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What is the result of a cell's inability to maintain its plasma membrane?
What is the role of plasma membrane pumps in many cases?
What is the consequence of a decrease in ATP generation?
What is the result of a reversible phase in a cell?
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What is the relationship between ATP and plasma membrane pumps?
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What is the consequence of plasma membrane damage?
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What is the result of a cell's ability to maintain its plasma membrane?
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What is the role of ATP in the context of plasma membrane pumps?
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What is the primary way infectious pathogens injure cells?
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What is the outcome of the disruption of metabolic pathways in cells?
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What is the role of eosinophils in the context of infectious pathogens?
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What is the result of the accumulation of glycerolyceride in cells?
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What is the primary mechanism by which infectious pathogens cause cell damage?
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What is the consequence of disrupting metabolic pathways in cells?
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What is the role of fatty changes in organs in the context of infectious pathogens?
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What is the outcome of the immune response triggered by infectious pathogens?
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What is the sequence of events in cell injury that culminate in necrosis or apoptosis?
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What are myelin figures composed of?
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What is often observed in mitochondria of cells undergoing necrosis?
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What is a consequence of RNA binding to the blue membrane staining?
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What occurs in the plasma membrane during cell injury?
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What is a consequence of DNA damage in cell injury?
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What can occur to the ER during cell injury?
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What can occur to nuclear chromatin during cell injury?
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What is the term for the process of calcium soap formation in fat necrosis?
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What is the term for the white chalky deposits seen in fat necrosis?
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What is the stage of cell injury shown in Fig. 1.2B?
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What is the characteristic feature of irreversible cell injury shown in Fig. 1.2C?
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What is the location of the tissue shown in Fig. 1.2A?
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What is the cause of the morphologic changes seen in Fig. 1.2B?
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What is the term for the breakdown of lipids in fat necrosis?
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What is the location of the fat necrosis shown in eFig. 1.1?
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What is the primary difference in cell size between necrosis and apoptosis?
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What is the typical outcome of enzymatic digestion in necrosis?
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Which process is often physiologic and eliminates unwanted cells?
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What is the typical outcome of nuclei in necrotic cells?
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What is the primary role of apoptosis in a cell?
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What is the characteristic feature of the plasma membrane in apoptotic cells?
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What is the typical outcome of adjacent inflammation in necrosis?
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What is the primary difference between necrosis and apoptosis in terms of physiological or pathological role?
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What is the characteristic feature of cellular contents in apoptotic cells?
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What is the outcome of nucleus fragmentation in apoptotic cells?
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Cell injury can be caused by genetic abnormalities, including mutations that impair cellular function.
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Immune-mediated reactions against self-antigens or environmental antigens can cause cell injury.
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Cells can adapt to stress and recover without injury.
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DNA damage can lead to the accumulation of damaged DNA or abnormal proteins in cells.
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Cell injury can be caused by the accumulation of damaged or abnormal proteins that cannot be repaired or corrected.
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Infectious pathogens can cause cell injury through various mechanisms, including immune-mediated reactions.
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Reversible cell injury can lead to cell death if the injurious stimulus is not removed.
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Cell injury can be caused by a failure to maintain proper cellular function, leading to the accumulation of damaged cellular components.
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Cell death due to hypoxia can lead to necrosis or apoptosis.
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Necrosis is always caused by a reversible phase in a cell.
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Damage to the plasma membrane can lead to cell death through necrosis.
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Infections are the primary mechanism of cell damage in all cases.
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Apoptosis is a form of cell death that always involves inflammation.
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Necrosis and apoptosis are two terms that describe the same process of cell death.
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Caseous necrosis is characterized by the accumulation of yellow-white debris.
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DNA damage can lead to the activation of proapoptotic proteins.
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Infections, especially viral infections, can activate the mitochondrial pathway.
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Caspases are involved in the killing of infected cells by cytotoxic T lymphocytes.
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Caseous necrosis is typically associated with fungal infections.
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Mitochondrial damage is a characteristic feature of apoptotic cells.
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Dry gangrene is caused by bacterial infections.
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Proapoptotic proteins are involved in the pathways leading to necrosis.
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Plasma membrane pumps are involved in the maintenance of cell membrane structure.
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Damage to the plasma membrane can lead to necrosis.
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Accumulation of misfolded proteins can activate proapoptotic pathways.
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Caseous necrosis is a type of reversible cell injury.
