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Year 2 EMS MoD > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Who was the ‘father of cellular pathology’, and what did he discover?

A

Virchow.

-cell injury is the basis of all disease

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2
Q

What happens to normal cells when they are put under stress?

A

They adapt.

-inability to adapt&raquo_space; cell injury

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3
Q

What happens if cell injury is irreversible?

A

Necrosis / apoptosis.

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4
Q

What is necrosis?

A

Cell death caused by enzymatic degradation.

-passive/unprogrammed, due to lethal cell injury

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5
Q

What is apoptosis?

A

Programmed cell death in multicellular organisms.

  • active
  • physiological and pathological
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6
Q

What is the difference between hyperplasia and hypertrophy?

A 
HYPERPLASIA = increased cell reproduction rate.
HYPERTROPHY = increased cell size.
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7
Q

What do hyperplasia and hypertrophy both lead to?

A

Enlargement of an organ or tissue.

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8
Q

What is atrophy?

A

Wasting away of an organ or tissue due to cell degradation.

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9
Q

What is metaplasia?

A

Change in cell type to an abnormal type for that tissue.

-reversible and non-cancerous

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10
Q

What is dysplasia?

A

Proliferation of cells of an abnormal type.

-early stage of cancer and irreversible

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11
Q

What happens to the cell type in the exocervix at puberty?

A

Changes from columnar epithelium to squamous epithelium.

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12
Q

What is Barrett’s oesophagus an example of?

A

Metaplasia.

-replacement of normal squamous epithelium with columnar glandular epithelium due to gastric reflux.

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13
Q

Give an example of physiological atrophy?

-NB not always pathological

A

Organ formation in embryology.

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14
Q

What is an increase in bone marrow cells at high altitude an example of?

A

Physiological hyperplasia.

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15
Q

What is an increased size of skeletal and heart muscle an example of?

A

Physiological hypertrophy.

-increased cell size

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16
Q

What are the main causes of cell injury? (6)

A
  • O2 availability
  • Physical trauma
  • Chemical agents
  • Infectious organisms
  • Irradiation
  • Genetic disorders
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17
Q

What is the difference between hypoxia and anoxia?

A 
HYPOXIA = lack of oxygen. 
ANOXIA = absence of oxygen.
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18
Q

What is a common cause of hypoxia/anoxia?

A

Ischaemia.

-lack of blood flow

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19
Q

What is generated when ischaemic tissues are reperfused?

A

Oxygen free radicals.

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20
Q

How does cyanide work on cells?

A

Inhibits cytochrome c oxidase, meaning cells are unable to use oxygen.
» hypoxia

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21
Q

What are the main types of physical trauma? (2)

A
  • Mechanical trauma (e.g. thrombosis)

- Temperature extremes (e.g. heat denaturation)

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22
Q

How can chemical agents lead to cell injury?

A
  • Denaturation
  • Breakdown of macromolecules
  • Interference with cellular metabolism
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23
Q

What toxic metabolite forms if someone takes a paracetamol overdose?

A

N-acetyl-p-benzoquinone imine (NAPQI).

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24
Q

How is paracetamol overdose treated?

A

N-acetylcysteine (NAC).

-precursor for glutathione; promotes normal conjugation of any remaining paracetamol

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25
Q

What are the 2 types of toxins produced by bacteria?

A

Endotoxins and exotoxins.

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26
Q

What is the difference between endotoxins and exotoxins?

A

ENDOTOXINS - secreted by bacterial cells.

EXOTOXINS - contained within bacterial cells, and released when it degenerate.

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27
Q

How does C. difficile cause cell injury?

A

Bacteria that produces exotoxins.

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28
Q

What is molluscum contagiosum?

A

Skin lesions produced by a pox virus infection.

-virions accumulate in cells

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29
Q

How does ionisation cause cell injury?

A

Generation of free radicals

|&raquo_space; damage to macromolecules, proteins and nucleic acids.

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30
Q

Which organs have high sensitivity for ionisation? (3)

A
  • Bone marrow
  • Gonads
  • Intestines

NB. high cell poliferation rate

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31
Q

Which organs have low sensitivity for ionisation? (3)

A
  • Uterus
  • Adrenals
  • Pancreas
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32
Q

What are the main targets of cell injury? (5)

A
  • Mitochondrial function
  • Membrane integrity
  • Protein synthesis
  • Cytoskeleton
  • Genetic apparatus
33
Q

What does mitochondrial damage cause?

A

Decreased oxidative phosphorylation&raquo_space; decreased ATP.

34
Q

What are the main consequences of mitochondrial damage? (5)

A
  • Cellular and ER swelling
  • Loss of microvilli
  • Decreased glycogen
  • Clumping of nuclear chromatin
  • Lipid deposition
35
Q

How does mitochondrial damage lead to cellular swelling and loss of microvilli?

A

Decreased ATP
» decreased Na pump activity
»influx of Ca, H2O and Na, and efflux of K
» cellular swelling and loss of microvilli

36
Q

How does mitochondrial damage lead to decreased glycogen?

A

Decreased ATP
» increased glycolysis
»decreased glycogen

37
Q

How does mitochondrial damage lead to clumping of nuclear chromatin?

A

Decreased ATP
» increased glycolysis
» decreased pH (lactic acid)
» clumping of nuclear chromatin

38
Q

How does mitochondrial damage lead to lipid deposition?

