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PP A > Session 1 Lecture 2 > Flashcards

Session 1 Lecture 2 Flashcards

1
Q

What does the degree of cell injury depend on?

A
  • Type of injury
  • Severity of injury
  • Type of tissue
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2
Q

What can severe changes in the environment lead to?

A

Cell adaptation, injury or cell death.

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3
Q

What kind of things can cause cell injury?

A
  • Hypoxia
  • Toxins
  • Physical agents
  • Radiation
  • Micro-organisms
  • Immune mechanisms
  • Dietary insufficiency and deficiencies
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4
Q

What physical agents can cause cell injury?

A

Direct trauma, extremes of temperature, changes in pressure and electric currents.

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5
Q

What is hypoxia?

A

Decreased oxygen supply to certain cells and tissues

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6
Q

What is ischaemia?

A

Decreased blood supply to the tissue

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7
Q

Which is worse, hypoxia or iscahemia? Why?

A

Ischaemia is worse because tissues isn’t getting oxygen and other nutrients such as glucose.

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8
Q

What are the different causes/types of hypoxia?

A

Hypoxaemic hypoxia, anaemic hypoxia, ischaemic hypoxia, histiocytic hypoxia.

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9
Q

What is hypoxaemic hypoxia?

A
  • Arterial content of oxygen is low

- Due to reduced oxygen in air (high altitude) or reduced absorption in lungs.

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10
Q

What is anaemic hypoxia?

A
  • Decreased ability of haemoglobin to carry oxygen

- Due to anaemia or CO poisoning

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11
Q

What is ischaemic hypoxia?

A
  • Interruption of blood supply

- Due to blockage of a vessel or heart failure.

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12
Q

What is histiocytic hypoxia?

A
  • Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes
  • Due to cyanide poisoning
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13
Q

What type of cell in the body is very sensitive to hypoxia and ischaemia?

A

Neurones

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14
Q

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

A
  • Hypersensitivity reactions

- Autoimmune reactions

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15
Q

What is a hypersensitivity reaction?

A

Host tissue is injured secondary to an overly vigorous immune reaction.

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16
Q

What is an autoimmune reaction?

A

Immune system fails to distinguish self from non-self.

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17
Q

Which cell components are most susceptible to injury?

A

Cell membrane, nucleus, proteins and mitochondria.

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18
Q

What is happening at a molecular level in hypoxia?

A

notes - check the notes that are in the folder

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19
Q

What about prolonged hypoxia?

A

Hypoxia is reversible but if it is prolonged, it does become irreversible.

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20
Q

What happens in a cell if it undergoes prolonged hypoxia?

A

The point which leads to cell death leads to a massive influx of calcium into the cell. Calcium activates lots of enzymes, eg proteases which break down cytoskeleton of the cell.

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21
Q

What are free radicals?

A

They are a reactive oxygen species.

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22
Q

What is the configuration of a free radical?

A

Single unpaired electron in an outer orbit - an unstable configuration hence react with other molecules, often producing further free radicals.

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23
Q

Which free radicals are of particular biological significance in cells?

A
  • OH (hydroxyl) - the most dangerous
  • O2 (superoxide)
  • H2O2 (hydrogen peroxide)
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24
Q

How are free radicals produced?

A
  • Normal metabolic reactions eg oxidative phosphorylation
  • Inflammation - oxidative burst of neutrophils
  • Radiation
  • Contact with unbound metals within the body
  • Drugs and chemicals eg paracetamol
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25
Q

How does the body control free radicals?

A
  • Antioxidant system; donate electrons to the free radical (vitamins A, C and E)
  • Metal carrier and storage proteins (transferrin, ceruplasmin) sequester iron and copper
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26
Q

Name some enzymes that neutralise free radicals

A

Superoxide dismutase, catalase, glutathione peroxidase

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27
Q

How do free radicals injure cells?

A
  • If the number of free radicals overwhelms the anti-oxidant system = oxidative imbalance
  • Most important target are lipid in cell membranes
  • Also oxidise proteins, carbohydrate and DNA
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28
Q

What effect can free radicals have on lipids in cell membrane?

A
  • Causes lipid peroxidation

- This leads to generation of further free radicals - autocatalytic chain reaction

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29
Q

What effect can free radicals have proteins, carbohydrates and DNA?

A
  • Oxidise them
  • The molecules become bent out of shape, broken or cross linked
  • Mutagenic and therefore carcinogenic
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30
Q

How else can the cell protect itself?

