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Pathological Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What kind of things can cause cell injury?

A
  • Hypoxia
  • Toxins
  • Physical agents (trauma, temperature, pressure, electricity)
  • Radiation
  • Micro-organisms
  • Immune mechanisms
  • Dietary insufficiency, deficiency, excess etc
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2
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia is due to a decreased O2 supply to certain cells and tissue.

Ischaemia is due to decreased blood supply (worse as there is no O2 or nutrients)

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3
Q

What is hypoxaemic hypoxia?

A

Arterial content of oxygen is low.

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4
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen.

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5
Q

What is ischaemic hypoxia?

A

Interruption to blood supply.

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6
Q

What might cause hypoxaemic hypoxia?

A

Reduced pO2 at altitude or reduced absorption secondary to lung disease.

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7
Q

Give a cause for anaemic hypoxia

A

Anaemia or carbon monoxide poisoning

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8
Q

Give a cause of ischaemic hypoxia

A

Blockage of a vessel or heart failure

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9
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes.

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10
Q

What causes histiocytic hypoxia?

A

Cyanide poisoning

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11
Q

Does hypoxia effect neurones and fibroblasts equally?

A

Different effects in different tissues. Neurones are much more sensitive to hypoxia and therefore only last a few minutes. Fibroblasts may last a few hours.

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12
Q

What is a hypersensitivity reaction?

A

Host tissue is injured secondary to an overly vigorous immune reaction

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13
Q

What is urticaria and what type of reaction is it an example of?

A

Hives = hypersensitivity reaction

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14
Q

What is an autoimmune reaction?

A

The immune system fails to distinguish self from non-self

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15
Q

Give an example of a autoimmune reaction

A

Grave’s disease of thyroid

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16
Q

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

A

Hypersensitivity and autoimmune reactions.

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17
Q

Which cell components are most susceptible to injury?

A

Cell membranes (plasma and organelles), DNA, enzymes and mitochondria (effecting ox phos)

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18
Q

What is happening at a molecular level in hypoxia?

A

Inadequate oxygen delivery to cells. Mitochondrial production of ATP will cease. ATP pump stops. Sodium and water seep into cell, cell swells. Anaerobic glycolysis will result in acidosis due to the accumulation of lactate. The acidosis promotes calcium influx. This is toxic and will catalyse reactions that destroy the cell.

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19
Q

What is happening in prolonged hypoxia?

A

Massive influx of calcium into the cell. Activates many enzymes e.g. ATPase (further reduction in ATP), phospholipase (attacks cell membrane), proteases (break down cell skeleton) and endonuclease (breaks down DNA).

Irreversible.

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20
Q

Other than hypoxia, give an example of a cause of cell damage.

A
  • Extreme cold attacks different key features (initially membranes) = frostbite
  • Free radicals damage membranes primarily

Mechanism of response is often similar

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21
Q

What are free radicals?

A

Reactive oxygen species with a single unpaired electron in outer orbit

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22
Q

Which free radicals are particularly significant in cells?

A

OH. (hydroxyl) = most dangerous
O2- (superoxide
H2O2 (hydrogen peroxide)

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23
Q

How are free radicals produced?

A

Metabolic reactions e.g. ox phos, oxidative burst, radiation (H20 -> OH.), contact with unbound metals within the body (iron and copper) and drugs and chemicals.

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24
Q

How does free radical damage occur in haemachromatosis?

A

Excess of iron produces free radicals via fenton reaction

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25
Q

What is Wilson’s disease and how does it cause damage?

A

Excess of copper produces free radicals.

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26
Q

How does the body control free radicals?

A
  • Anti-oxidant system: donate electrons to the free radical. Vitamins A, C & E (ace).
  • Metal carrier and storage proteins.
  • Enzymes neutralise free radicals
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27
Q

Which metal carrier/ storage proteins control free radicals?

A

Transferrin sequesters iron. Ceruloplasmin sequesters copper.

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28
Q

Which enzymes neutralise free radicals?

A

SOD

  • Superoxidase dismutase
  • Catalase
  • Glutathione Peroxidase
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29
Q

How do free radicals injure cells?

