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Pathological Processes > Session 1: Cell Injury > Flashcards

Session 1: Cell Injury Flashcards

1
Q

What does the degree of injury depend on?

A

Type of injury
Severity of injury
Type of tissue

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2
Q

What kind of things can cause cell injury?

A

Hypoxia
Toxins
Physical agents like direct trauma, extreme temperature, changes in pressure and electric currents.
Radiation
Micro-organisms
Immune mechanisms
Dietary insufficiencies and deficiencies.

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3
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia is purely when there is a deprivation of oxygen.

Ischaemia is when the blood supply is interrupted.

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4
Q

What causes of hypoxia are there?

A

Hypoxaemic hypoxia
Anaemic hypoxia
Ischaemic hypoxia
Histiocytic hypoxia

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5
Q

What is hyperaemic hypoxia? Give examples.

A

When the arterial content of oxygen is low.
This can happen at high altitudes where there is a reduction in inspiration due to the low pressure.
This can happen due to reduction of absorption secondary to lung disease.

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6
Q

What is anaemic hypoxia? Give examples.

A

The decreased ability of haemoglobin to carry oxygen.

Anaemia and CO poisoning.

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7
Q

What is ischaemic hypoxia? Give examples.

A

When the blood can’t reach its destination tissue due to interruption to blood supply.
This can happen in case of the blockage of a vessel or heart failure.

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8
Q

What is histiocytic hypoxia?

A

The inability to utilise oxygen in the cell itself. Usually due to disabled oxidative phosphorylation enzymes.
For example cyanide poisoning.

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9
Q

Which survives longer without oxygen; Neurones or fibroblasts? How long?

A 
Fibroblasts = few hours
Neurones = few minutes
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10
Q

How does the immune system damage the body’s cells?

A

By either hypersensitivity reactions or autoimmune reactions.

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11
Q

Explain hypersensitivity reactions.

A

Allergic reactions for example. When the host tissue is injured secondary to an overly vigorous immune reaction.

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12
Q

Explain autoimmune reactions.

A

When the immune system fails to distinguish self from non-self. An example is Grave’s disease of thyroid.

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13
Q

Which cell components are most susceptible to injury?

A

Cell membranes (plasma and organelles)
Nucleus (DNA)
Proteins (structural proteins and enzymes)
Mitochondria

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14
Q

Briefly explain what is happening at the molecular level in hypoxia.

A

Ischaemic hypoxia -> blockage of a vessel.
No oxygen to cell.
Disrupts oxidative phosphorylation which causes ATP concentration to go down.
When ATP goes down the a lot of the cell’s processes will fail to work properly. NA+/K+ ATPase will not work correctly which means there will be an accumulation of NA+ intracellularly. This causes an influx of Ca2+ or Ca2+ will not be able to be expelled. Influx of H2O as well.
Protein synthesis goes down.
Glycolysis however increases as anaerobic respiration. This produces an excess in lactate and pH and glycogen goes down. This causes climbing of nuclear chromatin.

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15
Q

What are the consequences of the influx of ions and water (efflux of K+)?

A 
Cellular swelling
Loss of microvilli
Blebs
ER swelling
Myelin figures
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16
Q

What are the consequences of increased cytosolic Ca2+?

A

ATPase goes up causing less ATP.
Phospholipase goes up causing decreased phospholipids.
Protease goes up causing disruption of membrane and cytoskeletal proteins.
Endonuclease goes up causing nuclear chromatin damage.

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17
Q

How do cell injuries that are a result of other causes than hypoxia differ?

A

The sequence of which the events occur might differ, however the outcome is often identical or very similar.
This means that other injuries might attack different key structures at the start like frostbite damages membranes initially.
Free radicals can also damage membranes primarily.

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18
Q

Why is the sequence of cell injury important?

A

If you know what type of injury generally attack a key structure primarily you might have a better idea of what has caused the injury.

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19
Q

What are free radicals?

A

Reactive oxygen species like O2-, OH* and H2O2.

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20
Q

When and where are free radicals produced?

A

In oxidative phosphorylation.
Inflammation due to oxidative burst of neutrophils.
Radiation: H2O -> OH*
Fenton reaction: Fe2+ + H2O2 -> OH- + OH* + Fe3+
Can be accumulation of iron in the body or copper as well.
Drugs and chemicals - e.g. in the liver during metabolism of paracetamol or carbon tetrachloride by P450 system.

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21
Q

What is haemochromatosis?

