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Pathological Processes (Milly's) > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What does the degree of cell injury depend on? (3)

A
  • type of injury
  • severity of injury
  • type of tissue
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2
Q

What is hypoxia and what can it cause?

A

Deficiency in the amount of oxygen reaching tissues

Can caused cell injury

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3
Q

What kind of things can cause cell injury? (9)

A 
Hypoxia
Toxin
Physical agents 
Radiation
Chemical agents and drugs 
Micro-organisms
Immune mechanisms 
Dietary insufficiencies and deficiencies/diet excess 
Genetic  (in born errors of metabolism)
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4
Q

Give some examples of the physical agents that might cause cell injury (4)

A

Direct trauma
Extreme temps
Changes in pressure
Electric currents

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5
Q

What is the difference between hypoxia and ischaemia? Which is worse?

A

Hypoxia is a deficiency in the amount of oxygen reaching tissue but ischaemia is a deficiency in the blood supply to tissue

Ischaemia is worse

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6
Q

Name and describe the 4 types of hypoxia

A
  • Hypoxaemic hypoxia (is arterial content of oxygen is low)
  • Anaemic hypoxia (decreased ability of haemoglobin to carry oxygen)
  • Ischaemic hypoxia (interruption to blood supply)
  • Histiocytic hypoxia (inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes)
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7
Q

Give a cause of Hypoxaemic hypoxia

A

Reduced inspired pO2 at altitude

Reduced absorption secondary to lung disease

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8
Q

Give a cause of anaemic hypoxia

A

Anaemia

CO poisoning

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9
Q

Give a cause of ischaemic hypoxia

A

Blockage of blood vessel

Heart failure

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10
Q

Give a cause of histiocytic hypoxia

A

Cyanide poisoning

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11
Q

The degree of damage caused by hypoxia varies in different tissues, how long can neurones and fibroblasts survive before they become damaged?

A

Neurone-few minutes

Fibroblasts-few hrs

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12
Q

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

A

Hypersensitivity reactions (host tissue is injured secondary to an overly vigorous immune reaction)

Autoimmune reactions (failure to distinguish self from foreign)

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13
Q

Give an example of a condition caused by hypersensitive reactions, when the immune system damages the body’s cells

A

Urticaria (hives)

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14
Q

Give an example of an autoimmune reaction, in which the immune system causes damage to the body’s cells

A

Grave’s disease of thryoid

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15
Q

Which cellular components are most susceptible to injury? (4)

A

Membranes (plasma/organellar)
Nucleus (DNA)
Proteins (structural/enzymes)
Mitochondria (oxidative phosphorylation)

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16
Q

What is happening at a molecular level in hypoxia?

A
  • oxygen levels are decreased
  • oxidative phosphorylation in mitochondria reduces
  • less ATP is produced (levels reach 5-10% of norm), causes many things:
    1) reduce in Na+/K+ ATPase = influx of Ca2+, H2O and Na+, efflux of K+ =cellular swelling, blebbing, myelin figures appear etc
    2) rate of glycolysis increases (anaerobic respiration)=pH is lowered + glycogen stores decrease
    3) other effect- detachments of ribosomes=decrease in protein synthesis=lipid deposition
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17
Q

What happens as result of prolonged hypoxia?

A

Irreversible results!

Increased cytosolic Ca2+ (due to lack of Na+ pump action)
Ca2+ inappropriately activates multiple enzymes:
1)ATPase=decreased ATP
2)phospholipase=decreased phospholipids
3)protease=disruption of membrane and cytoskeletal proteins
4)endonucleases=nuclear chromatin damage

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18
Q

Why do you often see the same result in cells in non hypoxia situations? Ie extreme cold- frostbite, free radicals

A

Often membranes can be damaged by extreme temps which allows for the influx of water and Ca2+ and causes the same issues

Free radicals cause damage to membranes also

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19
Q

What are free radicals?

