Cell Injury & Cell Death Flashcards
(30 cards)
Two main morphological correlates of reversible cell injury
Fatty Change & Cellular Swelling
3 Characterizations of Irreversible injury
Inability to restore mitochondrial function
Loss of structure and function of plasma membrane and intracellular membranes
Loss of DNA and chromatin structural integrity
Beginning of necrosis is initiated by
Injury to lysosomal membranes of injured cells.
Necrosis
“Accidental” cell injury
- occurs in diseased cells only
- Caused by toxins, infections, trauma and ischemia.
- elicits inflammation
- cells lose their membrane and cellular enzymes leak out and digest the cell and cytoplasmic organelles.
Apoptosis
“Regulated” cell death
- occurs in healthy or diseased cells
- occurs via therapeutic agents, genetic mutations, and infections.
- cells do not lose their membrane
- no inflammation
Pyknosis
Breakdown of DNA and chrome in characterized by nuclear shrinkage and increased basophila.
Karyorrhexis
Fragmentation of the pyknotic nucleus
Karyolysis
Digestion of DNA via DNase activity inside a pyknotic nucleus.
Coagulative necrosis
Underlying tissue architecture tube is preserved while the inside cells undergo necrosis.
- marked increase in eosinophilia
Liquefactive necrosis
Rapid accumulation of leukocytes “liquify” the tissue
- seen in bacterial and some fungal infections
Gangrenous Necrosis
Coagulative necrosis that is marked via a Loss of blood supply
- when combined with a bacterial infection, becomes liquefactive necrosis. “Wet gangrene”
Caseous Necrosis
Possess a yellow-white cheese like appearance from TB infections.
Fat necrosis
Fat destruction, typically caused via pancreatic lipase.
Fibrinoid necrosis
Caused via immune reactions and mostly found in blood vessels
Mitochondrial pathway of apoptosis
Most used form
Mitochondria releases cytochrome c, which triggers caspase: the initiator of apoptosis.
Proteins that control cytochrome c permeability
Bcl-2
- holds the Bax and Bak pathways back
Death Receptor pathway of apoptosis
Type 1 TNF and FAS (CD95) receptors are unregulated on infected cells.
CD-8 T cells posses fas-L and bind to these receptors, activating caspase: the initiator of apoptosis
Oxidative stress
Damage to the cell is generated via Reactive oxygen species (ROS)
Can be upregulated with additional stress factors
Can induce apoptosis or necrosis
Ways of cellular adaption to stress
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Autophagy
Lysosomal digestion of the cells own organelles and components
- done it times of severe nutrient deprivation
Pyroptosis
Inflammasome activation causes caspase activation
- produces cytokines and is essentially inflammation mixed with apoptosis
Necroptosis
TNF receptor triggering causes RIP kinases to activate.
Causes membrane dissolution and apoptosis bodies. Is essentially necrosis mixed with apoptosis.
4 pathways of abnormal intracellular accumulations
Defects in packaging/transport mechanisms
Genetic or acquired defects in protein folding
Failure to degrade a metabolite via enzyme deficiencies
Enzyme and transport failure altogether
Abnormal metabolism
Can’t metabolize products in cells
Ex: steatosis: accumulation of triglycerides writhing parenchyma cells