A

Any cause that results in an accumulation of iron in the body. An increased concentration of iron in the body can cause Fenton reaction to occur and increase the free radical production and subsequent damage.

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22
Q

Explain how the body can control free radicals from damaging the body.

A

Anti-oxidant scavengers which donate electrons to the free radical. (Vitamin A, C and E)
Metal carrier and storage proteins like transferrin and ceruloplasmin.
Enzymes that neutralise free radicals:
Catalase
Superoxide dismutase
Glutathione peroxidase

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23
Q

How do free radicals injure cells?

A

Oxidative imbalance
Lipid peroxidation (chain reaction called autocatalytic chain reaction).
Oxidation of proteins, carbohydrates and DNA.

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24
Q

What are consequences of the oxidation of proteins, carbohydrates and DNA?

A

The molecules become malformed, broken or cross-linked.

Can also cause mutation and down the line also cancer.

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25
Q

Are there any other ways for the cell to protect itself from injury?

A

Yes by heat shock proteins.

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26
Q

What are heat shock proteins?

A

In cell injury proteins will become misfolded and will not work anymore. Heat shock proteins mend the misfolded proteins by unfolding them and then refolding them to the correct setup. This is done by heat shock proteins such as unfoldases and chaperonins.
An example is ubiquitin.

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27
Q

What is pyknosis?

A

Irreversible condensation of chromatin of a cell undergoing cell death. The cell will appear to have shrunk under a microscope.

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28
Q

What is karyorrhexis?

A

Usually the predecessor of pyknosis where the nucleus becomes fragmented. Chromatin and nuclear information will have leaked out into cytoplasm and extracellular space. Cell will look like it might have multiple nuclei.

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29
Q

What is karyolysis?

A

The complete dissolution of chromatin in the cell. Under a microscope there will be no more staining by haematoxylin to see DNA so the cell appears completely empty.

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30
Q

What are indications of reversible injury of a cell?

A 
Blebs
Generalised swelling
Clumping of nuclear chromatin
Autophagy by lysosomes
ER swelling
Dispersion of ribosomes
Mitochondrial swelling
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31
Q

What are indications of irreversible injury of a cell?

A

Rupture of lysosomes following autophagy
Nuclear pyknosis, karyorrhexis or karyolysis.
Defects in cell membrane causing leakage.
Myelin figures
Lysis of ER

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32
Q

Define oncosis.

A

Cell death with swelling. The spectrum of changes that occur in injured cells prior to death.
It is also called ischaemic cell death.

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33
Q

Define necrosis.

A

In a living organism the morphologic changes that occur after a cell has been dead some time. This can usually be seen after 12-24 hours.
This means necrosis is not a type of cell death, it is not a process but the appearance.

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34
Q

What types of necrosis are there?

A

Two main types:
Coagulative necrosis
Liquefactive necrosis

Two less common types:
Caseous necrosis
Fat necrosis

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35
Q

What is coagulative necrosis?

A

An example of coagulative necrosis is when there is ischaemia of a solid organ. Here there is protein denaturation and that makes them stick together.
Denaturation of proteins dominates over the release of active proteases. This means that the cellular architecture will be somewhat preserved.

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36
Q

Coagulative necrosis usually happens in organs, give an example of an organ that does not undergo coagulative necrosis.

A

The brain.

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37
Q

What is liquefactive necrosis?

A

This is when the release of active proteases and hence protein degradation is greater than the denaturation. This leads to enzymatic digestion and liquefaction of the tissue. There will be no cellular architecture preserved here. There is usually presence of many neutrophils, and can be a result of ischaemia in loose tissue.

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38
Q

What is caseous necrosis?

A

This is particularly associated with infections and especially tuberculosis. It contains structureless or amorphous debris. The cells are no long intact but look like small globules.
It looks ‘cheese-like’.

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39
Q

What is fat necrosis?

A

When there is for example an inflammation of the pancreas there can be a release of lipase. The lipase then goes down the abdominal cavity and fatty acids are released by the lipase reacting with lipids. Fatty acids then react with calcium to form ‘soaps’.

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40
Q

Define gangrene.

A

Necrosis that is visible to the naked eye. (An appearance of necrosis.)

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41
Q

Define infarction.

A

Necrosis caused by reduction in arterial blood flow. Infarction is a cause of necrosis and can result in gangrene.

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42
Q

Define infarct.

A

An area of necrotic tissue which is the result of loss of arterial blood supply. It is an area of ischaemic necrosis.

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43
Q

What is dry gangrene?

A

Necrosis modified by exposure to air (coagulative necrosis.