A

Decreased ATP
» detachment of ribosomes
» decreased protein synthesis
» lipis deposition

39
Q

Are the effects of mitochondrial damage reversible?

A

Yes, with the restoration of normal blood flow.

40
Q

What is sublethal cell injury?

A

Injury that is insufficient to cause death.

41
Q

What are the sublethal effects of alcohol on liver cells?

A
  • Cell swelling

- Fat accumulation (steatosis)

42
Q

What are free radicals?

A

Highly reactive, uncharged molecules with an unpaired electron.

43
Q

How does free radical toxicity cause cell injury?

A

Free radicals
» chain reaction in membranes to produce more free radicals
» damage proteins and nucleic acids
» apoptosis

44
Q

What can detoxify free radicals?

A
  • Superoxide dismutase

- Antioxidants (e.g. vitamins A,C,E)

45
Q

What does killing of bacteria by neutrophils and macrophages depend on?

A

Formation of superoxide.

46
Q

How can membrane defects cause cell injury?

A

Increased Ca due to loss of membrane can activate enzymes&raquo_space; harmful effects.

47
Q

What are the main enzymes that Ca activates following membrane defects? (4)

A
  • ATPases
  • Phospholipases
  • Proteases
  • Endonucleases
48
Q

What is the effect of activating ATPases?

A

Faster ATP depletion.

49
Q

What is the effect of activating phospholipases?

A

Causes membrane damage.

50
Q

What is the effect of activating proteases?

A

Break down membrane and cytoskeleton proteins.

51
Q

What is the effect of activating endonucleases?

A

DNA fragmentation.

52
Q

What causes cell death?

A

Irreversible breakdown of interactions between DNA, membranes and enzymes.
-not always pathological

53
Q

Which is passive and unprogrammed; necrosis or apoptosis?

A

Necrosis.

54
Q

Which is active and programmed; necrosis or apoptosis?

A

Apoptosis.

55
Q

What causes necrosis and what does it lead to?

A
  • Caused by lethal cell injury

- Leads to an inflammatory reaction

56
Q

What are the main morphological types of necrosis? (5)

A
  • Coagulative
  • Colliquative
  • Caseous
  • Gangrene
  • Fat, fibrinoid
57
Q

What is the most common type of necrosis?

A

Coagulative.

-typical of ischaemic injury

58
Q

Which type of necrosis does TB cause?

A

Caseous.

59
Q

Which type of necrosis is found in the brain?

A

Colliquative.

60
Q

Which type of necrosis is described as ‘wet and dry’?

A

Gangrene.

61
Q

What is the process of coagulative necrosis formation?

A

Denaturation of intracytoplasmic protein
» dead tissue becomes firm/swollen
» cellular proteins may leak into blood

62
Q

What type of protein are denatured to form coagulative necrosis?

A

Intracytoplasmic proteins.

63
Q

How can coagulative necrosis be detected by a blood test?

A

Detection of cellular protein in blood.

-e.g. myocardial infarction&raquo_space; creatine kinase (MB subtype) and troponin T and I

64
Q

What is colliquative necrosis?

A

Necrotic tissue in the brain&raquo_space; neutrophils release toxins&raquo_space; total liquefaction to form a cyst.

65
Q

Why does brain injury lead to colliquative necrosis?

A

It does not have a collagenous tissue framework.

66
Q

What is caseous necrosis?

A

Cells destroyed and surrounded by granulomatous inflammation, lacking structure.

  • ‘cheese like’
  • characteristic of TB
67
Q

What is gangrenous necrosis?

A

Caused by a critically insufficient blood supply.

  • can be wet (e.g. bowel infarct) or dry (e.g. diabetes)
  • skin looks black/dead
68
Q

What is fat necrosis?

A

Damaged cells release lipases&raquo_space; chalky free fatty acids and calcium deposits.
-e.g. acute pancreatitis

69
Q

What is fibrinoid necrosis?

A

Immune reactions in vessels&raquo_space; thickened vessel walls.

70
Q

Give 3 examples of physiological apoptosis.

A
  • Embryogenesis
  • Elimination of self-reacting lymphocytes
  • Involution
71
Q

Give 3 examples of pathological apoptosis.

A
  • DNA/protein damage
  • Viral infections
  • Cell death by cytotoxic T-cells
72
Q

Where are apoptosis initiating factor (AIF) and cytochrome C normally located?

A

In mitochondria.

73
Q

What do apoptosis initiating factor and cytochrome C activate when released into the cytosol?

A

Capases,

  • final effector molecules of apoptosis
  • amplify cell signal
74
Q

What are the mechanisms of apoptosis?

A

Intrinsic and extrinsic pathways.

75
Q

What does apoptosis cause?

A

Cell becomes fragmented and pieces are phagocytosed.

-no inflammatory reaction

76
Q

What role does P53 play in apoptosis?

A

Activated by DNA damage and causes the elimination of damaged cells by apoptosis.

77
Q

How can mutation in P53 lead to cancer?

A

Allows cells to accumulate genetic abnormalities and become malignant.

78
Q

What role does Bcl-2 have in apoptosis?

A

Bcl-2 isolates cytochrome C&raquo_space; inhibits apoptosis.

79
Q

How can Bcl-2 lead to cancer?

A

Bcl-2 overexpression&raquo_space; tumours gain ability to proliferate in uncontrolled way.

Year 2 EMS MoD (20 decks)

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