Necrosis sheril
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necrosis that is a programmed cell deathn apoptosis that is uncontrolled cell death are all necessary evil for both growth n development of the living organisms
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Cell injury-necrosis
Necrosis and apoptosis are both forms of cell death, but they differ significantly. Necrosis is premature cell death caused by external factors like infection, toxins, or physical trauma. It results in the uncontrolled release of cellular contents and causes inflammation. Apoptosis is programmed cell death that occurs as part of natural biological processes. It is an actively regulated and controlled process where cells play an active role in their own death, avoiding inflammation.
Lect.no.4
This document discusses different types of cell death, including apoptosis and necrosis. It describes necrosis as cell death resulting from external factors that cause irreversible injury. The key morphological changes seen with necrosis include increased cytoplasmic eosinophilia, nuclear pyknosis, karyorrhexis, and karyolysis. There are several patterns of necrosis depending on the mechanism and tissue involved, such as coagulative, liquefactive, caseous, and gangrene. Coagulative necrosis preserves tissue architecture while liquefactive necrosis destroys tissue structure. Gangrene refers to visible tissue necrosis, usually due to ischemia.
General pathology necrosis
Necrosis is the death of cells and living tissue. There are several types of necrosis that are characterized by the microscopic appearance of dead cells. Coagulative necrosis occurs due to ischemia and results in pale, swollen tissue on gross examination and swollen eosinophilic cells on microscopy. Liquefactive necrosis occurs due to infection and results in soft, cystic lesions containing debris. Caseous necrosis is seen in tuberculosis and resembles dry cheese with granular debris. Fat necrosis affects pancreatic and breast tissue, appearing as yellowish deposits containing calcium salts. Fibrinoid necrosis involves fibrin deposition in tissues damaged by immune processes.
Necrosis,gangrene and apoptosis
This document summarizes different types of cell death including autolysis, necrosis, gangrene, and apoptosis. It describes the morphology, causes, and characteristics of coagulative, liquefactive, caseous, fatty, fibrinoid, and gangrenous necrosis. The key differences between dry, wet, and gas gangrene are highlighted. The document also provides details on the initiation and execution phases of apoptosis, the role of caspases, and morphological and biochemical changes in apoptosis.
Cell injury
Cell injury can occur through various causes and results in either reversible or irreversible injury and cell death. Reversible injury involves changes that can be repaired if the stressor is removed, while irreversible injury leads to cell death through either necrosis or apoptosis. Necrosis is unprogrammed cell death that occurs due to external factors and results in cell contents leaking out and triggering inflammation. Apoptosis is programmed cell death where cells activate internal enzymes to degrade themselves without inflammatory response. The key differences between the two types of cell death include apoptosis affecting individual cells while necrosis affects groups of cells.
Causes of cell injury
This document discusses various causes of cell injury and death, including oxygen deprivation, physical agents, chemicals, infectious agents, immune reactions, genetic defects, and nutritional imbalances. It describes the morphological changes that occur in reversible cell injury, including swelling and fatty change, as well as irreversible cell injury known as necrosis. Necrosis results in loss of cell integrity and contents. The document outlines different patterns of tissue necrosis, such as coagulative, liquefactive, gangrenous, caseous, and fibrinoid necrosis.
Necrosis
Necrosis is irreversible injury and death of cells and living tissue. There are several patterns of necrosis that occur in tissues including coagulative, liquefactive, caseous, fat and gangrenous necrosis. Coagulative necrosis involves the maintenance of cell outlines but loss of cellular details. Liquefactive necrosis results in the disintegration and liquefaction of dead cells. Caseous necrosis converts dead tissue into a granular mass resembling cottage cheese.
Chronic inflammation
This document discusses chronic inflammation. It defines chronic inflammation as a prolonged inflammatory response lasting weeks or months where inflammation, tissue injury, and repair occur simultaneously. Chronic inflammation can be caused by persistent infections, hypersensitivity reactions, prolonged toxic exposures, or recurrent acute inflammation. It is characterized by mononuclear cell infiltration, tissue destruction or necrosis, and attempts at healing. Macrophages and lymphocytes are the major cell types involved. Macrophages play key roles through phagocytosis, tissue repair, and secreting inflammatory mediators. Chronic inflammation can also involve plasma cells, mast cells, and eosinophils and their mediators. Granulomatous inflammation is a specific type of chronic inflammation forming granulomas made of epithelio
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Cell injury-necrosis
Necrosis and apoptosis are both forms of cell death, but they differ significantly. Necrosis is premature cell death caused by external factors like infection, toxins, or physical trauma. It results in the uncontrolled release of cellular contents and causes inflammation. Apoptosis is programmed cell death that occurs as part of natural biological processes. It is an actively regulated and controlled process where cells play an active role in their own death, avoiding inflammation.
