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Mechanisms of Disease > Session 1 -> Cell injury > Flashcards

Session 1 -> Cell injury Flashcards

0
Q

Name some toxins which can cause cell injury

A
  • High O2
  • Narcotics
  • Pesticides
  • Glucose
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1
Q

Name some physical agents of cell injury

A
  • Trauma
  • Heat
  • Cold
  • Radiation
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2
Q

Name some chemical agents which can cause cell injury

A
  • Alcohol
  • Therapeutic drugs
  • Poisons
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3
Q

What are the two immune mechanisms of cell injury?

A
  • Hypersensitivity

- Autoimmune

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4
Q

How does hypersensitivity cause cell injury?

A

-An overly vigorous immune reaction ensues which injures cells

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5
Q

List the frequent targets of cell injury

A
  • Cell membranes
  • Nucleus
  • Proteins
  • Mitochondria
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6
Q

To what organelle in particular is membrane damage dangerous and why?

A
  • Lysosomes

- Leakage of contents -> contains hydrolases etc would damage cell

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7
Q

What is the main reason why damage to the mitochondria causes cell injury?

A

-Mitochondria cannot carry out oxidative phosphorylation -> no ATP produced

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8
Q

What is hypoxia?

A

-Oxygen deprivation

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9
Q

What is the first consequence of oxygen deprivation?

A

-Decreased aerobic respiration

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10
Q

Name a cell type which can tolerate hours of hypoxia

A

-Dermal fibroblasts

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11
Q

Is hypoxia reversible or irreversible?

A

-Both, initially reversible but cell injury passes a point of no return

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12
Q

What is the main consequence of decreased aerobic respiration (oxidative phosphorylation)?

A

-Decreased ATP levels

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13
Q

At what level of decreased ATP does cellular function become compromised?

A

-When levels reach 5-10%

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14
Q

What happens to lipid and protein in reversible hypoxia?

A

-Accumulates within the cell as there is no ATP for metabolism

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15
Q

What happens to the glycogen stores in reversible hypoxia?

A

-They are used up

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16
Q

Why is protein synthesis decreased during reversible hypoxia?

A

-Ribosomes fall off the rER as energy is required to anchor them there

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17
Q

Why does cell swelling (oncosis) occur during hypoxia?

A
  • NaK pump fails as this requires ATP
  • K+ leaves the cell down its concentration gradient
  • Na+ enters down its concentration gradient
  • Ca2+ enters and the imbalance of electrolytes draws in water causing swelling
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18
Q

Why does loss of microvilli, blebbing and myelin figure appearance occur in hypoxia?

A

-Due to the imbalance of electrolytes

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19
Q

Why does lactic acidosis occur in hypoxia?

A

-Anaerobic respiration takes over resulting in a build up of lactate

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20
Q

Why does enzyme denaturation occur in hypoxia?

A

-Due to the lactic acidosis

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21
Q

Why does clumping of nuclear chromatin occur in hypoxia?

A

-Due to the decrease in pH caused by anaerobic respiration causing a build up of lactate

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22
Q

What is the main factor which causes hypoxia to become irreversible?

A

-The cell membrane becomes increasingly permeable causing a further increase in the influx of Ca which is toxic to the cell

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23
Q

What is the result the of increasing intracellular calcium during irreversible hypoxia?

A

-There is increased activation of cellular enzymes, including ATPases, phospholipases, proteases and endonucleases

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24
Q

What is the consequence of activation of ATPases during irreversible hypoxia?

A

-The enzymes further reduce the levels of available ATP within the cell

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25
Q

What is the consequence of the activation of phospholipases in irreversible hypoxia?

A

-hydorlyses phospholipids in cell membrane, further adding to the membrane damage

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26
Q

What is the consequence of activation of proteases during irreversible hypoxia?

A

-Further increase the breakdown of membranes and cytoskeletal proteins

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27
Q

What is the consequence of activation of endonucleases during irreversible hypoxia?

