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Pathological Processes * > S1 Cell Injury > Flashcards

S1 Cell Injury Flashcards

1
Q

What do cells have to deal with changes in environmental conditions?

A

Effective mechanisms if the changes are mild

However if they’re severe cell adaptation, injury or death occurs

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2
Q

What does the degree of cell injury depend on?

A
  1. Type of injury
  2. Severity of injury
  3. Type of tissue
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3
Q

What things can cause cell injury?

A
  1. Hypoxia
  2. Toxins
  3. Physical agents
  4. Radiation
  5. Microorganisms
  6. Immune mechanisms
  7. Dietary insufficiencies and deficiencies or dietary excess
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4
Q

What are the 4 types of hypoxia?

A
  1. Hypoxaemic hypoxia - arterial content of oxygen is low e.g. at high altitude
  2. Anaemic hypoxia - decreased ability of Hb to carry oxygen e.g. anaemia or CO poisoning
  3. Ischaemic hypoxia - interruption of blood supply e.g. blacked of vessel
  4. Histiocytic hypoxia - inability to utilise oxygen inc ells due to disabled oxidative phosphorylation e.g. cyanide poisoning
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5
Q

What is hypoxia?

What is ichaemia?

A

Lack of oxygen only

Loss of blood supply to a tissue and the lack of oxygen and other molecules/SU strates

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6
Q

How long can neurones ad fibroblasts survive in hypoxia?

A

Neurones - a few minutes

Fibroblasts - a few hours

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7
Q

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

A
  • hypersensitivity reactions - host tissue is injured due to an overly vigorous immune reaction (secondary) e.g. hives (urticaria)
  • autoimmune reactions - immune system fails to distinguish self from non-self e.g. Grave’s disease
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8
Q

Which cell components are most susceptible to injury?

A
  1. Cell membranes - plasma membrane
  2. Nucleus - DNA
  3. Proteins - enzymes
  4. Mitochondria - oxidative phosphorylation
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9
Q

What happens in reversible hypoxia?

A
  1. Ischaemia occurs
  2. Decrease in oxidative phosphorylation and so less ATP produced
  3. Less ATP means reduced Na+ pump activity and increased glycolysis and detachment of ribosomes from ER
  4. Reduced Na+ pump meanings an influx of Ca2+, water and NA+ and K+ efflux which causes swelling, loss of microvilli, blebs, ER swelling and myelin figures
  5. Increased glycolysis leads to a decrease in pH and glycogen which causes clumping of nuclear chromatin
  6. Detachment of ribosomes means decrease protein synthesis which causes lipid deposition
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10
Q

What happens in irreversible/prolonged hypoxia?

A
  1. Injuries agent causes influx of Ca2+
  2. Increased cytosolic Ca2+ (from outside the cell, the mitochondria and ER)
  3. High levels of Ca2+ lead to increased ATPase, phospholipase, protease and endonuclease activity
  4. This causes decreased ATP, decreased phospholipids, disruption of membrane and cytoskeleton proteins and nuclear chromatin damage
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11
Q

What is an injurious agent?

A

Something that causes atherosclerosis

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12
Q

Other than hypoxia, what other ways can cells be injured?

A
  1. Free radicals
  2. A sequence of events for another injury that are different but cells can have limited responses to injury so the outcome is often similar
  3. Other forms of injury may attack different key structures e.g. frostbite damages cell membranes
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13
Q

What are free radicals?

A

Reactive oxygen species

Have an unpaired electron in the outer orbit so has an unstable configuration so reacts with other molecules

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14
Q

What are the 3 key free radicals with biological significance in cells?

A
  1. OH* - hydroxyl
  2. O2- - superoxide
  3. H2O2 - hydrogen peroxide
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15
Q

How are free radicals produced?

A
  1. By normal metabolic reactions e.g. oxidative phosphorylation
  2. Inflammation - oxidative burst of neutrophils
  3. Radiation - H2O —> OH*
  4. Contact with unbound metals in the body - iron (Fenton reaction) and copper
  5. Drugs and chemicals
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16
Q

How does the body control free radicals?

A
  1. Anti-oxidant scavengers - donate electrons to the free radical (vitamin A, C and E)
  2. Metal carrier and storage proteins - sequester iron and copper
  3. Enzymes that neutralise free radicals (superoxide dismutase, catalase, glutathione peroxidase)
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17
Q

How do free radicals injure cells?

A

If the number of free radicals overwhelms the anti-oxidant system it leads to oxidative imbalance

  • lipid peroxidation of lipids in cell membranes - leads to more free radicals being produced in an autocatalytic chain reaction
  • they can also oxidise proteins, carbs and DNA - molecules bent/broken/cross-linked they are mutagenic and so are carcinogenic
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18
Q

How is the cell able to protect itself against injury? What is an example of the protein?

A

Cells have heat shock proteins - the heat shock response aims to mend misfolded proteins and maintain cell viability

Ubiquitin

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19
Q

What are blebs?

A

A rounded outgrowth on the surface of a cell

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20
Q

What are the stages dead cells in hypoxia undergo?