Lect.no.4
This document discusses different types of cell death, including apoptosis and necrosis. It describes necrosis as cell death resulting from external factors that cause irreversible injury. The key morphological changes seen with necrosis include increased cytoplasmic eosinophilia, nuclear pyknosis, karyorrhexis, and karyolysis. There are several patterns of necrosis depending on the mechanism and tissue involved, such as coagulative, liquefactive, caseous, and gangrene. Coagulative necrosis preserves tissue architecture while liquefactive necrosis destroys tissue structure. Gangrene refers to visible tissue necrosis, usually due to ischemia.
General pathology necrosis
Necrosis is the death of cells and living tissue. There are several types of necrosis that are characterized by the microscopic appearance of dead cells. Coagulative necrosis occurs due to ischemia and results in pale, swollen tissue on gross examination and swollen eosinophilic cells on microscopy. Liquefactive necrosis occurs due to infection and results in soft, cystic lesions containing debris. Caseous necrosis is seen in tuberculosis and resembles dry cheese with granular debris. Fat necrosis affects pancreatic and breast tissue, appearing as yellowish deposits containing calcium salts. Fibrinoid necrosis involves fibrin deposition in tissues damaged by immune processes.
Necrosis,gangrene and apoptosis
This document summarizes different types of cell death including autolysis, necrosis, gangrene, and apoptosis. It describes the morphology, causes, and characteristics of coagulative, liquefactive, caseous, fatty, fibrinoid, and gangrenous necrosis. The key differences between dry, wet, and gas gangrene are highlighted. The document also provides details on the initiation and execution phases of apoptosis, the role of caspases, and morphological and biochemical changes in apoptosis.
Cell injury
Cell injury can occur through various causes and results in either reversible or irreversible injury and cell death. Reversible injury involves changes that can be repaired if the stressor is removed, while irreversible injury leads to cell death through either necrosis or apoptosis. Necrosis is unprogrammed cell death that occurs due to external factors and results in cell contents leaking out and triggering inflammation. Apoptosis is programmed cell death where cells activate internal enzymes to degrade themselves without inflammatory response. The key differences between the two types of cell death include apoptosis affecting individual cells while necrosis affects groups of cells.
Causes of cell injury
This document discusses various causes of cell injury and death, including oxygen deprivation, physical agents, chemicals, infectious agents, immune reactions, genetic defects, and nutritional imbalances. It describes the morphological changes that occur in reversible cell injury, including swelling and fatty change, as well as irreversible cell injury known as necrosis. Necrosis results in loss of cell integrity and contents. The document outlines different patterns of tissue necrosis, such as coagulative, liquefactive, gangrenous, caseous, and fibrinoid necrosis.
Necrosis
Necrosis is irreversible injury and death of cells and living tissue. There are several patterns of necrosis that occur in tissues including coagulative, liquefactive, caseous, fat and gangrenous necrosis. Coagulative necrosis involves the maintenance of cell outlines but loss of cellular details. Liquefactive necrosis results in the disintegration and liquefaction of dead cells. Caseous necrosis converts dead tissue into a granular mass resembling cottage cheese.