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44
Q

What is wet gangrene?

A

Necrosis modified by infection (neutrophils). This is liquefactive necrosis.

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45
Q

What is gas gangrene?

A

It is essentially wet gangrene where the infection is with anaerobic bacteria that produce gas.

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46
Q

What are the most common causes of infarction?

A

Thrombosis and embolism.

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47
Q

Explain thrombosis.

A

Abnormal blood clot forming that obstruct blood flow.

48
Q

Explain embolism.

A

Can be anything solid, liquid or gaseous. It is distant to its origin. This means that a thrombus might have some of its clot breaking off, traveling to the lung and getting stuck there. It is carried by blood to a site that is distant from its origin.

49
Q

What can ischaemic necrosis look like? (Infarcted tissue)

A

It can either appear white or red.

50
Q

Why would an infarct appear white?

A

A white infarct is an anaemic infarct. This mean that there is no more blood supply going to the area of necrosis, the infarct. So the reason it is white is because there is no blood flow and no bleeding into the infarct from adjacent vessels. Usually happens in solid organs and coagulative necrosis.

51
Q

Why would an infarct appear red?

A

A red infarct is an haemorrhagic infarct. This means that there is a lot of bleeding into the dead tissue.

52
Q

Give some factors that makes a haemorrhagic infarct more likely.

A

Loose tissue
Dual blood supply like in the lungs
A lot of anastomoses which means blood continues to flow.
Raised venous pressure.
Re-perfusion where you allow blood to once again go back into the dead tissue. This is either done by reperfusion therapy or if the clot would spontaneously break free.

53
Q

What factors influence the severity of an infarction?

A

Whether there is alternative blood supply like anastomoses.
The speed of ischaemia.
Which tissue is involved (heart or brain will be much more severe).
Oxygen content of the blood.

54
Q

Explain ischaemia-reperfusion injury.

A

If blood flow is restored to a damaged but not yet necrotic tissue the damage that follows might be become much worse than if the blood flow wasn’t restored at all.

55
Q

Why would restoration of blood flow be even more detrimental than letting the tissue die?

A

Due to an increased production of free radicals with reoxygenation.
Increased number of neutrophils restyling in inflammation and increased tissue injury (the injury spreads and becomes larger).
Delivery of complement proteins and activation of the complement pathway.

56
Q

What are the consequences of molecules leaking out of the cell as it is injured?

A

It can cause local and systemic effects such as:

  • Local inflammation
  • General toxic effects on the body
57
Q

How can you detect cell injury clinically if it is not visible to the naked eye?

A

The leakage of molecules means that some molecules may appear in high concentrations in the blood. This can aid diagnosis.
Examples:
Creatine kinase
Troponin I

58
Q

Give three important substances or molecules that can leak out of the cell.

A

Potassium which is rather low extracellular.
Enzymes like creatine kinase.
Myoglobin causing myoglobinuria as a result of for example rhabdomyolysis. If the myoglobin goes into the kidney tubules it can cause renal failure.

59
Q

What is tumour lysis syndrome?

A

If you would kill a lot of cells at the same time the release of molecules can be extremely high and cause damage.

60
Q

Define apoptosis.

A

Cell death with shrinkage that is induced by regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins. (Death from within).

61
Q

Apoptosis is an active process, what does this mean?

A

That it requires ATP.

62
Q

What characterises apoptosis?

A

That there is DNA breakdown. It is non-random and there is cleavage of DNA.

63
Q

What is the main difference between apoptosis and necrosis?

A

Necrosis is always pathological

Apoptosis can be either physiological or pathological

64
Q

How does apoptosis differ from necrosis?

A

Active process.
Enzymes are activated and degrade nuclear DNA and proteins.
The membrane integrity is maintained.
Lysosomal enzymes are not involved.
It is quick and the cells are gone in a few hours.

65
Q

When does apoptosis occur physiologically and why?

A

In order to maintain a steady state.
It is controlled by hormones.
In embryogenesis, for example sculpting in order to make fingers.

66
Q

When does apoptosis occur pathologically?

A

Cytotoxic T cell killing of virus-infected or neoplastic cells.
When cells are damaged, usually damage to DNA.
Graft versus host disease.

67
Q

What does apoptosis look like?

A

The membrane remains intact however it will split into smaller globules called apoptic bodies.

68
Q

Why is it important that the membrane remains intact in apoptosis?

A

This means that there will be no leakage of intracellular molecules and enzymes. This means that there will be no subsequent inflammation and necrosis. There’s no indication when doing a blood count as well.

