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Semester 2 - Mechanisms of Disease > Week 1 - Cell Injury > Flashcards

Week 1 - Cell Injury Flashcards

1
Q

If mild changes occur in a cells environment, what happens?

What happens if those changes are more severe?

A

Cell copes with mild changes via homeostasis
If the changes are more severe, it will adapt in order to remain viable
If the changes are very severe, the cell will become injured, first reversibly and then irreversibly. The ultimate consequence is cell death.

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2
Q

What are the major causes of cell injury?

A 
Hypoxia
Physical agents
Chemical agents
Microorganisms
Immune mechanisms
Dietary deficiencies/excess
Genetic abnormalities
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3
Q

What are the 4 principal targets of cell injury?

A

The nucleus
The membrane
The mitochondria
Cell proteins

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4
Q

What are the 4 types of hypoxia? Give an explanation of each.

A

Hypoxaemic - lack of arterial O2, e.g. at high altitudes
Anaemic - lowered ability to carry O2
Histiocytic - inability to USE the O2 provided due to disabled oxidative phosphorylation enzymes
Ischaemic - interruption to blood supply

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5
Q

Which is the most serious type of hypoxia? Why?

A

Ischaemic

Lack of blood supply means the cell is starved of nutrients as well as oxygen.

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6
Q

When a hypoxic injury occurs, the cell is starved of oxygen. What is the major consequence of this?

A

Lack of ATP as oxidative phosphorylation ceases

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7
Q

What are the 3 main consequences of reduced ATP within the cell?

A
  1. Reduced Na+/K+-ATPase activity
  2. Increased anaerobic respiration
  3. Detachment of ribosomes from the ER
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8
Q

Talk through the consequences of reduced Na+/K+-ATPase activity.

A

Na+ builds up within the cell, as it is not being pumped out. This causes water to be drawn into the cell, resulting in cell swelling.

Ca2+ also builds up, as NCX cannot function without the Na+ gradient. Ca2+ injures the cell as it is toxic.

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9
Q

During hypoxic cell injury, lactate builds up. What effects does this have on the cell?

A

Lactate causes the pH within the cell to decrease, which causes:

  1. Enzymes to denature
  2. Chromatin to clump
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10
Q

Are the changes associated with hypoxic injury reversible? What key event changes this?

A

Yes, until the membrane integrity is disturbed, after which the cell is irreversibly injured and will die.

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11
Q

What changes lead to cell death from hypoxia?

A

Membrane integrity is disrupted, causing increased permeability. This causes -

  • massive Ca2+ influx, which activates many potent enzymes
  • substances to leak out of cell into blood
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12
Q

Give an example of a heat shock protein

A

Ubiquitin

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13
Q

Discuss the cell’s response to injury in terms of protein synthesis

A

Protein synthesis of all proteins greatly decreases, except for synthesis of heat shock proteins, which greatly increases.

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14
Q

What is the job of heat shock proteins?

A

Recognise mis-folded and denatured proteins, and ensure they are correctly re-folded or destroyed.

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15
Q

When using a light microscope, what is the easiest technique to look for cell death?

A

Dye exclusion technique - if dye enters, cell membrane has been disrupted and hence cell is dead.

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16
Q

What are the 3 main changes visible with oncosis when viewing cells under a light microscope?

A
  1. Cytoplasmic
  2. Nuclear
  3. Abnormal intracellular accumulations
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17
Q

Discuss both reversible and irreversible cytoplasmic changes which may be viewed under a light microscope.

A

Reversible - reduced pink staining, as the increased water content dilutes the dye.

Irreversible - increased pink staining, as the ribosomes detach and protein accumulates.

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18
Q

Discuss both reversible and irreversible nuclear changes, as viewed under a light microscope.

A

Reversible - chromatin clumping

Irreversible - pyknosis, karryohexis and karryolysis

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19
Q

What is pyknosis?

A

Nuclear shrinkage

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20
Q

What is karryohexis?

A

Nuclear fragmentation

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21
Q

What is karryolysis?

A

Nuclear dissolution

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22
Q

Which reversible changes that occur with cell injury can be seen under an electron microscope?

A

Swelling
Cytoplasmic blebbing
Chromatin clumping
Ribosome detachment

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23
Q

Which irreversible changes associated with cell injury can be seen under an electron microscope?