A

Reactive oxygen species
Single unpaired electrons
V. Unstable configuration
React with other molecules to stabilise themselves but produce free radicals in the process

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20
Q

Name the 3 types of free radicals that are of particular biological significance in cells

A

Hydroxyl (most dangerous) OH
O2- (superoxide)
H2O2 (hydrogen peroxide)

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21
Q

Give some examples of chemical agents and drugs that can cause cell injury (9)

A 
Glucose/salt in hypertonic solutions
Oxygen in high conc
Poisons
Insecticides 
Herbicides
Asbestos
Alcohol
Illicit drugs
Therapeutic drugs
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22
Q

Give a summary of hypoxia cell injury (14 steps)

A

1)cell is deprived of oxygen
2)Mitochondrial ATP production stops.
3)The ATP-driven Na+ K+ ATPase pumps runs down.
4)Sodium and water seep into the cell.
5)The cell swells, and the plasma membrane is stretched.
6)Glycolysis enables the cell to limp on for a while (anaerobic respiration)
7)The cell initiates a heat-shock (stress) response, which
will probably not be able to cope if the hypoxia persists.
8)The pH drops as cells produce energy by glycolysis and lactic acid
accumulates.
9)Calcium enters the cell. (Voltage changes across membrane due to abnormal movement of ions)
10)Calcium activates enzymes which damage cell and organelles
11)The ER and other organelles swell. 12) Enzymes leak out of lysosomes and these enzymes attack cytoplasmic components.
13)All cell membranes are damaged and start to show blebbing.
14)At some point the cell dies, possibly killed by the burst of a bleb.

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23
Q

What is a free radical?

A

Something that has an unpaired electron- high energy

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24
Q

When are free radicals produced? (4)

A

Chemical and radiation injury
Ischaemia-repercussion injury
Cellular aging
High oxygen concentration

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25
Q

What in particular do free radicals attack within the cell?

A

The cell membranes causing lipid peroxidation (oxidation of lipids- being degraded)

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26
Q

What is the system that the body has to prevent injury from free radicals?

A

Anti-oxidant system

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27
Q

When is a tissue said to be in oxidative stress?

A

When there is a build up of free radicals

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28
Q

What 3 things does the anti-oxidant system consist of?

A

Enzymes
Free radical scavengers
Storage proteins

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29
Q

Give examples of enzymes in the anti-oxidative system

A

Superoxide dismutase (SOD): O2- -> H2O2

Catalase: H2O2->O2 + H20

Peroxidases: H2O2->O2 + H2O

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30
Q

Give examples of free radical scavengers

A

Vitamin A
Vitamin C
Vitamin E
Glutathione

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31
Q

The anti-oxidative system has storage proteins, what are these?

A

These are proteins that sequester transition metals in the extracellular matrix.

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32
Q

What mechanism can a cell use to repair injury to proteins within cells?

A

Heat shock proteins

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33
Q

What do heat shock proteins do? Give an example

A

Mend other proteins
Bind to and guide them through the process of refolding/repair

Also called unfoldases or chaperonins

Ubiquitous

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34
Q

What cell morphology would you see in hypoxia under a light microscope?

A
  • Cytoplasmic change
  • Nuclear changes
  • Abnormal cellular accumulation
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35
Q

Describe the appearance of a cell injured during hypoxia under a light microscope

A

Pale pink and swollen- membranes aren’t working so well and so water and Na+ gets in

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36
Q

Describe what you might see in a dead cell during hypoxia under a light microscope

A

cytoplasm goes pink- it is deeply stained as proteins have coagulated and clumped, therefore have picked up eosin stain strongly

There are nuclear changes also:
Pyknosis-Nucleus shrinks and becomes very dark
Karyorrhexis- nucleus breaks up (follows pyknosis)
Karyolysis- complete dissolution of nuclei (follows karyorrhexis)

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37
Q

Name the 3 types of nuclear changes one might observe when looking down a light microscope at a dead cell after hypoxia

A

Pyknosis- shrinking and darkening
Karyrrhexis- breaks up
Karyolysis- disappears

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38
Q

Under an electron microscope it is possible to view both reversible and irreversible cellular changes that occur during hypoxia. Describe some of the reversible changes that are visible (4)

A
  • swelling of cell and organelles (due to Na+/K+ pump failure)
  • blebbing (occurs as a result of swelling)
  • clumped chromatin (due to reduced pH)
  • ribosome separation from ER (due to failure of energy-dependent process of maintaining ribosomes in correct position)
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39
Q

Under an electron microscope it is possible to view both reversible and irreversible cellular changes that occur during hypoxia. Describe some of the irreversible changes that are visible (7)

A
  • increased cell swelling
  • nuclear changes (pyknosis, karyorrhexis, karyolysis)
  • swelling and rupture of lysosomes (reflects membrane damage)
  • membrane defects
  • appearance of myelin figures 9which are damaged membranes)
  • lysis (rupture) of ER due to membrane defects
  • amorphous densities of swollen mitochondria
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40
Q

Define oncosis

A

Cell death with swelling, the spectrum of changes that occur prior to death in cells injured by hypoxia and some other agents

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41
Q

Define apoptosis

A

Cell death with shrinkage, cell death induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins

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42
Q

Define necrosis

A

In a living organism the morphologic changes that occur after a cell has been dead some time (eg 24 hrs)

**NB: necrosis is an appearance and not a process- it is NOT a type of cell death

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43
Q

Why do you get blebbing during oncosis?

