Podcast
Questions and Answers
What is the fundamental basis of all diseases?
What is the fundamental basis of all diseases?
What is the common underlying feature of all diseases?
What is the common underlying feature of all diseases?
What is the result of environmental toxins on cellular function?
What is the result of environmental toxins on cellular function?
What is the relationship between cellular function and disease?
What is the relationship between cellular function and disease?
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What is the impact of radiation exposure on cellular structure?
What is the impact of radiation exposure on cellular structure?
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What is the role of environmental insults in disease development?
What is the role of environmental insults in disease development?
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What is the relationship between toxins and cellular function?
What is the relationship between toxins and cellular function?
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What is the underlying cause of individual susceptibility to disease?
What is the underlying cause of individual susceptibility to disease?
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What are the two major pathways of cell death?
What are the two major pathways of cell death?
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What is the result of exposure to a variety of injurious agents?
What is the result of exposure to a variety of injurious agents?
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What is the site of protein synthesis and folding that is affected in endoplasmic reticulum stress?
What is the site of protein synthesis and folding that is affected in endoplasmic reticulum stress?
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What is the term for the movement of water into a cell, resulting in swelling?
What is the term for the movement of water into a cell, resulting in swelling?
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What is the term for the breakdown of cellular components, resulting in cell death?
What is the term for the breakdown of cellular components, resulting in cell death?
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What is the term for the compression of capillaries, resulting in cell injury?
What is the term for the compression of capillaries, resulting in cell injury?
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What is the term for the changes in cellular structure and function that occur in response to injury?
What is the term for the changes in cellular structure and function that occur in response to injury?
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What is the term for the swelling of organelles, such as the endoplasmic reticulum, in response to injury?
What is the term for the swelling of organelles, such as the endoplasmic reticulum, in response to injury?
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What is a characteristic microscopic finding in necrosis?
What is a characteristic microscopic finding in necrosis?
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What is a common cause of necrosis?
What is a common cause of necrosis?
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What type of injury can cause necrosis?
What type of injury can cause necrosis?
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What is a common immune response to necrosis?
What is a common immune response to necrosis?
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What can lead to the release of enzymes from cells in necrosis?
What can lead to the release of enzymes from cells in necrosis?
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Where can necrosis occur?
Where can necrosis occur?
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What is a consequence of necrosis?
What is a consequence of necrosis?
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What can occur in response to necrosis?
What can occur in response to necrosis?
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What is the characteristic of dry gangrene?
What is the characteristic of dry gangrene?
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What is the result of damage to membrane lipids?
What is the result of damage to membrane lipids?
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What is an example of a superimposed bacterial infection?
What is an example of a superimposed bacterial infection?
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What is the characteristic of caseous necrosis?
What is the characteristic of caseous necrosis?
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What is the result of disruption of plasma membrane?
What is the result of disruption of plasma membrane?
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What is an example of a disease caused by caseous necrosis?
What is an example of a disease caused by caseous necrosis?
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What is the result of necrosis of cellular membranes?
What is the result of necrosis of cellular membranes?
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What is an example of an infection that can lead to necrosis?
What is an example of an infection that can lead to necrosis?
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What is the primary function of mechanisms of apoptosis?
What is the primary function of mechanisms of apoptosis?
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What are the two main pathways of apoptosis?
What are the two main pathways of apoptosis?
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What is the role of BCL-2 in apoptosis?
What is the role of BCL-2 in apoptosis?
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What is the significance of BCL-2 in tumors?
What is the significance of BCL-2 in tumors?
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What is the term for the process of programmed cell death?
What is the term for the process of programmed cell death?
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What is the name of the gene that regulates apoptosis?
What is the name of the gene that regulates apoptosis?
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How do growth factors promote cell survival?
How do growth factors promote cell survival?
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What is the term for the pathway that involves the activation of death receptors?
What is the term for the pathway that involves the activation of death receptors?
