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Mechanisms of disease > Session 1 > Flashcards

Session 1 Flashcards

1
Q

What does the failure of homeostasis cause?

A

Disease with consequent morphological and functional disturbances

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2
Q

What is hypoxia?

A

Body or some tissue is deprived of oxygen

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3
Q

What are the four types of hypoxia?

A

Hypoxaemic hypoxia, anaemic hypoxia, ischaemic hypoxia, and histiocytic hypoxia

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4
Q

What is hypoxaemic hypoxia?

A

Arterial content of oxygen is too low; reduced inspiration/reduced absorption

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5
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen; anaemia, CO poisoning

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6
Q

What is ischaemic hypoxia?

A

Interruption to blood supply; blockage of a vessel, heart failure

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7
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes; cyanide poisoning

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8
Q

What is ischaemia?

A

Loss of blood supply, resulting in a decrease of oxygen and substrate; it causes more rapid and severe injury than hypoxia

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9
Q

How long can cells tolerate hypoxia?

A

It varies; come neurones can only tolerate a few mintes, fibroblasts in the dermis can last hours

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10
Q

What are the two principle ways in which the immune system can damage cells?

A

Hypersensitivity reactions (overly vigorous immune reaction), autoimmune reactions (failure to distinguish self and non-self)

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11
Q

What are the principle structural targets for cell damage?

A

Hypersensitivity reactions (overly vigorous immune reaction), autoimmune reactions (failure to distinguish self and non-self)

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12
Q

If ischaemia occurs, what will happen to the mitochondrial output?

A

Reduced oxidative phosphorylation, and hence reduced ATP

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13
Q

How does a reduction in ATP affect the Na pump?

A

Reduction in Na pump activity, resulting in an influx of Ca2+, H2O and Na+, and an efflux of K+; this results in cellular swelling, loss of microvilli, blebs, ER swelling and myelin figures

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14
Q

How does ischaemic cause the clumping of nuclear chromatin?

A

Reduced ATP, hence increased anaerobic glycolysis, and therefore a reduced pH and glycogen; the reduction in pH causes the clumping of nuclear chromatin

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15
Q

What effect does a decrease in ATP have on proteins synthesis?

A

Reduced ATP causes detachment of ribosome and hence a reduction in protein synthesis – this causes lipid deposition

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16
Q

What is a key event in the point where hypoxic cell damage becomes irreversible?

A

Massive cystolic accumulation of calcium, especially from intracellular stores (mitochondria, ER)

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17
Q

Why is the massive cystolic accumulation (during hypoxic cell injury) of calcium important? What happens?

A

It activates a range of potent enzymes; ATPases (decrease ATP), phospholipases (decrease phospholipids), proteases (disrupt membrane and cytoskeleton) and endonucleases (damage nuclear chromatin)

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18
Q

What are reactive oxygen species?

A

Free radicals containing oxygen; single unpaired electron in outer orbit, this unstable and hence reacts with other molecules causing damage

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19
Q

How are reactive oxygen species produced?

A

Chemical and radiation injury, ischaemia-reperfusion injury, cellular aging, high oxygen concentrations, and as a by-product of oxidative phosphorylation

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20
Q

Name the 3 especially important free radicals associated with cell damage. Which is the most dangerous?

A

OH• (hydroxyl, they most dangerous), O2- (superoxide), H2O2 (hydrogen peroxide)

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21
Q

Name three ways in which OH• (hydroxyl) free radicals can be generated

A

Radiation can directly lyse water, the Fenton reaction, the Haber-Weiss reaction

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22
Q

Describe the Fenton reaction

A

Fe2+ reacts with hydrogen peroxide to from Fe3+, hydroxyl and OH-

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23
Q

Describe the Haber-Weiss reaction

A

Superoxide (O2-) reacts with H+ and hydrogen peroxide to from oxygen, water and hydroxyl

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24
Q

Describe two places in a cell where normal metabolic reactions yield free radicals

A

Oxidative phosphorylation in the mitochondria can yield both superoxide and hydrogen peroxide, as can cystolic reactions and p450 enzymes in the endoplasmic reticulum

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25
Q

What are the most important targets of free radical injury?

A

Lipid in cell membranes; unsaturated lipids can be attacked by free radicals leading to lipid peroxidation; this reaction leads to more free radicals

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26
Q

How can free radicals damage proteins and DNA?

A

Free radicals can cause protein fragmentation and cross-links and can cause single strand breaks in DNA, both genomic and mitochondrial

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27
Q

Name 3 ways in which free radicals are removed

A

Spontaneous decay, enzymes, free radical scavengers

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28
Q

Describe the removal of superoxide free radicals

A

Supeoxide dismutase(SOD) produced hydrogen peroxide from superoxide; catalases and peroxidases complete the process of removal, converting peroxide to water and oxygen

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29
Q

What are free radical scavengers? Give some examples

A

Antioxidant chemicals that help neutralise free radicals; vitamins A, C and E

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30
Q

How do cells limit the Fenton reaction?

