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MOD (Semester 2) > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What happens to cell when it’s environment changes?

A

It can undergo morphological changes in order to remain viable. Sometimes these are irreversible in which case the cell dies.

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2
Q

What is hypoxia?

A

Oxygen deprivation. This leads to reduced aerobic oxidative respiration.

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3
Q

Name three things that hypoxia can lead to.

A

Cell adaption (typically atrophy), cell injury and cell death

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4
Q

What does hypoxaemic mean?

A

This means that the oxygen content of arterial blood is low. This can be caused by high altitude.

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5
Q

What is the term used to describe a low oxygen carrying capacity of the blood?

A

Anaemia.

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6
Q

Name 4 causes of hypoxia.

A

Hypoxaemia, anaemia, histiocytic, ischaemia.

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7
Q

What is a histiocytic cell?

A

This is a cell that is unable to utilise oxygen effectively due to disabled oxidative phosphorylation enzymes.

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8
Q

What is pathology?

A

Pathology is the study of disease.

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9
Q

What is ischaemia?

A

Interruption of blood supply due to blockage of a vessel, hypotension or heart failure which leads to reduced o2 and nutrients being supplied to the tissue.

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10
Q

Name 6 causes of hypoxia.

A

Chemical agents, physical agents, immune mechanisms, microorganisms, genetic abnormalities, diet insufficiencies or excesses.

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11
Q

What are 4 common targets in a cell for injury?

A

Nucleus, cell membrane, proteins and mitochondria.

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12
Q

What happens when a cell is deprived of oxygen?

A

There is less oxidative phosphorylation in the mitochondria and therefore less energy production. This compromises vital cell functions.

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13
Q

What problem does lack of ATP cause to ionic concentrations in the cell?

A

Lack of ATP means that there is reduced activity of the sodium potassium pump. It is also the case that calcium may enter the cell and this San damage cellular components.

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14
Q

Hypoxic cells get chromatin clumping. Why is this?

A

Hypoxic cells have a lack of ATP and so there is an increased amount of anaerobic respiration and therefore accumulation of lactic acid. The pH of the cell decreases and this affects the function of many enzymes.

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15
Q

Explain why protein synthesis is interrupted in Hypoxic cells.

A

Ribosomes detach from the ER. There may be accumulations of fat and denatured proteins in Hypoxic cells.

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16
Q

When does irreversible Hypoxic injury occur?

A

In most cells this is when oncosis –> necrosis. This means that membrane integrity is compromised and so there is a massive influx of calcium into the cell.

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17
Q

How does calcium influx damage cellular components?

A

When calcium enters the cell it activates various enzymes including: endonuclease a, proteases, phospholipases, ATPases.

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18
Q

Why is damage to lysosomal membranes in hypoxia a problem?

A

Damage to lysosomal membranes leads to enzymes leaking into the cell which causes damage.

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19
Q

How can we test for irreversible Hypoxic injury?

A

If the membrane is sufficiently damaged for calcium influx then cellular components also move into the blood - can be tested for.

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20
Q

What is ischaemia reperfusion injury?

A

This is where the restoration of blood flow to a cell causes injury

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21
Q

Why can restored blood flow to a tissue cause injury?

A

Increase oxygen leads to free radical production. Increased neutrophils - inflammatory response and causes damage. Delivery of compliment proteins, activates the compliment pathway.

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22
Q

Give an example mod chemical injury to a cell.

A

Cyanide binds in the mitochrondria and blocks the oxidative phosphorylation pathway.

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23
Q

What is the most common site of injury from free radicals?

A

Free radicals attack lipids in the membrane - lipid peroxidation.

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24
Q

Name two common substrates for Hydroxyl radical production.

A

O2- and H2O2. It is important these are removed to prevent free radical formation.

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25
Q

What is the Fenton reaction and when does this occur?

A

This is a reaction which produces free radicals. It occurs when Iron is available following bleeding.
Fe2+ + H2O2 –> Fe3+ + OH- + .OH

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26
Q

3 H2O2 –> O2 + 2 H2O + 2.OH

What reaction is this?

A

This is the Haber-Weiss reaction and it produces free radicals.

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27
Q

Name two enzymes which are part of the anti-oxidant system.

A

Superoxide dismutase, peroxidases/ catalases

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28
Q

What are the three parts of the anti oxidant system?

A

Enzymes, free radical scavengers and storage proteins.

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29
Q

Name some free radical scavengers.

A

Vit A,C,E and glutathione.