A

The cytoskeleton is being broken down by proteases (triggered by Ca2+ influx, cell swells because membrane is no longer held tightly in shape

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44
Q

How is necrotic tissue removed?

A

By enzymatic degradation and phagocytosis by white cells

45
Q

What is dystrophic calcification?

A

Necrotic tissue that calcified having been left by white blood cells

46
Q

What are the two main types of necrosis? Give a brief description of the types

A

Coagulation- solid tissues (a lot of Connective tissue support) and liquifactive - loose tissues (little c.t), can happen in presence of many neutrophils (in areas of inflammation due to chemicals from immune cells)

47
Q

When a cell is dying its proteins can undergo one of 2 things, name the two processes that might happen and what kind of necrosis is seen as a result

A

Denaturation (and resulting proteins coagulate)= coagulative necrosis

Autolysis (proteins undergo dissolution by the cells own enzymes)= liquifactive necrosis

48
Q

What are the two less common types of necrosis?

A

Caseous (structureless debris- bot uniform ghost outlines though) - can look like cheese
associated with infection (especially TB)

fat necrosis (collections of fat)

49
Q

What does coagulative necrosis look like?

A
  • coagulation of proteins- dark staining

- ghost outlines

50
Q

What does liquefactive necrosis look like?

A

Very little left
Proteins and everything else has been all but dissolved
(Often looks like a hole)

51
Q

Define the term gangrene

A

Necrosis visible to the naked eye

52
Q

Define infarction

A

Necrosis caused by reduction in arterial blood flow (can lead to hypoxia )

A cause of necrosis
Can result in gangrene

53
Q

Define the term ‘infarct’

A

An area of necrotic tissue which is the result of loss of arterial blood supply

An area of ischaemic necrosis

54
Q

What is the difference between wet and dry gangrene? Which type does gas gangrene come under?

A

Dry- necrosis modified by exposure to air (coagulative necrosis)

Wet- necrosis modified by infection (liquefactive necrosis)

Gas gangrene is a type of wet gangrene

55
Q

Define the term gas gangrene

A

wet gangrene where the tissue has become infected with anaerobic bacteria that produce visible and palpable bubbles of gas within the tissues.
(bacteria spread quickly into blood supply)

Very dangerous!

56
Q

What are the two types of infarction? What do they refer to?

A

Red and white

Indicated how much haemorrhage there is into the infarct

57
Q

When might a white (anaemic) infarct occur?

A

In solid organs after conclusions of ‘end’ arteries

Often wedge shaped

Coagulative necrosis

58
Q

When might a red (haemorrhagic) infarct occur?

A

Where there is extensive haemorrhage into dead tissue

Loose tissue- often in tissues with a dual blood supply- there is a bleed into the infarct because the vessels aren’t well supported

59
Q

Many molecules are released by injured, dying and dead cells as their membranes lose integrity, what are the consequences of this release? (3)

the consequences may not necessarily be bad

A
  • cause local irritation and inflammation
  • general toxic effects on body
  • can appear high concentrations in the blood and can be measured- aid diagnosis
60
Q

Give an example of a molecule released during cell injury/death (3)

A
  • potassium
  • enzymes (can indicate organ involved and extent, Timing and evolution of the tissue damage)
  • myoglobin (releases form dead myocardium and striated muscle)
61
Q

What are the commonest causes of infarctions?

A

Thrombosis- blood clot within vessel

Embolism- lodging of an embolus (a blockage-causing piece of material, inside a blood vessel)

Putting external pressure on tissue- restricting blood flow

62
Q

What does the severity of infarction depend upon?

A
  • alternative blood supply
  • speed of ischeamia
  • tissue involved
  • oxygen content of the blood
63
Q

What is ischaemia-repercussion injury?