Chronic inflammation
This document discusses chronic inflammation. It defines chronic inflammation as a prolonged inflammatory response lasting weeks or months where inflammation, tissue injury, and repair occur simultaneously. Chronic inflammation can be caused by persistent infections, hypersensitivity reactions, prolonged toxic exposures, or recurrent acute inflammation. It is characterized by mononuclear cell infiltration, tissue destruction or necrosis, and attempts at healing. Macrophages and lymphocytes are the major cell types involved. Macrophages play key roles through phagocytosis, tissue repair, and secreting inflammatory mediators. Chronic inflammation can also involve plasma cells, mast cells, and eosinophils and their mediators. Granulomatous inflammation is a specific type of chronic inflammation forming granulomas made of epithelio
Ch 2 adaptations, cell injury, cell death
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Necrosis vs apaptosis
Necrosis is cell death resulting from progressive degenerative action of enzymes on lethally injured cells. It begins with impaired homeostasis leading to water and ion influx. Morphological changes include nuclear condensation or fragmentation, cytoplasmic eosinophilia, organelle damage, and membrane rupture. There are three main types - coagulative, liquefactive, and caseous. Coagulative necrosis occurs in solid organs from ischemia. Liquefactive necrosis results from enzymatic autolysis and hydrolysis. Caseous necrosis forms dry, cheesy material seen in tuberculosis. Necrosis causes inflammation while apoptosis is an orderly programmed cell death.
Pathology cell injury i
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
Cell injury : Intracellular accumulations
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
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The document discusses the outcomes of acute inflammation and their morphological patterns. There are three potential outcomes of acute inflammation: 1) complete resolution, 2) healing by fibrosis, or 3) chronic inflammation. It also describes four main morphological patterns of acute inflammation: serous, fibrinous, suppurative (abscess formation), and ulcerative. Each pattern is associated with different clinical presentations and histological features.
Necrosis
Necrosis is the morphologic changes that follow cell death in living tissues. It can be caused by ischemia, physical agents, chemical agents, or immunological injury. The main types of necrosis include coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis, and fibrinoid necrosis. Coagulative necrosis preserves tissue architecture with denatured proteins and enzymatic digestion of cells. Liquefactive necrosis results in a liquid viscous mass. Caseous necrosis is a type of coagulative necrosis seen in tuberculosis that leaves cheesy white tissue.
Chronic inflammation
This document discusses chronic inflammation. It describes chronic inflammation as inflammation of prolonged duration involving ongoing inflammation, tissue injury, and attempts at repair. Chronic inflammation is characterized by mononuclear cell infiltration, tissue destruction, and attempts at healing through fibrosis and angiogenesis. Macrophages are a key player in chronic inflammation by secreting cytokines, growth factors, enzymes, and other inflammatory mediators that can cause both inflammatory tissue injury and repair. Granulomatous inflammation is a distinctive pattern of chronic inflammation seen in some infectious and noninfectious conditions, where macrophages form aggregates surrounded by lymphocytes called granulomas in an attempt to control difficult to eradicate agents.
Apoptosis
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Cell injury and degenerations
This document discusses cell injury, adaptations, and degenerations in pathology. It begins by defining key terms like etiology, pathogenesis, and morphology. It then explains the causes of cell injury including hypoxia, physical agents, chemicals, microbes, and immune reactions. The document delves into the pathogenesis of cell injury, noting factors like the type, duration, and severity of the injurious agent and target cell characteristics. It also describes the mechanisms of cell injury such as ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects. Finally, it distinguishes between reversible and irreversible cell injury.
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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.
Chronic granulomatous inflammation
Chronic granulomatous inflammation is a distinctive pattern of chronic inflammation caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. It functions as a protective response, restricting inflammation and preventing the dissemination of chronic infections or foreign materials. Granulomas are nodular lesions containing giant cells and epithelioid cells that form around the chronic irritant. Common causes that can elicit granulomatous inflammation include tuberculosis, leprosy, schistosomiasis, histoplasmosis, blastomycosis, berylliosis, and sarcoidosis.
chronic inflammation
Chronic inflammation is a prolonged host response to persistent stimuli that involves lymphocytes, macrophages, plasma cells, and mast cells. It is characterized by infiltration of mononuclear cells and macrophages, tissue destruction by inflammatory cells, and attempts at healing through fibrosis and angiogenesis. Chronic inflammation can result from acute inflammation turning persistent, infections, hypersensitivity, or prolonged toxic exposure. It causes diseases like atherosclerosis, tuberculosis, and rheumatoid arthritis. Granulomatous inflammation is a form of chronic inflammation seen in diseases like tuberculosis that involves collections of epithelioid macrophages and giant cells forming granulomas.