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Match the following cellular components with their functions:
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Match the following cellular responses with their effects:
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Match the following terms with their effects on cells:
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Match the following cellular changes with their underlying causes:
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Match the following cellular components with their effects during cell injury:
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Match the following cellular changes with their corresponding cellular processes:
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Match the following microscopic findings with their corresponding cellular processes:
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Match the following cellular processes with their effects on cellular function:
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Match the following organelles with their changes during cell injury:
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Match the following cellular changes with their corresponding cellular processes:
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Match the following cellular structures with their responses to injury:
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Match the following cellular changes with their causes:
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Match the following cellular changes with their appearances:
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Match the following cellular structures with their functions:
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Match the following cellular responses with their triggers:
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Match the following cellular changes with their consequences:
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Match the following cellular components with their functions in apoptosis:
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Match the following cellular processes with their outcomes:
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Match the following cellular reactions with their triggers:
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Match the following cellular changes with their consequences in disease:
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Cells can adapt to stress, but never die.
Cells can adapt to stress, but never die.
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Environmental toxins can trigger an immune response.
Environmental toxins can trigger an immune response.
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Cell injury can be caused by genetic abnormalities.
Cell injury can be caused by genetic abnormalities.
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Cells can repair damaged DNA.
Cells can repair damaged DNA.
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Cell injury can lead to cell death.
Cell injury can lead to cell death.
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Inflammation can cause cell injury.
Inflammation can cause cell injury.
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Cellular responses to injury are always reversible.
Cellular responses to injury are always reversible.
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Environmental insults can trigger an immune response against self-antigens.
Environmental insults can trigger an immune response against self-antigens.
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Fat necrosis results in the release of activated pancreatic lipases into the bloodstream.
Fat necrosis results in the release of activated pancreatic lipases into the bloodstream.
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Receptors expressed by macrophages and other cell types recognize and respond to necrotic cell debris.
Receptors expressed by macrophages and other cell types recognize and respond to necrotic cell debris.
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Necrosis typically results in the release of enzymes from cells.
Necrosis typically results in the release of enzymes from cells.
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Pancreatic lipases are normally confined within pancreatic cells and only released upon cellular injury.
Pancreatic lipases are normally confined within pancreatic cells and only released upon cellular injury.
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Necrosis is typically a reversible process.
Necrosis is typically a reversible process.
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Necrotic cells are typically intact and functional.
Necrotic cells are typically intact and functional.
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Caseous necrosis is a type of necrosis typically seen in bacterial infections.
Caseous necrosis is a type of necrosis typically seen in bacterial infections.
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Dry gangrene is a type of necrosis characterized by moist, soft tissue.
Dry gangrene is a type of necrosis characterized by moist, soft tissue.
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Apoptosis can occur as a pathological event even when cells are not damaged.
Apoptosis can occur as a pathological event even when cells are not damaged.
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Physiological apoptosis occurs during development of organisms, such as replacing premature tissues with mature tissues.
Physiological apoptosis occurs during development of organisms, such as replacing premature tissues with mature tissues.
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Cell death can occur through only one pathway.
Cell death can occur through only one pathway.
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Apoptosis is a form of cellular suicide that eliminates cells that are no longer needed or are damaged beyond repair, eliciting an inflammatory response.
Apoptosis is a form of cellular suicide that eliminates cells that are no longer needed or are damaged beyond repair, eliciting an inflammatory response.
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Damage to cellular DNA or proteins can trigger apoptosis.
Damage to cellular DNA or proteins can trigger apoptosis.
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Coagulative necrosis is a form of cellular suicide.
Coagulative necrosis is a form of cellular suicide.
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Necrosis always occurs as a result of apoptosis.
Necrosis always occurs as a result of apoptosis.
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Necrosis can occur in response to various injurious agents, including environmental toxins and radiation exposure.
Necrosis can occur in response to various injurious agents, including environmental toxins and radiation exposure.
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Apoptosis can occur in response to immune responses.
Apoptosis can occur in response to immune responses.
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Apoptosis and necrosis are two forms of cellular injury that always involve an inflammatory response.
Apoptosis and necrosis are two forms of cellular injury that always involve an inflammatory response.