A

In the extracellular matrix, storage proteins sequester transition metals e.g. iron

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31
Q

What do heat shock proteins do?

A

Help protein folding get back on track when it goes astray; the general upkeep of cellular proteins

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32
Q

Why are heat shock proteins important in cell injury?

A

They play a key role in maintaining protein viability and thus maximising cell survival

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33
Q

What are ‘chaperones’? Name the two major families

A

Chaperones help proteins to refold, their synthesis is boosted by heat shock proteins in a feedback system; hsp60, hsp70

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34
Q

What is pyknosis?

A

Irreversible nuclear shrinkage

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35
Q

What is karryohexis?

A

Irreversible nuclear fragmentation

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36
Q

What is karryolysis?

A

Irreversible nuclear dissolution

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37
Q

Describe a reversible, subtle change to the nucleus in cell injury

A

Clumping of chromatin

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38
Q

Describe a reversible change in the cytoplasm of an injured cell

A

Accumulation of water resulting in reduced pink staining

39
Q

What happens to the cytoplasm that is irreversible when the cell is injured?

A

Increased pink staining due to detachment and loss of ribosomes and accumulations of denatured proteins

40
Q

What do abnormal accumulations in reversibly injured cells reflect?

A

Damaged proteins and accumulations of abnormal metabolites

41
Q

Give an example of a damaged protein seen in cell injury in alcoholic liver disease

A

Mallory’s hyaline; accumulation of altered keratin filaments

42
Q

Give an example of an accumulation of abnormal metabolites seen in cell injury in alcoholic liver disease

A

Fat

43
Q

Why does swelling occur in cell injury? Is it reversible or irreversible?

A

Na+/K+ pump failure; reversible

44
Q

Why does chromatin clumping occur in cell injury? Is it reversible or irreversible?

A

Reduced pH; reversible

45
Q

Why does ribosome dispersion occur in cell injury? Is it reversible or irreversible?

A

No ATP for process of maintaining them; reversible

46
Q

Why does autophagy occur in cell injury? Is it reversible or irreversible?

A

Catabolic response to low energy; reversible

47
Q

Why do cytoplasmic blebs form in cell injury? Is it reversible or irreversible?

A

Symptomatic of cell swelling; reversible

48
Q

Why does lysosome rupture occur in cell injury? Is it reversible or irreversible?

A

Occurs due to membrane damage; irreversible

49
Q

Why do myelin figures form during cell injury? Is it reversible or irreversible?

A

Due to membrane defects which occur due to cell injury; irreversible

50
Q

Why does lysis of endoplasmic reticulum occur in cell injury? Is it reversible or irreversible?

A

Due to membrane defects which occur due to cell injury; irreversible

51
Q

What is necrosis?

A

Morphological changes following cell death in living tissue, largely due to progressive degradative action of enzymes on lethally injured cell

52
Q

What determines whether coagulative or liquifactive necrosis occurs?

A

Balance between protein denaturation and release of enzymes

53
Q

What happens when denaturation is dominant in necrosis? What type of necrosis is this?

A

Proteins tend to clump, leading to solidity of dead cells and consequently dead tissue; coagulative necrosis

54
Q

What happens when enzyme release is dominant in necrosis? What type of necrosis is this?

A

Dead cells and consequently dead tissue liquefy, leading to liquefactive necrosis

55
Q

When the cause of death is ischaemia, in most solid organs which type of necrosis occurs?

A

Coagulative

56
Q

When cell death is associated with a large number of neutrophils, which type of necrosis is likely to occur?

A

Their released proteolytic enzymes lead to liquefactive necrosis

57
Q

Describe the histology of cells having undergone coagulative necrosis the first few days after occurrence

A

Cellular architecture is somewhat preserved, creating a ‘ghost’ outline of the cells

58
Q

What happens in coagulative necrosis after the first few days?

A

Immune response is incited by dead tissue, it is infiltrated by phagocytes

59
Q

What are the observable changes in the tissue after the first few days of coagulative necrosis?

A

Increased eosinophilia of cytoplasm, nuclei changed/lost, ghost outline of architecture

60
Q

What are the smaller cells between the dead ones in coagulatively necrosed tissue?

A

Neutrophils; acute inflammation

61
Q

Why is liquifactive necrosis seen in massive neutrophil infiltration?

A

They release proteases

62
Q

Why is liquifactive necrosis seen in the brain?

A

The brain is a fragile tissue without support from a robust collagenous matrix

63
Q

What is caseous necrosis? Which infection is it particularly linked with?

