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MoD > Cell injury/death > Flashcards

Cell injury/death Flashcards

1
Q

how can cell injury be visualised?

A

gross appearance

microscopic features

ultrastructural features

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2
Q

intercellular Ca2+ levels ….. during cell injury. Why?

A

Increase

b/c of low ATP levels, low Ca pump activity, and plasma membrane damage

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3
Q

How does cellular pH change during cell injury?

A

pH decreases

due to failure of aerobic glycolysis, ditch to anaerobic glycolysis and build up of lactic acid.

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4
Q

how does fat necrosis occur?

A

adipocytes destroyed due to trauma or release of lipases from damaged pancreatic tissues

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5
Q

intracellular Na+ ….. during cell injury. Why?

A

increase

b/c low ATP disrupts na/K pump, water build up in cell

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6
Q

How is apoptosis regulated?

A

Genes

inhibitors - growth factors, sex steroids, ECM

inducers - viruses, loss of matrix attachment

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7
Q

what condition would you see Mallory hyaline?

A

Alchohol lover diesease

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8
Q

in apoptosis cell size is ……..

A

reduced

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9
Q

in apoptosis plasma membrane is ………

A

intact

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10
Q

in necrosis cell size is ……….

A

enlarged

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11
Q

in necrosis plasma membrane is ……….

A

disrupted

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12
Q

necrosis is a …….. cause of cell death

A

pathological

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13
Q

what 2 mechanisms can lead to cell death?

A

necrosis

apoptosis

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14
Q

what are capsizes?

A

family of protease enzymes

essential role in programmed cell death

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15
Q

examples of physiological apoptosis

A

embryogenesis/fetal development

death of cells that have served purpose

hormone dependent involution - shedding of lining during menstruation

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16
Q

what are heat shock proteins?

A

family of chaperone proteins

induced during environmental, physical or chemical stress

limit damage and facilitate cellular recovery

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17
Q

example of heat shock protein?

A

ubiquitin

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18
Q

examples of apoptosis inducers?

A

growth factor withdrawal

glucocorticoids

free radicals

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19
Q

examples of apoptosis inhibitors

A

growth factors

sex steroids

viral proteins

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20
Q

examples of chemical agents and drugs that can cause cellular injury

A

Cyanide

alcohol or therapeutic drugs

O2 in high concentrations

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21
Q

examples of dietary imbalance that could cause cellular injury

A

insufficiency - anorexia, malnourished

excess - obesity or diabetes

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22
Q

What are some examples of enzymes that Ca2+ activates in irreversible injury?

A

Proteases
phospholipases
endonucleases
ATPases

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23
Q

What are some examples of immunological reactions that can cause cellular injury?

A

self antigen reaction

hypersensivity reactions

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24
Q

examples of infections that can cause cell injury

A

Worms

viruses

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25
Q

examples of pathological apoptosis

A

Neoplasia

Autoimmune

AIDS

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26
Q

examples of physical agents that can cause cell injury

A

direct trauma

extremes of temperature

radiation

electric shock

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27
Q

What are the 2 pathways for apoptosis?

A

Extrinsic - external death receptors activated by ligand

Intrinsic - withdrawal of growth factors/hormones, molecules released form mitochondria

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28
Q

What are the 2 types of calcification?

A

Dystrophic

Metastatic

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29
Q

What are the 3 main effects at a cellular level of reduced ATP?

A

Reduced activity of Na+ pumps

Increased anaerobic glycolysis

detachment of ribosomes

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30
Q

What are the 3 phases of apoptosis?

A

initiation

execution

degradation/phagocytosis

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31
Q

What are the 3 stages of nuclear change in irreversible injury?

A

Pyknosis - nuclei condensed and dense

karyorrhexis- nuclei break into fragments

karyolysis - nuclei dissolved

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32
Q

What are the external receptors in extrinisic apoptosis?

A

Fas Receptor

TNF receptor

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33
Q

What are the type of necrosis?