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Liquefactive necrosis occurs in the brain as a result of apoptosis.
Liquefactive necrosis occurs in the brain as a result of apoptosis.
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Programmed cell death can occur in response to cellular stress.
Programmed cell death can occur in response to cellular stress.
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Karyorrhexis is a type of apoptosis.
Karyorrhexis is a type of apoptosis.
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Pyknosis is a characteristic microscopic finding in apoptosis.
Pyknosis is a characteristic microscopic finding in apoptosis.
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Enzymes such as amylase are released from cells in necrosis.
Enzymes such as amylase are released from cells in necrosis.
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Apoptosis is a mechanism that eliminates cells that are no longer needed or are damaged, and it does not activate an immune response.
Apoptosis is a mechanism that eliminates cells that are no longer needed or are damaged, and it does not activate an immune response.
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The opening of the membrane permeability transition pore leads to decreased mitochondrial membrane permeability.
The opening of the membrane permeability transition pore leads to decreased mitochondrial membrane permeability.
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Caspase-9 is activated in the cytosol, where it initiates the caspase cascade.
Caspase-9 is activated in the cytosol, where it initiates the caspase cascade.
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Environmental toxins can cause damage to nuclear structures and lead to cell death.
Environmental toxins can cause damage to nuclear structures and lead to cell death.
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Apoptosis is a mechanism of cell death that is characterized by cell swelling and inflammation.
Apoptosis is a mechanism of cell death that is characterized by cell swelling and inflammation.
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The endoplasmic reticulum is a site of protein synthesis and folding that is affected in endoplasmic reticulum stress.
The endoplasmic reticulum is a site of protein synthesis and folding that is affected in endoplasmic reticulum stress.
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Necrosis is a form of programmed cell death that is characterized by cell membrane disruption.
Necrosis is a form of programmed cell death that is characterized by cell membrane disruption.
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The release of enzymes from cells is a characteristic of apoptosis.
The release of enzymes from cells is a characteristic of apoptosis.
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Apoptosis can occur in response to cellular stress, such as DNA damage or oxidative stress.
Apoptosis can occur in response to cellular stress, such as DNA damage or oxidative stress.
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What is the primary mechanism of cell injury caused by hypoxia and ischemia?
What is the primary mechanism of cell injury caused by hypoxia and ischemia?
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What is the role of endoplasmic reticulum stress in cell injury?
What is the role of endoplasmic reticulum stress in cell injury?
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What is the characteristic of apoptosis that distinguishes it from necrosis?
What is the characteristic of apoptosis that distinguishes it from necrosis?
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What is the result of oxidative stress on cellular components?
What is the result of oxidative stress on cellular components?
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What is the term for the accumulation of abnormal protein aggregates in cells?
What is the term for the accumulation of abnormal protein aggregates in cells?
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What is the role of cellular adaptations in response to stress?
What is the role of cellular adaptations in response to stress?
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What is the consequence of DNA damage on cellular function?
What is the consequence of DNA damage on cellular function?
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What is the term for the process of cellular aging?
What is the term for the process of cellular aging?
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What is the outcome of the leakage of lysosomal enzymes in cell death?
What is the outcome of the leakage of lysosomal enzymes in cell death?
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What is the role of damage-associated molecular patterns (DAMPs) in cell death?
What is the role of damage-associated molecular patterns (DAMPs) in cell death?
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What is the source of ATP in necrosis?
What is the source of ATP in necrosis?
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What is the characteristic of the necrotic focus on microscopy?
What is the characteristic of the necrotic focus on microscopy?
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What is the result of the release of uric acid in necrosis?
What is the result of the release of uric acid in necrosis?
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What is the consequence of the disruption of plasma membrane in necrosis?
What is the consequence of the disruption of plasma membrane in necrosis?
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What is the role of ATP in the context of necrosis?
What is the role of ATP in the context of necrosis?
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What is the characteristic of eosinophilic necrosis?
What is the characteristic of eosinophilic necrosis?
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What is the result of cellular injury caused by genetic abnormalities, mutations, and chromosomal abnormalities?