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Wet gangrene is typically associated with bacterial infections.
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Necrosis is a reversible process.
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Disruption of metabolic pathways can lead to cell injury.
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Infectious pathogens can cause cell injury by disrupting the plasma membrane.
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Severe DNA damage can lead to the formation of apoptotic bodies.
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Necrosis is a physiological process that eliminates unwanted cells.
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Certain viruses can trigger immune responses that destroy infected cells.
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In apoptosis, the cell membrane remains intact.
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BAX and BAK proteins are normally activated by anti-apoptotic molecules.
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The accumulation of misfolded proteins can lead to ER stress.
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In necrosis, the cell's contents are released into the surrounding environment.
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Apoptosis is a rapid process that leads to cell death within minutes.
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What is the primary consequence of a cell's inability to maintain its plasma membrane, leading to a decrease in ATP generation?
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What is the role of plasma membrane pumps in many cases, and how does it relate to ATP generation?
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What is the outcome of a reversible phase in a cell, if the injurious stimulus is not removed?
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How do infectious pathogens cause cell injury, and what is the primary mechanism involved?
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What is the term used to describe the death of soft tissue and the resulting loss of blood supply and subsequent coagulative necrosis?
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What is the consequence of disrupting metabolic pathways in cells, and how does it relate to ATP generation?
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What is the result of severe injury to cells, leading to a pathologic process in which cells spill their contents into the extracellular milieu?
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What is the role of ATP in maintaining the plasma membrane, and how does it relate to cell injury?
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What is the outcome of a cell's inability to maintain its plasma membrane, and how does it relate to ATP generation?
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What is the term used to describe the process of cell death resulting from severe injury, such as ischemia, and characterized by a loss of blood supply and subsequent coagulative necrosis?
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What is the primary mechanism by which a cell's inability to maintain its plasma membrane leads to cell injury?
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What is the outcome of cell injury that leads to local inflammation?
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What is the term used to describe the death of cells resulting from a lack of blood supply, such as in diabetic vascular disease?
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What is the process by which cells die due to severe injury, leading to a loss of blood supply and subsequent necrosis?
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What is the outcome of the disruption of metabolic pathways in cells injured by infectious pathogens?
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How do infectious pathogens injure cells by producing toxins?
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What is the role of eosinophils in the context of infectious pathogens?
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What is the consequence of cell membrane damage caused by infectious pathogens?
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How do infectious pathogens disrupt metabolic pathways in cells?
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What is the outcome of the immune response triggered by infectious pathogens?
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How do fatty changes in organs occur in the context of infectious pathogens?
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What is the primary mechanism by which infectious pathogens cause cell damage?
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What is the primary mechanism of cell injury resulting from the disruption of plasma membrane structure and function?
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What is the consequence of severe cell injury, particularly in cases where the injury is not removed or corrected?
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What is the role of ATP in maintaining plasma membrane structure and function?
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What is the characteristic feature of reversible cell injury?
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What is the primary mechanism of infectious pathogens causing cell injury?
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What is the consequence of DNA damage in cell injury?
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What is the role of calcium in cell injury, particularly in cases of fat necrosis?
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What is the primary difference between necrosis and apoptosis in terms of physiological or pathological role?
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What is the characteristic feature of caseous necrosis?
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What is the outcome of DNA damage in cell injury?
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What is the mechanism by which certain viral infections cause cell injury?
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What is the role of cytotoxic T lymphocytes in cell injury caused by infections?
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What is the outcome of the accumulation of misfolded proteins in cells?
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What is the characteristic feature of necrotic cells?
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What is the role of apoptosis in eliminating unwanted cells?
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What is the outcome of nucleus fragmentation in apoptotic cells?
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Necrosis and apoptosis are two main forms of cell __________.
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The __________ phase of necrosis is cumulatively severe, leading to irreversible damage.
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Injury can cause necrosis, leading to the breakdown of __________ membrane integrity.
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Necrosis can be triggered by excessive __________ exposures.
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A characteristic feature of necrosis is a local __________ response.
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Necrosis can lead to the __________ of cellular components, making it difficult for the cell to recover.
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Apoptosis is often characterized by __________ morphological changes.
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The primary difference between necrosis and apoptosis is their __________ consequences.
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Infectious pathogens, which ______________ cells by producing toxins, can cause cell injury.
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Fatty changes in organs can lead to the accumulation of ______________, which disrupts metabolic pathways.
