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level: Cell Death

Questions and Answers List

level questions: Cell Death

Question	Answer
Loss of nucleus	Morphologic hallmark of cell death
Nuclear condensation/ Shrinking of nucleus ("ink dot")	Pyknosis
Breaking up/fragmentation of nucleus	Karyorrhexis
Breaking down of nuclear fragments to basic building blocks	Karyolysis
Necrosis and apoptosis	Mechanisms of cell death
Death of large group of cells followed by inflammation brought about by pathologic processes	Necrosis
Firm necrotic tissue with absent nuclei and preserved cell shape and organ structure due to protein coagulation	Coagulative Necrosis
Associated with coagulative necrosis (Exception: Brain)	Ischemic infarction
Blood re-entry to a loosely organized tissue (eg. pulmonary/testicular infarction)	Red infarction
Liquefied necrotic tissue due to enzymatic lysis of cells and protein	Liquefactive necrosis
Liquefactive necrosis due to proteolytic enzymes from microglia	Brain infarction
Coagulative necrosis characteristic of ischeme of lower limb and GIT	Dry gangrene
Liquefactive necrosis due to superimposed infection	Wet gangrene
Coagulative + Liquefactive necrosis; characteristic of granulomatous inflammation from TB and fungal infection	Caseous necrosis
Caseous necrosis	Cottage cheese-like appearance
Fat necrosis; appearance brought about by calcium deposition	Chalky white appearance
Necrotic adipose tissue brought about by saponification	Fat necrosis
Reaction of fatty acids with calcium deposits; type of dystrophic calcification	Saponification
Normal calcium and phosphate levels; necrotic tissue forms nidus for calcium deposit	Dystrophic calcification
High calcium and phosphate levels lead to calcium deposition in normal tissue	Metastatic calcification
Necrotic damage to blood vessel wall; malignant hypertension and vasculitis	Fibrinoid necrosis
ATP-dependent genetically programmed cell death	Apoptosis
Mediator of apoptosis	Caspase
Breaks down cytoskeleton	Protease
Breaks down DNA	Endonuclease
Cellular injury, DNA damage and loss of hormonal stimulation cause inactivation of Bcl2 -> cytochrome c release -> caspase activation	Intrinsic mitochondrial pathway
Inhibits release of cytochrome c from inner mitochondrial matrix	Bcl2
Activator of caspases	Cytochrome c
FAS ligand, TNF binds to corresponding receptors, activating caspases	Extrinsic receptor-ligand pathway
Binds to FAS death receptor to activate caspases in extrinsic apoptotic pathway	FAS ligand
FAS death receptor	CD95
FAS ligand-mediated apoptosis of T-cells which have too avid or strong binding of self antigen	Negative selection (Thymus)
CD8+ T cells release perforin and granzyme to stimulate apoptosis (eg. virally infected cells)	Cytotoxic CD8 + T-cell mediated pathway
Inserts pores on the membrane of the target cell	Perforin
Enters pores on the membrane and activates caspases	Granzyme