Parsa Flashcards
karyolysis
basophilia fades
pyknosis
nuclear shrinkage, increased basophilia
karyorrhexis
nuclear fragmentation
coagulative necrosis
ischemia of solid organs
hemorrhagic necrosis
venous vessel obstructed or artery plugged in softer tissue
liquefactive necrosis
abscess filled with enzymes or neutrophils create pus
gangrenous necrosis
blockage of blood vessels in leg
caseous necrosis
tuberculosis
gumma necrosis
syphilis
enzymatic fat necrosis
acute pancreatitis
fibrinoid necrosis
immune complex deposition in vascular walls
mercury chemical injury
binds cell membrane proteins to increase permeability (direct)
cyanide chemical injury
inhibits mitochondrial oxidative phosphorylation (direct)
CCl4
creates free radical *CCl3 (toxic metabolite)
acetaminophen
creates NAPQI (toxic metabolite)
fatty change in liver
normal endogenous substance produced excessively or removed inadequately
lysosomal storage disease
defects in metabolic enzymes lead to accumulation of normal endogenous substance
silicosis
cell can’t degrade or transport abnormal endogenous substance
a1-antitrypsin in liver
defects in protein folding and degradation lead to accumulation of abnormal endogenous substance
fatty liver causes
alcoholism, diabetes, obesity, starvation
proteinuria
protein leakage across glomerulus, increased reabsorption of protein into vesicles (hyaline droplets)
diabetic liver
glycogen accumulates
dystrophic calcification
occurs locally in dying tissues
metastatic calcification
hypercalcemia (disturbance in calcium metabolism)
hypertrophy/hyperplasia causes
increased demand/stimulation (growth factors, hormones)
atrophy causes
decreased demand/stimulation
metaplasia causes
chronic irritation (physical/chemical)
reversible injury effects
cellular swelling, fatty change
irreversible injury (cell death) effects
necrosis, apoptosis
cellular aging causes
cumulative sublethal injury over a long lifespan