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30
Q

How do storage proteins act as antioxidants?

A

They sequester transition metals which would otherwise act as catalysts for free radical formation.

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31
Q

What happens to a cell when it is under stress (in regards to protein synthesis)?

A

The cell stops synthesising proteins and focuses on making heat shock proteins.

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32
Q

What is a Heat shock protein and what is its function?

A

A heat shock protein is produced by a cell in a stress response. It recognises incorrectly folded proteins and refolds them.

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33
Q

Why are Heat Shock proteins important for maximising cell survival?

A

They play a key role in protein viability.

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34
Q

How can we tell if a cell is dead or not in microscopy?

A

Morphologically it is hard to tell, however with dye exclusion, only the dead cells will soak up the dye.

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35
Q

What is oncosis?

A

Cell death with swelling.

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36
Q

If the cytoplasm is seen to be less or more stained pink, what does this say about the cell?

A

If it is less stained then there is a higher water content in the cytoplasm. If it is more stained then this indicates detached ribosomes or denatured proteins.

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37
Q

What is a reversible change which can occur in the nucleus?

A

The chromatin can become subtly clumped.

38
Q

What is pyknosis?

A

Shrinkage of the nucleus.

39
Q

What is the term used to describe when the nucleus become fragmented?

A

Karryohexis

40
Q

What term is given to describe dissolution of the nucleus?

A

Karyolysis

41
Q

Name the reversible changes which can be seen on an electron micrograph of a cell.

A

Cytoplasmic blebs, clumped chromatin and ribosome separation.

42
Q

Give some examples of irreversible cellular changes

A

Lysosome rupture, membrane defects, nuclear changes, ER lysis, amorphous densities in swollen mitochondria.

43
Q

What is apoptosis?

A

It is cell death with shrinkage. The cell activates its own mechanisms and so there is breakdown of its DNA and proteins by enzymes.

44
Q

What is necrosis?

A

This is the appearance of a cell which has been dead for a long time, caused by the action of enzymes on the cell components.

45
Q

How is necrotic tissue removed?

A

Enzymatic degradation followed by phagocytosis.

46
Q

What is dystrophic calcification?

A

This is where the necrotic tissue remains and then calcifies.

47
Q

What two processes can happen to proteins when a cell dies?

A

Denature - this leads to coagulations of proteins (coagulative necrosis). Auto lysis - proteins dissolution by enzymes (liquefactive necrosis)

48
Q

Where does coagulative necrosis occur?

A

This tends to occur in solid organs.

49
Q

When cell death is associated with neutrophils, what type of necrosis is this?

A

Liquefactive

50
Q

What is the process of coagulative necrosis?

A

Denaturation of proteins dominates over release of active proteases, and this leads to a solid white appearance of tissue. After a few days this changes due to an acute inflammatory response.

51
Q

What is liquifactive necrosis?

A

This is where there is infiltration of neutrophils which release enzymes which break down proteins. This leads to the tissue become a viscous mass.

52
Q

caseous necrosis has amorphous, structure less debris and is associated with infections such as TB. What is it commonly associated with?

A

Granulomatous.

53
Q

What type of necrosis is destruction of adipose tissue? How does it occur?

A

Fat necrosis. This leads to release of free fatty acids which react with calcium leaving deposits. It is caused by release of lipases from damaged acinar cells (e.g. In acute pancreatitis) or can be a result of direct trauma.

54
Q

What is the term used to describe necrosis visible to the naked eye?

A

Gangrene

55
Q

Name the three different types of gangrene

A

Dry - e.g. Umbilical cord of a baby
Wet - e.g. Infected necrosis (liquifactive)
Gas - e.g. Anaerobic bacteria produce gases seen as bubbles under skin.

56
Q

What is an infarction?

A

This is an area of tissue death caused by obstruction to the blood supply by an embolism or thrombus.

57
Q

What type of infarct is seen where there is end artery occlusion in a solid organ?

A

White. This is because the solid organ prevents haemorrhage and so there is just tissue death.

58
Q

What accompanies red infarct?

A

Excessive haemorrhage into the dead tissue. This typically occurs where there is a dual blood supply, although the second is insufficient to keep the tissue alive. This is more common in loose tissue.

59
Q

What affects how severe the consequences of infarct are?

A

How susceptible the tissue is to hypoxia, how quickly ischaemia occurred, whether there is alternative blood supply and the oxygen content of the blood.

60
Q

Name two things that can be caused by molecules released from dying tissue.

A

Local irritation and inflammation and general toxic effects on the body.