A
  • Lipid peroxidation in cell membranes causing the generation of further free radicals (autocatalytic chain reaction). Taking one electron causes the atom to take a neighbouring electron and so on.
  • Oxidise proteins, carbohydrates and DNA so that these molecules become bent out of shape/ broken/ cross linked (mutagenic.. carcinogenic)
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30
Q

What is oxidative imbalance?

A

When the number of free radicals overwhelms the anti-oxidant system

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31
Q

How can the cell protect itself from injury?

A
  • Heat shock proteins mend mis-folded proteins

- Unfoldases or chaperonins e.g. ubiquitin

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32
Q

What do injured cells look like under a microscope?

A

Pale and swollen due to influx of water.

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33
Q

Which processes do dying cells undergo?

A

Pyknosis, karyorrhexis and karyolysis.

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34
Q

What is pyknosis?

A

Shrinking and darkening of the nucleus.

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35
Q

What is karyorrhexis?

A

Nuclear fragmentation.

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36
Q

What is karyolysis?

A

Dissolution of a cell nucleus.

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37
Q

What do dead cells look like under the microscope?

A

Very pink cytoplasm (eosinophilic), proteins have denatured and coagulated so pick up eosin stain very strongly, with pyknosis, karyorrhexis and karyolysis.

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38
Q

What do injured cells look like under an electron microscope?

A
  • Cytoskeleton has been broken down by proteases so there is blebbing of membrane (one may eventually burst)
  • Generalised swelling
  • Clumping of nuclear chromatin
  • Autophagy by lysosomes
  • ER swelling
  • Dispersion of ribosomes
  • Mitochondrial swelling
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39
Q

What do dying cells look like under an electron microscope?

A
  • Rupture of lysosomes and autolysis
  • Nucleus: pyknosis/ karyolysis/ karyorrhexis
  • Holes in the cell membrane
  • Myelin figures
  • Lysis of ER
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40
Q

How can you diagnose cell death?

A

Dye excision test
Put cells in fluid with dye/ fluorescence and if the cell membrane has holes the dye will go into the cell. Therefore these cells are dead.

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41
Q

What is oncosis?

A

Cell death with swelling, the spectrum of changes that occur in injured cells prior to death

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42
Q

What is necrosis?

A

The morphological changes that occur after a cell has been dead for some time (12-24 hours)

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43
Q

What are the two main types of necrosis?

A

Coagulative and liquefactive

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44
Q

What are the other two special types of necrosis?

A

Caseous and fat necrosis

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45
Q

Why are there two types of necrosis?

A

In cell death sometimes there is denaturation of protein (leading to coagulative necrosis) and sometimes there is destruction rather than coagulation of proteins (liquefactive necrosis)

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46
Q

What does coagulative necrosis look like?

A

Denaturation of proteins dominates over release of active proteases. Cellular architecture is somewhat preserved, “ghost outline” of cells. Progressive loss of nuclear staining and a loss of cytoplasmic detail.

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47
Q

What does liquefactive necrosis look like?

A

Enzyme degradation is substantially greater than denaturation. Leads to enzymatic digestion (liquefaction) of tissues.

48
Q

Where does liquefactive necrosis occur?

A

Mostly in the brain due to its lack of any substantial supporting stroma.

49
Q

What is caseous necrosis?

A

A pattern of necrosis in which the dead tissue is structureless. Contains amorphous (structureless) debris and is particularly associated with TB.

50
Q

What are the causes of fat necrosis?

A
  • Direct trauma to adipose tissue and extracellular liberation of fat (may cause palpable mass e.g. in breast)
  • Enzymatic lysis of fat due to release of lipases
51
Q

What does fat necrosis look like?

A

Fat droplets with lots of macrophages

52
Q

How does fat necrosis occur in pancreatitis?

A

Release of pancreatic lipase, as a result fat cells have their stored fat split into fatty acids which then combine with calcium to precipitate out as white soaps.

53
Q

What is gangrene?

A

Necrosis visible to the naked eye

54
Q

What is infarction?

A

Necrosis caused by reduction in arterial blood flow

55
Q

What is an infarct?

A

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

56
Q

What is dry gangrene?