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Infectious pathogens can cause cell injury by stimulating the ______________ response.
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Eosinophils play a role in the ______________ response to infectious pathogens.
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Infectious pathogens can cause cell injury by damaging the ______________ membrane.
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The ______________ of metabolic pathways can lead to cell injury and death.
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Infectious pathogens can cause cell injury by producing ______________, which can damage cells.
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The accumulation of ______________ in cells can disrupt metabolic pathways and lead to cell injury.
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Hypoxia is a result of reduced ______ supply.
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Ischemia is a result of reduced ______ supply.
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During cell injury, swelling of the ______ reticulum and mitochondria may occur.
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Myelin figures are composed of ______ and other lipids.
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The ______ staining of nuclei during cell injury may be indicative of DNA damage.
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During cell injury, the ______ of chromatin in the nucleus may occur.
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Membrane ______ may be a characteristic feature of irreversible cell injury.
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Cell injury can lead to ______ and eventually cell death.
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Apoptosis is a process of programmed cell ______.
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Phagocytosis of apoptotic cells and fragments is performed by ______.
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By ______, apoponenomena: the ability to restore mitochondrial function (oxidative and ive stress) is mediated by defined molecular pathways.
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______ is the process of calcium soap formation in fat necrosis.
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In ______, the cell size is reduced due to shrinkage.
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______ is the typical outcome of enzymatic digestion in necrosis.
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The ______ of the plasma membrane is disrupted in necrosis.
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In ______, the nucleus undergoes fragmentation into nucleosome-sized fragments.
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The ______ of cellular contents is intact in apoptosis, but may be released in apoptotic bodies.
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In ______, the adjacent inflammation is frequent.
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______ is often physiologic and eliminates unwanted cells.
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The ______ of nucleus fragmentation in apoptotic cells is the formation of nucleosome-sized fragments.
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Fig. 1.2B shows the stage of _____________ cell injury.
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The process of _____________ formation in fat necrosis is also known as saponification.
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In Fig. 1.2C, the _____________ of nuclei is a characteristic feature of irreversible cell injury.
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The white chalky deposits seen in fat necrosis are also known as _____________.
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The _____________ of lipids in fat necrosis leads to the formation of calcium soap.
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The location of the tissue shown in Fig. 1.2A is the _____________.
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The fat necrosis shown in eFig. 1.1 is located in the _____________.
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The primary difference between necrosis and apoptosis is in their _____________ or pathological role.
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Match the following terms with their descriptions related to cell injury:
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Match the following terms with their descriptions related to cell injury and adaptation:
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Match the following figures with the corresponding stage of cell injury:
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Match the following types of gangrene with their causes:
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Study Notes
Cell Injury and Cell Death
Reversible Cell Injury
- Reversible cell injury occurs when cells are stressed or damaged, but can recover if the injurious stimulus is removed.
- Characteristics of reversible cell injury include:
- Cell swelling
- Bleb formation
- Increased eosinophilia of cytoplasm
- Loss of cellular function
- Reversible cell injury can be caused by various factors, such as:
- Ischemia (lack of blood flow)
- Hypoxia (lack of oxygen)
- Infections
- Toxins
- Nutrient deficiency
Irreversible Cell Injury (Necrosis)
- Irreversible cell injury occurs when cells are severely damaged and cannot recover, leading to cell death.
- Characteristics of irreversible cell injury include:
- Loss of cell membrane integrity
- Disruption of cellular organelles
- Release of cellular contents
- Nuclear fragmentation
- Inflammation
- Irreversible cell injury can be caused by various factors, such as:
- Severe ischemia or hypoxia
- Viral infections
- Bacterial toxins
- Chemical toxins
- Radiation
Apoptosis
- Apoptosis is a form of programmed cell death that occurs when cells are damaged or unwanted.
- Characteristics of apoptosis include:
- Cell shrinkage
- Nuclear fragmentation
- Formation of apoptotic bodies
- Intact cell membrane
- No inflammation
- Apoptosis is a physiological process that helps eliminate unwanted cells, but it can also be induced by disease or injury.
