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Patho chp 2
| Term | Definition |
|---|---|
| Atrophy | A wasting or diminution of size, often accompanied by a decrease in function, of a cell, tissue, or organ |
| Hypertrophy | The enlargement or overgrowth of an organ that is due to an increase in the size of its cells rather than the number of its cells |
| Hyperplasia | An abnormal multiplication or increase in the number of normal cells of a body part |
| Metaplasia | Change in type of adult cells in a tissue to a form that is not normal for that tissue |
| Dysplasia | The alteration in size, shape, and organization of adult cell types |
| Apoptosis | A mechanism of programmed cell death, marked by shrinkage of the cell, condensation of chromatin, formation of cytoplasmic blebs, and fragmentation of the cell into membrane-bound bodies eliminated by phagocytosis |
| Infarction | Necrosis or death of tissues due to local ischemia resulting from obstruction of blood flow |
| Necrosis | Localized tissue death that occurs in groups of cells or part of a structure or an organ in response to disease or injury |
| Cell injury can be caused by a number of agents, including | physical agents, chemicals, biologic agents, and nutritional factors |
| Among the physical agents that generate cell injury are | mechanical forces that produce tissue trauma, extremes of temperature, and electrical forces |
| Ionizing radiation | can directly break chemical bonds, whereas nonionizing radiation exerts its harmful effects by causing vibration and rotation of atoms and molecules |
| Chemical agents | can block enzymatic pathways, cause coagulation of tissues, or disrupt the osmotic or ionic balance of the cell |
| Biologic agents | differ from other injurious agents in that they are able to replicate and continue to produce injury |
| Among the nutritional factors that contribute to cell injury are | excesses and deficiencies of total energy, as well as individual nutrients |
| Injurious agents | exert their effects largely through generation of reactive oxygen species (ROS) and free radicals, promotion of cell hypoxia, or impaired regulation of intracellular calcium levels |
| Free radicals are | an important cause of cell injury in hypoxia and after exposure to radiation and certain chemical agents |
| Lack of oxygen | underlies the pathogenesis of cell injury in hypoxia and ischemic, can result from inadequate oxygen in the air, cardiopulmonary disease, cardiorespiratory disease, anemia, or the inability of the cells to use oxygen |
| Increased intracellular calcium | activates a number of enzymes with potentially damaging effects |
| Injurious agents | may produce sublethal and reversible cellular damage or may lead to irreversible cell injury and death |
| Cell death | can involve two mechanisms |
| Apoptosis | involves controlled cell destruction and is the means by which the body removes and replaces cells that have been produced in excess, developed improperly, have genetic damage, or are worn out |
| Necrosis | refers to cell death that is characterized by cell swelling, rupture of the cell membrane, and inflammation |
| A number of body functions decline with age, including | muscle strength, cardiac reserve, vital capacity, nerve conduction time, and glomerular filtration rate |
| At the cellular level | oxidative phosphorylation by the mitochondria is reduced, as is the synthesis of nucleic acids and transcription factors, cell receptors, and structural and enzymatic proteins |
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