Lec 1 Flashcards

1
Q
List four pathogenesis of a cell injury:
1)
2)
3)
4)
A

Loss of Ca homeostasis.
Reduced ATP/synthesis.
Free radicals.
Disrupted membrane permeability.

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2
Q

When can cell injury be first viewed, and does this mean reversible or irreversible is apparent for the cell?

A

The cell injury can be first seen by nuclear and cytoplasmic changes.
The cell injury will be irreversible

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3
Q

What mechanism does hypoxia lead to, for cell dead to occur?

A

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

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4
Q

What is hypoxaemia?

A

Oxygen absorbing problems are apparent in the haemoglobin.

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5
Q

Lower in ATP will cause?
1)
2)
3)

A

Nuclear clumping
Protein synthesis decrease
ER swelling

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6
Q

Membrane damage are from what two main causes, in an injured cell?

A

Increase in phospholipid enzyme activity.

Cytoskeletal damage to the cell

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7
Q

Heat shock gene are for what purpose in cell injury?

A

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.

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8
Q

What is a mechanism which Ca ion influx will occur?

A

Trauma -> loss to regulate cell environment -> Ca influx -> over activation of enzymes -> membrane damage, nuclear damage and decrease ATP

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9
Q

Give 3 necrotic specific cell characteristics:

A

Mitochondria, ER swelling
Membrane blebbing
Adjacent influence inflammation

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10
Q

Give 3 main apoptotic specific cell injury characteristics:

A

Condensation of chromatin
Reduction in cell size
Cause mainly by physiological injury

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11
Q

What are the 4 type of necrosis?

A

Caseous necrosis
Coagulative necrosis (most common)
Liquefactive necrosis (neutrophil infiltration, in brain)
Infarction (red or white)

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12
Q

Apoptosis has an extrinsic and intrinsic pathways. Briefly explain the differences between the two:

A

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

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