69
Q

What are the phases of apoptosis?

A

Initation
Execution
Degradation and phagocytosis

70
Q

How is initiation triggered?

A

It is triggered either intrinsically or extrinsically. Both will result in activation of caspases.

71
Q

What are caspases?

A

Enzymes that control and mediate apoptosis. They cause cleavage of DNA and proteins of the cytoskeleton.

72
Q

What are the most common triggers of the intrinsic trigger?

A

Irreparable DNA damage

Withdrawal of growth factors or hormones.

73
Q

Briefly explain the intrinsically triggered pathway of apoptosis.

A

Following DNA damage p53 is activated and that causes the mitochondrial membrane to become leaky. Mitochondria releases cytochrome C which causes the activation of caspases.

74
Q

What the most common triggers of the extrinsic trigger?

A

Cells that are a danger, like tumour cells and virus-infected cells. They are recognised.

75
Q

Briefly explain the extrinsically triggered pathway of apoptosis. Give an example since there are more than one.

A

TNFalpha is a signal secreted by T killer cells. It binds to cell membrane receptors called death receptors. This causes the activation of caspases.

76
Q

What are apoptotic bodies?

A

They are the result of execution from both the intrinsic and the extrinsic pathway. This is the shrinkage of the cell and the cell breaking up into smaller globules called apoptotic bodies.

77
Q

What is the fate of the apoptotic bodies?

A

They will be phagocytosed.

78
Q

How does phagocytosis of apoptotic bodies happen?

A

Apoptotic bodies have proteins on their surface which can be recognised by phagocytes and neighbouring cells. The neighbouring cell or the phagocyte will then engulf the apoptotic body and degrade it.

79
Q

How does apoptosis differ from oncosis.

A

Apoptosis is shrinkage of the cell and the membrane remains intact.
Oncosis is swelling of the cell and blebs disrupt the cell membrane. Leakage and inflammation ensues.

80
Q

Look at the table on page 60 for a full summary of Apoptosis vs Oncosis/Necrosis.

A

.

81
Q

Explain abnormal cellular accumulation.

A

It occurs when the cell can’t metabolise something meaning it will remain in the cell. They often occur with sublethal or chronic injury. It can be reversible as well.

82
Q

What can abnormal cellular accumulation derive from?

A

The cell’s own metabolism
The extracellular space like spilled blood.
The outer environment of the body like dust.

83
Q

What are the five main groups of intracellular accumulation?

A 
Water and electrolytes
Carbohydrates
Proteins
Lipids
Pigments
84
Q

When does fluid accumulate in cells?

A

This is called hydronic swelling and often occurs when energy supplies are cut off like the case of hypoxia.
Sodium ions and water flows into the cell. It indicates severe cellular distress and can be a big problem in the brain.

85
Q

What is steatosis?

A

The accumulation of triglycerides.

86
Q

Where does steatosis most commonly occur? What are the causes?

A

Mostly seen in the liver. (Fatty liver)

It can be causes by alcohol, diabetes mellitus, obesity and toxin such as carbon tetrachloride.

87
Q

What are the main lipids that accumulate in cells?

A

Triglycerides (TAGs) and cholesterol.

88
Q

When does cholesterol accumulate in cells?

A

It can only be eliminated though the liver to produce bile salts. LDL as they are being oxidised can accumulate in smooth muscle cells by macrophages and form atherosclerotic plaques called foam cells.

89
Q

What does cholesterol accumulation look like?

A

Discoloration on eyelids
Nodules on knuckles and elsewhere
Corneal arcus

90
Q

In what conditions do proteins accumulate in cells?

A

Alcoholic liver disease like Mallory’s hyaline which is damaged keratin filaments.
Alpha1-antitrypsin deficiency.

91
Q

Explain alpha1-antitrypsin deficiency.

A

The liver produces incorrectly folded alpha1-antitrypsin which is a protease inhibitor.
Misfolded proteins can’t be packaged by the ER and will instead accumulate in the ER and will not be secreted. This means that there will be a systemic deficiency of the inhibitor.
Proteases in the lung can therefore roam free and act on elastase which causes emphysema.
It can also cause abnormal liver function causing cirrhosis.

92
Q

What do accumulated proteins look like?

A

Eosin stains proteins. The accumulated proteins are seen as something called eosinophilic droplets in the cell. Small red spots in the cell which are gathered.

93
Q

What are pigments?

A

Carbon/coal dust and soot as examples.

94
Q

When do exogenous pigments accumulate in cells?