A

Reperfusion (reoxygenation) injury is the tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen (anoxia, hypoxia).

Only occurs if the tissue is not yet necrotic

64
Q

What are the possible causes of an ischaemia-reperfusion injury?

A
  • increased production of oxygen free radicals
  • increased number of neutrophils resulting in more inflammation and increased tissue injury (can cause necrosis)
  • delivery of complement proteins and activation of the complement pathway
65
Q

What ion build up can tumour lysis syndrome cause?

A

Hyperkalaemia

66
Q

What is rhabdomyolysis? What is a sign of this?

A

condition in which damaged skeletal muscle breaks down rapidly

Happens during massive trauma/extreme exercise/extreme conditions

-The urine may be dark, often described as “tea-colored”, due to the presence of myoglobin.

67
Q

When might apoptosis occur?

A

When there is damage affecting the cell’s DNA (irreversible damage)

68
Q

Describe the appearance of a cell going through apoptosis under a light microscope

A

Shrunken and appear intensely eosinophilic, there is chromatin condensation, pyknosis (non-random, internucleosomal cleavage of DNA) and karyorrhexis are seen.

69
Q

Describe the appearance of a cell undergoing apoptosis under an electron microscope

A

Budding of apoptotic bodies (which will be removed by macrophage phagocytosis)

70
Q

What are the 3 key stages of apoptosis?

A

Initiation
Execution
Degradation/phagocytosis

71
Q

When might apoptosis occur physiologically?

A
  • maintain steady state
  • hormone controlled involuted now (eg women in menopause- smaller ovaries, hormones stopped)
  • embryogenesis (formation of limbs and fingers)
72
Q

When does apoptosis occur pathologically?

A
  • cytotoxic T cell killing of virus-infected or neoplastic cells
  • when cell has damage
  • graft versus host disease
73
Q

Initiation and execution of apoptosis is triggered by two mechanisms, name those mechanism

A

Intrinsic and extrinsic

74
Q

How is the intrinsic pathway in apoptosis initiated?

A

Initiating signals from within the cell

75
Q

What is a trigger for the intrinsic pathway of apoptosis?

A
  • irreparable DNA damage

- withdrawal of growth factors or hormone (like in ovaries of menopausal women)

76
Q

How is the apoptotic intrinsic pathway carried out?

A
  • p53 is activated
  • outer mitochondrial membrane becomes leaky
  • cytochrome C is released
  • causes activation of caspases (family of protease enzyme)
77
Q

How is the apoptotic extrinsic pathway initiated?

A

By extracellular signal

78
Q

Why would the apoptotic extrinsic pathway be triggered?

A

Cells that are a danger eg tumour cells, virus infected cells

79
Q

How is the apoptotic extrinsic pathway carried out- use TNF alpha as an example

A
  • TNF alpha secreted by T killer cells
  • bind to cell membrane receptors (death receptor)
  • results in activation of caspases
80
Q

How are apoptotic bodies phagocytosed?

A

By phagocytes or neighbouring cells, because they can recognise the proteins expressed on the apoptotic body’s membrane

81
Q

What are the difference between oncosis/necrosis and apoptosis, in terms of pattern of cells involved?

A

Oncosis- contiguous groups of cells

Apoptosis-single cells

82
Q

What are the difference between oncosis/necrosis and apoptosis, in terms of cell size?

A

Oncosis- enlarged

Apoptosis- reduced

83
Q

What are the difference between oncosis/necrosis and apoptosis, in terms of the plasma membrane?

A

Oncosis- disrupted, early lysis , blebbing

Apoptosis- in tact, budding

84
Q

What are the difference between oncosis/necrosis and apoptosis, in terms of cellular contents?

A

Oncosis- enzymatic digestion, leak out of cell

Apoptosis- intact, realised in apoptotic bodies

85
Q

What are the difference between oncosis/necrosis and apoptosis, in terms of adjacent inflammation?

A

Oncosis- frequent

Apoptosis- none

86
Q

What are the difference between oncosis/necrosis and apoptosis, in terms of physiological or pathological role?

A

Oncosis- invariably pathologic

Apoptosis- often physiologic- means of elimination unwanted cells, may be pathology after some form of cell injury

87
Q

What do abnormal cellular accumulations derive from?

A
  • cell’s own metabolism
  • the extracellular space (spilled blood eg)
  • the outer environment (dust eg)
88
Q

What are the 5 main groups of intracellular accumulations?

