Flashcards in MOD S1&2 Cell Injury Deck (49)
What is cell injury?
When the cell can no longer adapt to changes in its environment, it begins to show evidence of cell injury.
How may a cell be injured?
What are heat shock proteins?
Produced in response to cell injury due to heat
They refold denatured proteins correctly
Misfolded proteins are destroyed
What are the main targets of cell injury?
What is ischaemia reperfusion injury?
When blood flow is reinstated to an area of ischaemic tissue, the damage sustained is worse that it would have been without circulation.
The interruption of blood supply
Name the types of hypoxia
What is hypoxia?
Often due to ischaemia
What are some reversible changes to cells caused by hypoxia?
Reduced oxidative phosphorylation
Reduced protein synthesis due to ribosome detachment
The spectrum of changes that occur in a injured cell prior to death
What are irreversible changes to cells brought about by hypoxia?
Accumulation of cytosolic Ca2+
Activation of certain enzymes - these result in cell death
Do all cells react the same way to ischaemia?
Eg nerve cells would last a few minutes in ischaemic conditions whereas fibroblasts could last for hours
What reversible structural changes may be seen in an ischaemic cell under an electron microscope?
What are blebs?
Small bumps on the cell membrane where the cytoskeleton has detached
What irreversible effects may be seen with an electron microscope in an ischaemic cell?
Endoplasmic reticulum rupture
Programmed cell death
What are the stages of apoptosis?
What are the two methods of initiation of apoptosis?
Name an inhibitor of apoptosis
What is necrosis?
The changes which occur after cell death in living tissue
Name a death ligand and a death receptor (involved in extrinsic apoptosis)
What are caspases?
Important effector molecules of apoptosis eg caspase 3
What are the important mediators of apoptosis?
Cytochrome c, APAF, caspase 9
Give some examples of types of necrosis
Describe coagulative necrosis
More protein denaturation that enzyme release
Consistency of tissue remains solid
Cell structure is somewhat preserved, leaving a "ghost outline"
Tend to be due to infarcts (not in brain)
Describe liquefactive necrosis
More enzyme release than protein denaturation
Tissue becomes a viscous mass
Tissue is lysed and disappears
Tends to be due to infarction (eg in brain)
Also seen in massive neutrophil invasions
Describe caseous necrosis
Tissue appears amorphous
Halfway between coagulative and liquefactive
Describe fat necrosis
Occurs in cases of cell death in adipose tissue
The fatty acids released react with calcium to form chalky deposits (calcium soaps)
What is p53?
Very important protein in apoptosis
Mediates apoptosis in response to DNA damage