A

-DNA becomes irreparably damaged

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28
Q

What are the four groups of causes of hypoxia?

A
  • Hypoxaemic
  • Anaemic
  • Ischaemic
  • Histiocytic
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29
Q

What is hypoxaemic hypoxia? Give an example

A
  • hypoxia causes by low arterial pO2
  • altitude
  • hypoxia secondary to lung disease
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30
Q

What is anaemic hypoxia? Give an example

A
  • Hypoxia caused by the decreased ability of Hb to carry oxygen
  • CO poisoning
  • Anaemia
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31
Q

What is ischaemic hypoxia? Give an example

A
  • Hypoxia caused by the interruption of a blood supply
  • Heart failure
  • Occlusion
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32
Q

What is histiocytic hypoxia? Give an example

A
  • Hypoxia caused by the inability of the tissues to utilise oxygen
  • Cyanide poisoning (inhibits cytochrome system)
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33
Q

Define ischaemia

A

-Inadequate flow of blood to part of the body caused by constriction or blockage of the blood vessel supplying it

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34
Q

What may cause there to be a decreased arterial supply?

A
  • Occlusion
  • Low BP
  • Reduced venous drainage
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35
Q

Why is cell injury caused by ischaemia more rapid and severe than hypoxia?

A

-There is reduced metabolic substrates as well as a reduced oxygen supply

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36
Q

When does ischaemic reperfusion injury occur?

A

-When bloodflow is re-established to damaged tissue which has not yet become necrotic

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37
Q

How can reperfusion of tissue be dangerous?

A
  • The returning bloodflow causes an increase in superoxide radical production
  • Increased neutrophils which illicit an increased inflammatory response
  • Blood contains complement factors which are activated leading to further damage from inflammatin
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38
Q

What is the main target of free radicals?

A

-Cell membranes

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39
Q

Why are free radicals dangerous?

A

-They are very unstable, highly reactive molecules which react with other stable molecules, often producing a chain reaction involving the production of more free radicals

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40
Q

What are the three main free radicals in the body?

A
  • OH•
  • O2•
  • H2O2
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41
Q

How is O2• produced by radiation?

A

-Directly lyses water

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42
Q

What is the fenton reaction?

A

-The reaction of H2O2 with Fe to produce O2•

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43
Q

When does the fenton reaction become significant?

A

-During bleeding as this provides a free source of Fe which can be used

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44
Q

Why is the haber-weiss reaction useful?

A

-Although it produces -OH•, it uses O2•

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45
Q

What overdose causes death by liver failure due to reactive oxidative species production?

A

-Paracetamol

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46
Q

What is lipid peroxidation?

A

-The reaction of lipids with free radicals to generate a lipid peroxide

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47
Q

Where are the lipids, which are targeted in lipid peroxidation usually located?

A

-In cell membranes

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48
Q

Why is lipid peroxidation so dangerous?

A

-It is an autocatalytic chain reaction

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49
Q

What are the three main mechanisms of free radical removal?

A
  • Enzymes (SOD)
  • Vitamins (ACE)
  • Storage proteins (copper/iron)
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50
Q

What is the function of heat shock proteins during cell injury?

A

-To locate and repair mis-folded proteins in order to maintain cell vibility

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51
Q

What happens to protein/hsp production during cell injury

A
  • Protein production decreased

- HSP production increased

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52
Q

How do reversibly injured cells appear under a light microscope?

A
  • Swollen
  • Cytoplasm is reduced in pink (accumulation of water)
  • Pyknosis
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53
Q

What is pyknosis?

A

-Chromosome clumping

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54
Q

How does irreversible cell injury appear under a light microscope?

A
  • Karryohexis

- Karyolysis

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55
Q

What is karryohexis?

A

-Chromosomal lysis

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56
Q

What is karyolysis?

A

-Cell disintergration

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57
Q

How do reversibly injured cells appear under an electron microscope?

A
  • Swollen
  • Pyknosis
  • Autophagy
  • ER swelling
  • Blebbing
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58
Q

What is blebbing?

