Apoptosis is a tightly regulated and genetically programmed form of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins. Cells undergoing apoptosis break into fragments called apoptotic bodies that are phagocytosed without eliciting inflammation. Apoptosis eliminates damaged or unneeded cells and plays an important role in development, tissue homeostasis, and the removal of infected or abnormal cells. It involves cell shrinkage, chromatin condensation, blebbing of the cell membrane, and the formation of apoptotic bodies that are phagocytosed without inflammatory response.
This document discusses cellular aging and theories of aging. It covers several key points:
1) Cellular senescence and the Hayflick limit, where cells stop dividing after a certain number of divisions.
2) Theories of aging including the free radical theory, somatic mutation theory, and telomere loss theory.
3) Types of cell death including apoptosis, necrosis, necroptosis, and pyroptosis. Programmed cell death limits inflammation while necrosis causes damage and inflammation.
This document provides an overview of cellular injury and cell death. It defines cell injury and explains the processes of reversible and irreversible injury. The mechanisms of cellular injury include impaired cell membrane function, decreased energy production, genetic alterations, and metabolic imbalances. Causes of injury include hypoxia, physical and chemical agents, infections, and free radicals. The document describes necrosis as irreversible cell injury involving enzymatic degradation and protein denaturation. Apoptosis is defined as a vital process of programmed cell death to eliminate unwanted cells. Morphological changes of necrosis and apoptosis are compared.
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.
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.
Apoptosis is a tightly regulated and genetically programmed form of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins. Cells undergoing apoptosis break into fragments called apoptotic bodies that are phagocytosed without eliciting inflammation. Apoptosis eliminates damaged or unneeded cells and plays an important role in development, tissue homeostasis, and the removal of infected or abnormal cells. It involves cell shrinkage, chromatin condensation, blebbing of the cell membrane, and the formation of apoptotic bodies that are phagocytosed without inflammatory response.
This document discusses cellular aging and theories of aging. It covers several key points:
1) Cellular senescence and the Hayflick limit, where cells stop dividing after a certain number of divisions.
2) Theories of aging including the free radical theory, somatic mutation theory, and telomere loss theory.
3) Types of cell death including apoptosis, necrosis, necroptosis, and pyroptosis. Programmed cell death limits inflammation while necrosis causes damage and inflammation.
This document provides an overview of cellular injury and cell death. It defines cell injury and explains the processes of reversible and irreversible injury. The mechanisms of cellular injury include impaired cell membrane function, decreased energy production, genetic alterations, and metabolic imbalances. Causes of injury include hypoxia, physical and chemical agents, infections, and free radicals. The document describes necrosis as irreversible cell injury involving enzymatic degradation and protein denaturation. Apoptosis is defined as a vital process of programmed cell death to eliminate unwanted cells. Morphological changes of necrosis and apoptosis are compared.
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.
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.
11.20 (dr. yasmeen hashim) apoptosis (mechanism in normal tissues. programmed...Fati Naqvi
1. Apoptosis and necrosis are two main types of cell death. Apoptosis is programmed cell death that plays an important role in development and maintaining tissue homeostasis, while necrosis is unregulated cell death caused by external factors like injury.
2. Cancer develops due to mutations in genes that regulate cell growth, allowing cells to proliferate uncontrollably. Cancer cells evade apoptosis and are able to metastasize, or spread to other parts of the body. Abnormalities in apoptosis may contribute to diseases like cancer, neurodegeneration, and autoimmune disorders.
NECROSIS AND APOPTOSIS POWERPOINT PRESENTATIONJeenaRaj10
This document discusses different types of cell death: necrosis, apoptosis, and necroptosis. Necrosis is unprogrammed cell death due to external factors like toxins or hypoxia. Apoptosis is programmed cell death that helps eliminate unwanted cells through activation of genes and enzymes. Necroptosis shares characteristics of both necrosis and apoptosis - it is caspase-independent cell death triggered by signaling pathways involving the kinases RIPK1 and RIPK3, which phosphorylate MLKL leading to plasma membrane disruption and cell rupture in a programmed manner. Necroptosis plays roles in processes like bone growth, diseases like pancreatitis, and host defense against viruses.
This document discusses apoptosis and necrosis. It begins by outlining the objectives of describing the differences between necrosis and apoptosis, the mechanisms and pathways of apoptosis, and implications of cellular aging. Necrosis is defined as progressive cell disintegration initiated by overwhelming stress, while apoptosis is a tightly regulated suicide program. The intrinsic mitochondrial pathway and extrinsic death receptor pathway converge in the execution phase through caspase activation, resulting in DNA fragmentation and phagocytosis of apoptotic bodies without inflammation. Physiologic and pathologic examples of apoptosis are provided.