Necrosis
Necrosis is the death of cells and living tissue. There are several types of necrosis including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the preservation of the basic cellular structure but loss of cellular details. Liquefactive necrosis results in the transformation of tissue into a liquid mass where all cellular and architectural details are lost. Caseous necrosis converts dead tissue into a cheesy-like granular mass where no cellular or architectural details remain. The document further describes the characteristics, causes, and microscopic appearance of each type of necrosis.
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.
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.
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Healing and repair
1. Tissue repair involves regeneration of injured tissue or replacement by connective tissue scarring. It involves cell proliferation and interaction between cells and the extracellular matrix.
2. Tissues are divided into continuously dividing, stable, and permanent groups based on their ability to proliferate. Continuously dividing tissues like skin regenerate easily while permanent tissues like neurons cannot regenerate after injury.
3. Growth factors and the extracellular matrix play important roles in tissue repair by stimulating cell growth and movement. Repair occurs through regeneration in labile tissues and scarring in others when injury is too severe for regeneration.
Cell Injury
This document outlines different types of cell injury and death. It begins by defining cell injury as occurring when stress exceeds a cell's ability to adapt. Reversible cell injury involves swelling while irreversible injury involves membrane damage, ultimately leading to cell death via either necrosis or apoptosis. Necrosis is unprogrammed cell death from pathology, resulting in inflammation, while apoptosis is genetically programmed single-cell death without inflammation. Various patterns of necrosis are described, including coagulative, liquefactive, and caseous necrosis. Apoptosis involves cell and nuclear shrinkage followed by organized nuclear fragmentation and removal of apoptotic bodies by macrophages.
Necrosis and apoptosis
This document discusses necrosis and apoptosis. It defines necrosis as the premature death of cells in living tissue due to irreversible injury. Necrosis can be caused by ischemia, physical agents, chemicals, or immunological injury. There are several types of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis. Treatment involves debridement and excision of dead tissue. Apoptosis is programmed cell death that occurs as part of normal development and tissue homeostasis. It is mediated by caspases and involves cell shrinkage, chromatin condensation, and fragmentation into apoptotic bodies that are phagocytosed. Dysregulation of apoptosis can contribute to diseases.
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This is a presentation on the topic of Adaptations, Cell injury and cell death, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Necrosis vs apaptosis
Necrosis is cell death resulting from progressive degenerative action of enzymes on lethally injured cells. It begins with impaired homeostasis leading to water and ion influx. Morphological changes include nuclear condensation or fragmentation, cytoplasmic eosinophilia, organelle damage, and membrane rupture. There are three main types - coagulative, liquefactive, and caseous. Coagulative necrosis occurs in solid organs from ischemia. Liquefactive necrosis results from enzymatic autolysis and hydrolysis. Caseous necrosis forms dry, cheesy material seen in tuberculosis. Necrosis causes inflammation while apoptosis is an orderly programmed cell death.
Pathology cell injury i
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
Cell injury : Intracellular accumulations
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
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Necrosis
Necrosis is the morphologic changes that follow cell death in living tissues. It can be caused by ischemia, physical agents, chemical agents, or immunological injury. The main types of necrosis include coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis, and fibrinoid necrosis. Coagulative necrosis preserves tissue architecture with denatured proteins and enzymatic digestion of cells. Liquefactive necrosis results in a liquid viscous mass. Caseous necrosis is a type of coagulative necrosis seen in tuberculosis that leaves cheesy white tissue.
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This document discusses chronic inflammation. It describes chronic inflammation as inflammation of prolonged duration involving ongoing inflammation, tissue injury, and attempts at repair. Chronic inflammation is characterized by mononuclear cell infiltration, tissue destruction, and attempts at healing through fibrosis and angiogenesis. Macrophages are a key player in chronic inflammation by secreting cytokines, growth factors, enzymes, and other inflammatory mediators that can cause both inflammatory tissue injury and repair. Granulomatous inflammation is a distinctive pattern of chronic inflammation seen in some infectious and noninfectious conditions, where macrophages form aggregates surrounded by lymphocytes called granulomas in an attempt to control difficult to eradicate agents.