A
  • Heat shock proteins aim to ‘mend’ misfolded proteins and maintain cell viability
  • Unfoldases or chaperonins eg ubiquitin
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31
Q

In hypoxia, what does an injured/dying cell look like under a microscope?

A

Cytoplasmic changes, nuclear changes, abnormal accumulations

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32
Q

Describe what an injured cell looks like under a microscope

A

Cell become pale and swollen (membrane not working properly)

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33
Q

Describe what you see in the cytoplasm when the cell has died

A

When the cell dies, the cytoplasm looks very pink because the proteins have been denatured and they have clumped and clotted together hence stain strongly.

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34
Q

What can happen to a dead cell’s nucleus?

A
  • Pyknosis - nucleus shrinks and becomes dark
  • Karyorrhexis - nucleus breaks up into little bits
  • Karyolysis - nucleus disappears (shrinks to nothing)
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35
Q

What does a reversible injury of a cell look like under an electron microscope?

A

Blebs form, generalised swelling, clumping of nuclear chromatin, ER swelling, mitochondria swelling and autophagy by lysosomes.

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36
Q

What does an irreversible injury of a cell look like under an electron microscope?

A

Rupture of lysosomes and autolysis, nuclear changes, lysis of ER, mitochondrial swelling, defects in cell membrane

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37
Q

How can we diagnose cell death?

A

A good of way of knowing when a cell is dead is by testing its function. ( can use a dye exclusion test )

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38
Q

What is a dye exclusion test?

A

If the membrane has holes in it, the dye will enter the cell. The cells that are alive will keep the dye out.

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39
Q

What is the actual PROCESS of cell death called?

A

Oncosis

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40
Q

Define oncosis

A

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

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41
Q

Define necrosis

A

In a living organism the morphologic changes that occur after a cell has been dead some time (seen after 12-24 hours)

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42
Q

What are the different types of necrosis?

A
  • Two main types - coagualative and liquefactive

- Two special types - caseous and fat necrosis

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43
Q

Why are there two types of necrosis?

A

Depend on the tissue, you get protein denaturation or enzyme release. Protein denaturation leads to clumping but what often dominates is enzyme release from lysosomes.

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44
Q

Where is coagulation necrosis found?

A

Happens when you have ischaemia of solid organs (organs with lots of connective tissue eg kidney)

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45
Q

Where is liquifactive necrosis found?

A

Happens when you have ischaemia in loose tissues or in the presence of many neutrophils eg during infection.

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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 preserves “ghost outline” of cells.
47
Q

What does liquefactive necrosis look like?

A
  • Enzyme degradation is substantially greater than denaturation
  • Leads to enzymatic digestions (liquefaction) of tissues.
48
Q

What is caseous necrosis?

A
  • Contains amorphous (structureless) debris

- Particularly associated with infections, especially TB

49
Q

What does caseous necrosis look like?

A

Caseous necrotic dermis looks like cheese.

50
Q

What is fat necrosis?

A

Fat necrosis is a form of necrosis characterised by the action upon fat by digestive enzymes.

51
Q

What does fat necrosis look like?

A

White dots seen. Under microscope - big white spaces.

52
Q

Define gangrene

A

Necrosis visible to the naked eye

53
Q

Define infarction

A

Necrosis caused by reduction in arterial blood flow. (A cause of necrosis, can result in gangrene)

54
Q

Define infarct

A

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

55
Q

What is dry gangrene?

A

Necrosis modified by exposure to the air (coagulative necrosis)

56
Q

What is wet gangrene

A

Necrosis modified by infection (liquefactive necrosis)

57
Q

What is gas gangrene?

A

Type of wet gangrene where the infection is with anaerobic bacteria that produce gas.

58
Q

What are the commonest causes of infarction?

A
  • Thrombus

- Embolism

59
Q

How else can tissue become infarcted?

A

Something like testicular torsion - spermatic cord can twist itself and cut off the blood supply.

60
Q

What does infarcted tissue look like?

A

White or red

61
Q

Why are some infarcts white?

A
  • Coagulative necrosis
  • Happens in solid organs
  • Happen s when you haven’t got blood supply to it.
62
Q

Why are some infarcts red?

A
  • Liquefactive necrosis
  • Loose tissue
  • Dual blood supply
  • Numerous anastomoses
  • Prior congestion
  • Raised venous pressure
  • Re-perfusion
63
Q

What is the consequence of infarction

A
  • No consequences to death
64
Q

What does the consequence of infarction depend on?