A

-Bumps on the membrane surface when the cytoskeleton has detached

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59
Q

How does an irrervsibly injured cell appear under an electron microscope?

A
  • Karryohexis
  • Karyolysis
  • ER Lysis
  • Lysosomal lysis
  • Mitochondrial swelling
  • Accumulation of denatured proteins
60
Q

Define oncosis

A

-Cell death with swelling

61
Q

What types of cell injury is oncosis typically associated with?

A
  • Hypoxia

- Anaemia

62
Q

Why does swelling occur in oncosis?

A

-Due to changes in ionic gradients drawing water in

63
Q

What is necrosis?

A

-The morphological changes which occur after cell death (4-24hrs)

64
Q

What happens to the plasma membrane during necrosis?

A

-Ruptures

65
Q

What other process is often seen alongside necrosis?

A

-Inflammation

66
Q

Do cells swell of shrink in necrosis?

A

-Swell

67
Q

What are the 4 types of necrosis?

A
  • Coagulative
  • Liquefactive
  • Caseous
  • Fat necrosis
68
Q

What happens to the proteins in coagulative necrosis?

A

-They undergo denaturation rather than degredation resulting in protein clumping

69
Q

With what type of cell injury is coagulative necrosis often seen?

A

-Ischaemia

70
Q

How does coagulative necrosis appear to the naked eye?

A

-Firm and white

71
Q

Why does coagulative necrosis stain intensely pink?

A

-Due to extensive protein denaturation

72
Q

Why is coagulative necrosis said to have a ghost outline?

A

-The architecture of the cells is preserved

73
Q

What happens to the proteins in liquefactive necrosis?

A

-Proteins are autolysed and dissolved as protein degrdation > protein denaturation

74
Q

How does liquefactive necrosis appear to the naked eye?

A

-The dead tissue liquefies

75
Q

Why does the dead tissue liquify?

A

-Due to enzymatic digestion of the tissue

76
Q

Liquefactive necrosis is often associated with what other process?

A

-Inflammation

77
Q

Where does liquefactive necrosis often occur?

A
  • Areas of soft tissue with low supporting cells eg brain
  • Abscesses
  • Infections
78
Q

What does excessive neutrophil infiltrate lead to in liquefactive necrosis?

A

-Purulent pus in exudate

79
Q

When does caseous necrosis occur?

A
  • Often during infections such as TB

- Associated with granulomatous inflammation

80
Q

What does caseous necrosis appear like to the naked eye?

A

-Cheese-like

81
Q

What similarity does caseous necrosis share with coagulative necrosis?

A

-The cells retain there architecture leaving a ghost outline

82
Q

When does fat necrosis occur?

A

-During injury to adipocytes or fatty tissue

83
Q

What organ typically undergoes fat necrosis and when?

A

-Pancreas during acute pancreatitis

84
Q

What does fat necrosis release?

A

-Free FA

85
Q

What is the association between calcium and fat necrosis?

A

-Calcium deposits in abdomen

86
Q

What is apoptosis?

A

-Programmed cell death with shrinkage

87
Q

Why is apoptosis described as an active process?

A

-Requires ATP

88
Q

What are caspases?

A

-Enzymes which are activted during apoptosis and degrade the cell’s DNA and proteins in an organised and scheduled manner

89
Q

How is apoptosis activated intrinsically to the cell?

A
  • Leakage of cytochrome C from mitochondria
  • Interacts wih APAF1 and Caspase-9 to form apoptosome
  • Apoptosome activates downstream caspases
90
Q

What is the usual cause of intrinsic activation of apoptosis?

A
  • DNA damage

- Hormone withdrawal

91
Q

Describe extrinisic activation of apoptosis

A

-Binding of death ligand to death ligand receptor activates caspases

92
Q

When are death ligand receptors expressed on a cell?

A

-In response to damage

93
Q

Name 2 death ligands

A
  • TRAIL

- FAF

94
Q

What is the differences between blebbing and budding?

