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Pathology > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

what does the degree of cell injury depend on

A

type of injury, severity of injury and type of tissue

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2
Q

what is hypoxia

A

decreased oxygen supply

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3
Q

what is ischaemia

A

decreased blood supply

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4
Q

Give 4 causes of hypoxia

A
  1. Hypoxaemic
  2. Anaemic
  3. Ischaemic
  4. Histiocytic
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5
Q

what is hypoxaemic hypoxia

A

when the arterial content of oxygen is low e.g from reduced oxygen in higher altitudes

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6
Q

what is anaemic hypoxia

A

decreased ability of haemoglobin to carry oxygen

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7
Q

what is ischaemic hypoxia

A

interruption to blood supply

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8
Q

what is histiocytic hypoxia

A

inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

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9
Q

what type of hypoxia is cyanide poising an example of

A

histiocytic hypoxia

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10
Q

what 2 ways does the immune system damage the bodys cells

A
  1. Hypersensitivity reactions

2. Autoimmune reactions

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11
Q

what are hypersensitivity reactions

A

where the host tissue id injured due to an overly vigorous immune reaction

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12
Q

what is an autoimmune reaction

A

where the immune system fails to distinguish self from non self

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13
Q

which parts of the cell are most susceptible to injury

A

cell membranes, DNA, proteins and mitochondria

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14
Q

what happens during reversible injury caused by hypoxia

A

during a lack of oxygen there will be a lack of oxidative phosphorylation in the mitochondria decreasing atp production. This means the Na,K,ATPase stops. Na, Ca and water move into the cell. Ribosomes also detach from RER reducing protein synthesis. Glycolysis will increase, decreasing the pH of the cell.

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15
Q

why do you get a fatty liver in hypoxia

A

the ribosomes fall off RER, so hepatocytes cant make the proteins which metabolise fats so they accumulate in the liver cells

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16
Q

what happens if hypoxia is prolonged

A

there is a massive influx of calcium which activates enzymes such as:

  1. ATPase - so less ATP is produced
  2. Proteases - breaks down cytoskeleton
  3. Endonucleases - DNA is degraded
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17
Q

what are free radicals

A

reactive oxygen species with a single unpaired electron in their outer orbit

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18
Q

what is the most dangerous type of free radical

A

hydroxyl (OH)

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19
Q

what 3 free radicals are particularly significant in cells

A

hydroxyl, superoxide (O2-) and hydrogen peroxide

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20
Q

how are free radicals produced (5)

A
  1. oxidative phosphorylation
  2. Inflammation (neutrophils produce free radicals in oxygen dependant phagocytosis)
  3. radiation
  4. contact with iron or copper
  5. drugs
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21
Q

what is hemachromatosis

A

excess of iron

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22
Q

what is Wilson’s disease

A

excess of copper

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23
Q

how does the body control free radicals (3)

A
  1. vitamins A, C and E donate electrons to free radical
  2. metal carrier and storage proteins which bind to iron and copper
  3. enzymes neutralise free radicals
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24
Q

which metal carrier and storage proteins bind to iron and copper

A

transferrin and ceruloplasmin

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25
Q

what enzymes neutralise free radicals

A

superoxide dismutase, catalase

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26
Q

how do free radicals injure cells

A

causes lipid peroxidation, oxidises proteins, carbohydrates and DNA causing their shape to change and breakage of cross links

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27
Q

what is lipid peroxidation

A

when a free radical take an electron from a lipid, causing a chain reaction generating further free radicals

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28
Q

how do cells protect against injury

A

heat shock proteins try to help misfolded proteins reform (chaperone proteins)

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29
Q

give an example of a heat shock protein

A

ubiquitin

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30
Q

what is pyknosis

A

when the cytoplasm of injured cells looks very pink under a microscope as the proteins denature and clump together. the nucleus shrinks and become dull

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31
Q

what is karyorrhexis

A

when the nucleus begins to dissolves

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32
Q

what is karyolysis

A

when the nucleus is fully dissolved

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33
Q

what changes can be seen in reversible injury under an electron microscope

A

the cell swells and forms blebs as the cytoskeleton is broken down by proteases (due to calcium). The chromatin clumps. Lysosomes start to leak content. Ribosomes detach

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34
Q

what changes can be seen in irreversible cell injury under an electron microscope

A

lysosomes erupt releasing digestive enzymes, holes for in the membrane, nucleus dissolves and myelin figures form

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35
Q

how do you diagnose cell death

A

test their function. dead cells will have holes in their membrane so by putting cells in a dye and seeing which cells take up the die will show which cells are dead

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36
Q

what is oncosis

A

cell death with swelling

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37
Q

what is necrosis

A

the morphologic changes that occur after a cell has died (12-24 hours after)

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38
Q

what are the 2 main types of necrosis

A

coagulative and liquefactive

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39
Q

what are the 2 specialised types of necrosis

A

caseous and fat necrosis

40
Q

what causes coagulative necrosis

A

ischaemia of solid organs (organs with lots of CT support)

41
Q

what causes liquefactive necrosis

A

ischaemia of loose organs (e.g. the brain)

42
Q

what happens in coagulative necrosis

A

protein denature and clump, so cytoplasm looks more pink. Architecture of cells is preserved

43
Q

what happens in liquefactive necrosis

A

enzymes are released from lysosomes causing digestion of tissues

44
Q

what is caseous necrosis

A

necrosis associated with infections (TB). Cells break down and lose their architecture

45
Q

what is fat necrosis

A

when enzymes (especially digestive enzymes in the pancreas) break down lipids to give fatty acids which then react with calcium to from calcium soap depositions