What is the result of cellular injury caused by genetic abnormalities, mutations, and chromosomal abnormalities?
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How do cells respond to stress, and what are the possible outcomes?
How do cells respond to stress, and what are the possible outcomes?
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What is the role of immune responses in cell injury?
What is the role of immune responses in cell injury?
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What is the common underlying mechanism of cell injury and death?
What is the common underlying mechanism of cell injury and death?
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What is the relationship between environmental toxins and cellular function?
What is the relationship between environmental toxins and cellular function?
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What is the consequence of cellular injury, and how does it relate to disease?
What is the consequence of cellular injury, and how does it relate to disease?
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What is the role of inflammation in cell injury?
What is the role of inflammation in cell injury?
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How do cellular responses to injury impact disease development?
How do cellular responses to injury impact disease development?
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What is the characteristic of reversible cell injury?
What is the characteristic of reversible cell injury?
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What do adaptations enable cells to do?
What do adaptations enable cells to do?
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What is the result of cellular responses to injury?
What is the result of cellular responses to injury?
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What is the common underlying feature of all diseases?
What is the common underlying feature of all diseases?
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What is the role of adaptations in cellular responses to injury?
What is the role of adaptations in cellular responses to injury?
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What is the consequence of reversible cell injury?
What is the consequence of reversible cell injury?
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What are the three broad categories of cell injury?
What are the three broad categories of cell injury?
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What is the result of cellular adaptations to stress?
What is the result of cellular adaptations to stress?
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What is the characteristic of coagulative necrosis?
What is the characteristic of coagulative necrosis?
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What is the role of an immune response in necrosis?
What is the role of an immune response in necrosis?
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What is the result of the release of enzymes from cells in necrosis?
What is the result of the release of enzymes from cells in necrosis?
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What is the common underlying feature of necrosis and apoptosis?
What is the common underlying feature of necrosis and apoptosis?
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What is the effect of lipid peroxidation on cellular membranes?
What is the effect of lipid peroxidation on cellular membranes?
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What is the characteristic of gangrenous necrosis?
What is the characteristic of gangrenous necrosis?
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What is the role of exotoxins and endotoxins in cellular injury?
What is the role of exotoxins and endotoxins in cellular injury?
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What is the term for the process of cellular injury that leads to necrosis?
What is the term for the process of cellular injury that leads to necrosis?
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La necrosis se caracteriza por la muerte de ______ celular.
La necrosis se caracteriza por la muerte de ______ celular.
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La gangrena seca es un tipo de necrosis que se caracteriza por la presencia de ______ tejido muerto.
La gangrena seca es un tipo de necrosis que se caracteriza por la presencia de ______ tejido muerto.
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La membrana plasmática es un tipo de membrana que se puede dañar debido a la ______ de membrana lipídica.
La membrana plasmática es un tipo de membrana que se puede dañar debido a la ______ de membrana lipídica.
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La necrosis caseosa se asocia con la ______ tuberculosis.
La necrosis caseosa se asocia con la ______ tuberculosis.
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La necrosis puede ocurrir debido a la ______ de membranas celulares, lo que conduce a la liberación de enzimas.
La necrosis puede ocurrir debido a la ______ de membranas celulares, lo que conduce a la liberación de enzimas.
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La infección bacteriana superpuesta puede ser una causa de ______ gangrena.
La infección bacteriana superpuesta puede ser una causa de ______ gangrena.
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La necrosis puede ser causada por la ______ de toxinas ambientales en la función celular.
La necrosis puede ser causada por la ______ de toxinas ambientales en la función celular.
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La necrosis puede ocurrir en respuesta a la ______ de injurias, como la exposición a radiación.
La necrosis puede ocurrir en respuesta a la ______ de injurias, como la exposición a radiación.
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La liberación de enzimas ______ causa daños en la célula.
La liberación de enzimas ______ causa daños en la célula.
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Elicroscópicamente, el foco necrótico se caracteriza por una ______ de células.
Elicroscópicamente, el foco necrótico se caracteriza por una ______ de células.
