localised area of death of tissue
followed by degradation of tissue by hydrolytic
enzymes liberated from dead cells; it is invariably
accompanied by inflammatory reaction.
It can be caused by various agents such as hypoxia,
chemical and physical agents, microbial agents,
immunological injury, etc.
Two essential changes characterise irreversible cell
injury in necrosis of all types
1. Cell digestion by lytic enzymes.
2. Denaturation of proteins.
32. Types of Necrosis
1. COAGULATIVE NECROSIS
2. LIQUEFACTION NECROSIS
3. CASEOUS NECROSIS
4. FAT NECROSIS
5. FIBRINOID NECROSIS
1. COAGULATIVE NECROSIS:- It caused by irreversible
focal injury, mostly from sudden cessation of blood flow
and less often from bacterial and chemical agents. The
organs commonly affected are the heart, kidney, and
spleen.
33. 2. LIQUEFACTION NECROSIS:- It occurs commonly due to ischaemic injury and
bacterial or fungal infections. It occurs due to degradation of tissue by the
action of powerful hydrolytic enzymes. The common examples are infarct brain
and abscess cavity.
3. CASEOUS NECROSIS:- It is found in the centre of foci of TB infections. It
combines features of both coagulative and liquefactive necrosis.
4. FAT NECROSIS:- It is a special form of cell death occurring at two
anatomically different locations but morphologically similar lesions. These are
Acute pancreatic necrosis
traumatic fat necrosis
In the case of pancreas, there is liberation of pancreatic lipases from injured or
inflamed tissue that results in necrosis of the pancreas as well as of the fat
depots throughout the peritoneal cavity.
Fat necrosis hydrolyses neutral fat present in adipose cells into glycerol and free
fatty acids. The damaged adipose cells assume cloudy appearance. The leaked
out free fatty acids complex with calcium to form calcium soaps.
5. FIBRINOID NECROSIS:- It is characterized by deposition of fibrin-like
material which has the staining properties of fibrin. It is encountered in
examples of immunologic tissue injury, arterioles in hypertension, peptic ulcer
etc.
34. APOPTOSIS
It is a form of ‘coordinated and internally programmed
cell death’ having significance in a variety of
physiologic and pathologic conditions (apoptosis is a
Greek word meaning ‘falling off’ or ‘dropping off’).
The term was first introduced in 1972 as distinct from
necrosis by being a form of cell death which is
controlled and regulated by the rate of cell division;
when the cell is not needed, pathway of cell death is
activated (‘cell suicide’) and is unaccompanied by any
inflammation and collateral tissue damage.
35. APOPTOSIS IN BIOLOGIC PROCESSES:- Apoptosis is responsible for mediating
cell death in a wide variety of physiologic and pathologic processes as under:
Physiologic Processes:
1. Organized cell destruction in sculpting of tissues during development of embryo.
2. Physiologic involution of cells in hormone-dependent tissues
3. Normal cell destruction followed by replacement proliferation such as in intestinal
epithelium.
4. Involution of the thymus in early age.
Pathologic Processes:
1. Cell death in tumours exposed to chemotherapeutic agents.
2. Cell death by cytotoxic T cells in immune mechanisms
3. Progressive depletion of CD4+T cells in the pathogenesis of AIDS.
4. Cell death in viral infections e.g. viral hepatitis.
5. Pathologic atrophy of organs and tissues on withdrawal of stimuli e.g. prostatic
atrophy, atrophy of kidney
6. Cell death in response to injurious agents involved in causation of necrosis e.g.
radiation, hypoxia and mild thermal injury.
7. In degenerative diseases of CNS e.g. in Alzheimer’s disease, Parkinson’s disease, and
chronic infective dementias.
8. Heart diseases e.g. heart failure, acute myocardial infarction
36.
37. MOLECULAR MECHANISMS OF APOPTOSIS Several physiologic and
pathologic processes activate apoptosis in a variety of ways. However, in general
the following events sum up the sequence involved in apoptosis:
Initiators of apoptosis:- Triggers for signalling programmed cell death act at the
cell membrane, either intracellularly or extracellularly
i) Withdrawal of signals required for normal cell survival
(e.g. absence of certain hormones, growth factors, cytokines).
ii) Extracellular signals triggering of programmed cell death (e.g. activation of FAS
receptor belonging to TNF-R family).
iii) Intracellular stimuli e.g. heat, radiation, hypoxia etc.
Process of programmed cell death:- After the cell has been initiated into self-
destruct mode, the programme inbuilt in the cell gets activated as under:
i) Activation of caspases
ii) Activation of death receptors
iii) Activation of growth controlling genes (BCL-2 and p53)
iv) Cell death.
Phagocytosis:- The dead apoptotic cells develop membrane changes which
promote their phagocytosis. Phosphatidylserine and thrombospondin
molecules which are normally present on the inside of the cell membrane,
appear on the outer surface of the cells in apoptosis, which facilitate their
identification by adjacent phagocytes and promotes phagocytosis.
38. GANGRENE
It is a form of necrosis of tissue with superadded putrefaction.
Coagulative necrosis due to ischaemia (e.g. in gangrene of the
bowel, gangrene of limb).
Gangrenous inflammation is characterised by primarily
inflammation provoked by virulent bacteria resulting in massive
tissue necrosis.
The end-result of necrotising inflammation and gangrene is the
same but the way the two are produced.
Examples of necrotising inflammation are: gangrenous
appendicitis, gangrenous stomatitis.
There are 2 main forms of gangrene—
1. dry gangrene
2. wet gangrene
3. variant form of wet gangrene called gas gangrene.
39. Dry Gangrene
It begins in the distal part of a limb due to ischaemia.
Example is the dry gangrene in the toes and feet of an old patient
due to arteriosclerosis.
Other causes of dry gangrene foot include
1. Buerger’s disease
2. Raynaud’s disease
3. trauma
4. ergot poisoning
Gangrene spreads slowly upwards until it reaches a point where
the blood supply is adequate to keep the tissue viable.
A line of separation is formed at this point between the
gangrenous part and the viable part.
40. Wet Gangrene
It occurs in naturally moist tissues and organs such as the mouth,
bowel, lung, cervix, vulva etc.
Diabetic foot is another example of wet gangrene due to high sugar
content in the necrosed tissue which favours growth of bacteria.
Bed sores occurring in a bed-ridden patient due to pressure on sites like
the sacrum, buttocks and heels are the other important clinical
conditions included in wet gangrene.
Wet gangrene usually develops rapidly due to blockage of venous, and
less commonly, arterial blood flow from thrombosis or embolism.
The affected part is stuffed with blood which favours the rapid growth
of putrefactive bacteria. The toxic products formed by bacteria are
absorbed causing profound systemic manifestations of septicaemia,
and finally death.
The spreading wet gangrene generally lacks clear-cut line of
demarcation and may spread to peritoneal cavity causing peritonitis.
41. GAS GANGRENE
It is a special form of wet gangrene caused by gas-
forming clostridia (gram-positive anaerobic bacteria)
which gain entry into the tissues through open
contaminated wounds, especially in the muscles, or as
a complication of operation on colon which normally
contains clostridia.
Clostridia produce various toxins which produce
necrosis and oedema locally and are also absorbed
producing profound systemic manifestations.