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Pathological Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is cyanosis ?

A

Bluish discolouration of skin & nails

Sign of hypoxia/increase in deoxygenated haemoglobin

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2
Q

What is is the difference between hypoxia & ischaemia ?

Which is worse ?

A

Hypoxia - reduced oxygen to tissue
Ischaemia - reduced blood supply to tissue

Ischaemia is worse

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3
Q

What is hypoxaemic hypoxia?

A

Low oxygen in arteries

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4
Q

What is anaemic hypoxia ?

A

Hypoxia causes by reduced functional haemoglobin

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5
Q

What is ischaemic hypoxia?

A

Hypoxia caused by disrupted blood supply to tissue

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6
Q

What is histiocytic hypoxia?

A
  • Enough oxygen available to tissue but cells unable to use it
  • due to inhibited oxidative phosphorylation enzymes (eg cytochrome oxidase)
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7
Q

What are 2 causes of hypoxaemic hypoxia?

A
  • high altitude = reduced inspiration of o2

- lung disease = reduced o2 absorption

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8
Q

What are 2 causes of anaemic hypoxia?

A
  • Anaemia

- CO poisoning

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9
Q

What are 2 causes of ischaemic hypoxia?

A
  • local blockage of blood supply eg thrombus/embolus

- heart failure = low perfusion pressure = global ischaemia

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10
Q

What is a cause of histiocytic hypoxia ?

A

Cyanide poisoning - inhibits oxidative phosphorylation enzyme

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11
Q

Which cells would be disabled first without o2?

A

Neurones within few mins

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12
Q

How long can fibroblasts last without o2?

A

Few hours

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13
Q

What are urticaria? And what causes them ?

A

Hives

Hypersensitivity reaction

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14
Q

What is a hypersensitivity reaction?

A

Over active immune system injuring host tissue

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15
Q

What is an auto immune condition?

A

Failure of immune system to distinguish self from non self.

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16
Q

Which components of the cell are most susceptible to injury?

A
  • membrane
  • nucleus
  • structural proteins - enzymes
  • mitochondria (oxidative phosphorylation)
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17
Q

At a molecular level, how can Low ATP be detrimental to a cell?

A

1) inactive na+/k+ ATPase pump = na+, ca2+, h2o influx = swelling
2) increase in glycolysis = increase pyruvic acid = lower PH
3) detachment of ribosomes = reduced protein synthesis = reduced lipid transportation = lipid deposition.

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18
Q

How does increased ca2+ in the cytoplasm of a cell damage the cell?

A

Activates enzymes which will break up molecules/structures in the cell

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19
Q

What enzymes does increased cytosolic ca2+ active?

A
  • Proteases
  • Phospholipases
  • ATPases
  • Endonucleases
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20
Q

What do endonucleases do ?

A

Break down DNA

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21
Q

What are free radicals?

A

Molecules that have one or more unpaired electrons in their outer orbit

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22
Q

What is the most common type of free radicals in the body?

A

Reactive oxygen species

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23
Q

What are the 3 main reactive oxygen species in the cells?

A

Hydroxyl radical
Superoxide 02^-
Hydrogen peroxide h2o2

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24
Q

What is the most dangerous reactive oxygen species ?

A

Hydroxyl radical

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25
Q

How are free radicals produced ?

A

Slide 16 lecture

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26
Q

How are ROS produced in normal, daily biochemistry of cell?

A
  • oxidative phosphorylation (as oxygen is reduced along electron transport chain)
  • intermediates in enzyme reactions
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27
Q

What is Haemachromatosis?

A

Hereditary disorder in which iron salts are deposited in the tissues. Leads to

  • liver damage
  • diabetes
  • bronze skin

Free radial damage occurs in this condition

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28
Q

What is Wilson’s disease?

A

Autosomal recessive
Copper deposits in tissues

= free radicals

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29
Q

How can free radicals be overproduced in cells?

A
  • inflammation
  • radiation
  • iron deposits - Fenton reaction
  • copper deposits
  • drug and chemical metabolism in liver
  • hypoxia
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30
Q

Which vitamins protect against free radicals?

A

A
C
E
Donate electrons to free radicals

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31
Q

What are antioxidants ?

