Cell Death and Perfusion Disorders III Flashcards
autolysis
cell destruction that occurs after death (by a cells own enzymes)
putrefaction
decomposition of dead tissues by microorganisms
ischemia
decrease in blood supply to a tissue with resultant hypoxia, decreased glucose and other nutrients and decreased removal of metabolic waste
infarct
local area of peracute ischemia that causes coagulative necrosis
what is the time progression of necrosis types
coagulative -> caseous -> liquifactive
common causes of coagulative necrosis
hypoxia, ischemia, toxins
common cause of caseous necrosis
infectious agents
common area of liquefactive necrosis
nervous tissue
gangrenous necrosis occurs at
extremities or dependent portions of organs
dry gangrenous necrosis resembles
coagulative necrosis
wet gangrenous necrosis resembles
liquefactive necrosis
gross appearance of coagulative necrosis
pale tan to gray, sharply demarcated, solid
histologic appearance of coagulative necrosis
retained architecture, cytoplasmic eosinophilia
gross appearance of caseous necrosis
dry or moist, crumbly, granular or laminated, may have central exudate
histologic appearance of caseous necrosis
architecture lost, lysed cells, granular to amorphous debris, nuclear debris
gross appearance of liquefactive necrosis
pale to translucent, soft to liquid, cavitated
histologic appearance of liquefactive necrosis
architecture lost, parenchymal cells lost, space filled with inflammatory cells
gross appearance of dry gangrene
dry, leathery
histologic appearance of dry gangrene
(coagulative necrosis): cytoplasmic eosinophilia, architecture retained
gross appearance of wet gangrene
red-black, wet
histologic appearance of wet gangrene
(liquefactive necrosis): architecture lost, parenchyma lost, inflammatory cells
describe what hematogenous agents would cause a zonal pattern and what would cause a random multifocal pattern
toxins would cause zonal patterns; bacteria would cause a random multifocal pattern
what pattern would inhaled pathogens cause on the lung
cranioventral distribution
what would the presence of fibrin in a lesion tell you
the lesion was an ulcer (reached the blood vessels) as opposed to an erosion
what layers does erosion go through vs an ulcer
erosion: just mucosa; ulcer: mucosa, submucosa, muscularis
what part of the kidney is most susceptible to NSAID overdose
medulla; specifically the medullary capillary plexus
what is a clinical sign of growth plate necrosis
affected limb is shorter than non-affected limb
anemic hypoxia would impact what part of the liver first
zone III (last to receive oxygen)
causes of oxygen deprivation (4)
- inadequate blood oxygenation
- inadequate oxygen-carrying capacity of blood
- inadequate delivery of oxygenated blood to tissue
- inhibition of cellular respiration enzymes
what is reperfusion syndrome
reperfusion of tissues -> ROS/free-radical generation -> further damage to tissue
how does ischemia of watershed zones appear
segmental
example of end-artery ischemia
coagulative necrosis of a renal pyramid
difference between arterial and venous occlusion
arterial causes an immediate infarction, whereas venous first causes congestion and edema, which promotes the infarction
what would cause a pale and non-swollen infarct
ACUTE arterial infarct
what would cause a dark red/swollen infarct
venous infarct; slightly later arterial infarct with damage of blood vessels in the infarcted tissue and backflow of blood from other tissues
what would cause a pale, swollen, red-rimmed infarct
cell swelling and necrosis that pushes blood out of the infarct, macrophage cleaning
red rim = hyperemia/hemorrhage/acute inflammation
what would cause a multicoloured infarct
RBC breakdown, inflammation, neovascularization
what would cause a white and contracted infarct
chronic infarction with subsequent scarring
what is the endpoint of infarction
scarring with contraction
what is DIC
loss of localization of the coagulation process and generation of excess thrombin, with widespread microvascular thrombi
name 3 causes of DIC
sepsis, shock, extensive trauma
DIC sequela
bleeding due to consumption of all coagulation factors; ischemic tissue damage
