Cell Responses to Injury Flashcards
Reversible; cell gets bigger (no new cells!)
hypertrophy
ex/ uterus during pregnancy!
Reversible; increase in number of cells
hyperplasia
may be precancerous, or may be normal - like during period
Two basic ways to get hyperplasia:
1) growth factor
2) stem cells
Cyclosporin is a medication that can cause:
hyperplasia
Occurs in tissues that are incapable of cell division
hypertrophy
Reversible; changes in ion concentration & water influx
hydropic swelling
When nuclear membrane starts to break down:
karyorrhexis
When there is continuous injury, the nucleus becomes dark purple and looks like shriveled raisin. This is called:
pyknosis
When the nucleus totally breaks up:
karyolysis
Increase in cell volume characterized by pale cytoplasm and normal nucleus
hydropic swelling
reflection of acute, reversible injury
When cells aren’t able to maintain membrane and the contents leak out:
necrosis
elicits an inflammatory response
What are the six types of necrosis? (CCFFGL)
- Coagulative
- Caseous
- Fat
- Fibrinoid
- Gangrenous
- Liquefactive
Type of necrosis that preserves the architecture of the tissue
Coagulative
Type of necrosis associated with TB
Caseous
Type of necrosis where there is leakage of enzymes into abdomen
Fat
Type of necrosis that can be seen in oral cavity, and it is immunologically mediated vasculitis in blood vv walls
Fibrinoid
Type of necrosis that involves both coagulation and liquefaction
Gangrenous
Type of necrosis that occurs with cerebral infarction and bacterial infections
Liquefactive
What is the type of necrosis that occurs in heart attacks?
Coagulative necrosis
Type of necrosis where pus is seen
Liquefactive
When mitochondria doesn’t get enough oxygen, what happens to ATP levels?
Decrease
low oxidative phosphorylation = low ATP
Ischemia changes are reversible or irreversible?
Reversible! But must be taken care of quickly
Why is apoptosis preferred and not necrosis?
Necrosis -> releases cell contents; INFLAMMATION
Apoptosis -> cells break down in packets so contents stay contained; NO inflammation
Too much calcium in the cell disrupts:
ATP generation, so apoptosis is induced because damaging enzymes are activated
What ROS can cause pathologic effects, like membrane damage or mutations?
OH (hydroxyl radical)
Hypoxia vs. Ischemia?
Hypoxia = deficiency of oxygen Ischemia = loss of blood supply, which causes lack of oxygen (more severe than hypoxia)
What enzymes are activated in apoptosis?
caspases
Mitochondrial intrinsic pathway for apoptosis is more common. It is run by a group of effectors called:
BCL-2
TNF receptor + Fas =
Apoptosis
they’re in extrinsic pathway
Between necrosis and apoptosis, what is the main difference in regards to loss of plasma membrane?
Loss of plasma membrane occurs first in necrosis & last in apoptosis
Killer lymphocytes inject ____ through perforin
granzyme
What is the cell death rheostat?
BCL-2
