Weissman - Cell Injury Flashcards
WHy might you have a decrease in size?
Decrease in stress or trophic factors leads to a decrease in the size of the organ
- Decreased hormones
- Disuse
- Decreased nutrients or blood supply
Decreased number of cells due to apoptosis
Decrease in cell size due to decreased protein synthesis or increased degradation
Metaplasia
Change in cell type in response to an adverse environment. On the one hand this serves as a benefit because it can protect the tissue to conform to its new environment. On the other hand, that tissue loses its old function.
- examples are changing from columnar to squamous in the respiratory tract of a smoker. A second example is a change from squamous to columnar in Barrett’s esophagus.
Hyperplasia vs. hypertrophy
Hyperplasia. - cell division to make more cells
Hypertrophy - cells grow
What are the three major types of adaptations?
Growth, atrophy, Metaplasia
Reversible changes vs irreversible changes
Reversible: Decreased ATP, so cell swelling due to inability of Na+/K+ pump to work adequately.
Irreversible: Extensive membrane damage (plasma, lysosomal, and mitochondrial), severe mitochondrial damage.
Reversible. Vs. irreversible on microscope
Under a microscope you Can’t really tell the difference at all in irreversible damage. With reversible you can somewhat see the delineation between cells. In the reversible you should also be able to see cell swelling.
In general what happens if you have an increased amount of calcium in the cell?
- Increased membrane permeability
- activation of many damaging cellular enzymes
WHat happens when there. Is an excessive amount of misfolded Proteins due to DNA/protein damage?
The cell can either adapt or not. If it adapts it will make more chaperone proteins and the misfolded proteins will work themselves out. If the cell can’t handle it then it will apoptose.
Gangrenous necrosis
Loss of blood supply to an organ - common in the lower leg
Intrinsic Pathway of apoptosis
Bcl2 is responsible for keeping the cell from apoptosing. Bcl2 keeps cytochrome c in the mitochondria. If Cyto c gets out into the cytosol, it will act on the various caspases to cause apoptosis. Bcl2 also inhibits Apaf-1, which keeps the caspases in check.
Extrinsic pathway of apoptosis
FAS ligand will activate the death receptor on the outside of the cell, which will activate the caspases downhill.
Necroptosis
Morphologically looks like necrosis but it is genetically programmed.
- It doesn’t involved caspases
- Typical ligand is TNFR1, which recruits RIP1 and RIP3.
- you will see membrane permeabilization, ROS, mitochondria damage, decreased ATP.
Autophagy
Occurs under stress conditions such as nutrient deprivation.
- the cell begins to teat itself. It makes a vacuole and fuses with a vacuole and self-destructs in it.
Dystrophic vs metastatic calcification
Dystrophic would be in a tissue that is abnormal you would see mineralizations.
Metastatic would be a normal tissue but because of hypercalcemia you get these deposits.