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La respuesta inflamatoria local se activa en respuesta a la liberación de ______ de las células muertas.
La respuesta inflamatoria local se activa en respuesta a la liberación de ______ de las células muertas.
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La necrosis se caracteriza por la ______ de células y la liberación de enzimas.
La necrosis se caracteriza por la ______ de células y la liberación de enzimas.
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La ______ de células puede llevar a la formación de un granuloma.
La ______ de células puede llevar a la formación de un granuloma.
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La lesión asociada con la liberación de ATP y ácido úrico se conoce como ______.
La lesión asociada con la liberación de ATP y ácido úrico se conoce como ______.
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La necrosis puede ser causada por la ______ de células debido a la lesión del miocardio.
La necrosis puede ser causada por la ______ de células debido a la lesión del miocardio.
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El examen microscópico de la necrosis often shows una ______ de células.
El examen microscópico de la necrosis often shows una ______ de células.
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La necrosis puede ocurrir en áreas del ______ y del tejido adiposo.
La necrosis puede ocurrir en áreas del ______ y del tejido adiposo.
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Los receptores se expresan en macrófagos y ______ células.
Los receptores se expresan en macrófagos y ______ células.
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La ______ es una característica microscópica común en la necrosis.
La ______ es una característica microscópica común en la necrosis.
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La liberación de enzimas de las células se puede deber a la ______ de las células pancreáticas.
La liberación de enzimas de las células se puede deber a la ______ de las células pancreáticas.
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El ______ es un ejemplo de infección bacteriana que puede llevar a la necrosis.
El ______ es un ejemplo de infección bacteriana que puede llevar a la necrosis.
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La necrosis puede ocurrir en respuesta a la ______ de células pancreáticas.
La necrosis puede ocurrir en respuesta a la ______ de células pancreáticas.
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La ______ es un tipo de necrosis seca caracterizada por la formación de una masa seca y quebradiza.
La ______ es un tipo de necrosis seca caracterizada por la formación de una masa seca y quebradiza.
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La ______ es un tipo de necrosis caracterizada por la formación de una masa caseosa.
La ______ es un tipo de necrosis caracterizada por la formación de una masa caseosa.
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La necrosis grasa se caracteriza por la formación de jabón cálcico en sitios de ______ de lípidos.
La necrosis grasa se caracteriza por la formación de jabón cálcico en sitios de ______ de lípidos.
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La lesión celular irreversible se conoce como ______.
La lesión celular irreversible se conoce como ______.
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La Figura 1.2 muestra cambios morfológicos en ______ celular reversible y irreversible.
La Figura 1.2 muestra cambios morfológicos en ______ celular reversible y irreversible.
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La lesión celular puede ser causada por la exposición a agentes lesivos, como ______.
La lesión celular puede ser causada por la exposición a agentes lesivos, como ______.
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La necrosis puede ocurrir en cualquier parte del cuerpo, incluyendo el ______.
La necrosis puede ocurrir en cualquier parte del cuerpo, incluyendo el ______.
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La ______ de células puede llevar a la liberación de enzimas y la muerte celular.
La ______ de células puede llevar a la liberación de enzimas y la muerte celular.
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La respuesta inmune común a la necrosis es la ______.
La respuesta inmune común a la necrosis es la ______.
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La consecuencia de la necrosis puede ser la ______ de tejido.
La consecuencia de la necrosis puede ser la ______ de tejido.
