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Cell Injury, Cell Death, and Adaptations - Coggle Diagram
Cell Injury, Cell Death, and Adaptations
CELLULAR ADAPTATIONS TO STRESS
Hypertrophy
increased cell and organ size, often in
response to increased workload
induced by growth
factors produced in response to mechanical stress or
other stimuli
occurs in tissues incapable of cell division
Hyperplasia
increased cell numbers in response to hormones and other growth factors
occurs in tissues whose cells areable to divide or contain abundant tissue stem cells
Atrophy
decreased cell and organ size, as a result of
decreased nutrient supply or disuse
associated with decreased synthesis of cellular building blocks and increased breakdown of cellular organelles
Metaplasia
change in phenotype of differentiated cells
often in response to chronic irritation, that makes cells better able to withstand the stress
usually induced by
altered differentiation pathway of tissue stem cells
may result in reduced functions or increased propensity for malignant transformation
CELL INJURY AND CELL DEATH
Morphologic Alterations in Injured Cells and Tissues
Reversible cell injury
cell swelling
fatty change
plasma
membrane blebbing
loss of microvilli
mitochondrial
swelling
dilation of the ER
eosinophilia
Necrosis
increased eosinophilia
nuclear shrinkage
fragmentation
dissolution
breakdown of plasma membrane and organellar membranes
abundant myelin figures
leakage and enzymatic digestion of cellular contents
Patterns of tissue necrosis
Under different conditions,
necrosis in tissues may assume specific patterns
coagulative
liquefactive
gangrenous
caseous
fat
fibrinoid
Mechanisms of Cell Injury
ATP depletion
failure of energy-dependent functions →
reversible injury → necrosis
Mitochondrial damage
ATP depletion → failure of energydependent cellular functions → ultimately, necrosis
under some conditions, leakage of mitochondrial proteins that cause apoptosis
Influx of calcium
activation of enzymes that damage cellular components and may also trigger apoptosis
Accumulation of reactive oxygen species
covalent modification of cellular proteins, lipids, nucleic acids
Increased permeability of cellular membranes
may affect plasma membrane, lysosomal membranes, mitochondrial membranes;
typically culminates in necrosis
Accumulation of damaged DNA and misfolded proteins
triggers apoptosis
APOPTOSIS
Regulated mechanism of cell death that serves to eliminate unwanted and irreparably damaged cells, with the
least possible host reaction
Characterized by enzymatic degradation of proteins and DNA, initiated by caspases; and by recognition and removal of dead cells by phagocytes
Initiated by two major pathways:
Mitochondrial (intrinsic) pathway
triggered by loss of
survival signals, DNA damage and accumulation of misfolded proteins (ER stress)
associated with leakage of pro-apoptotic proteins from mitochondrial membrane into the cytoplasm, where they trigger caspase activation; inhibited by anti-apoptotic members of the Bcl family, which are induced by survival signals including growth factors.
Death receptor (extrinsic) pathway
responsible for elimination of self-reactive lymphocytes and damage by
cytotoxic T lymphocytes
is initiated by engagement of death receptors (members of the TNF receptor family) by ligands on adjacent cells