GNUR 293: Patho basics: Cellular
Response to Injury
Atrophy - ANS-cells shrink and reduce their differentiated functions in response to
normal and injurious factors
cause of atrophy (5) - ANS--disuse
-poor nutrition
-denervation
-ischemia
-persistent cell injury
2 biochemical pathways for atrophy - ANS-1. ubiquitin- proteosome system
2. lysosomes
Hypertrophy - ANS-increased cell mass accompanied by an augmented functional
capacity in response to physiologic and pathophysiologic demands
-muscle cells enlarge
-cells do not divide
causes of hypertrophy - ANS--increased cellular protein content
-muscle protein synthesis (rebuilding of muscle tissue)
-over use
hyperplasia - ANS-increase in functional capacity related to an increase in cell number
due to mitotic division
-increase in size because influx in NEW cells (proliferation)
-provoked by excessive cell inflammation
-cells divide
causes of hyperplasia - ANS--increased physiologic demand or hormonal stimulation
-persistent cell injury
-chronic irritation of epithelial cells
Metaplasia - ANS-replacement of one differentiated cell type with another
-adapt to help (ex: smoking)
, causes of metaplasia - ANS--adaption to persistent injury, with replacement of a cell
type that is better suited to tolerate injurious stimulation
-fully reversible when injurious stimulation is removed
Dysplasia - ANS-disorganized appearance of cells because of abnormal variations in
size, shape, and arrangement
-may transform into cancerous cells (low or high grade)
reversible cell injury - ANS--mild or short lived injury
-withstands assault
-returns to normal function
irreversible cell injury - ANS--severe or prolonged injury
-results in cell death
Hypoxic cell injury (5) - ANS--ischemia
-hypoxia (CO2 can cause this)
-anoxia (severe hypoxia)
-cellular responses
-reperfusion injury
cellular response in cell injury - ANS--decrease ATP due to lack of O2, causing failure of
Na/K pump & Na/Ca exchange(leads to increase Na & K)
-cellular swelling (increased Na & H2O)
reperfusion injury in cell injury - ANS--restoration of O2 generates highly reactive O2
radicals which cause further membrane damage & Ca overload of the mitochondria
(does not response well to excess Ca)
-subsequent inflammation
Reperfusion injury following an ischemic episode results in increased free radical
production and leads to further tissue damage due to: - ANS-excessive intracellular
calcium
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