A
  • Blebbing is disorganised disruption of the cell membrane and the blebs do not contain cellular material
  • Budding is organised rearrangement of cytoskeleton and the apoptotic bodies may contain cellular material
95
Q

What happens to the nuclear fragments and apoptotic bodies produced by apoptosis?

A

-They are phagocytosed by phagocytes or removed by neighbouring cells

96
Q

Is apoptosis pathological or physiological?

A
  • Often physiological eg eliminating unwated cells

- Can be pathologic after some forms of cell injury

97
Q

Do the cells disintegrate in apoptosis like in necrosis?

A

-No, there is chromatin condensation and nuclear fragmentation

98
Q

What is chracteristic of the membrane throughout apoptosis?

A

-Stays intact

99
Q

Does apoptosis occur in groups of cells or singly?

A

-Single cells

100
Q

What is gangrene?

A

-Grossly visible necrosis

101
Q

What is the treatment for gangrene?

A

-The dead tissue needs to be removed

102
Q

What is dry gangrene?

A

-Coagulative necrosis modified by the air to become dry gangrene

103
Q

Give an example of dry gangrene

A

-Umbilical cord after birth

104
Q

What is wet gangrene?

A

-Liquefactive necrosis modified by bacteria to form wet gangrene

105
Q

Why is wet gangrene more dangerous than dry gangrene?

A

-The bacteria can leak into the blood and cause septicaemia

106
Q

What is gas gangrene?

A

-Necrotic tissue becomes infected with anaerobic bacteria which produce gas which appears as bubbles/blisters under the skin

107
Q

When is gas gangrene frequently seen?

A

-In motorbike injuries as soil/gravel/dirt enters the wound upon impact

108
Q

What is an infarct?

A

-Necrosis due to ischaemia

109
Q

What are the frequent causes of infarcts?

A
  • Thrombosis
  • Embolism
  • Compressional twisting
110
Q

Give examples of compressional twisting

A
  • Twisting of colon
  • Haemorrhoid
  • Testicular torsion
111
Q

What determines the type of necrosis which occurs during an infarct?

A
  • Whether there is an alternative blood supply
  • The speed of ischaemia
  • The tissues involved
112
Q

What detemines whether the infarct is white or red?

A

-The level of haemorrhaging

113
Q

Why is the occlusion of an end artery a white infarct?

A

-No peripheral blood vessels which leaves the area entirely without blood and thus there is no haemorrhaging

114
Q

In what type of organs does white infarct occur and why?

A

-Solid organs as the amount of haemorrhage that occurs from adjacent capillaries is limited

115
Q

Why does red infarct occur in tissues with dual blood supply?

A

-Occlusion of one vessel, the other vessel is not sufficient to maintain cells and tissue dies with haemorrhaging occuring

116
Q

Why does red infarct occur in loose tissue?

A

-There is poor stromal support for adjacent capillaries and they burst

117
Q

How does venous insufficiency cause red infarct?

A

-Increased venous pressure decreases arterial blood flow which leads to ischaemia and infarct however blood flow is still present, just not sufficient

118
Q

What is hyperaemia and what type of infarct occurs?

A
  • Increased blood flow to a specific tissue

- Red

119
Q

What type of infarct occurs if there is reperfusion?

A

-Red

120
Q

Why is high levels of potassium in the blood extremely dangerous?

A

-Stops the heart beating

121
Q

Under what pathlogical conditions is it possible to get high levels of potassium in the blood?

A
  • Large myocardial infarction (high levels of local potassium release)
  • Severe burns (high levels of cellular necrosis)
  • Tourniquet shock (removed quickly after several hours)
  • Tumour lysis syndrome
122
Q

What is tumour lysis syndrome?

A

-Paradoxical effect form successful chemotherapy ->High number of cancerous cells killed and broken down at once releasing lots of potassium

123
Q

How are enzymes in the blood useful after cell injury?