A 
Increased swelling
ER lysis
Swelling/rupture of lysosomes
Membrane defects
Pyknosis, karryohexis and karryolysis
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24
Q

What are the two types of cell death?

A

Oncosis and apoptosis

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25
Q

Define oncosis

A

Cell death with swelling

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26
Q

Define apoptosis

A

Cell death with shrinkage

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27
Q

Which of oncosis and apoptosis is ATP-dependent and which is not?

A

Oncosis is not

Apoptosis is

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28
Q

Give 3 characteristic features of apoptosis

A
  1. Induced by a regulated intracellular programme
  2. Occurs in single cells or groups of a few cells only
  3. Can be a normal physiological process as well as occurring in injured cells.
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29
Q

What structural changes occur in apoptosis?

A
  • Chromatin condensation

- Cell fragments into apoptotic bodies

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30
Q

What is an apoptotic body?

A

A cell fragment containing cytoplasm, organelles and nuclear fragments.

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31
Q

How are apoptotic bodies removed?

A

By phagocytosis

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32
Q

What are the 3 stages of apoptosis?

A
  1. Initiation
  2. Execution
  3. Degradation/phagocytosis
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33
Q

What is a caspase, and when are they activated?

A

Caspase = protease that cleaves proteins to break up the cytoskeleton and initiate DNA degradation.

Activated by both intrinsically and extrinsically triggered apoptosis.

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34
Q

What is p53?

A

A protein that mediates apoptosis

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35
Q

Give the sequence of events of intrinsically triggered apoptosis.

A 
DNA damaged
p53 activated
Increased mitochondrial permeability
Cytochrome C released from mitochondria
Interacts with APAF1 and caspase 9 --> forms aptosome, which activates further caspases
36
Q

How may intrinsic apoptosis be inhibited?

A

By Bcl-2 - prevents release of cytochrome C from the mitochondria

37
Q

How does extrinsic apoptosis occur?

A

External ligand binds to a “death receptor” on the cell - leads to caspase activation.
E.g. TRAIL binds to TRAIL-R

38
Q

What is all disease a consequence of?

A

Failed homeostasis

39
Q

What is necrosis? (and what is it not?)

A

The morphological changes that occur after a cell has been dead for some time - i.e. it is an appearance rather than a process.

It is NOT a type of cell death

40
Q

What must be present in order for necrosis to occur?

A

A blood supply around the dead tissue

41
Q

What are the 4 types of necrosis?

A
  • Coagulative
  • Liquefactive
  • Caseous
  • Fat necrosis
42
Q

What is coagulative necrosis characterised by?

A

Denaturation of proteins dominates over release of active enzymes

43
Q

In coagulative necrosis, the dominant factor is denatured proteins. What is the significance of this?

A
  • Denatured proteins clump

- Denatured proteins uncoil - less soluble

44
Q

What is left behind in areas of coagulative necrosis? Why?

A

Ghost cells

Cell architecture remains intact but the cell contents is destroyed.

45
Q

In which sorts of organs does coagulative necrosis tend to occur?
What would usually have caused cell death?

A

Solid organs

Ischaemia

46
Q

What characterises liquefactive necrosis?

A

Active enzyme degradation dominates over protein denaturation

47
Q

What happens to the tissues in liquefactive necrosis?

Why is this process referred to as autolysis?

A

They are digested enzymatically to form a viscous mass.

The digestion occurs via the cell’s own enzymes, hence autolysis.

48
Q

When/where does liquefactive necrosis tend to occur? Why?

A

Tends to occur in bacterial infections, as the neutrophils present release protealytic enzymes
Tends to occur in the brain - low stromal support

49
Q

What characterises caseous necrosis?

A

Amorphous debris

Particularly associated with granulomatous infection

50
Q

What is fat necrosis?

Why does it usually occur?

A

Destruction of the adipose tissue

Usually secondary to pancreatitis - leases lipases which act on the adipose.

51
Q

Why does fat necrosis result in chalky deposits?

A

The free fatty acids released from the breakdown of the adipose tissue react with calcium - forms chalky deposits.

52
Q

What is gangrene (and what is it not)?

A

Gangrene describes necrosis that is visible to the naked eye.
It is NOT a type of necrosis.

53
Q

What is dry gangrene?

A

Coagulative necrosis exposed to the air

54
Q

What is wet gangrene?

