Cell Injury- Calcification and Amyloidosis Flashcards
Disease
abnormal body process with a characteristic set of signs or symptoms that may affect the whole body or any of its parts. The fundamental disease process regardless of etiology begins at the molecular and cellular level.
Injury
refers to damage or pathologic alterations in molecules and structure can occur in cells and extracellular components of tissue. Injury to a cell can result in loss of normal cell functions and loss of tissue function.
adaptation
changes in function and structure that maintain a homeostatic state and maintain cell viability. Cells may revert to previous structure and function when the stress or injury is removed.
Reversible injury
pathologic alterations in cell molecules and structure that are associated with abnormal function and with loss of homeostatic state. Removal of stress or injury results in cell recovery and return to normal function.
Irreversible injury and cell death
damage to cell reaches magnitude or duration where the cell passes a “point of no return.” Despite removal of injury or stress, the cell cannot recover and dies.
Necrosis
a pattern of cell death that often follows hypoxic, toxic and some microbial injuries and that is characterized by cell swelling and membrane changes as well as nuclear changes such as pyknosis and karyorrhexis.
Apoptosis
a pattern of cell death that is induced by a tightly regulated intracellular program in which cells induced to die activate enzymes that degrades the cells’ own nuclear DNA and nuclear and cytoplasmic proteins leading to nuclear fragmentation without loss of plasma membrane integrity.
Hypoxia/hypoxemia
cardio respiratory failure and neuronal necrosis. Renal vein thrombosis and renal tubular necrosis.
Physical agents
trauma. Thermal induced skin necrosis.
Chemicals/drugs
lead toxicity and neuronal and renal tubular necrosis. Glucocorticoid- induced lymphocyte apoptosis.
Infectious agents
adenovirus-induced epithelial cell necrosis. Endotoxin-induced apoptosis of lymphocytes and hepatocytes in gram-negative bacteremia.
Immunologic reactions
complement-mediated hemolysis in autoimmune hemolytic anemia in dogs. T-lymphocytes-induced cell apoptosis in viral infection.
Genetic defects
copper storage disease of bedlington terrier dogs results in hepatocyte necrosis. Purkinje cells necrosis in cerebellar abiotrophy of calves.
Nutritional inbalances
vitamin E deficiency and hepatocellular necrosis in pigs. High dietary copper and hemolysis in sheep.
Swelling
Gross morphology: organ may be enlarged, pale or discolored.
Light microscopic morphology: lipidosis may occur because of decreased protein synthesis.
Electron microscopic changes: cell swelling with ER dilation
Pyknosis
nuclear shrinkage with increased basophilia
Karyorrhexis
fragmentation of chromatin
karyolysis
dissolution of chromatin
Gangrenous necrosis
ischemic necrosis of distal extremities toes, feet, ears
Fat necrosis
necrosis of adipocytes and chalky-white lesions in fat characterized by cleaveage of neutral fat by lipase to triglycerides and FA and precipitation of the FA by calcium to form FA soaps.
Patterns of necrosis
coagulative, liquefactive, caseous.
Physiologic apoptosis
embryogenesis and development involution. Hormone dependent cycling. Cell depletion in proliferating populations. Deletion of autoreactive Tcells.
Pathologic induction of apoptosis
endotoxin-induced apoptosis of lymphocytes and hepatocytes. Corticosteroid-induced apoptosis of lymphocytes. Lentiviral-induced apoptosis of lymphocytes. Tumor necrosis factor of apoptosis in many cells.
Pathologic inhibition of apoptosis
the failure of cells to undergo apoptosis is a feature of many neoplastic diseases. Inhibition of apoptosis is an important feature of several viral diseases that induce proliferative lesions.