Features of Necrosis and Apoptosis
- Table 1.1 summarizes the key features of necrosis and apoptosis:
- Cell size: Necrosis - enlarged, Apoptosis - reduced
- Nucleus: Necrosis - pyknosis, karyorrhexis, karyolysis, Apoptosis - fragmentation
- Plasma membrane: Necrosis - disrupted, Apoptosis - intact
- Cellular contents: Necrosis - enzymatic digestion, Apoptosis - intact
- Adjacent inflammation: Necrosis - frequent, Apoptosis - no
Fat Necrosis
- Fat necrosis is a type of necrosis that occurs in adipose tissue, characterized by the formation of calcium soap deposits.
- Figure 1.1 shows an example of fat necrosis in the mesentery.
Morphologic Changes in Reversible and Irreversible Cell Injury
- Figure 1.2 shows the morphologic changes in reversible and irreversible cell injury:
- A: Normal kidney tubules with viable epithelial cells
- B: Early reversible ischemic injury with surface blebs, increased eosinophilia, and swelling of occasional cells
- C: Necrotic (irreversible) injury with loss of nuclei, fragmentation of cells, and leakage of contents.
Cell Injury
- Cells can adapt to stress, but may also be injured reversibly or irreversibly, leading to cell death.
- Reversible cell injury can be caused by various factors, including genetic abnormalities, mutations, and environmental toxins.
- Irreversible cell injury can lead to cell death, which can be caused by factors such as DNA damage, oxidative stress, and mitochondrial dysfunction.
Necrosis
- Necrosis is a type of cell death characterized by cell membrane damage, leading to an influx of Ca2+ and activation of proteases.
- Necrosis can be caused by various factors, including DNA damage, oxidative stress, and mitochondrial dysfunction.
- Characteristic features of necrosis include:
- Disruption of cellular membranes, including the plasma membrane and lysosomal membranes
- Release of cellular contents, including enzymes and proteins
- Inflammation and immune response
- Cell death and tissue damage
Apoptosis
- Apoptosis is a type of programmed cell death that occurs in response to certain stimuli, such as DNA damage or viral infections.
- Apoptosis is characterized by a series of cellular changes, including:
- Condensation of chromatin
- Fragmentation of DNA
- Activation of caspases
- Release of apoptotic bodies
- Apoptosis can be initiated through various pathways, including:
- Intrinsic pathway: involving mitochondrial dysfunction and release of cytochrome c
- Extrinsic pathway: involving activation of death receptors by ligands
- Apoptosis plays a crucial role in various biological processes, including:
- Development and tissue homeostasis
- Immune response and defense against infections
- Cancer and tumor suppression
Pathologic Consequences of Cell Injury
- Cell injury can lead to various pathologic consequences, including:
- Inflammation and tissue damage
- Fibrosis and scarring
- Cancer and tumorigenesis
- Organ dysfunction and failure
- Cell injury can be caused by various factors, including:
- Genetic abnormalities and mutations
- Environmental toxins and chemicals
- Infections and viral diseases
- Cancer and chemotherapy
Cellular Adapations and Physiological Responses
- Cellular adaptations and physiological responses associated with injury are summarized at the end of the chapter.
- The early changes associated with injury mostly affect the plasma membrane, leading to a reversible injury phase.
Reversible Injury
- Reversible injury refers to structural and functional abnormalities that can be corrected if the injurious agent is removed.
- It is characterized by changes in the plasma membrane, cellular swelling, and abnormal mitochondrial function.
Irreversible Injury
- Irreversible injury leads to cell death and is often caused by severe or prolonged injury.
- It is characterized by irreversible mitochondrial damage, nuclear chromatin clumping, and eventual cell death.
Cellular Death
- Cellular death can occur due to various mechanisms, including ATP depletion, plasma membrane damage, and increase in intracellular calcium.
- It can lead to the release of cellular contents, causing inflammation and tissue damage.
Necrosis
- Necrosis is a pathologic process that results in cell death due to severe injury or ATP depletion.
- It is characterized by the release of cellular contents, causing inflammation and tissue damage.
- Necrosis can be classified into different types, including coagulative necrosis, caseous necrosis, and gangrenous necrosis.
Causes of Necrosis
- Infectious pathogens, such as viruses, bacteria, and fungi, can cause necrosis by producing toxins or inducing immune responses.
- Fatty change in organs, such as the liver, can disrupt metabolic pathways and lead to necrosis.
- Eosinophilic necrosis, characterized by the accumulation of eosinophils, can occur due to various causes, including infections and allergic reactions.
Consequences of Necrosis
- Necrosis can lead to the release of cellular contents, causing inflammation and tissue damage.