Apoptosis
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
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This document discusses cell injury, adaptations, and degenerations in pathology. It begins by defining key terms like etiology, pathogenesis, and morphology. It then explains the causes of cell injury including hypoxia, physical agents, chemicals, microbes, and immune reactions. The document delves into the pathogenesis of cell injury, noting factors like the type, duration, and severity of the injurious agent and target cell characteristics. It also describes the mechanisms of cell injury such as ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects. Finally, it distinguishes between reversible and irreversible cell injury.
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Chronic granulomatous inflammation
Chronic granulomatous inflammation is a distinctive pattern of chronic inflammation caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. It functions as a protective response, restricting inflammation and preventing the dissemination of chronic infections or foreign materials. Granulomas are nodular lesions containing giant cells and epithelioid cells that form around the chronic irritant. Common causes that can elicit granulomatous inflammation include tuberculosis, leprosy, schistosomiasis, histoplasmosis, blastomycosis, berylliosis, and sarcoidosis.
chronic inflammation
Chronic inflammation is a prolonged host response to persistent stimuli that involves lymphocytes, macrophages, plasma cells, and mast cells. It is characterized by infiltration of mononuclear cells and macrophages, tissue destruction by inflammatory cells, and attempts at healing through fibrosis and angiogenesis. Chronic inflammation can result from acute inflammation turning persistent, infections, hypersensitivity, or prolonged toxic exposure. It causes diseases like atherosclerosis, tuberculosis, and rheumatoid arthritis. Granulomatous inflammation is a form of chronic inflammation seen in diseases like tuberculosis that involves collections of epithelioid macrophages and giant cells forming granulomas.
Necrosis
Necrosis is the death of cells and living tissue. There are several types of necrosis including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the preservation of the basic cellular structure but loss of cellular details. Liquefactive necrosis results in the transformation of tissue into a liquid mass where all cellular and architectural details are lost. Caseous necrosis converts dead tissue into a cheesy-like granular mass where no cellular or architectural details remain. The document further describes the characteristics, causes, and microscopic appearance of each type of necrosis.
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.
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.
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1. Tissue repair involves regeneration of injured tissue or replacement by connective tissue scarring. It involves cell proliferation and interaction between cells and the extracellular matrix.
2. Tissues are divided into continuously dividing, stable, and permanent groups based on their ability to proliferate. Continuously dividing tissues like skin regenerate easily while permanent tissues like neurons cannot regenerate after injury.
3. Growth factors and the extracellular matrix play important roles in tissue repair by stimulating cell growth and movement. Repair occurs through regeneration in labile tissues and scarring in others when injury is too severe for regeneration.
Cell Injury
This document outlines different types of cell injury and death. It begins by defining cell injury as occurring when stress exceeds a cell's ability to adapt. Reversible cell injury involves swelling while irreversible injury involves membrane damage, ultimately leading to cell death via either necrosis or apoptosis. Necrosis is unprogrammed cell death from pathology, resulting in inflammation, while apoptosis is genetically programmed single-cell death without inflammation. Various patterns of necrosis are described, including coagulative, liquefactive, and caseous necrosis. Apoptosis involves cell and nuclear shrinkage followed by organized nuclear fragmentation and removal of apoptotic bodies by macrophages.
Necrosis and apoptosis
This document discusses necrosis and apoptosis. It defines necrosis as the premature death of cells in living tissue due to irreversible injury. Necrosis can be caused by ischemia, physical agents, chemicals, or immunological injury. There are several types of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis. Treatment involves debridement and excision of dead tissue. Apoptosis is programmed cell death that occurs as part of normal development and tissue homeostasis. It is mediated by caspases and involves cell shrinkage, chromatin condensation, and fragmentation into apoptotic bodies that are phagocytosed. Dysregulation of apoptosis can contribute to diseases.
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Tooth development begins with the formation of the primary epithelial band in the embryo. This band gives rise to the dental lamina, from which tooth buds develop. The buds grow through the bud, cap, and bell stages as the enamel organ and dental papilla form and differentiate. Teeth then continue developing through the formation of dentin, enamel, and cementum to erupt in the mouth at the appropriate time.
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NECROSIS by Shabistan.pptx
The term necrosis is derived from a greek word nekros which means dead body.
Definition: Necrosis is defined as local or focal death of cells along with degradation of tissues by hydrolytic enzymes released from lysosome of the cell.
It is often associated with surrounding inflammatory reaction.