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La necrosis caseosa se caracteriza por una área grande de ______ amarillo-blanco
La necrosis caseosa se caracteriza por una área grande de ______ amarillo-blanco
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La activación de proteínas proapoptóticas puede ser causada por ______ de DNA
La activación de proteínas proapoptóticas puede ser causada por ______ de DNA
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La necrosis caseosa se asocia con infecciones, especialmente ______ virales
La necrosis caseosa se asocia con infecciones, especialmente ______ virales
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La muerte de células infectadas se produce mediante la activación de ______ por parte de linfocitos T citotóxicos
La muerte de células infectadas se produce mediante la activación de ______ por parte de linfocitos T citotóxicos
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El estrés del retículo endoplásmico puede causar la acumulación de ______ plegados incorrectamente
El estrés del retículo endoplásmico puede causar la acumulación de ______ plegados incorrectamente
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La activación de la vía mitocondrial puede ser directa mediante la activación de ______ por proteínas virales
La activación de la vía mitocondrial puede ser directa mediante la activación de ______ por proteínas virales
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La necrosis caseosa se caracteriza por una zona de ______ con un contenido amarillo-blanco
La necrosis caseosa se caracteriza por una zona de ______ con un contenido amarillo-blanco
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La activación de receptores de muerte puede ser causada por ______ de citotoxicidad
La activación de receptores de muerte puede ser causada por ______ de citotoxicidad
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Study Notes
Cell Injury and Death
- Cell injury and death can occur due to various insults, including toxins, radiation, and physical trauma, leading to diseases.
- Environmental toxins, some therapeutic agents, and abnormal cellular processes can cause cell injury and death.
Mechanisms of Cell Injury
- Cell injury can occur through multiple mechanisms, including:
- Disruption of cellular membranes, including plasma membrane and lysosomal membranes.
- Activation of phospholipases, leading to damage to membrane lipids.
- Disruption of cellular ion balance, leading to changes in cellular function.
- Inhibition of cellular metabolism, leading to energy depletion.
Types of Cell Death
- There are two major types of cell death:
- Necrosis: characterized by cell swelling, membrane rupture, and release of cellular contents.
- Apoptosis: characterized by cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
Causes of Necrosis
- Necrosis can occur due to various causes, including:
- Ischemia (reduced blood flow)
- Infection (bacterial, viral, or fungal)
- Toxins (environmental or therapeutic)
- Physical trauma (mechanical injury)
- Radiation
- Genetic mutations
Mechanisms of Apoptosis
- Apoptosis can occur through two pathways:
- Mitochondrial (intrinsic) pathway: initiated by mitochondrial dysfunction, leading to release of cytochrome c and activation of caspases.
- Death receptor (extrinsic) pathway: initiated by binding of ligands to death receptors, leading to activation of caspases.
Regulation of Apoptosis
- Apoptosis is regulated by various molecules, including:
- BCL-2 family proteins: anti-apoptotic proteins that regulate mitochondrial permeability.
- Caspases: enzymes that cleave cellular proteins, leading to apoptosis.
- Death receptors: transmembrane proteins that initiate apoptosis in response to ligand binding.
Importance of Apoptosis
- Apoptosis is essential for maintaining tissue homeostasis, as it eliminates damaged or unwanted cells.
- Dysregulation of apoptosis has been implicated in various diseases, including cancer and autoimmune disorders.
Cell Injury and Death
- Cellular injury can be caused by various factors, including environmental toxins, physical trauma, radiation exposure, and infections.
- The major cellular adaptations and physiological responses to injury are summarized at the end of the chapter.
Cellular Injury
- Cellular injury can result in reversible or irreversible damage to cells.
- Reversible cell injury can be corrected by removing the injurious agent, and the cell can recover its normal structure and function.
- Irreversible cell injury can lead to cell death, which can be divided into two types: necrosis and apoptosis.
Necrosis
- Necrosis is a type of cell death characterized by cellular swelling, rupture of the plasma membrane, and release of cellular contents.
- It is often accompanied by inflammation and can lead to tissue damage.
- Necrosis can be caused by various factors, including toxins, radiation, and physical trauma.
Apoptosis
- Apoptosis is a type of cell death characterized by cellular shrinkage, nuclear fragmentation, and the formation of apoptotic bodies.
- It is a programmed cell death that occurs naturally in various physiological processes, such as embryonic development and tissue homeostasis.
- Apoptosis can be triggered by various stimuli, including DNA damage, oxidative stress, and withdrawal of growth factors.
Cellular Responses to Injury
- Cellular injury can trigger various responses, including:
- Inflammation: a response to tissue damage characterized by the activation of immune cells and the release of inflammatory mediators.