Apoptosis is a tightly regulated process of programmed cell death where cells activate enzymes to degrade their own DNA and proteins. The plasma membrane remains intact but becomes a target for phagocytes. The dead cell and fragments are rapidly consumed before contents can leak out, preventing inflammation. Apoptosis eliminates damaged, unneeded, or harmful cells and occurs during development, tissue remodeling, and to limit damage from infections or DNA damage. It is characterized by cell shrinkage, chromatin condensation, and fragmentation into membrane-bound apoptotic bodies.
Cell death occurs through two main forms: apoptosis and necrosis. Apoptosis is programmed cell death where cells undergo changes like DNA fragmentation and shrinkage in a way that avoids damaging nearby cells. Necrosis is unprogrammed cell death due to external factors like injury or internal issues. During necrosis, cells lose metabolic function and membrane integrity, organelles swell, and cell contents may leak out. Necrosis can occur through several types including coagulative, liquefactive, and gangrenous necrosis. Autophagy is a process where cells digest damaged organelles through the formation and fusion of vesicles to maintain cellular homeostasis.
This document provides an introduction to general pathology, which is concerned with the study of cellular and tissue-level changes that underlie disease. It discusses the causes of cell injury, including physical, chemical, infectious, immunological, nutritional, and genetic factors. Reversible cell injury features swelling and changes to organelles that are repairable, while irreversible injury leads to cell death through necrosis or apoptosis. Necrosis is characterized by loss of membrane integrity and digestion of cellular contents, resulting in increased eosinophilia and nuclear changes like karyolysis, pyknosis, and karyorrhexis. Different types of necrosis include coagulative, liquefactive, caseous, and fibrinoid.
There are two main forms of cell death: apoptosis and necrosis. Apoptosis is programmed cell death that occurs during normal cell turnover or in response to DNA damage. It involves nuclear fragmentation and formation of apoptotic bodies that are phagocytosed without inflammation. Necrosis is unregulated cell death due to injury and involves cell contents leaking out, triggering inflammation. There are several patterns of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis.
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.
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.
This document discusses various types of cellular adaptations, injuries, and deaths. It describes adaptations like hypertrophy and hyperplasia that occur in response to stress. It also discusses different types of cell injuries and deaths including necrosis, apoptosis, necroptosis, and pyroptosis. Various intracellular accumulations are also summarized such as lipids, proteins, glycogen, and pigments.
This document describes patterns of acute cell injury, including reversible and irreversible injury. Reversible injury includes cellular swelling and fatty change. Irreversible injury results in cell death through either necrosis or apoptosis. Necrosis is unprogrammed cell death that results from external factors and leads to inflammation. Apoptosis is programmed cell death that occurs physiologically during development and pathologically to remove damaged cells, resulting in cell shrinkage and fragmentation without inflammation.
Cell death can occur through two main processes: apoptosis and necrosis. Apoptosis is programmed cell death that occurs under normal physiological conditions, triggered by intracellular signals. The cell shrinks and fragments into apoptotic bodies that are phagocytosed, avoiding inflammation. Necrosis is accidental cell death due to external factors like trauma or toxins, where the cell lyses and releases intracellular contents, potentially causing tissue damage and inflammation. Both processes are important for development, tissue homeostasis, and removal of damaged cells.
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
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.
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.
Cell injury can be reversible or irreversible, leading to cell death. Reversible injury causes pathological changes that can be reversed when the stressor is removed, while irreversible injury causes permanent changes and cell death. Cell injury is caused by various stressors like hypoxia, physical/chemical agents, microbiological agents, genetic defects, and nutritional imbalances. The key targets of injury are the mitochondria, cell membrane, proteins, cytoskeleton, and DNA. Injury disrupts cellular energy production and increases reactive oxygen species, calcium influx, and damage to membranes and DNA/proteins. This can lead to either reversible injury or the irreversible processes of necrosis or apoptosis.
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.
This document summarizes different aspects of cell injury, inflammation, and cell death:
Cell injury can be lethal or non-lethal, with non-lethal injury causing cell degeneration and lethal injury resulting in cell death through apoptosis or necrosis. Necrosis is unprogrammed cell death that can take various forms depending on the affected cells. Inflammation is the body's response to injury and aims to remove damaged tissue to promote healing. The causes of cell injury and inflammation are also the causes of tissue damage, and inflammation is characterized by cardinal signs like pain, redness, heat, and swelling.