Necrosis is a series of morphological changes that follows cell death due to the irreversible cell injury/lethal cell injury/pathological cell injury.
Difference between Apoptosis versus Necrosis and Types of Necrosis.pptx
Apoptosis Versus Nercosis
Apoptosis Necrosis
Predefined cell suicide or programmed cell death. Natural physiological Process. Involve one cell at a time. Cell shrinkage (Dense eosinophilic cytoplasm) Pyknosis (Condensation) and Karyorrhexis (fragmentation) of nuclear material Formation of membrane blebs and apoptotic bodies
Phagocytosis of apoptotic bodies by Macrophages
Caspase dependent pathway
No Inflammation (no immune response) Premature, unprogrammed cell death always pathological. Involve many cells Cell Swelling (Swelling of endoplasmic reticulum and mitochondria) and membrane blebs Pyknosis (condensation), Karyorrhexis (Fragmentation) and Karyolysis (lysis)of the nucleus. Breakdown of the plasma membrane, organelles (enzymatic digestion), leakage of cellular contents
Increased eosinophilia, Accumulation of Myelin figures (whorled precipitated Phospholipids)
Initiate Inflammation (Strong immune response)
Necrosis and apoptosis
This document provides an overview of necrosis and apoptosis. It defines necrosis as cell death resulting from external injury to cells, characterized by swelling and organelle breakdown. Apoptosis is defined as tightly regulated programmed cell suicide. The document discusses the morphology of necrosis under light microscopy and different types of necrosis. It then covers the mechanism, morphology, and triggers of apoptosis. Key differences between necrosis and apoptosis are that necrosis elicits inflammation while apoptosis does not and apoptosis is a tightly regulated process.
necrosis-160906190127.pptx
Necrosis is irreversible injury and death of cells and living tissue. There are several patterns of necrosis that can occur in tissues including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the maintenance of cell outlines but loss of cellular details. The dead tissues remain in the body for a long period. Liquefactive necrosis results from the rapid dissolution of dead cells, often leading to abscess formation. Caseous necrosis converts dead tissue into a granular mass resembling cottage cheese, associated with tuberculosis lesions.
Cell death.pptx
Cellular injury and cell death can occur through necrosis or apoptosis. Necrosis is unregulated cell death due to external factors like hypoxia or toxins. It is characterized by cellular swelling, membrane rupture, and inflammatory responses. Apoptosis is regulated cell death that occurs normally or in response to DNA damage. The cell shrinks and fragments into membrane-bound vesicles that are phagocytosed without inflammation. Both can result from ATP depletion, calcium flux, reactive oxygen species, or endoplasmic reticulum stress. The pattern of necrosis in tissue provides clues to the underlying cause, such as coagulative necrosis from ischemia.
cell necrosis , apoptosis presentation.pdf
Cellular injury and cell death can occur through several mechanisms:
1. Reversible injury may occur when cells are stressed but can still adapt through changes like swelling. Irreversible injury leads to cell death.
2. Necrosis is caused by severe damage where cell contents leak out. Apoptosis is a programmed form of cell death where the cell dismantles itself. Autophagy is a process where cells digest their own components.
3. The causes of cellular injury include hypoxia, physical and chemical agents, infectious agents, immunological reactions, and genetic or nutritional factors. Cell death is identifiable through morphology changes in microscopy.
cell injury.pptx
Reversible cell injury results in cellular swelling and fatty change due to failure of ion pumps and appearance of lipid vacuoles. If injury persists, irreversible changes occur like membrane damage, mitochondrial damage, calcium influx, and reactive oxygen species accumulation leading to cell death by necrosis or apoptosis. Necrosis involves loss of membrane integrity while apoptosis is a regulated pathway of cell fragmentation and phagocytosis.
Cell death.pptx
Cell death can occur through two main processes: necrosis and apoptosis. Necrosis is unregulated cell death caused by external factors like trauma or toxins. It involves the premature death of cells and tissue damage. Apoptosis is a tightly regulated form of programmed cell death that eliminates unnecessary or potentially dangerous cells. It involves changes to the cell like nuclear fragmentation, blebbing of the cell membrane, and formation of apoptotic bodies that are then cleared by phagocytes without inducing inflammation. Apoptosis plays an important role in development, homeostasis, and eliminating infected or damaged cells.
