Cellular Injury and Cell Death Flashcards
causes of cellular injury
[PHINGIC]
physical agents
hypoxia
infectious agents
nutritional imbalances
genetic abnormalities
immunologic reactions
chemical agents
morphologic alterations in cell injury
generalized swelling of cells and organelles
blebbing of plasma membrane
detachment of ribosomes from ER
clumping of nuclear chromatin
earliest manifestation of cell injury
generalized swelling of cells and organelles
plasma membrane protrudes due to
increased free radicals
nucleus in apoptosis
fragmentation into nucleosome-size fragments
pyknosis
clumping
karyorrhexis
fragmentation
karyolysis
dissolution
marker for cells undergoing apoptosis
caspases
cysteine proteases that can cleave aspartic acid residue
caspases
benefits of a necrosis death
none
types of necrosis according to location/extent
focal
massive
types of necrosis according to morphology
[CLGCFF]
coagulative
liquefactive
gangrenous
caseous
fat
fibrinoid
tissue is firm; eosinophilic; occurs when vessel is obstructed; infarct; looks dull and dirty/cooked
coagulative
viscous, microbial infection pus formation, rapid desolution, digestion of dead cells, creamy yellow, affects the CNS
liquefactive
due to ischemia, superimposed with bacterial infection, coagulation + liquid infection
gangrenous
two types of gangrene
dry and wet
sterile type, due to arterial occlusion, ischemic, less foul odor, discoloration (black or blood pigments)
dry gangrene
venous occlusion, foul odor, increase bacterial action + ischemic injury
wet gangrene
friable white appearance of necrotic area, soft whitish gray debris, TB and granuloma
caseous
forms an amorphous proteinaceous
caseous
due to destruction of pancreatic lipase
fat
splits fat into fatty acids and glycerol without affecting the membrane
lipase
FATTY ACIDS + CALCIUM =
FAT SAPONIFICATION (chalky white areas)