A
  1. Pyknosis - condensation of chromatid
  2. Karyorrhexis - fragmented nucleus
  3. Karyolysis - nucleus no longer present
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21
Q

In reversible injury, what does cell injury look like?

A
  • blebs form
  • generalised swelling occurs
  • clumping of nuclear chromatin
  • autophagy by lysosomes
  • mitochondrial swelling
  • dispersion of ribosomes
  • ER swelling
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22
Q

In irreversible injury, what does cell injury/death look like?

A
  • rupture of lysosomes and autolysis
  • nucleus undergoes pyknosis, karyolysis or karyorrhexis
  • defects in the cell membrane
  • myelin figures (aggregation of lipids at the membrane)
  • lysis of the ER
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23
Q

How can we diagnose cell death?

A

Look at the function of the organ that has cells that have possibly died

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24
Q

What is oncosis?

A

Cell death with swelling - the changes that occur in injured cells prior to death

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25
Q

What necrosis?

A

The morphological changes that occur after a cell has been dead some time e.g. 12 to 24 hours

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26
Q

What are the types of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat necrosis
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27
Q

What is coagulative necrosis? What happens in this type of necrosis?

A

Ischaemia of solid organs e.g. heart, kidney and spleen

Desaturation of proteins dominates release of active proteases.
There is a ‘ghost outline’ of cells.

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28
Q

What is liquefactive necrosis? What happens in this type of necrosis?

A

Ischaemia in loose tissues e.g. lungs and brain

Involves the presence of many neutrophils

Enzyme degradation (proteases) is greater than denaturation.
It leads to enzymatic digestion (liquefaction) of tissues - cells fall apart
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29
Q

What is caseous necrosis?

A

Results in amorphous (structureless) debris

Associated with infections like TB

30
Q

What is fat necrosis?

A

Release of free fatty acid when it reacts with calcium e.g. in breast tissue after trauma

31
Q

What is gangrene?

A

Necrosis that is visible to the naked eye - it is the appearance of necrosis

32
Q

What is an infarction?

A

Necrosis caused by reduction in arterial blood flow - a cause of necrosis that can result in gangrene

33
Q

What is an infarct?

A

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

34
Q

What is dry gangrene?

A

Necrosis affected by exposure to air (happens in coagulative necrosis)

35
Q

What is wet gangrene?

A

Necrosis affected by infection (happens in liquefactive necrosis)

36
Q

What is gas gangrene?

A

A type of wet gangrene where the infection occurs due to anaerobic bacteria that produce gas e.g. bacteria get into body after an accident that leads to surgery

37
Q

What are the two most commonest causes of infarction?

A

Thrombosis and embolism

38
Q

What is an embolism?

A

A bit of a thrombus that breaks away and travels to another part of the body

39
Q

What is a third way a tissue can become infarcted?

A

Torsion

40
Q

Why are some infarcts white?

A

These are anaemic infarcts that occurs in coagulative necrosis due to the blockage of an end artery

(Often wedge-shaped)

41
Q

Why are some infarcts red?

A

These are haemorrhage infarcts that occurs in liquefactive necrosis.
Happens if there is a dual blood supply, numerous anastomoses, raised venous pressure or reperfusion(when blood returns to a tissue ischaemia))

42
Q

What do the consequences of infarction depend on?

A
  1. Is there an alternative blood supply?
  2. How quickly does the ischaemia occur?
  3. What tissue is involved?
  4. What is the oxygen content of the blood?
43
Q

What is ischaemia-reperfusion injury?

A

If blood flow is returned to a damaged (but no necrotic) tissue, it can worsen the damage

44
Q

What are possible causes of ischaemia-reperfusion?

A
  1. Increased production of oxygen free radicals with reoxygenation
  2. Increased number of neutrophils which causes more inflammation and increased tissue injury
  3. Delivery of complement proteins and activation of the complement pathway (immune response that increases activity of immune cells)
45
Q

Can molecules leak out of leaky membranes? What does this cause?

A

Yes
Local and systemic effects can occur

  1. Local inflammation
  2. General toxic effects
  3. High concentrations in the blood can aid diagnosis
46
Q

What are some important molecules/particles that leak out of cell if it is damaged?

A
  1. Potassium
  2. Enzymes/proteins - troponin, creatine kinase, ALT and AST
  3. Myoglobin
47
Q

What is apoptosis?

A

Cell death with shrinkage induced by a regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins (membrane integrity remains)

“Cell suicide”

It can be pathological or physiological

48
Q

Why does apoptosis happen physiologically?

A
  • to maintain a steady state
  • hormone-controlled involution - shrinkage of cells with old age
  • in embryogenesis - hand is initially a “paw” need to remove cells between fingers by apoptosis to produce fingers - ‘sculpting’
49
Q

Why does apoptosis happen pathologically?

A
  • when cytotoxic T cells kill virus-infected/neoplastic cells
  • when cells are damaged e.g. have damaged DNA
  • in graft vs host disease (from transplant - antibodies attack transplanted tissue)
50
Q

Does apoptosis induce inflammation?