A

Necrosis modified by exposure to air (coagulative)

57
Q

What is wet gangrene?

A

Necrosis modified by infection (liquefactive)

58
Q

What is gas gangrene?

A

Wet gangrene where the infection is with anaerobic bacteria that produce gas

59
Q

Why are some infarcts white?

A

Solid organs e.g. kidney
Occlusion of an end artery
Often wedge shaped
Coagulative necrosis

60
Q

Why are some infarcts red?

A
  • Loose tissue
  • Dual blood supply (e.g. bronchial and pulmonary artery)
  • Numerous anastomoses
  • Prior congestion (infarct followed by re-perfusion)
  • Raised venous pressure
  • Re-perfusion
61
Q

What is ischaemia reperfusion injury?

A

If blood flow is returned to a damaged but not yet necrotic tissue, damage sustained can be worse than if the blood flow hadn’t be been returned.

62
Q

What are the possible causes of ischaemia-reperfusion injury?

A
  • Increased production of oxygen free radicals with reoxygenation
  • Increased number of neutrophils resulting in more inflammation and increased tissue injury
  • Delivery of complement proteins and activation of the complement pathway
63
Q

What is apoptosis?

A

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

64
Q

Describe DNA breakdown in apoptosis

A

Non random, internucleosomal (same length) cleavage of DNA

65
Q

When does apoptosis occur physiologically?

A
  • Maintaining steady state (removal of old cells)
  • Hormone controlled involution (ovaries in menopausal women are much smaller)
  • Embryogenesis of limbs
66
Q

When does apoptosis occur pathologically?

A
  • Cytotoxic T cell killing of virus-infected or neoplastic cells
  • When cells are damaged
  • Graft versus host disease
67
Q

Describe the process of apoptosis

A

Condensation of chromatin, broken down into clumps (karyhorrexis), budding of membrane, formation of apoptotic bodies containing cell fragments.

68
Q

Describe the microscopic appearance of apoptotic bodies

A

Dark staining due to chromatin and DNA

69
Q

What are the three phases of apoptosis?

A

Initiation, execution, degradation & phagocytosis

70
Q

Describe the initiation and execution of apoptosis

A

Triggered by intrinsic and extrinsic mechanisms. Both result in the activation of caspases (control and mediate apoptosis) causing the cleavage of DNA and proteins of the cytoskeleton.

71
Q

How is the intrinsic pathway of apoptosis carried out?

A
  • Initiating signal comes from within the cell
  • Triggers irreparable DNA damage and withdrawal of growth factors/ hormones
  • P53 protein is activated and this results in the outer mitochondrial membrane becoming leaky
  • Cytochrome C is released from the mitochondria and this causes activation of caspases.
72
Q

How is the extrinsic pathway of apoptosis carried out?

A
  • Initiated by extracellular signals
  • Triggered by cells that are a danger e.g. tumour cells
  • One of the signals is TNFa which is secreted by T killer cells, binds to cell membrane receptor and results in the activation of caspases.
73
Q

Why are the apoptotic bodies phagocytosed?

A

Apoptotic bodies express proteins on their surface that can be recognised by phagocytes and are different to cell antigens.

74
Q

Describe the key differences between apoptosis and oncosis

A

Apoptosis

  • Shrinkage and chromatin condensation
  • Budding
  • Apoptotic bodies phagocytosed with no inflammation
  • Plasma membrane intact
  • Cellular contents intact
  • No adjacent inflammation

Necrosis

  • Swelling
  • Blebbing with disruption of cell membrane
  • Release of proteolytic enzymes with important inflammatory reaction
75
Q

What kind of things can accumulate in cells?

A
  • Water and electrolytes
  • Lipids
  • Carbohydrates
  • Proteins
  • ‘Pigments’
76
Q

Where do abnormal cellular accumulations come from?

A
  • Cells own metabolism
  • Extracellular space e.g. spilled blood
  • Outer environment e.g. dust

They accumulate because the body can’t metabolise them.

77
Q

When does fluid accumulate in cells?