A

Substances that remove damaging reactive oxygen species

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32
Q

What are 2 Functions of transferrin?

A
  • transport iron in the serum

- thus controls amount of free radicals in body

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33
Q

What is Ceruloplasmin?

A

Copper carrying protein

Involved in iron metabolism

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34
Q

Which enzymes neutralise free radicals?

A

Superoxide dismutase
Catalase
Glutathione peroxidase

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35
Q

Which part of the cell do free radicals target the most?

A

Phospholipids in memebrane

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36
Q

What causes lipid peroxidation?

A

Free radicals

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37
Q

What is the name of the process in which free radicals attack cell membranes?

A

Lipid peroxidation

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38
Q

What are 3 ways in which free radicals attack a cell?

A

1) lipid peroxidation - target membranes
2) oxidise proteins, carbohydrates = alter shape/cross link them
3) mutagenic = oxidise DNA = carcinogenic

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39
Q

What are heat shock proteins?

A

Proteins that mend mis-folded/damaged proteins during cell injury

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40
Q

What are other names for heat shock proteins?

A

Unfoldases

Chaperonins

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41
Q

Give an example of a heat shock protein?

A

Ubiquitin

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42
Q

What is ubiquitin?

A

A heat shock protein/chaperone protein/unfoldases

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43
Q

What is pyknosis?

A

Condensation of chromatin in nucleus after cell death during necrosis & apoptosis

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44
Q

What is karyorrhexis?

A

Rupture of the nucleus during apoptosis and necrosis

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45
Q

What is karyolysis?

A

Nucleus dissolves after cell death

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46
Q

Using a light microscope what structures will be visible during cell death?

A

Cell membrane and nucleus

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47
Q

What can happen to the nucleus during cell death?

A
  • pyknosis : enlarges
  • karyorrhexis : breaks up
  • Karyolysis : dissolves
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48
Q

What can be seen under an electron microscope during reversible cell injury and how can it be reversed if hypoxia was the cause?

A
  • blebs : disruption to cytoskeleton by proteases activated by ca2+
  • swelling of cell
  • swelling of organelles

Reversed by o2 if hypoxia is the cause

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49
Q

What can be seen in a irreversibly injured cell?

A
  • lysis of organelles
  • autolysis of cell from lysosome enzymes
  • holes in membrane
  • myelin figures : fat deposits in and around cell
  • nucleus changes: pyknosis, karyorrhexis, karyolysis
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50
Q

What is oncosis and necrosis ?

A

Oncosis: changes that occur to cell before cell death (cell swelling)

Necrosis: changes that occur to cell after cell death

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51
Q

What are 4 types of necrosis?

A

Main

  • Coagulative
  • Liquefactive

Special type

  • Caseous
  • Fat necrosis
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52
Q

Describe coagulative necrosis

A
  • involves solid tissues/organs eg heart, kidney
  • denatured proteins
  • cell architecture preserved
  • can lead to dry necrosis
  • white infect
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53
Q

Describe liquefactive necrosis

A

Involves liquid areas/areas with less connective tissue eg brain

  • enzymatic digestion of tissue
  • cell architecture lost
  • can lead to wet necrosis
  • red infarct
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54
Q

Which infection is caseous necrosis associated with?

A

Tuberculosis

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55
Q

Describe caseous necrosis

A

Amorphous debris
Associated with infections
Cottage cheese appearance around lung in TB

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56
Q

What does fat necrosis look like?

A

Candle wax

57
Q

Describe fat necrosis and in a condition that it can be seen

A
  • Fatty acids produced from breakdown of triglycerides by enzymes
  • Fatty acids react with ca2+ to form calcium soaps = candle wax appearance

Seen in pancreatitis

58
Q

What is Gangrene?

A

Visible necrosis

59
Q

What is an infarction?

A

Necrosis of a tissue caused by ischaemia

60
Q

What is an infarct?

A

Area of ischaemic necrosis on a tissue

61
Q

In which type of necrosis would you see dry gangrene?

A

Coagulative necrosis

62
Q

In which type of necrosis would you see wet gangrene?

A

Liquefactive necrosis

63
Q

What is dry gangrene?

A

Visible necrosis modified by air

64
Q

What is wet gangrene ?