This document discusses cell injury and cell death. It begins by introducing pathology and defining etiology and pathogenesis. It then describes the cellular responses to stress, including adaptation and reversible injury. If stress is severe or persistent, it can lead to irreversible injury and cell death through necrosis or apoptosis. The document outlines the mechanisms and morphologies of different types of necrosis and apoptosis. It also discusses other pathways of cell death like necroptosis and pyroptosis. Causes of cell injury discussed include hypoxia, ischemia, oxidative stress, toxins, DNA damage, and inflammation. Reversible injury and cell death are important concepts for understanding disease pathogenesis.
11.20 (dr. yasmeen hashim) apoptosis (mechanism in normal tissues. programmed...Fati Naqvi
1. Apoptosis and necrosis are two main types of cell death. Apoptosis is programmed cell death that plays an important role in development and maintaining tissue homeostasis, while necrosis is unregulated cell death caused by external factors like injury.
2. Cancer develops due to mutations in genes that regulate cell growth, allowing cells to proliferate uncontrollably. Cancer cells evade apoptosis and are able to metastasize, or spread to other parts of the body. Abnormalities in apoptosis may contribute to diseases like cancer, neurodegeneration, and autoimmune disorders.
NECROSIS AND APOPTOSIS POWERPOINT PRESENTATIONJeenaRaj10
This document discusses different types of cell death: necrosis, apoptosis, and necroptosis. Necrosis is unprogrammed cell death due to external factors like toxins or hypoxia. Apoptosis is programmed cell death that helps eliminate unwanted cells through activation of genes and enzymes. Necroptosis shares characteristics of both necrosis and apoptosis - it is caspase-independent cell death triggered by signaling pathways involving the kinases RIPK1 and RIPK3, which phosphorylate MLKL leading to plasma membrane disruption and cell rupture in a programmed manner. Necroptosis plays roles in processes like bone growth, diseases like pancreatitis, and host defense against viruses.
This document discusses apoptosis and necrosis. It begins by outlining the objectives of describing the differences between necrosis and apoptosis, the mechanisms and pathways of apoptosis, and implications of cellular aging. Necrosis is defined as progressive cell disintegration initiated by overwhelming stress, while apoptosis is a tightly regulated suicide program. The intrinsic mitochondrial pathway and extrinsic death receptor pathway converge in the execution phase through caspase activation, resulting in DNA fragmentation and phagocytosis of apoptotic bodies without inflammation. Physiologic and pathologic examples of apoptosis are provided.
Apoptosis is a tightly regulated process of programmed cell death where cells activate enzymes to degrade their own DNA and proteins. The plasma membrane remains intact but becomes a target for phagocytes. The dead cell and fragments are rapidly consumed before contents can leak out, preventing inflammation. Apoptosis eliminates damaged, unneeded, or harmful cells and occurs during development, tissue remodeling, and to limit damage from infections or DNA damage. It is characterized by cell shrinkage, chromatin condensation, and fragmentation into membrane-bound apoptotic bodies.
Cell death occurs through two main forms: apoptosis and necrosis. Apoptosis is programmed cell death where cells undergo changes like DNA fragmentation and shrinkage in a way that avoids damaging nearby cells. Necrosis is unprogrammed cell death due to external factors like injury or internal issues. During necrosis, cells lose metabolic function and membrane integrity, organelles swell, and cell contents may leak out. Necrosis can occur through several types including coagulative, liquefactive, and gangrenous necrosis. Autophagy is a process where cells digest damaged organelles through the formation and fusion of vesicles to maintain cellular homeostasis.
This document provides an introduction to general pathology, which is concerned with the study of cellular and tissue-level changes that underlie disease. It discusses the causes of cell injury, including physical, chemical, infectious, immunological, nutritional, and genetic factors. Reversible cell injury features swelling and changes to organelles that are repairable, while irreversible injury leads to cell death through necrosis or apoptosis. Necrosis is characterized by loss of membrane integrity and digestion of cellular contents, resulting in increased eosinophilia and nuclear changes like karyolysis, pyknosis, and karyorrhexis. Different types of necrosis include coagulative, liquefactive, caseous, and fibrinoid.
There are two main forms of cell death: apoptosis and necrosis. Apoptosis is programmed cell death that occurs during normal cell turnover or in response to DNA damage. It involves nuclear fragmentation and formation of apoptotic bodies that are phagocytosed without inflammation. Necrosis is unregulated cell death due to injury and involves cell contents leaking out, triggering inflammation. There are several patterns of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis.
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.
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.
This document discusses various types of cellular adaptations, injuries, and deaths. It describes adaptations like hypertrophy and hyperplasia that occur in response to stress. It also discusses different types of cell injuries and deaths including necrosis, apoptosis, necroptosis, and pyroptosis. Various intracellular accumulations are also summarized such as lipids, proteins, glycogen, and pigments.