- Oxidative stress: an imbalance between the production of reactive oxygen species and the body's ability to detoxify them.
- DNA damage: damage to the genetic material of the cell, which can trigger various responses, including apoptosis.
- Cellular adaptation: changes in cellular structure and function to compensate for the injury.
Cellular Components and Injury
- Plasma membrane damage: a critical component of cellular injury, which can lead to cell death.
- Mitochondrial damage: mitochondria are critical for cellular energy production, and damage to them can lead to cellular injury and death.
- Endoplasmic reticulum (ER) stress: the ER is responsible for protein synthesis and folding, and stress on the ER can lead to cellular injury and death.
- Nuclear damage: damage to the genetic material of the cell, which can trigger various responses, including apoptosis.
Cell Death and Disease
- Cell death can contribute to various diseases, including cancer, neurodegenerative disorders, and cardiovascular disease.
- Apoptosis can be dysregulated in cancer, leading to the formation of tumors.
- Necrosis can lead to tissue damage and organ failure in various diseases, including cardiovascular disease and neurodegenerative disorders.
Overview of Cell Injury
- Cell injury can result from various factors, including genetic abnormalities, mutations, and environmental agents.
Types of Cell Injury
- Reversible cell injury: cells can adapt to stress, recover, or be injured reversibly, often by triggering inflammation.
- Irreversible cell injury: cells can be damaged beyond repair, leading to cell death.
Causes of Cell Injury
- Genetic abnormalities, mutations, and environmental agents can cause cell injury.
- Immune responses, such as autoimmune diseases or allergies, can also lead to cell injury.
Consequences of Cell Injury
- Cell injury can lead to cell death, either through necrosis or apoptosis.
- Necrosis: a form of cell death that results in the release of cellular components, leading to an inflammatory response.
- Apoptosis: a form of programmed cell death that eliminates damaged or unwanted cells without eliciting an inflammatory response.
Apoptosis
- Apoptosis is a form of cellular suicide that eliminates cells that are damaged beyond repair or no longer needed.
- It occurs during development, when old cells are replaced by mature cells, and during immune responses, when damaged cells are eliminated.
- Apoptosis can also occur in response to DNA damage or protein misfolding.
Necrosis
- Necrosis is a form of cell death that results from severe cell injury, often due to environmental toxins, infections, or inflammation.
- It leads to the release of cellular components, causing an inflammatory response.
Pathological Consequences of Cell Injury
- Cell injury can lead to various diseases, such as cancer, cardiovascular disease, and neurodegenerative disorders.
- Apoptosis and necrosis can both contribute to disease progression, depending on the context.
Cellular Response to Injury
- Cells respond to injury by activating signaling pathways that trigger repair or death.
- The response depends on the severity and type of injury, as well as the cellular context.
Regulation of Cell Death
- Cell death is regulated by a balance between pro-death and anti-death signals.
- The Bcl-2 protein family plays a key role in regulating apoptosis.
Molecular Mechanisms of Apoptosis
- Apoptosis involves the activation of caspases, which are enzymes that break down cellular components.
- The Bcl-2 protein family regulates the activation of caspases.
- Cytochrome c release from the mitochondria can trigger apoptosis.
Importance of Cell Death
- Cell death is essential for development, tissue homeostasis, and the elimination of damaged or unwanted cells.
- Apoptosis helps to maintain tissue integrity and prevent disease.
Cell Injury and Death
- Cell injury can be reversible or irreversible, and can lead to cell death if not repaired or corrected.
- Causes of cell injury include genetic abnormalities, oxidative stress, hypoxia, ischemia, toxin-mediated injury, and endoplasmic reticulum (ER) stress.
- Cellular adaptations to stress can occur, including increased muscle mass in response to increased workload.
Reversible Cell Injury
- Characterized by functional and structural changes in cells that are not permanent.
- Can be caused by factors such as increased muscle mass, leakage of lysosomal enzymes, and local inflammation.
- Examples of reversible cell injury include increased muscle mass in response to increased workload, and leakage of lysosomal enzymes.
