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Mechanisms of disease > Session 1 > Flashcards

Session 1 Flashcards

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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
What are the most important targets of free radical injury?
Lipid in cell membranes; unsaturated lipids can be attacked by free radicals leading to lipid peroxidation; this reaction leads to more free radicals
26
How can free radicals damage proteins and DNA?
Free radicals can cause protein fragmentation and cross-links and can cause single strand breaks in DNA, both genomic and mitochondrial
27
Name 3 ways in which free radicals are removed
Spontaneous decay, enzymes, free radical scavengers
28
Describe the removal of superoxide free radicals
Supeoxide dismutase(SOD) produced hydrogen peroxide from superoxide; catalases and peroxidases complete the process of removal, converting peroxide to water and oxygen
29
What are free radical scavengers? Give some examples
Antioxidant chemicals that help neutralise free radicals; vitamins A, C and E
30
How do cells limit the Fenton reaction?
In the extracellular matrix, storage proteins sequester transition metals e.g. iron
31
What do heat shock proteins do?
Help protein folding get back on track when it goes astray; the general upkeep of cellular proteins
32
Why are heat shock proteins important in cell injury?
They play a key role in maintaining protein viability and thus maximising cell survival
33
What are ‘chaperones’? Name the two major families
Chaperones help proteins to refold, their synthesis is boosted by heat shock proteins in a feedback system; hsp60, hsp70
34
What is pyknosis?
Irreversible nuclear shrinkage
35
What is karryohexis?
Irreversible nuclear fragmentation
36
What is karryolysis?
Irreversible nuclear dissolution
37
Describe a reversible, subtle change to the nucleus in cell injury
Clumping of chromatin
38
Describe a reversible change in the cytoplasm of an injured cell
Accumulation of water resulting in reduced pink staining
39
What happens to the cytoplasm that is irreversible when the cell is injured?
Increased pink staining due to detachment and loss of ribosomes and accumulations of denatured proteins
40
What do abnormal accumulations in reversibly injured cells reflect?
Damaged proteins and accumulations of abnormal metabolites
41
Give an example of a damaged protein seen in cell injury in alcoholic liver disease
Mallory’s hyaline; accumulation of altered keratin filaments
42
Give an example of an accumulation of abnormal metabolites seen in cell injury in alcoholic liver disease
Fat
43
Why does swelling occur in cell injury? Is it reversible or irreversible?
Na+/K+ pump failure; reversible
44
Why does chromatin clumping occur in cell injury? Is it reversible or irreversible?
Reduced pH; reversible
45
Why does ribosome dispersion occur in cell injury? Is it reversible or irreversible?
No ATP for process of maintaining them; reversible
46
Why does autophagy occur in cell injury? Is it reversible or irreversible?
Catabolic response to low energy; reversible
47
Why do cytoplasmic blebs form in cell injury? Is it reversible or irreversible?
Symptomatic of cell swelling; reversible
48
Why does lysosome rupture occur in cell injury? Is it reversible or irreversible?
Occurs due to membrane damage; irreversible
49
Why do myelin figures form during cell injury? Is it reversible or irreversible?
Due to membrane defects which occur due to cell injury; irreversible
50
Why does lysis of endoplasmic reticulum occur in cell injury? Is it reversible or irreversible?
Due to membrane defects which occur due to cell injury; irreversible
51
What is necrosis?
Morphological changes following cell death in living tissue, largely due to progressive degradative action of enzymes on lethally injured cell
52
What determines whether coagulative or liquifactive necrosis occurs?
Balance between protein denaturation and release of enzymes
53
What happens when denaturation is dominant in necrosis? What type of necrosis is this?
Proteins tend to clump, leading to solidity of dead cells and consequently dead tissue; coagulative necrosis
54
What happens when enzyme release is dominant in necrosis? What type of necrosis is this?
Dead cells and consequently dead tissue liquefy, leading to liquefactive necrosis
55
When the cause of death is ischaemia, in most solid organs which type of necrosis occurs?
Coagulative
56
When cell death is associated with a large number of neutrophils, which type of necrosis is likely to occur?
Their released proteolytic enzymes lead to liquefactive necrosis
57
Describe the histology of cells having undergone coagulative necrosis the first few days after occurrence
Cellular architecture is somewhat preserved, creating a ‘ghost’ outline of the cells
58
What happens in coagulative necrosis after the first few days?
Immune response is incited by dead tissue, it is infiltrated by phagocytes
59
What are the observable changes in the tissue after the first few days of coagulative necrosis?
