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Immunology and Microbiology > 1.I Etiology, injury and cell death > Flashcards

1.I Etiology, injury and cell death Flashcards

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1
Q

What can a cell do during stress?

A

Respond to stimuli and trigger adaptation mechanisms

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2
Q

Is cell death always a pathological condition?

A

No there can also be physiological death

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3
Q

What is path-physiologic death of cells?

A

Outcome of cell damage or missed adaptation to injurious stimuli

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4
Q

What is physiologic cell death?

A

Intrinsic property of normal cells underlying tissue regulation

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5
Q

What is necrosis?

A

Accidental cell death

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6
Q

What is apoptosis?

A

Regulated cell death

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7
Q

What are the two types of cell death?

A

Necrosis
Apoptosis

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8
Q

What does irreversible injury of cells lead to?

A

Cell death

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9
Q

2 models for cell death

A

Conversion model
Competition model

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10
Q

What is the conversion model?

A

All or nothing

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11
Q

What is the competition model?

A

Signals promoting and inhibiting cell death start at the same time

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12
Q

What kind of cell death are the conversion and competition model relevant for?

A

Both apoptosis and necrosis

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13
Q

Different name for accidental cell death

A

Passive necrosis

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14
Q

What is passive necrosis?

A

Pathological event not controlled or modified by the cell

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15
Q

What causes passive necrosis?

A

Severe exogenous/endogenous injury

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16
Q

What can cause passive necrosis?

A

Chemical
Physical
Biological

External factors

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17
Q

Why does passive necrosis typically involve a group of cells?

A

Because it is random and caused by an external factor

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18
Q

What characterises passive necrosis?

A

Massive protein denaturation (like by lowering pH)
ATP depletion
Cell and organelle swelling
Increased membrane permeability

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19
Q

What does increased membrane permeability cause?

A

Leakage of the intracellular content (damp) which causes inflamation

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20
Q

Is apoptosis an inflammatory trigger?

A

No

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21
Q

Why is apoptosis not an inflammatory trigger?

A

Because there is compartmentalisation, there is no damage in the membran and no leakage of intracellular content

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22
Q

What cleans up after apoptosis?

A

Phagocytes clean up the fragments

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23
Q

What cleans up after necrosis?

A

Macrophages and Nucleophiles which cause inflammation

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24
Q

What is the main event of passive necrosis?

A

Irreversible cell damage

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25
Q

Measuring levels of which enzyme in the blood can show signs of necrosis?

A

LDH

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26
Q

Why can LDH levels show signs of necrosis?

A

Because it typically lives inside the cell which means that if high levels are detected in the blood there is tissue damage somewhere

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27
Q

What is coagulative necrosis caused by?

A

Massive protein denaturation

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28
Q

Where does coagulative necrosis often happen?

A

In tissue with singular vascularisation

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29
Q

What causes caseous necrosis?

A

Massive protein denaturation in lungs

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30
Q

What causes colliquative necrosis?

A

Protein lysis

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31
Q

What causes pyogenic infection?

A

Bacteria

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32
Q

What is the key event of necrosis?

A

Fall of ATP

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33
Q

What happens with the fall of ATP?

A

Loss of energy to maintain the hydro-osmotic equilibrium and cell membrane integrity

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34
Q

What does osmotic imbalance cause?

A

Cells to swell

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35
Q

What does the influx of Ca2+ cause?

A

Over activation of enzymes that cause lipid degradation which causes membrane degradation

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36
Q

Where does the influx of Ca2+ come from?

A

ER and mitochondria

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37
Q

What is apoptosis useful for?

A

Eliminate damaged and infected cells through the activation of a genetic program

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38
Q

Can the same stimuli that trigger necrosis also trigger apoptosis?

A

Yes, depends on intensity and length of stimuli

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39
Q

What is apoptosis important to prevent?

A

Overreactive T cells

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40
Q

What happens to T-cells that bind with high affinity to self epitope antigen-MHC complexes?

A

Apoptosis

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41
Q

Does apoptosis involve a group of cells

A

Not always, can be very specific to one single cell

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42
Q

2 pathways of apoptosis singalling

A

Extrinsic pathway
Intrinsic pathway

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43
Q

Which apoptosis signalling pathway is receptor dependant ?

A

Extrinsic

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44
Q

What activates the intrinsic pathway of apoptosis signalling?

