Cell Injury and Death II Flashcards
Necrosis
cell death that is not controlled by the cell, does not require the signals or activation of genes
cytoplasmic changes in necrosis
eosinophilia, glassy appearance, vacuolation
nuclear changes in necrosis
pyknosis, karyorrhexis, karolysis
6 types of necrosis
coagulative liqufactive caseous enzymatic fat fibrinoid gangrenous
coagulative necrosis
seen in death due to ischemia, hypoxia, reperfusion injury
basic outline of cell preserved but with no nuclei (ghost like)
liquefactive necrosis
death of brain tissue
abscesses where the center is made of pus.
amoorphous, granular under microscope
caseous necrosis
accumulation of mononuclear cells that mediate the chronic inflammatory reaction and granuloma formation. looks cheesy.
caseous necrosis is characteristic of what
TB
certain fungi
enzymatic fat necrosis
due to action of lipases
fatty acids that are released reach with calcium to form a soap-like substance
what does enzymatic fat necrosis look like under a microscope
material in fat cells
what does enzymatic fat necrosis look like in gross
white, chalky
If there is enough calcium the deposits in enzymatic fat necrosis will be _____-
basophilic
what is enzymatic fat necrosis seen in
pancreatitis
fibrinoid necrosis
injury in blood vessels with accumulation of plasma proteins causing wall to stain eosiohpilic
gangrenous necrosis
affects multiple types of tissue, happens when there is no blood going to that tissue. not a specific pattern of cell death
what is gangrenous necrosis often applied to
a limb lost from diabetes
wet gangrene
gangrene + bacterial infection
ischemia
caused by reduction of available oxygen, leads to tissue death
reperfusion
blood flow/oxygenation of tissue is restored, leads to large amount of ROS damage
what does ROS react with
lipid peroxide radicals
oxidation of proteins
oxidation of DNA
other findings in ischemia/reperfusion injury
accumulation of neutrophils
activation of complement pathway
roles of apoptosis (non-pathological)
em bryogenesis
hormone dependent involution
cell deletion in proliferating cell population
immune defense
removal of self-reactive lymphocytes
removal of cells that have served their purpose
apoptosis (pathologic)
cell death in tumors DNA damages transplant rejection atrophy after duct obstruction some viral diseases
stages of apoptosis
signaling pathways
intracellular signals
execution phase
removal of dead cells
In DNA damage what activates proapoptic forms of Bcl-2
p53
stimulation of proapoptic forms of Bcl-2 stimulates
Bax and Bak
apoptosis extrinsic pathway
Fas, TNF activate adaptor proteins which bind caspases
Apoptosis instrinsice pathway
Bax and Bak dimerize and form channels in the mitochondrial membrane leading to permeability of cytochromc C leakage and activation of caspases
cell size of necrosis
enlarges
cell size of apoptosis
reduces
nuclues of necrosis
pyknosis, karyorrhexis, karyolysis
nucleus of apoptosis
fragmentation
plasma membrane of necrosis
disrupted
plasma membrane of apoptosis
intact
cellular contents of necrosis
enzymatic digestion, may leak out of cell
cellular contents of apoptosis
intact
acetaminophen
it’s metabolite is a highly reactive quinone that reacts with protein, DNA< causes oxygen stress - massive liver necrosis
CCl4
reacts with membrane and ER
heavy metals and cyanide
act on mitochondria
reduce ATP
phalloidin, paclitaxel
act on cytoskeletal
prevent cell from replicating
chemotherapeutic alkylating agents
damage DNA directly
