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Cell injury
| Term | Definition |
|---|---|
| physiological hypertrophy is | An increase in the size of skeletal muscle cells observed in body builders as a result of regular exercise |
| cause of cell injury | acquired, genetic, congenital |
| acquired | developed after birth,external factors eg ischemia |
| genetic | family inherited, abnormalities in DNA, sickle cell disease |
| congenital | present from birth, develop during foetal life, trisomy 21 |
| ischemia is | lack of blood flow through the tissue, disturbs oxidative metabolism, cause blood clots that result in brain stroke. |
| sickle cell disease | red blood cells have abnormal shape, whih blocks and slow down the flow of oxygenated blood to th tissues, causing pain |
| trisomy 21 | extra copy of a chromosome on chromosome 21, mental retardation, weak muscles. |
| cellular adaptation | changes in cell in order to become stable in new environment, increased, decreased or change in cellular activity |
| increased | hypertrophy and hyperplasia |
| decreased | atrophy |
| change in cell type/position | metaplsia and dysplasia |
| hypertrophy | increase in cell size, usually tissue type incapable of division, back to normal when stimuli is removed |
| hyperplasia | increase in cell number, in cells undergoing mitotic division. 3 subtypes- physiologic, compensatory |
| Atrophy | shrinkage of the cell by loss of cellular substance. |
| metaplasia | substitution of 1 adult cell for another which leads to loosing it protective mechanism. |
| dysplasia | loss of architecture between cells, abnormal development in tissue |
| necrosis | cell death by injury - mechanical damage or exposed to chemical agents |
| apoptosis | cell death by suicide: - internal and external signals |
| series of cellular changes in necrosis | 1. mitochondria swells up and rupture 2. plasma membrane ruptures 3. cell content spillage outside the cell and affect neighbour cells 4. cell lysis and inflammatory response |
| Coagulative necrosis | lost nucleus, highly acidophillic cytoplasm, cell outline remains. hardening of tissue due to protein denaturation. ALmost all tissue type, due to ischemia/ chemical agents |
| Liquefaction necrosis | softening/liquefying tissue (brain). Dead cell digestion leading to turbid liquid |
| caseous necrosis | featureless appearance of the tissue (lump of cheeses) tuberculosis disease . |
| fat necrosis | in sites rich of fat eg female breast. release of lipase breaks adipose into fatty acids causing fat saponification in connection with calcium producing glossy white areas. |
| gangrenous necrosis | superimposed infection caused by bacteria, notable clostridia. iron suphide is deposited from haemoglobin and affected area turns black, loss blood supply, gut as a center area of attack |
| why apoptosis take place | proper development, cells with DNA damage activate p53 for dna repair, if it failsinduce apoptosis for elimination; , infected with viruses to stop the proliferation |
| process of apoptosis | 1. signal from control gene 2. activation of death genes in nucleus 3. diffusion of death gene product through the cell. 4a. cell surface breakdown 4b. fragmentation of chromatin 4c. mitochondria shutdown |
| series of cellular changes in apoptosis | dna fragments, cytoplasm shrink and membrane bleps, content is packed in apoptotic bodies, receptor of phagocytic cells engulf the cell fragments |