6 cell injury2
This document discusses various types of cell injury and growth disturbances. It describes reversible cell injury known as degeneration, which includes cloudy swelling and hydropic change caused by mild injury and accumulation of water in cells. Prolonged or severe injury can lead to irreversible necrosis or programmed cell death known as apoptosis. Fatty change is also a type of reversible degeneration caused by accumulation of lipids in cells. Different types of necrosis like coagulative, liquefactive, and caseous are outlined. The document also discusses cellular changes seen in apoptosis. Various growth disturbances like atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, and neoplasia are defined and examples provided.
1590180412.pptx
Necrosis is the death of cells and living tissue. It is characterized by cellular swelling, breakdown of organelles, and denaturation of proteins. The main types of necrosis include coagulative, caseous, fat, liquefactive, and fibrinoid necrosis. Coagulative necrosis occurs from ischemia and results in preservation of cell outlines. Caseous necrosis is seen in tuberculosis and has a cheesy appearance. Fat necrosis involves destruction of fat cells. Liquefactive necrosis causes tissue liquefaction by hydrolytic enzymes. Fibrinoid necrosis features deposition of fibrin-like material in blood vessels. Necrosis can lead to inflammation, fibrosis, calcification, or cyst formation over time.
Necrosis.pathology lecture slideshare.pptx
Necrosis is cell death caused by external factors like lack of oxygen, toxins, burns or trauma. There are several types of necrosis including coagulative where tissue structure is preserved, liquefactive where cells are digested, and gangrenous which often involves bacterial infection. Necrotic cells appear eosinophilic on staining and show features like nuclear dissolution or fragmentation. Clinical signs include pain, swelling and spreading skin redness.
Pathology Cell Injury and cell adaptation
Cell injury and cell adaptation--Mbbs / Bams 2nd year Pathology topic
Cell injury l2 medical sept. 2018
This document provides an overview of cell injury, specifically necrosis and apoptosis. It discusses several types of necrosis including coagulative, liquefactive, caseous, gangrenous, fibrinoid, and fat necrosis. Apoptosis is defined as programmed cell death that is regulated by death pathway genes and involves cell shrinkage, chromatin condensation, blebbing, and phagocytosis without inflammation. Key differences between necrosis and apoptosis are highlighted, such as necrosis resulting from irreversible injury and inflammation, while apoptosis is a regulated process without inflammation.
APOPTOSIS NECROSIS.pptx
The document discusses various types of cell death including apoptosis, necrosis, autolysis, and gangrene. It provides details on the morphology, causes, and characteristics of each type. Apoptosis is defined as programmed cell death that is tightly regulated. It involves cell shrinkage, nuclear fragmentation, blebbing and formation of apoptotic bodies that are then phagocytosed. Necrosis is unregulated cell death caused by external factors like toxins and hypoxia. It results in cell swelling and lysosomal enzyme release. The document contrasts the features of apoptosis and necrosis and discusses the molecular pathways and caspase activation involved in apoptosis.
Causesofcellinjury
This document discusses various causes of cell injury and death, including oxygen deprivation, physical agents, chemicals, infectious agents, immune reactions, genetic defects, and nutritional imbalances. It describes the morphological changes that occur in reversible cell injury, including swelling and fatty change, as well as the changes that characterize irreversible injury or necrosis, such as increased eosinophilia, loss of structure, and membrane breakdown. Different patterns of tissue necrosis are also outlined, such as coagulative, liquefactive, gangrenous, and caseous necrosis.
cell injury apotosis necrosis.pptx
Cell injury can result from various causes like hypoxia, infections, chemicals, or genetic abnormalities. Injured cells may adapt, die through necrosis or apoptosis, or experience reversible injury. Necrosis is unprogrammed cell death where the cell loses membrane integrity and undergoes physical changes like swelling and nuclear fragmentation. Apoptosis is programmed cell death where the cell remains intact until phagocytosis in a non-inflammatory manner. Different types of necrosis include coagulative, liquefactive, caseous, and gangrenous necrosis.