A
  • Hydropic swelling (intracellular oedema)
  • Occurs when energy supplies are cut off e.g. hypoxia
  • Indicates severe cellular distress
  • Na+ and water flood into cell
  • Particular problem in the brain due to ICP
78
Q

When do lipids accumulate in cells?

A
  • Steatosis (accumulation of triglycerides)

- Cholesterol may accumulate in smooth muscle cells

79
Q

What does steatosis look like?

A

Organ will swell, appear fatty/ greasy and heavy. Hepatocytes will be filled with fat droplets causing the nucleus to be pushed to one side.

80
Q

What is steatosis?

A

Steatosis (accumulation of triglycerides) is often seen in the liver (major organ in fat metabolism). Caused by alcohol, diabetes, obesity and toxins.

81
Q

How does cholesterol accumulate in cells?

A
  • Only eliminated in liver, excess stored in cell vesicles
  • Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques = foam cells
  • Present in macrophages in skin and tendons of people with hereditary hyperlipidaemias (xanthomas)
82
Q

What do protein accumulations look like microscopically?

A

Seen as eosinophilic droplets or aggregations in the cytoplasm

83
Q

In what conditions do proteins accumulate in cells?

A
  • Alcoholic liver disease (leads to Mallory’s hyaline, damaged keratin filaments/ collection of proteins in cell due to alcohol toxicity)
  • A1-antitrypsin deficiency
84
Q

How does a1-antitrypsin deficiency lead to the accumulation of proteins?

A
  • Liver produces incorrectly folded a1-antitrypsin protein
  • Cannot be packaged by ER, accumulates within the ER and is not secreted
  • Systemic deficiency - proteases in lung act unchecked resulting in emphysema
85
Q

When do pigments accumulate in cells?

A
  • Carbon/coal dust/ soot (air pollution)
  • Tattoo (ink remains in dermis macrophages)
  • Haemosiderin due to excess of iron
86
Q

How do air pollutants lead to disease?

A
  • Inhaled and phagocytosed by alveolar macrophages
  • Anthracosis and blacked peribronchial lymph nodes
  • Usually harmless in moderation
  • Fibrosis and emphysema (coal workers pneumoconiosis)
87
Q

What is haemosiderin?

A
  • Iron storage molecule
  • Derived from haemoglobin (yellow/brown)
  • Forms when there is a systemic or local excess of iron e.g. bruise
88
Q

What is haemosiderosis?

A

Systemic overload of iron causing haemosiderin to be deposited in many organs. Seen in haemolytic anaemias, blood transfusions and hereditary haemochromatosis.

89
Q

What is hereditary haemochromatosis?

A

Genetically inherited disorder - results in increased intestinal absorption of dietary iron

90
Q

What does hereditary haemochromatosis look like?

A

Tanned skin. Liver stain for iron (blue spots).

91
Q

What is accumulating in jaundice?

A

Bilirubin (bright yellow), the breakdown produce of heme that is formed in all cells of the body and must be eliminated by bile.

92
Q

How is bilirubin eliminated from the body?

A

Taken from tissues by albumin to liver, conjugated and excreted in bile, if bile flow is obstructed or overwhelmed, bilirubin in blood rises and jaundice results. Deposited in tissues extracellularly or in macrophages.

93
Q

Describe the key mechanisms of intracellular accumulations

A
  • Abnormal metabolism
  • Alterations in protein folding and transport
  • Enzyme deficiency
  • Inability to degrade phagocytosed particles
94
Q

Describe the two ways in which tissues can be calcified within the body?

A

Localised (dystrophic)
Generalised (Metastatic)
Deposition of calcium salts within tissues

95
Q

What is dystrophic calcium deposition?

A

More common than metastatic, occurs in an area of dying tissue, atherosclerotic plaques, agent or damaged heart valves, in TB lymph nodes, some malignancies.

96
Q

Why does dystrophic calcification occur?

A
  • No abnormality in calcium metabolism or serum calcium or phosphate concentration
  • Local change favours nucleation of hydroxyapatite crystals (calcium salt)
  • Can cause oran dysfunction e.g. atherosclerosis or calcified heart valves.
97
Q

Why does metastatic calcification occur?

