Lec 1 Flashcards
List four pathogenesis of a cell injury: 1) 2) 3) 4)
Loss of Ca homeostasis.
Reduced ATP/synthesis.
Free radicals.
Disrupted membrane permeability.
When can cell injury be first viewed, and does this mean reversible or irreversible is apparent for the cell?
The cell injury can be first seen by nuclear and cytoplasmic changes.
The cell injury will be irreversible
What mechanism does hypoxia lead to, for cell dead to occur?
Decrease in O2 consumption which in turn lowers ATP production. This means the cell metabolite process decreases and waste accumulation will occur in the cell
What is hypoxaemia?
Oxygen absorbing problems are apparent in the haemoglobin.
Lower in ATP will cause?
1)
2)
3)
Nuclear clumping
Protein synthesis decrease
ER swelling
Membrane damage are from what two main causes, in an injured cell?
Increase in phospholipid enzyme activity.
Cytoskeletal damage to the cell
Heat shock gene are for what purpose in cell injury?
They help the cell survive a stressful environment, by cleaning up damaged proteins and produce more protein chaperone for the protein function to still occur during injury.
What is a mechanism which Ca ion influx will occur?
Trauma -> loss to regulate cell environment -> Ca influx -> over activation of enzymes -> membrane damage, nuclear damage and decrease ATP
Give 3 necrotic specific cell characteristics:
Mitochondria, ER swelling
Membrane blebbing
Adjacent influence inflammation
Give 3 main apoptotic specific cell injury characteristics:
Condensation of chromatin
Reduction in cell size
Cause mainly by physiological injury
What are the 4 type of necrosis?
Caseous necrosis
Coagulative necrosis (most common)
Liquefactive necrosis (neutrophil infiltration, in brain)
Infarction (red or white)
Apoptosis has an extrinsic and intrinsic pathways. Briefly explain the differences between the two:
Intrinsic: Cell injury occurs -> BLC2 sensors -> Bax activates -> cytochrome c produced from mitochondria -> apoptosis occurs
Extrinsic: FasL from T cell is presented -> Fas or TNF receptor activated -> initiator caspases form -> executioner caspases activate -> apoptosis