Necrosis.pptx definition, types, examples
Necrosis is irreversible cell injury that can occur through several mechanisms and patterns. It involves severe damage to cell membranes leading to loss of integrity and contents leaking out. Morphological changes include nuclear changes like pyknosis, karyorrhexis, and karyolysis as well as cytoplasmic changes like dense eosinophilic cytoplasm and vacuolization. The main patterns discussed are coagulative necrosis, where architecture is preserved; liquefactive necrosis, where tissues digest into pus; and caseous necrosis, seen in tuberculosis as cheesy white areas.
02-Necrosis and apoptosis-1.ppt
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Necrosis
The spectrum of morphological changes that leads to cell death within a living tissue
Cell death due to an irreversible cell injury
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Necrosis sheril
- 1. Necrosis By- Sheril S. Philip 15BCB0120
- 2. • Define necrosis and apoptosis • List the different types of necrosis, examples of each and its features • List the different conditions associated with apoptosis, its morphology and its mechanism • Know the difference between apoptosis and necrosis CONTENTS
- 3. Define necrosis and apoptosis List the different types of necrosis, examples of each and its features List the different conditions associated with apoptosis, its morphology and its mechanism Know the difference between apoptosis and necrosis
- 4. Cell Death Death of cells occurs in two ways: 1. Necrosis--(irreversible injury) changes produced by enzymatic digestion of dead cellular elements 2. Apoptosis--vital process that helps eliminate unwanted cells--an internally programmed series of events effected by dedicated gene products
- 5. Morphology of necrosis : 1. Cellular swelling or rupture 2. Denaturation and coagulation of cytoplasmic proteins 3. Breakdown of cell organelles 4. Breakdown of nuclear DNA
- 6. Patterns of Necrosis In Tissues or Organs As a result of cell death the tissues or organs display one of these six macroscopic changes: 1. Coagulative necrosis 2. Liquifactive necrosis 3. Caseous necrosis 4. Fat necrosis 5. Gangrenous necrosis 6. Fibrinoid necrosis
- 7. Patterns of Necrosis In Tissues or Organs 1. Coagulative necrosis: the outline of the dead cells are maintained and the tissue is somewhat firm. Example: myocardial infarction 1. Liquefactive necrosis: the dead cells undergo disintegration and affected tissue is liquefied. Example: cerebral infarction.
- 8. Patterns of Necrosis In Tissues or Organs 3. Caseous necrosis: a form of coagulative necrosis (cheese-like). Example: tuberculosis lesions. 4. Fat necrosis: enzymatic digestion of fat. Example: necrosis of fat by pancreatic enzymes. 5. Gangrenous necrosis: Necrosis (secondary to ischemia) usually with superimposed infection. Example: necrosis of distal limbs, usually foot and toes in diabetes. 6. Fibrinoid necrosis: typically seen in vasculitis and glomerular autoimmune diseases
- 9. Coagulative Necrosis Changes in the cytoplasm and the nucleus Karyolysis Pyknosis Karyorrhexis
- 10. Necrosis of the liver induced by herpesvirus. Herpesvirus invades liver cell nuclei producing nuclear ('ground glass') mildly basophilic inclusions.
- 11. Acute renal tubular necrosis (ischemia) : increased eosinophilia and pyknosis in necrotic cells Normal Necrotic
- 12. Ischemic neuronal injury:acidophilic cytoplasm & nuclear pyknosis
- 13. … a mess - so many cells have died - the tissue is not recognizable. Nuclei have become pyknotic (shrunken and dark), undergone karorrhexis (fragmentation) and karyolysis(dissolution) Necrotic myocardium
- 14. Kidney: ischemia and infarction (loss of blood supply and resultant tissue anoxia). Coagulative necrosis Removal of the dead tissue leaves behind a scar
- 15. Infarcts (vascular distribution) are wedge-shaped with a base on the organ capsule. Coagulative necrosis: is due to loss of blood supply Spleen
- 16. Depending on circumstances: 1. necrotic tissue may be walled off by scar tissue, 2. totally converted to scar tissue, 3. get destroyed (producing a cavity or cyst), 4. get infected (producing an abscess or "wet gangrene"), 5. or calcify. If the supporting tissue framework does not die, and the dead cells are of a type capable of regeneration, you may have complete healing. Remember: True coagulation necrosis involves groups of cells, and is almost always accompanied, by acute inflammation (infiltrate)