patho final ch. 3

fever, increased heart rate, pain, increase in leukocytes, presence of cellular enzymes

manifestations of cellular injury

what is the effect of reactive oxygen radicals?

these can cause further membrane damage and mitochondrial calcium overload

reperfusion injury

tissue injury resulting from the restoration of oxygen after an interval of hypoxia or anoxia

dysplasia

abnormal changes in the size, shape, and organization of mature cells

apoptosis

an active process of cellular self-destruction called programmed cell death

hypertrophy

an increase in size of cells and consequently in the size of the affected organ

hyperplasia

an increase in the number of cells resulting from an increased rate of cellular division. occurs when the injury has been severe and prolonged enough to have caused cell death

cellular aging

characteristics of aging include atrophy, decreased function, and loss of cells-possibly caused by apoptosis

lead, carbon monoxide, ethanol, mercury

chemical agents that can cause cellular injury or death

atrophy

a decrease or shrinkage in cellular size

metastatic calcification

consists of mineral deposits that occur in undamaged normal tissue as the result of hypercalcemia.

calcium accumulation

damage occurs when calcium salts cluster and harden, interfering with normal cellular structure and function.

intracellular accumulation of proteins

damages the cells in two ways: metabolites, produced when the cell tries to digest some proteins, are enzymes that can damage the organelles. second, excessive amounts of protein in the cytoplasm push against cellular organelles, disrupting organelle function and intracellular communication

atherosclerosis, cancer, diabetes, iron overload

diseases that are linked to oxygen-derived free radicals

accumulation of urate (uric acid)

high levels result in hyperuricemia and the deposition of sodium urate crystals in the tissues, leading to painful disorders collectively called gout. chronic hyperuricemia results in the deposition of urate in tissues, cell injury, and inflammation

pigment accumulation

may be normal or abnormal, endogenous (produced within the body) or exogenous (produced outside the body). endogenous proteins are made from amino acids and contain melanin. exogenous include mineral dusts containing silica and iron particles, lead, silver salts, and dyes for tattoos.

cellular swelling

most common degenerative change. caused by the shift of extracellular water into the cells.

intracellular lipid accumulation

most common site of this happening is in liver cells. as lipids fill the cells, vaculolation pushes the nucleus and other organelles aside. the outward appearance is yellow and greasy. alcohol abuse is one of the most common causes of this cellular injury

dystrophic calcification

occurs in dying and dead tissues, chronic tuberculosis of the lungs and lymph nodes, advanced atherosclerosis, and heart valve injuries.

intracellular accumulation of glycogen

seen in genetic disorders called glycogen storage diseases, and in disorders of glucose and glycogen metabolism. accumulation results in excessive vacuolation of the cytoplasm. most common cause of this is the disorder of glucose metabolism, aka diabetes.

coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis, gangrenous necrosis, gas gangrene

six types of necrosis

what causes cells to swell during hypoxic cell injury?

sodium and water can freely enter the cell which results in increased concentrations of sodium, water, and chloride

progressive stiffness or rigidity

the most common tissue change in the aging person

metaplasia

the reversible replacement of one mature cell type by another, sometimes less differentiated, cell type

necrosis

the sum of cellular changes after local cell death and the process of cellular self-digestion