- It can disrupt metabolic pathways, leading to the accumulation of toxic substances and further tissue damage.
- Necrosis can also lead to scarring and tissue remodeling, which can impair organ function.
Cell Injury and Cell Death
- Infectious pathogens can injure cells by producing toxins, leading to cell damage and disrupting metabolic pathways in organs.
- Fatty change in organs, such as the liver, can occur due to toxic injury, disrupting metabolic pathways and leading to rapid accumulation of triglycerides and lipid droplets.
- Eosinophilic degeneration of cells appears as red, eosinophilic, and degenerated cells with vacuolization in the cytoplasm.
Reversible Cell Injury
- Hypoxia (reduced oxygen supply) and ischemia (reduced blood supply) can cause reversible cell injury.
- Cell injury can lead to swelling of the endoplasmic reticulum and mitochondria, causing damage to the plasma membrane.
- Reversible cell injury can be recovered from, and the cell can return to its normal state.
Cell Death
- There are two main forms of cell death: necrosis and apoptosis.
- Necrosis is a result of severe cell injury, causing cell death and disruption of the plasma membrane.
- Apoptosis is a regulated process of cell death, where the cell undergoes programmed cell death.
- Necrosis is often associated with inflammation, whereas apoptosis is not.
Necrosis
- Necrosis is a result of severe cell injury, causing cell death and disruption of the plasma membrane.
- The cell undergoes karyorrhexis, karyolysis, and enzymatic digestion, leading to leakage of cell contents.
- Necrosis is often associated with inflammation and is a pathologic process.
Apoptosis
- Apoptosis is a regulated process of cell death, where the cell undergoes programmed cell death.
- The cell undergoes fragmentation, and the nucleus breaks down into nucleosome-sized fragments.
- Apoptosis is often a physiologic process, but can be pathologic in certain cases.
Morphologic Changes
- Reversible cell injury can lead to surface blebs, increased eosinophilia, and swelling of cells.
- Irreversible cell injury (necrosis) can lead to loss of nuclei, fragmentation of cells, and leakage of cell contents.
- Fat necrosis can lead to the formation of calcium soap deposits in the mesentery.
Cell Injury and Death
- Cell injury can be reversible or irreversible, leading to cell death.
- Reversible cell injury can be corrected once the injurious agent is removed.
Causes of Cell Injury
- Diverse insults, such as chemical, physical, or biological agents, can cause cell injury or death.
- Insults can lead to disease, including necrosis, apoptosis, and other cell death mechanisms.
Types of Cell Death
- Necrosis: a type of cell death characterized by cellular swelling, rupture, and inflammatory response.
- Apoptosis: a type of programmed cell death, also known as "cell suicide," where the cell undergoes a controlled process of self-destruction.
Mechanisms of Cell Death
- Plasma membrane damage: leads to cell death due to the loss of cellular contents and uptake of extracellular substances.
- Lipid breakdown: can lead to fat necrosis, characterized by the formation of calcium soap deposits.
- Mitochondrial damage: can disrupt cellular energy production and lead to cell death.
- Endoplasmic reticulum (ER) stress: can lead to cell death through the activation of apoptotic pathways.
Cellular Responses to Injury
- Cellular stress responses: can activate various signaling pathways to respond to injury, including the unfolded protein response (UPR) and the heat shock response.
- Inflammation: a response to tissue injury, characterized by the activation of immune cells and the release of pro-inflammatory molecules.
Apoptotic Pathways
- The intrinsic (mitochondrial) pathway: involves the activation of pro-apoptotic proteins, such as BAX, to trigger apoptosis.
- The extrinsic (death receptor) pathway: involves the activation of death receptors, such as Fas, to trigger apoptosis.
Consequences of Cell Death
- Tissue damage: can lead to organ dysfunction and disease.
- Inflammation: can lead to tissue damage and disease.
- Immune responses: can lead to autoimmune disorders or immunodeficiency diseases.
Examples of Cell Death
- Fat necrosis: a type of cell death characterized by the formation of calcium soap deposits.
- Fibrinoid necrosis: a type of cell death characterized by the deposition of fibrin and protein in the affected tissue.
- Caseous necrosis: a type of cell death characterized by the formation of cheesy, granular material, often seen in tuberculosis.
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This quiz assesses knowledge on cellular respiration, ATP production, and related biochemical processes. It covers the role of adenosine in energy transfer and the mechanism of ATP synthesis.