A

Liquefactive necrosis infected with bacteria.

55
Q

What is gas gangrene?

A

Wet gangrene where the infective agent is anaerobic bacteria that produce gas bubbles in the tissues.

56
Q

What is an infarct?

A

An area of ischaemic necrosis - i.e. an area of tissue that has died due to an obstruction to blood supply.

57
Q

Is ischaemic necrosis coagulative or liquefactive?

A

Could be either - depends where it is

58
Q

How are infarcts classified?

A

According to colour - white or red

59
Q

What is another name for a white infarct?

A

Anaemic infarct

60
Q

Where might a white infarct occur, and what causes it?

A

Occurs in solid organs

Caused by occlusion of an end artery

61
Q

Why is a red infarct “red”?

A

There has been extensive haemorrhage within dead tissue

62
Q

Give 3 reasons as to why a red infarct would occur.

A
  1. Organ has dual blood supply/anastomoses - blood fills dead tissue (but not enough to keep it alive)
  2. Tissue has low stromal support
  3. Venous pressure is raised, hence the arterial pressure is low, causing ischaemia whilst tissue is engorged.
63
Q

Give three molecules which may be released by injured/dying cells.

A
  1. Potassium
  2. Enzymes
  3. Myoglobin
64
Q

Why is myoglobin release during muscle cell death a particular danger?

A

Can block the renal tubules causing renal failure

65
Q

What are the 5 main groups of abnormal cellular accumulations that occur during oncosis?

A 
Carbohydrates
Lipids
Proteins
Fluid
Pigments
66
Q

What is a build up of triacylglycerides called?

A

Steatosis

67
Q

In terms of lipids, which substances may accumulate abnormally?

A

TAGs
Cholesterol
Phospholipids

68
Q

How does TAG and cholesterol accumulation differ?

A

TAGs accumulate as droplets, but cholesterol accumulates as membrane-bound droplets.

69
Q

How do proteins accumulate?

A

As eosinophilic droplets

70
Q

What is Mallory’s hyaline?

A

A “body” seen inside hepatocytes in alcoholic liver disease. They are formed from the accumulation of altered keratin filaments.

71
Q

Outline a1-antitrypsin deficiency

A

a1-antitrypsin is not folded correctly, and therefore cannot be packaged by the ER. Hence it accumulates in the cell, but is deficient elsewhere.

72
Q

Where in the body is a fluid accumulation particularly serious, and why?

A

The brain - cannot expand due to the skull

73
Q

Name two exogenous pigments that may accumulate within the body.

A
  1. Carbon

2. Tattoos

74
Q

Name 3 endogenous pigments that may accumulate within the body

A
  1. Lipofuscin
  2. Haemosiderin
  3. Bilirubin
75
Q

What is lipofuscin?

A

Harmless brown pigment seen in ageing cells

76
Q

What is haemosiderin?

A

An iron storage molecule derived from Hb.

77
Q

When may there be be an accumulation of haemosiderin?

A

When there is excess iron in the blood - haemosiderin “mops up” iron and accumulates in the organs

78
Q

How is bilirubin deposited?

A

Either in tissues in macrophages or extracellularly

79
Q

Define pathological calcification

A

Abnormal deposition of calcium salts within the tissues

80
Q

What are the 2 ways in which pathological calcification can occur?

A
  1. Dystrophic

2. Metastatic

81
Q

What is dystrophic pathological calcification?

A

Localised deposition of calcium salts - i.e. no change in serum Ca2+
Occurs in dying tissues

82
Q

When does metastatic calcification occur?

A

When there is hypercalcaemia - hydroxyapatite crystials deposited in normal tissue. Body wide.

83
Q

What 3 things occur as cells age?

A
  1. Lipofuscin accumulation
  2. Damage to DNA
  3. Abnormally folded proteins
84
Q

What is replicative senescence?

A

As a cell ages, its ability to replicate diminishes as the telomeres shorten.

85
Q

Which cells may rebuild their telomeres?

A

Germ cells, stem cells and some cancer cells

86
Q

Give the 3 stages of alcoholic liver disease. Which are reversible?

A
  1. Steatosis and hepatomegaly –> reversible
  2. Acute alcoholic hepatitis –> reversible
  3. Cirrhosis –> irreversible

Semester 2 - Mechanisms of Disease (5 decks)

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