3: Cell Death Flashcards
leaking cellular contents
necrosis
cell fragmentation and phagocytosis
apoptosis
cytoplasmic changes with necrosis
esoinophilia
glassy appearance
vauolation
nuclear changes with necrosis
pyknosis
karyorrhexis
karyolysis
pyknosis
shrinkage of nucleus
karyolysis
fading of nuclear fragments
karyorrhexis
fragmentation of nucleus
usually seen in death due to ischeia, hypoxia, reperfusion injury in most organs except brain
coagulative necrosis
basic outline of cell preserved but with no nuclei
coagulative necrosis
death of brain tissue, typically
liquefactive necrosis
seen in abscess where the center is made up of enzymatic digested PMNs (pus)
liquefactive necrosis
amorhpous, granular under the microscope with loss of cells and tissue structure
liquefactive necrosis
accumulation of mononuclear cells that mediate the CHRONIC inflammatory rxn and GRANULOMA formation
caseous necrosis
lipid in wall of the organism can’t be fully broken down
caseous necrosis
dead cell persist indefinitely as amorphous, coarsely granular, eosinophilic debris
caseous necrosis
caseous necrosis is characteristic of what organisms
TB and fungi
fat is changed due to action of lipases
enzymatic fat necrosis
FA released from enzymatic fat necrosis react with calcium to form
soap like substance that appears white, chalky
why can you see some enzymatic fat necrosis on x-ray
enough calcium deposition (this will also make them basophilic)
where is enzymatic fat necrosis most commonly seen
pancreatitis
injury in blood vessels with accumulation of plasma prtn (cause wall to stain eosinophilic)
fibrinoid necrosis
vasculitis is associated with…
fibrinoid necrosis
not specific pattern of cell death usually applied to limb died due to loss of circulation or bowel
gangrenous necrosis
wet gangrene
combination of gangrene with superimposed bacterial infection
associated with diabetes
gangrene
reduction of available oxygen
ischemia
TPA
tissue plasminogen activator
- given to help reperfusion during first 30 min of heart attack/stroke or transplantation
blood flow/oxygenation of tissue is restored
reperfusion
clinical observations during a heart attack
- lavine sign
- no ‘P’
- ST elevation
- elevations in creatine kinase CK-MB
- elevations in troponin I or T (TnI or TnT)
physiological roles of apoptosis
- embryogenesis
- hormone dependent involution
- cell deletion in proliferating cell population
- normal immune defense against infected/transformed cells
- removal of self-reactive lymph clones
pathologic apoptosis conditions
- cytotoxic anticancer drugs
- low doses of radiation, temp. drugs
- transplant rejection
- duct obstruction atrophy
- some viruses
basic outline of apoptosis
- signaling pathways initiate apoptosis
- itnracellular signals further commit cell to apoptotic pathway
- execution caspases catabolize cytoskeleton and activate endonucleases (DNA breakdown)
- removal of dead cells
apoptotic pathway from within the cell
mitochondrial intrinsic pathway
apoptotic pathway that uses receptors
death receptor extrinsic pathway
Bax and Bak
proapoptotic family members of Bcl-2 family
action of Bax and Bak
dimerize and form holes in mitochondria
what role does cytochrome c play in apoptosis
leaks out of holey mitochondria and stimulates initiator capsases
Bcl-2 and Bcl-x
anti-proapoptotic prtns (block proapoptotic prtns)
describe the extrinsic pathway of apoptosis
Bcl-2 family sensors recognize cell injury
- Bax and bak attack mitochondria
- cytochrome c activates initiator capsaes which activate executioner capsases which do the degrading
describe the intrinsic pathway of apoptosis
receptor-ligand interactions with Fas and TNF receptor activate adapter proteins
- adapter prtns activates initiator capsases which activate executioner capsases which do the degrading
wher do the intrinsic and extrinsic apoptotic pathways converge
initiator capsases
how does p53 respond to DNA damage
p53 will activate pro-apoptotic forms of the Bcl-2 family (Bax and Bak)
low v. high doses of radiation
low= apoptosis (gets the proliferationg cells) high= necrosis (gets all cells)
do viruses induce apoptosis or necrosis
both
if nutrient deficiency or complement activation… necrosis
if changes in p53, granzyme, or Tcells…. apoptosis
tylenol suicide
massive liver necrosis
acetaminophen
highly reactive quinone metabolite that reacts w/ prtn, DNA and causes oxygen stress
carbon tetrachloride CCL4
metabolite CCl3- reacts with membrane and ER
heavy metals and cyanide
injure the mitochondria
phalloidin, paclitaxel
injure cytoskeleton and prevent replication
chemoterapeutic alkylating agents
direct damage to DNA
most vulnerable liver zone for necrosis
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