A
  • Concentrations of specific enzymes in the blood indicate which organs have been effected severly and for how long
  • Small enzymes released first as the gaps in membranes are small, as damage progresses the gaps become bigger and larger enzymes can leak out
124
Q

Why are high levels of myoglobin in the blood dangerous after cell injury?

A
  • Released from dead myocardium and striated muscle

- Rhabdomyolysis -> myoglobin plugs renal tubules and leads to renal failure

125
Q

What are common causes of rhabdomyolysis?

A
  • Trauma
  • Burns
  • Alcohol/drug abuse
126
Q

What is the result of abnormal accumulation of water and electolytes?

A

-Swelling and oedema

127
Q

What is the result of abnormal lipid accumulation?

A
  • Hepatic steatosis (fatty liver)
  • Cholesterol in atherosclerotic plaques
  • Xanthomas
128
Q

What is a result of abnormal protein accumulation due to alcoholic liver disease?

A

-Mallory’s hyaline (an accumulation of keratin in the liver)

129
Q

How does a-1 antitrypsin deficiency lead to liver cirrhosis?

A

-Abnormal folding of proteins leads to accumulation of protein in the liver which leads to cirrhosis

130
Q

Name 2 exogenous abnormal accumulations of pigment

A
  • Coal dust picked up by alveolar marcrophages (pneumoconiosis)
  • Tattoos (pigment can be taken to lymph nodes)
131
Q

What is lipofuscin?

A
  • An endogenous pigment which appears with age in the myocardium, neurones and hepatocytes
  • Has no pathological consequences
132
Q

What is haemosiderin?

A

-Iron storage molecule

133
Q

What is haemosiderosis?

A

-The accumulation of haemosiderin in various tissues

134
Q

What is hereditary haemochromatosis?

A
  • Bronze diabetes

- Increased intestinal absorbtion of iron leads to deposition in skin, liver pancreas and heart

135
Q

What is pathological calcification?

A

-Abnormal deposition of calcium salts in tissues

136
Q

What is dystrophic calcification?

A

-Local calcium deposition which occurs in areas of dying tissue (eg damaged heart valves)

137
Q

What causes dystrophic calcification?

A

-There is no abnormality in calcium metabolism, it is caused by local changed which promote hydroxyapatite depositions in tissues

138
Q

What are the outcomes of dystrophic calcification?

A

-Can cause organ dysfunction but can also be harmless

139
Q

What valve never calcifies?

A

-Pulmonary

140
Q

What is metastatic calcification?

A

-Hydroxyapatite deposition whih is systemic when there is hypercalcaemia

141
Q

What are the main causes of metastatic calcification?

A
  • Oversecretion of PTH (parathyroid adenoma, renal failure with retention of phosphate causing high levels of PTH)
  • Ectopic secretion of PTHrp from malignant tumours (esp. lung)
  • Destruction of bone tissue (primary tumours, padgets disease)
142
Q

What is replication senescence?

A

-Cells loose their ability to replicate as they age

143
Q

What happens to telomeres as cells age?

A

-They reduce in size per each round of replication

144
Q

What are telomerases and which cells have them?

A
  • Enzymes which can re-lengthen telomeres so replication can be indefinite
  • Stem cells, germ cells and some cancer cells
145
Q

What are the stages of liver disease from chronic excessive alcohol intake?

A
  • Steatosis
  • Acute alcoholic hepatitis
  • Cirrhosis
146
Q

What are the features of alcoholic liver disease?

A
  • Focal hepatocyte necrosis
  • Mallory body formation
  • Accumulation of neutrophils
  • fever
  • Liver tenderness
  • Nausea
  • Vomiting
  • Jaundice
147
Q

Describe a cirrhotic liver

A

-Hard, shrunken nobbly liver with micronodules of regenerating hepatocytes separated by scar tissue

148
Q

What stage of liver damage becomes irreversible?

A

-Cirrhosis

Mechanisms of Disease (11 decks)

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