61
Q

Name three substances released from dead cells

A

Myoglobin, enzymes and potassium

62
Q

Why is potassium release from dead cells a problem?

A

Potassium is at much higher concentrations intracellularly. If there is massive necrosis then this potassium can get to the heart causing MI.

63
Q

What is the clinical significance of enzyme release from dead tissue?

A

We can test in the blood for these enzymes which gives us a measure of necrosis.

64
Q

What substance, lost from dead tissue, can cause renal failure?

A

Myoglobin. It is able to block the tubules.

65
Q

Describe DNA breakdown in Apoptosis.

A

It is internucleosomal cleavage.

66
Q

When does apoptosis occur?

A

It is a normal physiologically process and occurs in embryogenesis, but it also occurs in damaged tissue - particularly when DNA is affected.

67
Q

What happens in the cell during apoptosis?

A

The membrane remains intact, whilst the cell activates enzymes which degrade DNA and proteins.

68
Q

Does apoptosis use lysosomal enzymes?

A

No

69
Q

What can be seen under a light microscope in apoptosis?

A

Cells are shrunken and eosinophilic. The nuclei show chromatin condensation,pyknosis and Karryohexis.

70
Q

Why is there no inflammation associated with apoptosis?

A

Cytoplasmic budding leads to fragmentation and cellular components are contained within vesicles which are then removed by macrophages. There is no leaks and therefore no inflammation.

71
Q

In initiation and execution of apoptosis, what is activated?

A

Caspases.

72
Q

What is intrinsic initiation of apoptosis?

A

In this mitochondria are a central player. P53 is an important trigger and thus and others leads to increased permeability of mitochondria and release of cytochrome C. This interacts with caspase 9.

73
Q

What is external activation of apoptosis?

A

External ligand Bing to death receptors leading to activation of caspases.

74
Q

Give an example of a death ligand and death receptor.

A

TRAIL and TRAIL-R

75
Q

What two forms of fluid accumulation can lead to cell swelling?

A

Diffuse water logging of the entire cell or discrete droplets.

76
Q

What is hydropic swelling?

A

This is due to osmotic disturbances and occurs when energy supplies to the cell are cut off.

77
Q

What problems can be associated with cellular swelling?

A

When a cell swells this can cause compression of blood vessels and so reduced blood flow.

78
Q

What is Steatosis?

A

This is fatty change. It commonly occurs I. The liver due to alcohol abuse. It is reversible and leads to the liver having a yellow appearance rather than red.

79
Q

Cholestrol cannot be broken down. Where does it accumulate in the body?

A

It accumulates in foam cells in the walls of blood vessels. This leads to an artherosclerotic plaque which is a fatty streak.

80
Q

What is Mallorys Hyaline?

A

This is seen in liver disease and bis a damaged protein. It leads to accumulation of keratin fragments.

81
Q

What is a1 anti trypsin deficiency?

A

This is where the protein is mis folded and so accumulates in the ER. This means proteins in the lungs act unchecked and this leads to emphysema.

82
Q

Give two examples of exogenous pigments.

A

Carbon/ soot and tattoo ink.

83
Q

What is lipofuscin?

A

This is a brown endogenous pigment and is a result of age, wear and tear. It is a sign of lipid peroxidation and previous free radical damage.

84
Q

What is Haemosiderin?

A

This is an iron storage molecule which is seen present after iron excess - e.g. After haemorrhage. When systemic iron is high this also can accumulate in organs.

85
Q

What is jaundice?

A

This is accumulation of bilirubin in cells leading to a yellow colour. It can be caused by obstructed bile flow. It is toxic and taken by albumin to the liver for excretion.

86
Q

What is the difference between dystrophic and metastatic calcification?

A

Dystrophic calcification is a local tissue change whilst metastatic is body wide.

87
Q

What can cause regression of metastatic calcification?

A

This is second to high calcium levels so if hypercalcaemia is corrected then this leads to regression.

88
Q

What happens to cells as they age?

A

As cells age they contain more damaged constituents. They also can undergo replication senescence- thought to be due to the length of the telomeres.

89
Q

What maintains telomere length in germ cells/ stem cells?

A

Telomerase.

90
Q

Name three conditions caused by excessive alcohol intake.

A

Fatty change, acute alcohol hepatitis and cirrhosis

91
Q

What is cirrhosis?

A

This is a hard shrunken liver as hepatocytes become surrounded by collagen bundles. It is irreversible and a serious condition.

MOD (Semester 2) (12 decks)

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