A

Coagulative - protein denaturation
Liquefactive - degradation of tissue by enzymes
Caseous necrosis - chess like
Fat necrosis
Fibrinoid necrosis

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34
Q

What are the types of gangrene

A

wet gangrene - bacteria

Dry gangrene - air

Gas gangrene - gas forming bacteria

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35
Q

What are white deposits made of in fat necrosis

A

Fatty acids and calcium

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36
Q

What are white infarcts

A

Arterial insufficiency due to robust stromal support preventing haemorrahage entering necrotic area

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37
Q

what can cause a Hypoxaemic hypoxia

A

low arterial O2 content

high altitude

cardiorespiratory failure

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38
Q

What can cause an infarction

A

Thrombosis

Embolism

External compression of vessel

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39
Q

what can cause anaemic hypoxia

A

low O2 carrying capacity

anaemia

CO poisoning

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40
Q

causes of cell injury (7)

A

Hypoxia
chemical agents and drugs
Infections
immunological reactions
dietary imbalance
genetics
physical agents

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41
Q

what can cause histiocytic hypoxia

A

disabled oxidative phosphorylation

cyanide
paracetamol poisoning

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42
Q

what can cause hypoxia(4)

A

Hypoxaemic hypoxia
anaemic hypoxia
ischaemic hypoxia
histiocytic hypoxia

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43
Q

What can cause ischaemic hypoxia

A

interruption to blood supply

blocked vessel
heart failure

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44
Q

What can cause metastatic calcification

A

Parathyroid overactivity
Vitamin D overdose
Maligant tumour (PTHrp)
Prolonged immobilisation

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45
Q

What can occur to a cell that cannot adapt to a stress

A

Cell injury occurs

46
Q

What can occur to a cell that cannot adapt to a stress

A

Cell injury occurs

47
Q

What caspase do both extrinsic and intrinsic pathway for apoptosis activate

A

Caspase 3

48
Q

What colour urine seen in myoglobinuria

A

Brown

breakdown of muscle cause damage to kidneys

49
Q

What do the consequences of infarct depend on

A

if tissue has alternative blood supply

How quickly ischaemia occured

How vulnerable tissue is to hypoxia

Oxygen content of blood

50
Q

What factors released from mitochondria in intrinsic apoptosis

A

Bcl2
Bax
p53

51
Q

What is apoptosis

A

Energy dependant programmed cell death

52
Q

What is calcification

A

Abnormal deposition of calcium salts in tissues

53
Q

What is gangrene

A

clinical term to describe visible necrosis

54
Q

What is haemosiderin

A

iron storage complex
iron released from heme stored as haemosiderin

55
Q

What is infarction

A

obstruction of blood vessel to organ or region of tissue

56
Q

What is ischaemia-Reperfusion injury

A

Return of blood to ischemic tissue results in production of O2 -derived free radicals, which further damage tissue.

57
Q

What is mallory’s hyaline

A

Damaged protein seen in hepatocytes

58
Q

what is oncosis

A

Cell death with swelling which eventually leads to necrosis

59
Q

What is Steatosis

A

abnormal retention of fat (lipids) within a cell or organ

60
Q

What is the appearance in fibrinoid necrosis

A

Bright pink and amorphous appearance

61
Q

What is the apperance of caseous necrosis

A

Cheese like appearance

62
Q

What is the effect of detachment of ribosomes in cell injury

A

Decreased protein synthesis

lipid deposition

63
Q

What is the function of caspase 3

A

Cleave proteins leading to chromatin condensation
nuclear fragmentation and blebbing occurs

64
Q

What is the gross apperance in coagulative necrosis

A

Firm

Pale wedge of tissue

65
Q

What is the morphological hallmark of cell death?

A

Loss of the nucleus

66
Q

What is the morphological hallmark of irreversible cellular injury?

A

Membrane damage

67
Q

What is the morphological hallmark of reversible cell injury?

A

Cellular swelling

68
Q

most dangerous/reactive free radical?

A

Hydroxyl

69
Q

What is the only organ that does not yield coagulative necrosis following an ischaemic infarct?

A

Brain

70
Q

What is the role of Bcl2?

A

Prevent cytochrome C release from mitochondria hence inhibits apoptosis

71
Q

What molecules are released by cells due to cell injury and death

A

Potassium
Enzymes
myoglobin

72
Q

What molecules can accumulate intracellularly(5)

A

Water
lipids
proteins
carbohydrates
pigments

73
Q

What occurs if cell injury is severe and progressive

A

Irreversible injury occurs

74
Q

What occurs to a cell when the stress applied is mild

A

Injury can be reversible and homeostasis can be returned

75
Q

What pattern of necrosis is characteristic of pancreatitis-mediated damage of peripancreatic fat?

A

Fat necrosis

76
Q

What pattern of necrosis is characteristically seen in Tuberculosis?

