Lecture 2 Flashcards
What causes ischemia ?
- Vessel Spasm
- Thrombus
- Embolus
- Atherosclerosis/Plaque
- Outside Pressure (Tumour etc.)
Hypoxia can be caused by…
- Ischemia
2. Erythrocyte Impairment (Anemia OR CO poisoning)
The causes of cell injury are…
- Biological Agents
- Immune Reactions
- Inadequate Nutrition
- Chemical Agent
- Physical Injury
- Genetic Abnormalities
- Hypoxia (Most Common)
What is superoxide dismutase ?
An antioxidant that inactivates ROS as a protective mechanism against free radical injury.
Describe the process of hypoxic cell injury.
Decreased O2 levels -> Decreased oxidative phosphorylation by mitochondria -> Decreased ATP production -> Decreased function of Sodium Pump -> Accumulation of sodium in the cell -> Cell swells and there are “blebs” in the plasma membrane.
- ER swells and stops making proteins.
- Increased glycolysis increases intracellular lactic acid, leading to PH decrease.
- Calcium accumulation in the cell (extracellular and from mitochondria) activates enzymes like phospholipase and leads to cell damage + decreased ATP.
What is Free Radical Injury ?
When the cell undergoes hypoxic injury, it releases ROS from the mitochondria. This leads to Free Radical Injury, which includes lipid peroxidation of the membrane, protein misfiling, DNA mutations, etc.
What are the different types of cell death ?
- Apoptosis
2. Necrosis
What is the main difference between apoptosis and necrosis ?
Necrosis triggers an inflammatory reaction while apoptosis doesn’t.
What are the key features of necrosis ?
- Triggers an inflammatory reaction.
- Triggers autolysis
- Is irreversible
What are the different types of necrosis ?
- Coagulative necrosis : cell death and scarring occur at the same time.
- Liquefactive necrosis: cells die and liquefy.
- Caseous necrosis: formation of “cheese-like” texture.
What is gangrene ?
Coagulative necrosis followed by a bacterial attack.
What is the internal mechanism of apoptosis?
Bcl2 normally inhibits Bax/Bak channel, but when there’s DNA damage, there’s inhibition of Bcl2 , which increases Bax/Bak channel action, which increases cytochrome c, which then activates caspase -> triggers apoptosis.
What is the external mechanism of apoptosis?
Fas in the membrane gets activated by extracellular compounds (e.g. TNF), trimerizes to form the FADD domain intracellularly, which activates cascade -> triggers apoptosis.
Note : NFkB can inhibit this process.
What is lipofuscin ?
A compound that accumulates in cells with aging, and can’t come out.