A

Visible necrosis modified by infection

Involves anaerobic bacteria that produce gas

65
Q

What causes an infarction ?

A

Thrombosis

Embolism

66
Q

What’s the difference between thrombosis and an embolism ?

A

Thrombosis - formation of clot inside intact blood vessel

Embolus - travelling clot

67
Q

What results in white infarct?

A

Solid tissue
Occlusion of end artery
No haemorrhage
Coagulation infarction

68
Q

What causes red infarcts?

A 
Loose tissue
Dual blood supply to tissue 
Numerous anastomoses 
Raised venous pressure (congestion of blood in venous end)
Liquefactive infarction
69
Q

What is it called when oxygen is returned to a damaged (not yet necrotic) tissue resulting in even more damaged tissue?

A

Ischaemia - reperfusion injury

70
Q

What are the causes of ischaemia-reperfusion injury ?

A
  • increased reactive oxygen species
  • increased inflammation from cells in blood
  • activation of complement pathway
71
Q

How is cell death caused in necrosis ?

A

Cell swelling

72
Q

During necrosis what things can leak out from the dead cell?

A
  • k+ : stops heart beating
  • proteins : CK, troponin
  • myoglobin : skeletal muscle break down, brown urine
73
Q

What can lead to myoglobin in urine?

A

Brown urine

  • Caused by breakdown of skeletal muscle
  • Extreme exercise without enough water
74
Q

How does apoptosis cause cell death?

A
  • Regulated and controlled Shrinkage of cell

- non random degradation of DNA and proteins

75
Q

Does apoptosis require energy?

A

Yes

76
Q

Is membrane integrity maintained in apoptosis?

A

Yes

77
Q

Are lysosomes involved in apoptosis?

A

No

78
Q

Is apoptosis pathological or physiological ?

A

Can be both

79
Q

When does apoptosis occur physiologically?

A

Metamorphosis of limbs during embryonic development

80
Q

When does apoptosis occur pathologically?

A
  • via cytotoxic T cells
  • DNA mutated cells
  • grafts/transplants
81
Q

Name the 2 mechanisms that can initiate apoptosis

A

Intrinsic pathway

Extrinsic pathway

82
Q

Which enzymes are activated in apoptosis and what do they do?

A

Caspases

Cleave proteins and DNA

83
Q

What is formed at the end of apoptosis?

A

Apoptic bodies

84
Q

What can trigger intrinsic apoptosis of a cell ?

A
  • DNA damage

- withdrawal of growth factors/hormones

85
Q

What is P53?

A

Tumour suppressor protein

86
Q

In which pathway for apoptosis is p53 activated?

A

Intrinsic

87
Q

What does the activation of p53 in a cell do during intrinsic apoptosis ?

A

Makes outer mitochondrial membrane more Permeable so that cytochrome C can be released.

Cytochrome C activates caspases which cleaves proteins and DNA

88
Q

What is cytochrome C?

A

Protein found in mitochondria involved in oxidative phosphorylation and apoptosis

89
Q

How is Cytochrome C involved in intrinsic apoptosis ?

A

Activates caspases which cleave DNA and protein

90
Q

What proteins are involved in intrinsic apoptosis ?

A

P53
Cytochrome C
Caspases

91
Q

What are some triggers of the extrinsic pathway ?

A
  • tumour cells

- virus infected cells

92
Q

What is TNFalpha ?

A

Tumour necrosis factor alpha
Cell signalling protein (cytokines)
Involved in extrinsic pathway of apoptosis

93
Q

Where does TNFalpha come from ?

A

Secreted by T killer cells

94
Q

How is TNF alpha involved in extrinsic apoptosis ?

A

Secreted by T killer cells
Binds to cell membrane receptor
Activates caspases which cleave DNA and proteins

95
Q

In Apoptosis what happens to the apoptotic bodies produced?

A

Phagocytosed

96
Q

Give 7 ways in which necrosis and apoptosis differ?

A

See table in lecture

97
Q

What are the 5 main groups of intracellular accumulation ?

A 
Water & electrolytes 
Lipids
Proteins
Fats
Pigment
98
Q

How does hypoxia result in cerebral oedema ?

