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level: Cell Death

Questions and Answers List

level questions: Cell Death

QuestionAnswer
Loss of nucleusMorphologic hallmark of cell death
Nuclear condensation/ Shrinking of nucleus ("ink dot")Pyknosis
Breaking up/fragmentation of nucleusKaryorrhexis
Breaking down of nuclear fragments to basic building blocksKaryolysis
Necrosis and apoptosisMechanisms of cell death
Death of large group of cells followed by inflammation brought about by pathologic processesNecrosis
Firm necrotic tissue with absent nuclei and preserved cell shape and organ structure due to protein coagulationCoagulative 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 proteinLiquefactive necrosis
Liquefactive necrosis due to proteolytic enzymes from microgliaBrain infarction
Coagulative necrosis characteristic of ischeme of lower limb and GITDry gangrene
Liquefactive necrosis due to superimposed infectionWet gangrene
Coagulative + Liquefactive necrosis; characteristic of granulomatous inflammation from TB and fungal infectionCaseous necrosis
Caseous necrosisCottage cheese-like appearance
Fat necrosis; appearance brought about by calcium depositionChalky white appearance
Necrotic adipose tissue brought about by saponificationFat necrosis
Reaction of fatty acids with calcium deposits; type of dystrophic calcificationSaponification
Normal calcium and phosphate levels; necrotic tissue forms nidus for calcium depositDystrophic calcification
High calcium and phosphate levels lead to calcium deposition in normal tissueMetastatic calcification
Necrotic damage to blood vessel wall; malignant hypertension and vasculitisFibrinoid necrosis
ATP-dependent genetically programmed cell deathApoptosis
Mediator of apoptosisCaspase
Breaks down cytoskeletonProtease
Breaks down DNAEndonuclease
Cellular injury, DNA damage and loss of hormonal stimulation cause inactivation of Bcl2 -> cytochrome c release -> caspase activationIntrinsic mitochondrial pathway
Inhibits release of cytochrome c from inner mitochondrial matrixBcl2
Activator of caspasesCytochrome c
FAS ligand, TNF binds to corresponding receptors, activating caspasesExtrinsic receptor-ligand pathway
Binds to FAS death receptor to activate caspases in extrinsic apoptotic pathwayFAS ligand
FAS death receptorCD95
FAS ligand-mediated apoptosis of T-cells which have too avid or strong binding of self antigenNegative 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 cellPerforin
Enters pores on the membrane and activates caspasesGranzyme