A

No

51
Q

What are the main overview stages in apoptosis?

A
  1. Normal cell
  2. Condensation
  3. Fragmentation
  4. Apoptic bodies
52
Q

What are the three phases of apoptosis?

A
  1. Initiation
  2. Execution
  3. Degradation and phagocytosis
53
Q

What happens in initiation and execution in apoptosis?

A
  1. Apoptosis is triggered by intrinsic (intracellular signal e.g. irreparable DNA) and extrinsic mechanisms (extracellular signal e.g. tumour cells, virus-infected cells)
  2. Both mechanisms results in activation of caspases (enzymes that control and mediate apoptosis by causing cleavage of DNA and proteins of the cytoskeleton)
54
Q

What happens in phagocytosis in apoptosis?

A
  1. Cells broken up into apoptotic bodies which express a protein on their surface
  2. The protein is recognised by phagocytes/neighbouring cells
  3. Degraded by phagocyte/neighbouring cells
55
Q

Compare the pattern, cell size, nucleus, plasma membrane, cellular contents, inflammation, physiologic/pathologic role of oncosis/necrosis (1) and apoptosis (2).

A
  • pattern - 1: contiguous cells 2: single cells
  • cell size - 1: swells 2: shrinks
  • nucleus - 1: undergoes pyknosis, karyorrhexis and karyolysis 2: fragmentation of nucleus that clump under the nuclear membrane
  • plasma membrane - 1: disrupted, early lysis 2: remains in tact
  • cellular contents - 1: undergo enzymatic digestion/leak out of cell 2: remain intact, released in apoptotic bodies
  • inflammation - 1: frequent 2: none
  • physiologic/pathologic role - 1: pathologic 2: physiologic but can be pathologic
56
Q

What kind of things can accumulate in cells?

A
  1. Water and electrolytes
  2. Lipids
  3. Carbs
  4. Proteins
  5. Pigments
57
Q

When does fluid accumulate in cells? Where is it a major problem?

A

An example is hydropic swelling (intracellular oedema) which occurs in e.g. hypoxia - indicates severe cellular distress - Na+ and water flood into the cell

Major problem in the brain

58
Q

When do lipids accumulate in cells (two examples)?

A

An example is steatosis (accumulation of triglycerides)

Another example is cholesterol - forms atherosclerotic plaques or xanthomas

59
Q

What can cause TAG accumulation in cells?

A
  • alcohol (reversible)
  • diabetes mellitus
  • obesity
  • toxins
60
Q

Where is this accumulation of TAGs often seen? What if it’s mild?

A

The liver

It is asymptomatic

61
Q

What conditions lead to protein accumulation in cells?

A
  • alcoholic liver disease - damaged keratin filaments
  • alpha-1 antitrypsin deficiency - protein accumulates in the ER and isn’t secreted as it can’t be packaged due to incorrect folding
62
Q

What does alpha-1 antitrypsin deficiency lead to?

A

A systemic deficiency that means proteases in the lungs act unchecked resulting in emphysema (as the deficient enzyme is usually a protease inhibitor)

63
Q

Where do pigments accumulating in cells from?

A
  • carbon/coal dust/soot - air pollution
  • tattooing - pigments pricked into skin
  • haemosiderin - bruising
  • jaundice - bilirubin
64
Q

What happens to the pigments once they are in cells?

A

Phagocytosed by macrophages which keeps the pigment suspended wherever they are

65
Q

What is haemosiderin?

A

An iron storage molecule derived from Hb that forms when there is systemic or local excess of iron (e.g. from a bruise)

66
Q

What is hereditary haemochromatosis?

A

A genetic disorder which results from in increased intestinal absorption or dietary iron leading to iron being deposited in skin, liver, pancreas, heart and endocrine organs

67
Q

How is bilirubin eliminated? What happens if this is obstructed or overwhelmed?

A

Eliminated in bile

If bile flow is obstructed/overwhelmed the bilirubin blood levels rise and jaundice occurs. Bilirubin is deposited in tissues extracellularly or in macrophages

68
Q

How does calcification of tissues occur?

A
  • dystrophic - local change favours nucleation of hydroxyapatite crystals which can cause organ dysfunction e.g. atherosclerosis and calcified heart valves
  • metastatic - due to hypercalcaemia due to disturbances in calcium metabolism, hydroxyapatite crystals are deposited in tissues throughout the body usually asymptomatic but can be lethal (reversible)
69
Q

What can cause hypercalcaemia?

A
  • increased PTH secretion leading to bone resorption (primary - parathyroid hyperplasia/tumour, secondary - renal failure or ectopic - PTH relented protein secreted by malignancy tumours)
  • destruction of bone tissue (bone marrow tumours, skeletal metastases, accelerated bone turnover, immobilisation)
70
Q

Can cells live forever?

A

After a number of divisions cells reach replicative senescence (when telomeres can no longer be shortened without damage to the cell)

However germ cells, stem cells and cancer cells have the enzyme telomerase which maintains the original length of the telomeres allowing continual replication

Pathological Processes * (10 decks)

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