A
  • Alternative blood supply
  • Speed of ischaemia
  • Tissue involved
  • Oxygen content of the blood
65
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 blood flow hadn’t been returned.

66
Q

Why does return of blood to a ischaemic are bad?

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
67
Q

When membranes are leaky, can molecules leak out as well as in?

A

Yes and they can have both local and systemic effects

  • can cause local inflammation
  • may have general toxic effects on body
  • may appear in high concentrations in blood and can aid in diagnosis
68
Q

When the cell membrane is damaged, what can leak out of the cell?

A
  • Potassium
  • Enzymes
  • Myoglobin
69
Q

What happens when potassium leaks out of the cell?

A

Potassium is in high concentration in the cell, so lots leaks out when the membrane is leaky. Can lead to cardiac arrest.

70
Q

What happens if myoglobin leaks out of the cell?

A
  • Myoglobin leaks when you have damage to skeletal muscle.

- Blocks glomeruline in the kidney and causes renal failure.

71
Q

Define apoptosis

A

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

72
Q

What does a cell undergoing apoptosis look like under a microscope?

A
  • Internucleosomal cleavage of DNA

- Membrane integrity is maintained

73
Q

When does apoptosis occur physiologically?

A
  • In order to maintain a steady state
  • Hormone controlled involution - ovaries of post menopausal woman are smaller
  • Embryogenesis
74
Q

When does apoptosis occur pathologically?

A
  • Cytotoxic T cell killing of virus-infected or neoplastic cells
  • When cells are damaged, particularly with damaged DNA
75
Q

What does apoptosis look like?

A
  • The chromatin gets broken down and it starts to clump.
  • Karyorrhexis occurs
  • Cell fragments into apoptotic bodies (due to budding)
76
Q

How does apoptosis occur?

A

Three phases

  • Initiation
  • Execution
  • Degradation & phagocytosis
77
Q

Describe initiation and execution of apoptosis

A
  • Triggered by two mechanisms - intrinsic and extrinsic

- Both result in activation of caspases

78
Q

What are caspases?

A
  • Enzymes that control and mediate apoptosis

- Cause cleavage of DNA and proteins of the cytoskeleton

79
Q

How is the intrinsic pathway initiated?

A
  • Initiating signal comes from within the cell

- Triggers: most commonly irreparable DNA damage and withdrawal of growth factors or hormones

80
Q

How is the intrinsic pathway carried out?

A
  • 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.
81
Q

How is the extrinsic pathway initiated?

A
  • Initiated by extracellular signals

- Trigger: cells that are a danger e.g. tumour cells, virus infected cells

82
Q

How is the extrinsic pathway carried out?

A

One of the signals is TNF alpha.

  • Secreted by T killer cells
  • Binds to cell membrane receptor
  • Results in activation of caspases
83
Q

What do both the intrinsic and extrinsic pathways cause the cell to do?

A

The cells shrink and break up into apoptotic bodies.

84
Q

Why and how are apoptotic bodies phagocytosed?

A
  • The apoptotic bodies express proteins on their surface
  • They can now be recognised by phagocytes or neighbouring cells
  • Finally degradation takes place within the phagocyte/neighbour.
85
Q

Where do abnormal cellular accumulations come from?

A
  • If a cell can’t metabolise something, it will remain within the cell.
  • They can derive from; cell own metabolism; the extracellular space and the outer environment.
86
Q

What kind of things can accumulate in cells?

A

There are five main groups of intracellular accumulations; water/electrolytes; lipids, carbohydrates, proteins and pigments.

87
Q

When does fluid accumulate in cells?

A
  • Hydropic swelling
  • Occurs when energy supplies are cut off (hypoxia)
  • Indicates severe cellular diseases
  • Na+ and water flood into cell
  • Particular problem in the brain
88
Q

When do lipids accumulate in cells?

A
  • Steatosis (accumulation of triglycerides)

Causes; alcohol, diabetes mellitus, obesity and toxins.

89
Q

Where is lipid accumulation often seen?

A

liver - major organ of fat metabolism

90
Q

In what conditions do proteins accumulate in cells?

