MOD S1&2 Cell Injury Flashcards Preview

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Flashcards in MOD S1&2 Cell Injury Deck (49)
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0

What is cell injury?

When the cell can no longer adapt to changes in its environment, it begins to show evidence of cell injury.

2

How may a cell be injured?

Hypoxia
Toxins
Heat
Cold
Trauma
Radiation
Microorganisms
Immune mechanisms
Dietary deficiency/insufficiency
Genetic abnormalities

3

What are heat shock proteins?

Produced in response to cell injury due to heat
They refold denatured proteins correctly
Misfolded proteins are destroyed

4

What are the main targets of cell injury?

Cell membranes
Nucleus
Proteins
Mitochondria

6

What is ischaemia reperfusion injury?

When blood flow is reinstated to an area of ischaemic tissue, the damage sustained is worse that it would have been without circulation.

8

Define ischaemia

The interruption of blood supply

9

Name the types of hypoxia

Hypoxaemic
Anaemic
Ischaemic
Histeocytic

11

What is hypoxia?

Reduced O2
Often due to ischaemia

13

What are some reversible changes to cells caused by hypoxia?

Reduced oxidative phosphorylation
Decreased pH
Na accumulation
Cell swelling
Reduced protein synthesis due to ribosome detachment

14

Define oncosis

The spectrum of changes that occur in a injured cell prior to death

15

What are irreversible changes to cells brought about by hypoxia?

Accumulation of cytosolic Ca2+
Activation of certain enzymes - these result in cell death

16

Do all cells react the same way to ischaemia?

No
Eg nerve cells would last a few minutes in ischaemic conditions whereas fibroblasts could last for hours

17

What reversible structural changes may be seen in an ischaemic cell under an electron microscope?

Swelling
Chromatin clumping
Autophagy
Ribosome dispersal
Blebs

18

What are blebs?

Small bumps on the cell membrane where the cytoskeleton has detached

19

What irreversible effects may be seen with an electron microscope in an ischaemic cell?

Nuclear changes
Lysosome rupture
Membrane defects
Endoplasmic reticulum rupture

21

Define apoptosis

Programmed cell death

22

What are the stages of apoptosis?

Initiation
Execution
Degradation/phagocytosis

23

What are the two methods of initiation of apoptosis?

Intrinsic (mitochondrial)
Extrinsic

24

Name an inhibitor of apoptosis

Bcl-2

25

What is necrosis?

The changes which occur after cell death in living tissue

26

Name a death ligand and a death receptor (involved in extrinsic apoptosis)

Ligand: TRAIL
Receptor: TRAIL-R

27

What are caspases?

Important effector molecules of apoptosis eg caspase 3

28

What are the important mediators of apoptosis?

Cytochrome c, APAF, caspase 9

29

Give some examples of types of necrosis

Coagulative
Liquefactive
Fat
Caseous

30

Describe coagulative necrosis

More protein denaturation that enzyme release
Consistency of tissue remains solid
Cell structure is somewhat preserved, leaving a "ghost outline"
Tend to be due to infarcts (not in brain)

31

Describe liquefactive necrosis

More enzyme release than protein denaturation
Tissue becomes a viscous mass
Tissue is lysed and disappears
Tends to be due to infarction (eg in brain)
Also seen in massive neutrophil invasions

32

Describe caseous necrosis

Tissue appears amorphous
Halfway between coagulative and liquefactive

33

Describe fat necrosis

Occurs in cases of cell death in adipose tissue
The fatty acids released react with calcium to form chalky deposits (calcium soaps)

34

What is p53?

Very important protein in apoptosis
Mediates apoptosis in response to DNA damage

35

What is pathological calcification?

Abnormal deposition of calcium salts within tissues