A

Intracellular signals from the mitochondria and damage of DNA

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45
Q

Different name for the intrinsic pathway of apoptosis signalling?

A

Mitochondrial pathway

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46
Q

What is the active form of cell death and why?

A

Apoptosis, because it requires ATP

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47
Q

What do all forms of extrinsic pathway death have?

A

Death domain

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48
Q

Different name for the extrinsic pathway of apoptosis

A

Receptor mediated

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49
Q

Receptors used in the extrinsic pathway of apoptosis

A

Fas and FasL (ligand)

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50
Q

Does the extrinsic pathway of apoptosis always trigger apoptosis?

A

No it can also trigger adapting proteins which trigger survival

51
Q

Which immunological phenomena are Fas-FasL mediated apoptosis involved with?

A

Homeostasis of T-cells
Cytotoxic activity of T-cells
Immune-privilege
Neoplastic cells

52
Q

Why is it important for apoptosis to control immune responses?

A

To avoid inflammation

53
Q

What is MOMP?

A

Mitochondrial outer membrane permeability

54
Q

Which effector protein is found in apoptosome complex?

A

CASPASE 9

55
Q

Which phases of the extrinsic and intrinsic pathways are the same?

A

The effector phases

56
Q

What does p53 do?

A

Stop reproduction of cells if there is DNA damage

57
Q

Example of diseases associated with inhibition of apoptosis

A

Cancer
Autoimmune
Glomerulonephritis
Viral infections

58
Q

Example of diseases associated with excessive stimulation of apoptosis

A

AIDS
Neurogenerative disorders
Myelodysplastic syndromes
Damage from schema
Toxic liver disease

59
Q

What is programmed Necrosis?

A

Mix between necrosis and apoptosis
Necrosis, but regulated

60
Q

Different name for programmed necrosis

A

Necroptois

61
Q

What is PARP?

A

Poly ADP-ribose polymerase

62
Q

Is there inflammation in necroptosis?

A

Yes

63
Q

What is the result of necroptosis the same as?

A

Necroses, there is a disruption of cell membrane and inflammation

64
Q

What is the biological meaning of autophagy?

A

To degrade cellular components that don’t work like unfolded proteins
Produce energy

65
Q

3 steps of autophagy

A

Nucleation
Formation of a vesicle
Maturation

66
Q

Name of the vesicle formed in autophagy

A

Autophagosome

67
Q

Is autophagy and apoptosis independant processes?

A

No

68
Q

What happen when the apoptotic pathway fails?

A

The cell might trigger alternative death process like for example autophagy

69
Q

2 things that can trigger autophagy

A

Nutrient deprivation
Depletion of growth factors

70
Q

What is inhibited during nutrient deprivation?

A

mTOR

71
Q

Can autophagy produce energy?

A

Yes

72
Q

Does autophagy need ATP to start?

A

Yes

73
Q

What way of death happens if ATP is present?

A

Apoptosis or autophagy

74
Q

Types of programmed cell death

A
75
Q

What is pyroptosis?

A

capase-1-dependant cell death subroutine

76
Q

What does pyroptosis amplify?

A

Inflammation

77
Q

What is entosis?

A

Cell death when 3 specific conditions are met

78
Q

What happens during the pyknosis phase of necrosis?

A

hyper chromatic nuclei are shrunk compared to normal cell

79
Q

What is the karyorrhexis phase of necrosis?

A

The random degradation of DNA

80
Q

What is the karyolysis phase of necrosis?

A

Complete loss of intracellular nuclei and DNA has been released due to activity of the endonuclease

81
Q

What is coagulative necrosis caused by?

A

Massive protein denaturation

82
Q

Example of coagulative necrosis

A

Cardiac myocyte during ischemic insult

83
Q

What is the cause of coagulative necrosis in ischemic insult?

A

Protein denaturing dur to lowering of intracellular pH

84
Q

What happens to the tissue texture in ischemic insult?

A

Texture is conserved which makes it difficult to distinguish living cells and necrotic cells

85
Q

What is the main difference in necrotic cells and living cells in coagulative necrosis caused by ischemic insult?

A

The absence of DNA due to absence degradation caused by necrosis

86
Q

What is liquefactive necrosis due to?

A

Causes are not completely clear
Protein lysis
Lack of extracellular matrix makes it possible that disruption of tissue is faster than repair

87
Q

What is fat necrosis due to?

