01 - Cellular response to stress Flashcards
Increase in SIZE of cells resulting in increased size of organ; cellular adaptation of non-dividing cells (i.e. myocardial fibers).
Hypertrophy
Increase in NUMBER of cells; examples: BPH, papilloma virus infection
Hyperplasia
Reduction in the size of an organ or tissue due to decrease in cell size and number; example: Alzheimer’s disease
Atrophy
A reversible change in which one differentiated cell type is replaced by another cell type; example: Barrett esophagus
Metaplasia
The first manifestation of almost all forms of injury to cells; due to influx of ions (and water) due to failure of energy-dependent ion pumps.
Cellular swelling
A type of reversible injury, characterized by appearance of lipid vacuoles in the cytoplasm; often seen in cells participating in fat metabolism (liver, heart).
Fatty change (Steatosis)
Type of cell death, which results from a pathologic cell injury; undergoes cellular swelling and eventual pyknosis, karyorrhexis, and karyolysis.
Necrosis
It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis; there is nuclear shrinkage with increased basophilia.
Pyknosis
It is the destructive fragmentation of the nucleus of a dying cell.
Karyorrhexis
It is the complete dissolution of the chromatin of a dying cell.
Karyolysis
Type of cell death, which is energy-dependent, tightly regulated, and associated with normal cellular functions; often physiologic; the cell undergoes shrinkage and fragmentation.
Apoptosis
Pathway of apoptosis triggered by loss of survival signals, DNA damage and accumulation of misfolded proteins; inhibited by anti-apoptotic members of the Bcl family.
Mitochondrial/Intrinsic pathway
Initiator caspase for intrinsic pathway of apoptosis.
Caspase 9
Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes; initiated by TNF receptors.
Death receptor/Extrinsic pathway
Initiator caspases for extrinsic pathway of apoptosis.
Caspase 8, 10
Executioner caspases.
Caspase 3, 6
Regulated cell death that results in necrosis (morphologically); caspase-independent; activates RIP1 and RIP3 complexes that lead to increased ROS and decreased mitochondrial ATP production.
Necroptosis
Type of apoptosis often seen in microbe-infected cells; caspase 1 releases IL-1, and together with caspase 11, causes cell injury.
Pyroptosis
It involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles that fuse with lysosomes and digest enclosed material; used as a survival mechanism under various stress conditions (i.e. nutrient deprivation).
Autophagy
Marker for autophagy; involved in formation of autophagosome.
LC3
A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved; affected tissues take on a firm texture; often seen in infarcts of all solid organs (heart, spleen, kidney) except the brain.
Coagulative necrosis
Characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass; often seen in infections (pus) and in hypoxic death of cells within the CNS.
Liquefactive necrosis
This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis with superimposed liquefactive necrosis involving multiple tissue layers.
Gangrenous necrosis
Friable, white appearance of necrosis; appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border (granuloma); “cheese-like”.
Caseous necrosis
Refers to focal areas of fat destruction, typically seen in acute pancreatitis; there is release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity; the foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits (saponification), surrounded by an inflammatory reaction.
Fat necrosis
A special form of necrosis usually seen in immune reactions involving blood vessels; deposits of immune complexes, together with fibrin that have leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists.
Fibrinoid necrosis
Abnormal calcium deposition occurring in the absence of calcium metabolic derangements; examples: Psammoma bodies in cancers with papillary architecture and meningioma
Dystrophic calcification
Effect of caloric restriction on longevity.
Increased due to decreased IGF-1 signaling
Calcium deposition in normal tissues occurring in the presence of hypercalcemia; example: calcinosis
Metastatic calcification
Proteins that are produced in response to food deprivation; with actions that lead to prolonged longevity (anti-apoptotic, anti-ROS).
Sirtuins