Increased eosinophilia of cytoplasm, nuclei changed/lost, ghost outline of architecture
60
What are the smaller cells between the dead ones in coagulatively necrosed tissue?
Neutrophils; acute inflammation
61
Why is liquifactive necrosis seen in massive neutrophil infiltration?
They release proteases
62
Why is liquifactive necrosis seen in the brain?
The brain is a fragile tissue without support from a robust collagenous matrix
63
What is caseous necrosis? Which infection is it particularly linked with?
‘cheese-like’ appearance, structureless debris; mycobacterium tuberculosis
64
What is fat necrosis most typically seen as a consequence of? Why?
Pancreatitis; causes release of lipases which act on fatty tissue of pancreas and abdominal cavity to cause fat necrosis;
65
Why can fat necrosis be seen on x-ray?
Causes release of fatty acids, which can react with calcium to form chalky deposits
66
What is gangrene?
Necrosis that is visible to the eye; it is not a type of necrosis
67
Why can gangrene be described as ‘wet’ or ‘dry’?
It can be liquifactive of coagulative
68
What is the most common cause of seeing gangrene in clinical practice?
Ischaemia in the limbs
69
What is an ‘infarction’?
Tissue death caused by obstruction of the tissue’s blood supply; it is a cause of necrosis
70
How do ‘white’ infarcts occur?
Occlusion of an ‘end’ artery; lack of blood in the tissue
71
How do ‘red’ infarcts occur?
Extensive haemorrhage into into dead tissue; can be due to dual blood supply (insufficient to save tissue, haemorrhagic necrosis), and rich anastomoses
72
Why do red infracts occur in the lung?
Poor stromal support for capillaries
73
How does raised venous pressure cause red infracts?
Increased pressure is transmitted to the capillary beds; arterial filling reduces, causing ischaemia and subsequent necrosis; the tissue is engorged with blood
74
What is apoptosis?
Single ‘programmed’ cell death
75
Give an example of physiological apoptosis
Embryonic development; removal of hand webbing
76
Describe three general changes of apoptosis histologically
Nuclear changes (fragmentation) with intense eosinophilia, cell shrinkage and fragmentation, phagocytosis of fragments by macrophages
77
Why is there no inflammation with apoptosis?
There is no leakage of cell contents
78
What are the three phases of apoptosis?
Initiation, execution, degradation and phagocytosis
79
Describe the basis of intrinsic apoptosis initiation
Stimuli (DNA damage, p53) cause increased mitochondrial permeability and the release of cytochrome c from the mitochondria
80
Describe the basis of intrinsic apoptosis execution
Cytochrome c interacts with APAF1 and caspase 9 to from the apoptosome; this activates caspases which mediat the cellular effects of apoptosis
81
What is the action of Bcl-2?
Prevents cytochrome c release from the mitochondria and hence inhibits apoptosis
82
Describe the basis of extrinsic apoptosis initiation
External ligands (e.g. TRAIL) bind to ‘death receptors’ (e.g. TRAIL-R)
83
Describe the basis of extrinsic apoptosis initiation
Death receptors cause activation of caspases independently of mitochondria
84
What is the difference in cell size between apoptosis and necrosis?
Necrosis causes cell swelling, apoptosis cause cell shrinkage
85
What is the difference in cell contents between apoptosis and necrosis?
Necrosis causes enzymatic digestion, apoptosis contents are intact and may be released in apoptopic bodies
86
Describe the basic metabolism of alcohol
Ethanol to acetaldehyde, by action of alcohol dehydrogenase, acetaldehyde to acetic acid by action of aldehyde dehydrogenase
87
Describe the effects of chronic alcohol intake on AST, ALT, MCV, PT, Gamma-GT, and ALP
All raised
88
What happens to paracetamol metabolism after overdose?
Phase II conjugation with glucuronide/sulphate saturated, paracetamol undergoes phase I metabolism, producing a toxic metabolite NAPQI
89
Why is NAPQI dangerous to hepatocytes?
It is toxic itself, but also undergoes phase II metabolism depleting glutathione
90
How long does liver failure take to occur after a paracetamol overdose?
36-96 hours
91
Which test gives a guide to the severity of liver damage with a paracetamol overdose?
Prothrombin time 24 hours after OD
92
What is an antidote for paracetamol OD? How is treatment with this drug determined?
N-acetylcysteine, increases availability of hepatic glutathione; measure serum paracetamol 4 hours after OD
93
How does an aspirin overdoes result in a fall in pH?
OD stimulates respiratory centre resulting in respiratory alkalosis; compensatory mechanisms result in a metabolic acidosis
94
How does aspirin overdoes affect the GI tract and cause petechiae?
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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