A

Low o2 = low ATP = inactive na+/k+ ATPase pump.
Na+ & h20 rush into cells
Brain becomes compressed against skull

99
Q

What is Steatosis and where is it seen the most?

A

Accumulation of triglycerides

Liver

100
Q

What is the major organ of fat metabolism?

A

Liver

101
Q

What are the causes of steatosis ?

A

Alcohol
Diabetes mellitus
Obesity
Toxins

102
Q

Can cholesterol be broken down? And is it insoluble or soluble

A

Cannot be broken down

Insoluble

103
Q

Which is the only organ that can eliminate cholesterol ?

A

Liver

104
Q

What happens to excess cholesterol in the liver?

A

Stored in cell vesicles

105
Q

What are foam cells?

A

Macrophages in atherosclerotic plaques

106
Q

What are xanthomas?

A

Fatty deposits under skin/tendons

Seen in hyperlipidaemias

107
Q

What are Mallorys hyaline?

A

damaged keratin filaments within the hepatocytes.

Seen in alcoholic liver disease

108
Q

Where is alpha 1 antitrypsin protein made?

A

Liver

109
Q

What is alpha 1 anti trypsin deficiency?

A

Liver producing incorrectly folded alpha 1 anti trypsin

Build up within ER

110
Q

What is alpha 1 anti trypsin protein?

A

Protease inhibitor

111
Q

What secondary disease can alpha 1 anti-trypsin deficiency lead to do ?

A

Emphysema in lungs

112
Q

When do pigments accumulate in cells ?

A
  • pollution

Tattoo

113
Q

Which cells do pigment accumulate in?

A

Macrophages

114
Q

What is Haemosiderin?

A

Iron storage molecule in cells formed when there is excess iron.

115
Q

What is haemosiderosis ?

A

Accumulate of iron storage molecule haemosiderin

Leading to excess of iron

116
Q

Give an example when haemosiderins are seen ?

A

Excess iron

So bruising

117
Q

What is cirrhosis ?

A

Scarring of the liver

118
Q

What is hereditary haemochromatosis?

A

Excess iron in a number of organs

Skin looks bronze

119
Q

What is the treatment of hereditary haemochromatosis?

A

Repeated bleeding

120
Q

What colour is bilirubin ?

A

Yellow

121
Q

What substance accumulates in jaundice?

A

Bilirubin

122
Q

What is bilirubin

A

Breakdown product of heme

123
Q

Where is bilirubin formed ?

A

All cells

124
Q

Where is bilirubin removed ?

A

In liver via bile

125
Q

How does bilirubin get from tissue to liver?

A

Via albumin

126
Q

What is jaundice ?

A

Build up of bilirubin in blood due to disruption of bile flow

127
Q

What is dystrophic calcification?

A

Local deposit of calcium salts within tissue

128
Q

Is dystrophic calcification caused by abnormal calcium metabolism/abnormal phosphate/abnormal serum calcium concentrations

A

No

129
Q

What is dystrophic calcification?

A

Local deposits of calcium salts in tissue

130
Q

Give 2 examples of dystrophic calcification

A
  • atherosclerosis

- calcified heart valves

131
Q

How is dystrophic calcification formed

A

Nucleation of hydroxyapatite crystals

132
Q

What is metastatic calcification?

A

Hydroxyapatite crystals deposited in tissue throughout the whole body

133
Q

What type of crystals are deposited in calcification of tissues ?

A

Hydroxyapatite crystals

134
Q

How does metastatic calcification occur?

A

Secondary to disturbances in calcium metabolism/ as a result of hypercalcaemia

135
Q

What does the parathyroid hormone do?

A

Increases calcium in the blood

136
Q

What are two causes of hypercalcaemia ?

A
  • increased secretion of parathyroid hormone (parathyroid tumour, renal failure)
  • destruction of bone tissue (cancer, Paget’s disease)
137
Q

What is pagets disease?

A

Excessive breakdown and formation of bone followed by disorganised bone remodelling

138
Q

When does an ageing somatic cell stop dividing?

A

When telomeres reach a critical length

139
Q

Which type of cells contain the enzyme telomerase ? What does telomerase do?

A

Germ cells, stem cells, some cancer cells

Maintains original length of telomeres

Pathological Processes (3 decks)

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