A
  • Seen as eosinophilic droplets or aggregation in the cytoplasm
  • Alcohol liver disease
  • alpha 1 antitrypsin deficiency
91
Q

Alpha 1 antitrypsin deficiency

A
  • Liver produces incorrectly folded alpha 1 antitrypsin protein
  • Can’t be packaged by ER, accumulates within ER and is not secreted
  • Systemic deficiency - proteases in lung act unchecked resulting in emphysema.
92
Q

Why do pigments accumulate in cells?

A
  • Carbon/coal dust/ soot
  • Inhaled and phagocytksed by alveolar macrophages
  • Anthracosis and blackened peribronchial lymph nodes
  • Usually harmless, unless in large amounts= fibrosis and emphysema
  • Tattooing
93
Q

Why does tattooing lead to pigment accumulation in cells?

A

The pigment is pricked into skin. It is phagocytosed by macrophages in dermis and remains there. Some pigment will reach draining lymph nodes.

94
Q

Give an example of the accumulation of endogenous pigments

A

Haemosidirin

95
Q

What is haemosiderin?

A
  • Iron storage molecule

- Derived from haemoglobin, yellow/brown

96
Q

What causes haemosiderin to form?

A

Forms when there is a systemic or local excess of iron e.g. bruise

97
Q

What is haemosiderosis?

A

With systemic overload of iron, haemosiderin is deposited in many organs, this leads to haemosiderosis.

98
Q

Where is haemosideris commonly seen?

A

Seen in haemolytic anaemias, blood transfusions and hereditary haemochromatosis.

99
Q

What is hereditary haemochromatosis?

A
  • Genetically inherited disorder
  • Increased intestinal absorption of dietary iron
  • Iron is deposited in the skin, liver, pancreas, heart and endocrine organs.
100
Q

What are the symptoms of hereditary haemochromatosis?

A

Liver damage, heart dysfunction and multiple endocrine failures, esp those of the pancreas

101
Q

What does hereditary haemochromatosis look like?

A
  • Darkening of the skin - patient looks permanently tanned
102
Q

What’s accumulating in jaundice?

A

Accumulation of bilirubin - bright yellow.

103
Q

How does bilirubin accumulate in the body?

A
  • Breakdown product of heme
  • Formed in all cells but must be eliminated in the bile
  • Bilirubin normally 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 cells extracellularly or in macrophages.
104
Q

What does jaundice look like?

A

Yellowing of the skin

- Good place to look for jaundice is in the sclera

105
Q

What are the different mechanisms of intracellular accumulations?

A
  • Abnormal metabolism
  • Alterations in protein folding and transport
  • Deficiency of critical enzymes
  • Inability to degrade phagocytosed particles
106
Q

What is calcification of tissues and what are the different types?

A
  • Abnormal deposition of calcium salts within tissues

- Can be localised (dystrophic) or generalised (metastatic)

107
Q

Dystrophic calcification

A
  • More common than metastatic
  • Occurs in an area of dying tissue, atherosclerotic plaques, raging or damaged heart valves, in tubercles lymph nodes and some malignancies.
108
Q

Why does dystrophic calcification occur?

A
  • No abnormality in calcium metabolism, or serum calcium or phosphate concentrations
  • Local change/disturbance favour nucleation of hydroxyapatite crystals
  • Can cause organ dysfunction e.g. atherosclerosis, calcified heart valves
109
Q

Why does metastatic calcification occur?

A
  • Due to hypercalcaemia secondary to disturbances in calcium metabolism
  • Hydroxyapatite crystals are deposited in normal tissues throughout the body
110
Q

What causes hypercalcaemia?

A
  • Increased secretion of parathyroid hormone (PTH) resulting in bone resorption
  • Destruction of bone tissue
111
Q

What are the causes of increased secretion of PTH?

A
  1. Primary - due to parathyroid hyperplasia or tumour
  2. Secondary - due to renal failure and the retention of phosphate
  3. Ectopic - secretion of PTH-related protein by malignant tumours
112
Q

What are the causes of destruction of bone tissue?

A
  • Primary tumours of bone marrow e.g. leukaemia
  • Diffuse skeletal masses
  • Paget’s disease of bone - when accelerated bone turnover occurs
  • Immobilisation
113
Q

Can cells live forever?

A
  • As cells are, they accumulate damage to cellular constituents and DNA
  • After certain number of divisions they reach replicative senescence
  • When telomeres reach a certain length the cell can no longer divide
114
Q

How do cancer cells manage to replicate multiple times?

A

Many cancer cells produce telomerase and this maintain the original length of the telomeres.

PP A (13 decks)

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