A

Triglyceride hydrolysis mediated by the release of lipolytic enzymes of the pancreas

88
Q

Example of would could cause triglyceride hydrolysis to trigger fat necrosis?

A

Trauma or pancreatitis

89
Q

What is the key event in necrosis?

A

Decrease of concentration of ATP in the intracellular space

90
Q

What is necrosis typical during?

A

Ischemic injuries where oxygen supply is interrupted and cells cannot perform respiration as it decreases the synthesis of ATP

91
Q

What happens as consequence of the concentration of ATP decreasing during necrosis?

A

Hydro-osmotic equilibrium is completely lost
Permeability to selective ions is lost

92
Q

Does necrosis involve a specific cut of DNA?

A

No

93
Q

What does selective ion permeability require?

A

Energy consumption (ATP)
Membrane integrity
Ion channel efficiency
Structural integrity (cytoskeleton)

94
Q

What is ischemia?

A

Restriction in blood supply causing shortage of oxygen and nutrients

95
Q

What happens to the control of calcium and sodium during ischemic cell death?

A

Loss of control in them between cell and extracellular space

96
Q

What does the disfunction of the sodium pump during ischemic cell death cause?

A

Inability to diffuse
Loss of osmotic balance which causes cell to swell

97
Q

What does the influx of calcium into the cell during ischemic cell death cause?

A

Over activation of enzymes that cause lipid degradation which causes membrane degradation and loss of permeability

98
Q

Where does the influx of calcium come from in ischemic cell death?

A

ER and mitochondria

99
Q

Can osmotic catastrophe be counteracted in patient with hyperglycaemia?

A

No

100
Q

Does programmed/regulated cell death require energy?

A

Yes

101
Q

7 types of programmed cell death

A

Apoptosis
Mitotic catastrophe
Paraptosis
Autophagy
Programmed necrosis
Condroptosis
Accelerated senscence

102
Q

What kind of phenomenon is Apoptosis?

A

Physiologic

103
Q

What is apoptosis important in?

A

Regulation of embryogenisi, cell turnover in high proliferating tissues (ex. epidermis), in intestine its crucial to maintain number of cells (homeostatic condition) and restore some dysfunctions

104
Q

Why is apoptosis important during inflammation?

A

Because it controls the activity of macrophages and neutrophils

105
Q

What is the signal that activates apoptosis called?

A

Priming

106
Q

Is there inflammation during apoptosis, why/why not?

A

No because there is no damage to the cell membrane

107
Q

Why does the cell shrink during apoptosis?

A

Water and electrolyte leakage

108
Q

What eliminates apoptotic bodies?

A

Phagocytes

109
Q

What cleaves DNA in apoptosis?

A

Ca/mg dependant endonuclease and degradation of chromatin-associated proteins by protease

110
Q

How does phagocytes recognise apoptotic bodies?

A

Exposure of thrombopadin, vitronecting and phosphatidylserine (flip-flop)

111
Q

What is the main executor of the apoptotic action?

A

Capases

112
Q

What kind of enzyme is camases?

A

Zymogen enzyme

113
Q

4 phases of apoptosis

A

Initiating the signal
Control the integration
Common executive phase (between the 2 phases)
Removal of the dead cells (apoptotic bodies)

114
Q

What is the phagocytosis of apoptotic bodies called?

A

Efferocytosis

115
Q

Differen name for the extrinsic pathway of apoptosis

A

Receptor dependant

116
Q

What activates the extrinsic pathway of apoptosis?

A

Interaction of extracellular membrane receptors w/their specific ligands which activates intracellular signalling pathway that actives the program controlling apoptosis

117
Q

Death signals of the extrinsic pathway of apoptosis

A

FAS
TNFR
TRAIL receptors (TRI-4)

118
Q

How can FasL exist?

A

In soluble form or integrated into the plasma membrane of killing cells

119
Q

What are the main target for cells carrying FasL?

A

Fas expressing cells

120
Q

What happens when the cells carrying FasL interacts with Fas expressing cells?

A

Fas expressing cells are killed

121
Q

What is FADD?

A

Fas death domain

122
Q

What does pro caspase-8 turn into when activated?

A

Active capase-8

123
Q

What 4 immunologic are Fas-FasL mediated apoptosis involved in?

A

Homeostasis of T-cells
Cytotoxic activity of T-cells
Immune-privilege
Neoplastic cells

124
Q
A

Immunology and Microbiology (11 decks)

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