A

‘cheese-like’ appearance, structureless debris; mycobacterium tuberculosis

64
Q

What is fat necrosis most typically seen as a consequence of? Why?

A

Pancreatitis; causes release of lipases which act on fatty tissue of pancreas and abdominal cavity to cause fat necrosis;

65
Q

Why can fat necrosis be seen on x-ray?

A

Causes release of fatty acids, which can react with calcium to form chalky deposits

66
Q

What is gangrene?

A

Necrosis that is visible to the eye; it is not a type of necrosis

67
Q

Why can gangrene be described as ‘wet’ or ‘dry’?

A

It can be liquifactive of coagulative

68
Q

What is the most common cause of seeing gangrene in clinical practice?

A

Ischaemia in the limbs

69
Q

What is an ‘infarction’?

A

Tissue death caused by obstruction of the tissue’s blood supply; it is a cause of necrosis

70
Q

How do ‘white’ infarcts occur?

A

Occlusion of an ‘end’ artery; lack of blood in the tissue

71
Q

How do ‘red’ infarcts occur?

A

Extensive haemorrhage into into dead tissue; can be due to dual blood supply (insufficient to save tissue, haemorrhagic necrosis), and rich anastomoses

72
Q

Why do red infracts occur in the lung?

A

Poor stromal support for capillaries

73
Q

How does raised venous pressure cause red infracts?

A

Increased pressure is transmitted to the capillary beds; arterial filling reduces, causing ischaemia and subsequent necrosis; the tissue is engorged with blood

74
Q

What is apoptosis?

A

Single ‘programmed’ cell death

75
Q

Give an example of physiological apoptosis

A

Embryonic development; removal of hand webbing

76
Q

Describe three general changes of apoptosis histologically

A

Nuclear changes (fragmentation) with intense eosinophilia, cell shrinkage and fragmentation, phagocytosis of fragments by macrophages

77
Q

Why is there no inflammation with apoptosis?

A

There is no leakage of cell contents

78
Q

What are the three phases of apoptosis?

A

Initiation, execution, degradation and phagocytosis

79
Q

Describe the basis of intrinsic apoptosis initiation

A

Stimuli (DNA damage, p53) cause increased mitochondrial permeability and the release of cytochrome c from the mitochondria

80
Q

Describe the basis of intrinsic apoptosis execution

A

Cytochrome c interacts with APAF1 and caspase 9 to from the apoptosome; this activates caspases which mediat the cellular effects of apoptosis

81
Q

What is the action of Bcl-2?

A

Prevents cytochrome c release from the mitochondria and hence inhibits apoptosis

82
Q

Describe the basis of extrinsic apoptosis initiation

A

External ligands (e.g. TRAIL) bind to ‘death receptors’ (e.g. TRAIL-R)

83
Q

Describe the basis of extrinsic apoptosis initiation

A

Death receptors cause activation of caspases independently of mitochondria

84
Q

What is the difference in cell size between apoptosis and necrosis?

A

Necrosis causes cell swelling, apoptosis cause cell shrinkage

85
Q

What is the difference in cell contents between apoptosis and necrosis?

A

Necrosis causes enzymatic digestion, apoptosis contents are intact and may be released in apoptopic bodies

86
Q

Describe the basic metabolism of alcohol

A

Ethanol to acetaldehyde, by action of alcohol dehydrogenase, acetaldehyde to acetic acid by action of aldehyde dehydrogenase

87
Q

Describe the effects of chronic alcohol intake on AST, ALT, MCV, PT, Gamma-GT, and ALP

A

All raised

88
Q

What happens to paracetamol metabolism after overdose?

A

Phase II conjugation with glucuronide/sulphate saturated, paracetamol undergoes phase I metabolism, producing a toxic metabolite NAPQI

89
Q

Why is NAPQI dangerous to hepatocytes?

A

It is toxic itself, but also undergoes phase II metabolism depleting glutathione

90
Q

How long does liver failure take to occur after a paracetamol overdose?

A

36-96 hours

91
Q

Which test gives a guide to the severity of liver damage with a paracetamol overdose?

A

Prothrombin time 24 hours after OD

92
Q

What is an antidote for paracetamol OD? How is treatment with this drug determined?

A

N-acetylcysteine, increases availability of hepatic glutathione; measure serum paracetamol 4 hours after OD

93
Q

How does an aspirin overdoes result in a fall in pH?

A

OD stimulates respiratory centre resulting in respiratory alkalosis; compensatory mechanisms result in a metabolic acidosis

94
Q

How does aspirin overdoes affect the GI tract and cause petechiae?

A

Aspirin OD causes erosive gastritis and GI bleeding; there is inhibition of platelet cyclo-oxygenase causing reduced platelet aggregation

Mechanisms of disease (3 decks)

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