This document describes patterns of acute cell injury, including reversible and irreversible injury. Reversible injury includes cellular swelling and fatty change. Irreversible injury results in cell death through either necrosis or apoptosis. Necrosis is unprogrammed cell death that results from external factors and leads to inflammation. Apoptosis is programmed cell death that occurs physiologically during development and pathologically to remove damaged cells, resulting in cell shrinkage and fragmentation without inflammation.
Cell death can occur through two main processes: apoptosis and necrosis. Apoptosis is programmed cell death that occurs under normal physiological conditions, triggered by intracellular signals. The cell shrinks and fragments into apoptotic bodies that are phagocytosed, avoiding inflammation. Necrosis is accidental cell death due to external factors like trauma or toxins, where the cell lyses and releases intracellular contents, potentially causing tissue damage and inflammation. Both processes are important for development, tissue homeostasis, and removal of damaged cells.
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
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.
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.
Cell injury can be reversible or irreversible, leading to cell death. Reversible injury causes pathological changes that can be reversed when the stressor is removed, while irreversible injury causes permanent changes and cell death. Cell injury is caused by various stressors like hypoxia, physical/chemical agents, microbiological agents, genetic defects, and nutritional imbalances. The key targets of injury are the mitochondria, cell membrane, proteins, cytoskeleton, and DNA. Injury disrupts cellular energy production and increases reactive oxygen species, calcium influx, and damage to membranes and DNA/proteins. This can lead to either reversible injury or the irreversible processes of necrosis or apoptosis.
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.
This document summarizes different aspects of cell injury, inflammation, and cell death:
Cell injury can be lethal or non-lethal, with non-lethal injury causing cell degeneration and lethal injury resulting in cell death through apoptosis or necrosis. Necrosis is unprogrammed cell death that can take various forms depending on the affected cells. Inflammation is the body's response to injury and aims to remove damaged tissue to promote healing. The causes of cell injury and inflammation are also the causes of tissue damage, and inflammation is characterized by cardinal signs like pain, redness, heat, and swelling.
This document discusses cell injury and cell death. It begins by introducing pathology and defining etiology and pathogenesis. It then describes the cellular responses to stress, including adaptation and reversible injury. If stress is severe or persistent, it can lead to irreversible injury and cell death through necrosis or apoptosis. The document outlines the mechanisms and morphologies of different types of necrosis and apoptosis. It also discusses other pathways of cell death like necroptosis and pyroptosis. Causes of cell injury discussed include hypoxia, ischemia, oxidative stress, toxins, DNA damage, and inflammation. Reversible injury and cell death are important concepts for understanding disease pathogenesis.
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1. Presented To : Dr Ishtiaq Ahmed
Presented By : Umer Farooq
Login Id : 2021-dvmje-033
General Veterinary Pathology
2. Types of cell death
Cell death is the event of a biological cell ceasing
to carry out its functions.
3 major types of cell death.
Apoptosis
Autophagic cell death
Necrosis
3. Apoptosis
Latin word meaning “ fall off”.
Process of programmed cell death.
During early development to eliminate unwanted
cells.
Eliminate dead cells.
If doesn’t happen lead to uncontrolled cell division
and cause development of tumor.
Hence absence of apoptosis cause cancer.
To much apoptosis lead to neurodegenerative
diseases. For example certain parts of lower part of
brain causing Parkinson disease.
4. Events of apoptosis
Blebbing
Cell shrinkage
Proteolysis
Nuclear DNA fragmentation
These are morphological changes occurring in cell
5.
6. Causes of apoptosis
Sudden removal of survival signal
Removal of disassociation from neighboring cells
Cellular stress like
• High heat conditions
• DNA damage by irradiation/chemotherapy
• Pathogenic infections
7. Autophagic cell death
Cell death that occurs in absence of chromatin
condensation but accompanied by large scale
autophagic vacuolization of cytoplasm.
Catabolic pathway
Maintains cellular homeostasis through recycling
selective intracellular organelles and molecules
Cellular contents are engulfed by autophagosomes
Degraded upon autophagosomes fusion with
lysosome
8. Occur in response to
• Apoptotic activity is reduced
• Fasting : body deprives of nutrients
• Calorie restriction
• Exercise
9. Necrosis
Accidental cell death
Too little blood flow to tissue leads necrosis
Can be from injury , radiation , chemicals ,
infections
Necrosis once happen cannot be reversed
When large areas of tissues die due to lack of
blood supply this condition called gangrene
10. Necrosis begins with
• Cell swelling
• The chromatin gets digested
• The plasma and organelles are disrupted
• ER vacuolizes
• The organelles breakdown completely
• Finally the cell lyses
• And spreads its intracellular contents