A

Due to environment. When those pigments which are common urban air pollutants are inhaled they are phagocytosed by alveolar macrophages.
This results in anthracosis and blackened peribronchial lymph nodes.
In excess exposure fibrosis and emphysema can follow like coal worker’s pneumoconiosis.
Tattooing where pigments are picked into the skin and phagocytosed by macrophages in dermis and will remain there.

95
Q

How does accumulation of endogenous pigments happen?

A

Haemosiderin is an iron storage complex. They are derived from haemoglobin. They are formed whiner there is a systemic or local excess of iron like following damage of tissue, bruise etc.
As there is an increase in iron or iron overload (haemochromatosis) haemosiderin will be deposited into many organs causing haemosiderosis (accumulation of haemosiderin).

96
Q

When can haemosiderosis be seen?

A

In the case of haemolytic anaemias, blood transfusions and hereditary haemochromatosis.

97
Q

What is hereditary haemochromatosis?

A

Genetically inherited
Increased intestinal absorption of dietary iron.
Iron is deposited into skin, liver, pancreas, heart and endocrine organs. Results in liver cirrhosis and also scarring of pancreas.

98
Q

What are symptoms of hereditary haemochromatosis?

A

Liver damage
Heary dysfunction
Endocrine failure (pancreas especially)
Pancreatic failure

99
Q

How do you treat hereditary haemochromatosis?

A

Repeated bleeding of the patient.

100
Q

What is accumulating in jaundice?

A

Bilirubin which is bright yellow.

101
Q

How does jaundice occur?

A

When red blood cells are broken down heme and stacks of broken porphyrin rings are produced. They are formed all over the body but they must be eliminated in bile. This means they will be transported from tissues by albumin to the liver and conjugated with bilirubin there.
If bile flow is obstructed or overwhelmed bilirubin in blood rises and jaundice ensues.
Bilirubin is then deposited into tissues extracellularly or in macrophages.

102
Q

What is pathological calcification of tissues?

A

Abornmal deposition of calcium salts within tissues.

103
Q

What is localised calcification of tissues called?

A

Dystrophic.

104
Q

What is generals calcification of tissues called?

A

Metastatic.

105
Q

What is most common, metastatic or dystrophic?

A

Dystrophic.

106
Q

Where does dystrophic calcification most commonly occur?

A

In an area of dying tissue, atherosclerotic plaques, paging, or damaged heart valves. In tubercles lymph nodes and some malignancies.

107
Q

Why does dystrophic calcification occur?

A

In dystrophic there is no abnormality in calcium metabolism or serum calcium or phosphate concentrations. This is because if there would be, it wouldn’t be localised.
It is due to a local change or disturbance that favours the nucleation of hydroxyapatite crystals.
It can cause organ dysfunction. e.g. atherosclerosis or calcified heart valves.

108
Q

Why does metastatic calcification occur?

A

Due to hypercalcaemia secondary to to disturbances in calcium metabolism. Hydroxyapatite crystal are deposited normal in all tissues here. The main problem is metabolism.
It is usually asymptomatic but it can be lethal.
It can regress if the cause of hypercalcaemia is corrected.

109
Q

What causes hypercalcaemia?

A

Increased secretion of PTH resulting in higher calcium levels in the body.
Destruction of bone tissue as well not related to PTH.

110
Q

What is primary PTH hypercalcaemia?

A

Du to parathyroid hyperplasia or tumour.

111
Q

What is secondary PTH hypercalcaemia?

A

Due to renal failure and the retention of phosphate.

112
Q

What is ectopic PTH hypercalcaemia?

A

Secretion of PTH-related protein by malignant tumours like carcinoma of the lungs.

113
Q

Give example of causes of hypercalcaemia not related to PTH.

A

Primary tumours of bone marrow, leukaemia and multiple myeloma.
Diffuse skeletal metastases
Paget’s disease of bone
Immobilisation

114
Q

What is replicative senescence?

A

A cell can only divide a certain number of times. This is related to the length of the chromosomes.

115
Q

What are telomeres and how to they relate to cell division?

A

The end of the chromosomes are called telomeres. With every replication of a cell the telomeres shorten. At a certain point of length of the telomeres the cell can no longer divide.

116
Q

Are there cells that can live forever and divide forever?

A

Germ cells and stem cells and cancer cells.

117
Q

How do they live forever?

A

They contain an enzyme called telomerase which maintains the original length of the telomeres to they can replicate indefinitely.

Pathological Processes (14 decks)

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