A
  • Due to hypercalcaemia secondary to disturbances in calcium metabolism
  • Hydroxyapatite crystals are deposited in normal tissues throughout body
  • Usually asymptomatic but can be lethal
  • Can regret if the cause of hypercalcaemia is corrected
98
Q

What causes hypercalcaemia?

A
  • Increased secretion of parathyroid hormone (PTH) resulting in bone resorption
  • Destruction of bone tissue
99
Q

What limits cell age?

A

At a certain number of divisions cells reach replicative senescence - related to the length of telomeres. When the telomeres reach a critical length the cell can no longer divide.

100
Q

How do germ cells continue to replicate?

A

Germ and stem cells contain an enzyme called telomerase which maintains the original length of the telomeres.

101
Q

What is the effect of excessive alcohol intake on the liver?

A

Steatosis (accumulation of triglycerides), the liver swells, appears fatty and heavy.

102
Q

What is the laboratory diagnosis of excessive alcohol intake?

A

Raised bilirubin, raised alkaline phosphatase, raised gamma GT.

103
Q

How does hepatitis present?

A

Can be acute or chronic. Chronic hepatitis is defined as over 6 months history with histology of inflammation and necrosis.

104
Q

What are the symptoms of Hep B?

A
  • Tiredness
  • General aches and pains
  • High temperature (fever) of 38C (100.4F) or above
  • General sense of feeling unwell
  • Loss of appetite
  • Feeling and being sick
  • Diarrhoea
  • Abdominal pain
  • Yellowing of the skin and eyes (jaundice)
105
Q

What is the laboratory diagnosis of Hep B?

A
  • Raised serum ALT, AST and LDH. These are cytosolic hepatocellular enzymes and their presence in the blood indicates poor hepatocyte integrity
  • Raised bilirubin
  • Decreased albumin, raised PT, raised ammonia = poor hepatocyte function
106
Q

What is the laboratory diagnosis of acute pancreatitis?

A
  • Raised serum amylase in first 24 hours

- Raised serum lipase from 72 - 96 hours

107
Q

How does hereditary haemochromatosis present?

A
  • Iron is deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas
  • Symptoms include liver damage, heart dysfunction and multiple endocrine failures, especially of the pancreas.
108
Q

How is hereditary haemochromatosis treated?

A

Repeated bleeding

109
Q

What complications are involved with hereditary haemochromatosis?

A

Complications include

  • Liver damage (cirrhosis)
  • Excessive iron in joints leads to arthritis
  • Excessive iron in heart = cardiomyopathy
110
Q

What is alpha-1 antitrypsin deficiency?

A

Autosomal recessive disorder with varying levels of severity in which there are low levels of alpha-1 antitrypsin (protease inhibitor) which deactivates enzymes released from neutrophils at the site of inflammation.

111
Q

Describe the pathophysiology of a-1 antitrypsin deficiency

A

The liver produces a version of the protein a-1 antitrypsin that is incorrectly folded. This cannot be packaged by the endoplasmic reticulum and accumulates within this organelle and is not secreted by the liver.

112
Q

Describe the presentation and complications of alpha 1 antitrypsin deficiency

A

The initial symptoms of alpha1-antitrypsin deficiency include cough, sputum production, and wheezing. The systemic deficiency of the enzyme means that proteases within the lung can act unchecked and patients with the condition develop emphysema as lung tissue is broken down. Liver disease also occurs as the accumulated abnormal version of the protein causes hepatocyte damage and eventually cirrhosis.

113
Q

What is coal-worker’s pneumoconiosis?

A

Caused by long term exposure to coal dust

114
Q

How does coal-worker’s pneumoconiosis present?

A

Miners with simple coal worker’s pneumoconiosis are usually asymptomatic. They may report cough or sputum production, but this is generally secondary to industrial bronchitis or smoking and not to the body’s reaction to coal. Complicated coal worker’s pneumoconiosis produces cough, dyspnea, and lung function impairment.

115
Q

What are the complications involved in coal-worker’s pneumoconiosis?

A
  • Chronic bronchitis
  • Chronic obstructive pulmonary disease (COPD)
  • Cor pulmonale (failure of the right side of the heart)
  • Respiratory failure

Pathological Processes (13 decks)

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