Cell Death
- Can occur through various pathways, including necrosis, apoptosis, and other mechanisms.
- Necrosis is characterized by the breakdown of dead tissue, leading to a cheesy consistency on gross examination.
- Microscopically, necrotic cells appear as a collection of fragmented or lysed cells with an amorphous granular pink appearance.
Necrosis
- Causes of necrosis include ischemia, exposure to toxins, and other forms of cellular injury.
- Fibrinoid necrosis is a characteristic microscopic finding seen in immune reactions.
- Examples of necrosis include pancreatitis, where enzymes leak out of cells and injure adjacent tissues.
Apoptosis
- A type of programmed cell death that occurs in response to various stimuli, including DNA damage and oxidative stress.
- Characterized by cell shrinkage, chromatin condensation, and the formation of apoptotic bodies.
Other Pathways of Cell Death
- Include autophagic cell death, where cells recycle their own components in response to stress, and mitotic catastrophe, where cells die during mitosis due to DNA damage.
- Other mechanisms of cell death include cellular senescence, where cells become quiescent and resistant to apoptosis, and pyroptosis, where cells die due to the formation of pores in the cell membrane.
Mechanisms of Cell Injury and Death
- Include oxidative stress, where cells are damaged due to the presence of reactive oxygen species, and ER stress, where cells are damaged due to the accumulation of misfolded proteins.
- Other mechanisms of cell injury and death include DNA damage, where cells are damaged due to the presence of damaged DNA, and hypoxia, where cells are damaged due to a lack of oxygen.
Cellular Adaptations to Stress
- Include changes in cellular metabolism, such as increased glucose uptake, and changes in cellular structure, such as increased muscle mass.
- Other adaptations to stress include the activation of cellular defense mechanisms, such as the production of antioxidants and heat shock proteins.
Pathologic Accumulations in Cells
- Include the accumulation of damaged DNA, misfolded proteins, and other abnormal cellular components.
- Examples of pathologic accumulations include the accumulation of beta-amyloid peptides in Alzheimer's disease, and the accumulation of alpha-synuclein in Parkinson's disease.
Cell Injury and Cell Death
- Necrosis is a type of cell death characterized by the release of intracellular contents, leading to inflammation and tissue damage.
- Types of necrosis:
- Dry gangrene: characterized by dead tissue that is dry and shrunk, often due to ischemia or lack of blood supply.
- Wet gangrene: characterized by dead tissue that is soft and moist, often due to bacterial infection.
- Caseous necrosis: characterized by dead tissue that is cheesy and soft, often due to tuberculosis.
- Fat necrosis: characterized by dead tissue that is fatty and soft, often due to pancreatitis.
Characteristics of Necrosis
- Dissolution of cell membranes, leading to the release of cellular contents.
- Leakage of lysosomal enzymes, leading to digestion of cellular components.
- Local inflammation in response to the release of cellular contents.
- Microscopically, necrotic cells appear as a collection of fragmented cells with an amorphous granular pink appearance (eosinophilic).
Molecular Mechanisms of Necrosis
- Release of damage-associated molecular patterns (DAMPs), including ATP, uric acid, and DNA, which stimulate an immune response.
- Activation of pro-inflammatory pathways, leading to the recruitment of immune cells and the production of pro-inflammatory cytokines.
- Inhibition of anti-inflammatory pathways, leading to the exacerbation of inflammation.
Morphologic Changes in Cell Injury
- Reversible cell injury: characterized by surface blebs, increased eosinophilia, and swelling of occasional cells.
- Irreversible cell injury (necrosis): characterized by the loss of nuclei, fragmentation of cells, and leakage of cellular contents.
Examples of Necrosis
- Tuberculosis: characterized by caseous necrosis, often in the lung.
- Pancreatitis: characterized by fat necrosis, often in the pancreas.
- Ischemic injury: characterized by dry gangrene, often due to lack of blood supply.
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Cell injury and death can occur due to various insults, including toxins, radiation, and physical trauma, leading to diseases. Explore the mechanisms of cell injury and its causes.