A

Caseous necrosis; with granulomas

77
Q

What physiological process does hypoxia affect

A

Oxidative phosphorylation

78
Q

What structural changes occur in irreversible cell injury

A

membrane blebbing
lysosomes rupture
swelling of ER and loss of ribosomes
swollen mitochondria
nuclear condensation
myelin figures appear

79
Q

What structural changes occur in reversible cell injury

A

clumping of chromatin
swelling of ER and mitochondria

80
Q

What two main processes are seen in necrosis

A

Denaturation of intracellular proteins

Enzymatic digestion by lysosomes

81
Q

What type of free radical is made through inflammation?

A

Superoxide Ions via NADPH Oxidase action

Made during oxygen-dependent killing by neutrophils.

82
Q

What type of free radicals are formed via ionising radiation?

A

Hydroxyl (OH) free radicals

via hydrolysis of water

83
Q

What type of free radicals are made via the Fenton Reaction?

A

Hydroxyl radicals

via Fe2+

84
Q

What type of tissue calcification is associated with normal serum Ca?

A

Dystrophic calcification

Metastatic calcification occurs in normal tissue.
Dystrophic calcification occurs in necrotic tissue.

85
Q

What ultrastructural components of the cell are involved in morphological changes in cell injury?

A

Cell membranes
nucleus
proteins
mitochondria

86
Q

Where are lipofuscin granules usually seen

A

liver and heart

87
Q

Where can free radicals be produced from(5)

A

Chemical and radiation injury
ischaemia-reperfusion
Cellular ageing
high O2 concentration
Phagocytosis

88
Q

Where do red infarcts occur

A

Organs with dual blood supply

Organs with loose stromal support

89
Q

Where do red infarcts occur

A

Organs with dual blood supply

Organs with loose stromal support

90
Q

Where is caseous necrosis seen in

A

Granulomatous

inflammation

91
Q

Where is dystrophic calcification seen

A

necrotic tissue

92
Q

Where is fat necrosis seen

A

Breast tissue where it can mimic a breast tumour

Pancreas in pancreatitis where lipase released from pancreas

93
Q

Where is fibrinoid necrosis usually seen

A

immune reactions with blood vessels

94
Q

Where is liquefactive necrosis usually seen

A

Brain and abscess formation

95
Q

Which enzyme functions to eliminate H2O2?

A

catalase

96
Q

Which enzyme functions to eliminate Superoxide Radicals?

A

superoxide dismutase

97
Q

Which enzyme functions to primarily eliminate Hydroxyl radicals (OH)?

A

Glutathione peroxidase

98
Q

Which enzyme secreted by CD8+ T cells functions to create pores in the membrane of target cells

A

perforin

99
Q

Which enzyme secreted by CD8+ T cells functions to enter the pores made by Perforin and activate Caspases?

A

granzyme

100
Q

Which mechanism of cell death is always followed by acute inflammation?

A

necrosis

101
Q

Which mechanism of cell death is associated with shrunken cells with more eosinophilic cytoplasm?

A

apoptosis

102
Q

Which mechanism of cell death is not followed by acute inflammation?

A

apoptosis

103
Q

Which metabolic process is the source of physiological generation of free radicals?

A

oxidative phosphorylation

104
Q

Which organs are white infarcts commonly seen

A

heart
Spleen
kidney

105
Q

Why does a cell swell in reversible injury

A

Reduced activity of Na pump
Na accumulates in cell
H2O follows Na
H2O retained by cell

106
Q

Why is necrotic material in liquefactive necrosis creamy yellow

A

Presence of dead leukocytes and is called pus

107
Q

Why is rhabdomyolysis serious

A

Myoglobin produced as a breakdown product of muscle and causes damage to kidneys and eventually renal failure

108
Q

…….. is a protein that leaks out of the inner mitochondrial matrix when Bcl2 is inactivated.

A

cytochrome c

then activates capsize and starts apoptosis

109
Q

……..is a cause of decreased O2 carrying capacity that classically presents with cyanosis and chocolate-coloured blood.

A

Methaemoglobinaemia

involves oxidation of haem Fe2+ to Fe3+, which cannot bind to O2.

110
Q

……..is a phenomenon seen in fat necrosis that involves the release of fatty acids via trauma or pancreatic lipase and subsequent joining of Ca with those fatty acids.

A

Saponification

MoD (8 decks)

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