Effect on injury on cells (W10) Flashcards
causes of cell injury
lack of O2
physical agents (temp, psi, electricity, radiation)
chemicals and drugs
infectious agents
immune reactions
genetic defects
nutrition
reversible cell injury features?
rapid changes
swelling due to loss of ion/fluid homeostasis
fat accumulation (steatosis)
when does reversible cell injury become irreversable
if experiences persistent injury - no defined ‘point of no return’
fatty change histology?
large pale spaces - fat globules
2 types of cell death
apoptosis and necrosis
apoptosis overview?
membrane stays in tact
energy spent from own cell
apoptotic bodies spread off from cell
phagocytosis of cell and fragments
apoptosis 2 stages
intrinsic
extrinsic (signal from outside cell - YOU MUST KILL YOURSELF!!!)
apoptosis - extrinsic regulation
receptor ligand interactions
leads to series of intracellular protein-protein interactions
activates initiator caspase 8
apoptosis - intrinsic pathway?
less BCL2 (anti-apoptotic proteins), more BAX and BAK (pro-apoptotic proteins)
this allows leakage of cytochrome C and SMAC out mitochondria
these lead to activation of caspase 9
initiator caspase for intrinsic apoptosis pathway
caspase 9
normal intrinsic pathway before apoptosis
growth factors cause transcription of more anti-apoptotic (BCL-2) proteins, outnumbering pro-apoptotic proteins therefore keeping cell alive
initiator caspase for extrinsic apoptosis pathway
activates initiator caspase 8
what do active initiator caspases act on in apoptosis? what does this cause?
activate executioner caspases (‘cut’ off inhibitory part) which then disassemble the cell
what is autophagy
recycling and turnover of cytoplasmic cell constituents
what regulates autophagy
autophagy-related genes (ATGs)