46
Q

what does gangrene mean

A

necrosis visible to the naked eye

47
Q

what is an infarction

A

necrosis caused by the reduction of arterial blood flow

48
Q

what is an infarct

A

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

49
Q

what is dry gangrene

A

necrosis modified by exposure to air (form of coagulative necrosis)

50
Q

what is wet gangrene

A

necrosis modified by infection (form of liquefactive necrosis)

51
Q

what is gas gangrene

A

where there is a bacterial infection that produces gas inside tissues anaerobically

52
Q

what is a thrombosis

A

formation of a blood clot inside a blood vessel

53
Q

what is an embolism

A

where part of a thrombus breaks off and blocks a blood vessel

54
Q

why are some infarcts white

A

occlusion of end arteries to solid organs (coagulative necrosis) means theres no blood so the area looks white

55
Q

why are some infarcts red

A

there is occlusion of a vessel in loose tissue but because of the anastomoses other vessels supply blood to this area which leaks out

56
Q

what is ischaemia reperfusion injury

A

when blood flow is returned to damage tissue and results in increased production of free radicals, increased number of neutrophils (causes inflammation) and delivery of complement proteins

57
Q

what happens if potassium leaks out of cells

A

can stop the heart from beating

58
Q

when does myoglobin leak out of cells

A

when there’’s damage to skeletal muscle. the myoglobin then blocks the glomerulus in the kidney and leaks out the in the urine

59
Q

what is Rhabdomyolysis

A

break down of skeletal muscle

60
Q

what is apoptosis

A

cell death with shrinkage induced by regulated intracellular signals to activate enzymes to degrade its own DNA and proteins

61
Q

what is the characteristical DNA break down in apoptosis

A

DNA is cleaved inbetween nucleosomes giving similar lengths of DNA

62
Q

true or false: apoptosis is a passive process

A

false - its an active process

63
Q

what happens in apoptosis

A

enzymes degrade DNA and proteins. Membrane integrity is maintained, lysosomal enzymes are not involved. Budding occurs and the apoptic bodies break off

64
Q

when does apoptosis occur physiologically

A
  1. embryogenesis to form digits

2. in response to hormone levels

65
Q

when do apoptosis occur pathologically

A
  1. cytotoxic T cells killed infected cells
  2. when cells are damaged
  3. Graft versus host disease (bone marrow transplant is seen as foreign)
66
Q

which 2 mechanism initiate apoptosis

A

intrinsic and extrinsic

67
Q

what do the 2 mechanisms of initiating apoptosis result in

A

activation of caspases which are enzymes which cause DNA and protein cleavage

68
Q

how is intrinsic apoptosis carried out

A

triggered by signals inside the cells (DNA damage or withdrawal of hormones). this activates the p53 protein making the outer mitochondrial membrane leaky. Cytochrome C is released from the mitochondria causes activation of capases

69
Q

how is the extrinsic apoptosis carried out

A

trigger by extracellular signals including the TNF alpha signal which is secreted by T killer cells and binds to death receptors on the cell membrane which activates caspases

70
Q

why are apoptotic bodies phagocytosed

A

they have proteins on their surface which are recognised by phagocytes

71
Q

true of false: apoptosis is the death of groups of cells

A

false - this is necrosis. apoptosis is the breakdown of single cells

72
Q

what happens to the nucleus in necrosis

A

it undergoes pkinosis, karyorrhexis and karyolysis

73
Q

what happens to the nucleus in apoptosis

A

fragments

74
Q

what is hydropic swelling

A

accumulation of fluid in cells

75
Q

what causes hydropic swelling

A

energy supply is stopped so sodium and water flood into the cell causing swelling

76
Q

what is steatosis

A

accumulation of triglycerides

77
Q

where is steatosis normally seen

A

in the liver

78
Q

what causes steatosis

A

alcohol, diabetes, obesity and toxins

79
Q

what does steatosis look like under a microscope

A

white gap as the prep for the slide dissolves the fat

80
Q

what cells does cholesterol accumulate in

A

smooth muscle cells and macrophages

81
Q

what is xanthomas

A

accumulation of cholesterol in people with hyperlipidaemia

82
Q

when do proteins accumulate in cells

A
  1. alcoholic liver disease (Mallory hyaline)
  2. alpha1 antitrypsin deficiency - protein is folded properly so accumulates in ER. Means that proteases aren’t broken down
83
Q

what pigments can accumulate in cells

A
  1. soot - taken up by alveoli macrophages

2. tattoos - phagocytosed by macrophages in dermis and some pigment will reach lymph nodes

84
Q

what is haemosiderin

A

iron storage molecule which forms when there an excess of iron.

85
Q

what is haemosiderosis

A

deposition of haemosiderin in organs due to an overload of iron

86
Q

what are the symptoms of haemochromatosis

A

liver damage, heart dysfunction, endocrine failure (especially pancreas)

87
Q

what accumulates in jaundice

A

bilirubin (breakdown product of heme)

88
Q

how is bilirubin excreted

A

taken from tissues by albumin to the liver where its conjugated and excreted in bile

89
Q

how does bilirubin levels rise

A

when bile flow is obstructed

90
Q

what is dystrophic calcification of tissues

A

localised depositions of calcium salts

91
Q

what is metastatic calcification of tissues

A

deposition of calcium salts around the body

92
Q

why does dystrophic calcification occur

A

local changes causes production of hydroxyapatite crystals

93
Q

what causes metastatic calcification

A

hypercalcaemia caused by disturbances in calcium metabolism depositing hydroxyapatite crystals throughout the body

94
Q

what causes hypercalcaemia

A

1, increased secretion of the Parathyroid hormone resulting in bone resorption
2. destruction of bone tissue

95
Q

what enzyme do germ cells and stem cells contain that allow them to divide indefinitely

A

telomerase

Pathology (13 decks)

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