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Pathology - Cellular death
Necrosis is an inadequately regulated kind of cell death characterized by the loss of membrane integrity, resulting in the spilling of cellular contents and an inflammatory reaction.
• Coagulative necrosis is the predominant type, marked by the absence of cell nuclei while maintaining the overall structural integrity. The necrotic tissue appears macroscopically pale and firm.
Liquefactive necrosis results in the total destruction of cellular architecture, transforming it into a mushy, semi-solid mass. This is commonly observed in the brain subsequent to cerebral infarction.
Caseous necrosis is a form of necrosis characterized by dead tissue that macroscopically resembles cream cheese. It can manifest in several diseases, but is predominantly linked to tuberculosis.
• Gangrene denotes necrotic tissues altered by air exposure, leading to desiccation (dry gangrene) or infection (wet gangrene). In cases of critical limb ischaemia, toes that experience blood deprivation typically exhibit dry gangrene.
Apoptosis is a regulated process of cellular demise when no intracellular components are expelled from the dying cell, hence preventing any inflammatory response. Apoptosis can occur naturally, such as in the elimination of cells during embryogenesis and those with DNA damage, or pathologically. Apoptosis can be initiated via two primary mechanisms: the activation of surface death receptors, such as Fas or TNF-α (extrinsic pathway), or through cellular damage (intrinsic pathway). The final outcome is the activation of protease enzymes known as caspases, which deconstruct the cell's cytoplasm and nucleus.
Apoptotic cells undergo shrinkage and fragmentation into apoptotic bodies, each maintaining an unbroken cell membrane. • Apoptotic entities are promptly eliminated by neighboring cells. • Dysregulated apoptosis is believed to play a crucial role in various significant disease mechanisms, especially carcinogenesis.
Necrosis is an inadequately regulated kind of cell death characterized by the loss of membrane integrity, resulting in the spilling of cellular contents and an inflammatory reaction.
• Coagulative necrosis is the predominant type, marked by the absence of cell nuclei while maintaining the overall structural integrity. The necrotic tissue appears macroscopically pale and firm.
Liquefactive necrosis results in the total destruction of cellular architecture, transforming it into a mushy, semi-solid mass. This is commonly observed in the brain subsequent to cerebral infarction.
Caseous necrosis is a form of necrosis characterized by dead tissue that macroscopically resembles cream cheese. It can manifest in several diseases, but is predominantly linked to tuberculosis.
• Gangrene denotes necrotic tissues altered by air exposure, leading to desiccation (dry gangrene) or infection (wet gangrene). In cases of critical limb ischaemia, toes that experience blood deprivation typically exhibit dry gangrene.
Apoptosis is a regulated process of cellular demise when no intracellular components are expelled from the dying cell, hence preventing any inflammatory response. Apoptosis can occur naturally, such as in the elimination of cells during embryogenesis and those with DNA damage, or pathologically. Apoptosis can be initiated via two primary mechanisms: the activation of surface death receptors, such as Fas or TNF-α (extrinsic pathway), or through cellular damage (intrinsic pathway). The final outcome is the activation of protease enzymes known as caspases, which deconstruct the cell's cytoplasm and nucleus.
Apoptotic cells undergo shrinkage and fragmentation into apoptotic bodies, each maintaining an unbroken cell membrane. • Apoptotic entities are promptly eliminated by neighboring cells. • Dysregulated apoptosis is believed to play a crucial role in various significant disease mechanisms, especially carcinogenesis.
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