A
  • water and electrolytes
  • lipid (triglycerides and cholesterol)
  • proteins (eg Mallory’ hyaline, alpha-1 antitrypsin)
  • ‘pigments’ (exogenous and endogenous)
  • carbohydrates
89
Q

What is the term used to describe local pathological calcification?

A

Dystrophic calcification

90
Q

What is the term used to describe general calcification?

A

Metastic calcification

91
Q

Where might dystrophic calcification occur? (4)

A
  • In areas of dying tissue
  • Artherosclerotic plaques
  • In aging or damaged heart valves
  • Tuberculous lymph nodes
92
Q

Why does dystrophic calcification occur?

A

Local change/disturbance causes the formation of hydroxyapatite crystals (which are mineral forms of Ca2+)

93
Q

Why does metastatic calcification occur?

A

Hypercalcaemia secondary to disturbances in calcium metabolism
(Hydroxyapatite crystals are deposited in normal tissues throughout the body)

94
Q

What causes hypercalcaemia?

A
  • Increased secretion of parathyroid hormone (PTH) resulting in bone reabsorption
  • destruction of bone tissue (eg being immobile for long periods of time)
95
Q

What is steatosis?

A

Accumulation of triglycerides (often seen in the liver- fatty liver)

96
Q

What is fluid accumulating in cells called?

A

Hydropic swelling

97
Q

Why does hydropic swelling occur? And where might this be a particular issue?

A

Loss of blood supply leads to decreased oxygen tension inside cell and results in ATP depletion. There is also loss of oxidative phosphorylation causing decreased ATP generation and failure of Na+K+ pump. This leads to increased intracellular sodium and water along with increased extracellular potassium, leading to cellular swelling.

Problem in brain

98
Q

Why are there very few proteins in injured cells?

A

Because there is a reduced level of ATP meaning ribosome are no longer held onto the ER and as a result there is little protein production within injured cells

99
Q

When does cholesterol accumulate in the cells?

A

When the liver is not functioning properly, (can only be eliminated by the liver).

100
Q

Cholesterol can often accumulate in smooth muscle cells and macrophages in artherosclerotic plaques, what does this form?

A

Foam cells

101
Q

What are foam cells?

A

Fat filled macrophages:
Foam cells are formed when the body sends macrophages to the location of a fatty deposit on the blood vessel walls. The macrophage surrounds the fatty material in an attempt to destroy it. The cell becomes filled with lipids (fats). The lipids surrounded by the macrophage give it a “foamy” appearance.

102
Q

What occurs when there is cholesterol build up in macrophages of the skin and tendons with people with hereditary hyperlipidaemias?

A

xanthomas

Yellow swellings-look like blisters

103
Q

What is Mallory’s hyaline? What is a cause of this?

A

Damaged keratin filaments- clumped together

Alcoholic liver disease

104
Q

Briefly describe what is mans to have a alpha1-antitrypsin deficiency, what is one possible outcome of this particular deficiency?

A

-Liver produces incorrectly folded a1-antitrypsin protein
-Cannot be packages in ER
-accumulates in ER
Systemic deficiency

Can lead to proteases in the lungs acting unchecked resulting in emphysema

(**under a microscope you would see a lot of pink proteins)

105
Q

Give some examples of pigments accumulating in the cells (2)

A

Carbon/coal dust soot

Tattooing ink

106
Q

You can get accumulation of endogenous pigments- for example haemosiderin, why might this accumulate?

A

Because there is a systemic/local excess of iron eg bruise- where blood leaks into tissues and haemosiderin is formed due to excess of iron

107
Q

What is hereditary haemochromatosis?

A
  • Inherited
  • results in increases intestinal absorption of dietary iron
  • iron is deposited around body, causing inflammation and scarring
  • patients often have golden colour to skin
  • treatment:repeated bleeding
  • symptoms: liver damage, heart dysfunction, multiple endocrine failures
108
Q

What is the cause of jaundice?

A
  • Accumulation of bilirubin (bright yellow)
  • excreted in bile
  • if bile flow is obstructed or overwhelmed, bilirubin in blood rises=jaundice
109
Q

What are the mechanisms of intracellular accumulations?q

A
  • abnormal metabolism
  • alteration in protein folding and transport
  • deficiency of critical enzymes
  • inability to degrade phagocytosed particles

Pathological Processes (Milly's) (21 decks)

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