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ESA 2 - Pathological Processes > Session 1: Cell Injury > Flashcards

Session 1: Cell Injury Flashcards

1
Q

What kind of things can cause cell injury?

A
  • hypoxia
  • toxins
  • physical agents (direct trauma, extremes of temperature, changes in pressure, electric currents)
  • radiation
  • microorganisms
  • immune mechanisms
  • dietary insufficiency and deficiencies, dietary excess
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2
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia - decreased oxygen supply

Ischaemia - decreased blood supply (can lead to hypoxia)

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3
Q

What are the different types of hypoxia? (4)

A
  1. hypoxaemic hypoxia
  2. Anaemia hypoxia
  3. Ischaemic hypoxia
  4. Histiocytic hypoxia
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4
Q

What are the causes of hypoxaemic hypoxia?

A
  1. Reduced inspired pO2 at altitude

2. Reduced absorption secondary to lung disease

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5
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen

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6
Q

What are the causes of anaemia hypoxia?

A
  1. Anaemia

2. CO poisoning

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7
Q

What are the causes of ischaemic hypoxia?

A
  1. Blockage of a vessel

2. Heart failure

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8
Q

What is histiocytic hypoxia?

A

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

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9
Q

What causes histiocytic hypoxia?

A

Cyanide poisoning

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10
Q

How does the immune system damage the body’s cells? (2)

A
  1. Hypersensitivity reactions - host tissue is injured secondary to an overly vigorous reaction
  2. Autoimmune reactions - immune system fails to distinguish self from non-self
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11
Q

Which cell components are most susceptible to injury? (4)

A
  1. Cell membranes
  2. Nucleus - DNA
  3. Proteins
  4. Mitochondria
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12
Q

What is happening at a molecular level in hypoxia when there is reversible injury? (3)

A

Level of oxidative phosphorylation decreases - ATP levels decrease

  1. Na-K pump functioning decreases - Na+ influx and H2O increases -> Cellular swelling
  2. Glycolysis increases - Anaerobic respiration increases lactic acid - pH falls -> clumping of nuclear chromatin
  3. Detachment of ribosomes - protein synthesis decreases - lipid deposition (fatty liver)
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13
Q

What happens at a molecular level in prolonged hypoxia when there is irreversible injury? (4)

A

Increased cytosolic Ca2+ levels activates many enzymes

  1. ATPase - decreased ATP
  2. Phospholipase - membrane digested
  3. Protease - disruption of membrane and cytoskeletal proteins (cell shape changes)
  4. Endonuclease - nuclear chromatin damage
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14
Q

What are free radicals?

A

Reactive oxygen species - single unpaired electron in outer orbit (want to gain an electron)

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15
Q

Give three examples of free radicals.

A
  1. OH. (hydroxyl)
  2. O2- (superoxide)
  3. H2O2
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16
Q

Where are free radicals usually locked away in cells?

A

Mitochondria

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17
Q

How are free radicals produced? (5)

A
  1. Normal metabolic reactions - oxidative phosphorylation
  2. Inflammation - oxidative burst of neutrophils
  3. Radiation
  4. Contact with unbound metals in the body (iron - haemachromatosis)
  5. Drugs and chemicals (liver’s P450 system
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18
Q

How does the body control free radicals? (3)

A
  1. Anti-oxidant system - Vitamins A, C, E ‘neutralise’ them
  2. Metal carrier and storage proteins - eg. transferrin
  3. Enzymes (neutralise them) - eg superoxide dismutase
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19
Q

How do free radicals injure cells? (3)

A
  1. Oxidative imbalance
  2. Lipids in cell membranes targeted - causes lipid peroxidation -> autocatalytic chain reaction
  3. Oxidation of proteins, carbohydrates and DNA (mutagenic, carcinogenic)
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20
Q

How can a cell protect itself against injury?

A
  1. Heat shock proteins - ‘mend’ mis-folded proteins and maintain cell viability
  2. Unfoldases or chaperonins
  3. eg ubiquitin
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21
Q

What do injured and dying cells look like under a light microscope?

A
  • Injured: pale and swollen cytoplasm
  • pyknosis: eosinophilic cytoplasm, clumped proteins
  • karyorrhexis: nucleus broken up into bits
  • karyolysis: nucleus dissolves away
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22
Q

What does reversible injury look like under an electron microscope? (7)

A
  1. Blebs - cytoskeleton broken down by proteases
  2. Generalised swelling
  3. Clumping of nuclear chromatin
  4. Autophagy by lysosomes (leakiness)
  5. ER swelling
  6. Dispersion of ribosomes
  7. Mitochondrial swelling
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23
Q

What does irreversible injury look like under an electron microscope? (5)

A
  1. Rupture of lysosomes and autolysis
  2. Nucleus (pyknosis, karyorrhexis or karyolysis)
  3. Lysis of ER
  4. Defects in cell membrane (holes)
  5. Myelin figures
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24
Q

How can cell death be diagnosed?

A

Dye exclusion test - cells with the dye in them are dead

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25
Q

What is oncosis?

A

Cell death with swelling - spectrum of changes that occur in injured cells prior to death

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26
Q

What is necrosis?

A

Morphological changes that occur in a living organism after a cell has been dead some time - seen after 12-24 hours

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27
Q

What are the different types of necrosis? (4)

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat necrosis
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28
Q

What are some characteristics of coagulative necrosis? (2)

A
  1. Ischaemia of solid organs - lots of connective tissue

2. Protein clumping

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29
Q

What are some characteristics of liquefactive necrosis? (4)

A
  1. Loose tissues
  2. Presence of neutrophils (infection)
  3. Enzyme release (lysosomes)
  4. More Destruction rather than clumping
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30
Q

What does coagulative necrosis look like?

A

Cellular architecture somewhat preserved - “ghost outline” of cells

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31
Q

What does coagulative necrosis look like under a microscope?

A
  • very pink staining of protein clumps
  • cant see nuclei properly
  • karyolysis
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32
Q

What is caseous necrosis?

A
  • ‘Cottage cheese’ appearance
  • between coagulative and liquefactive necrosis
  • characteristic of tuberculosis
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33
Q

What does fat necrosis look like?

A

Little drops of wax

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34
Q

What is gangrene?

A

Necrosis visible to the naked eye

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35
Q

What is an infarction?

A

Ischaemic hypoxia results in reduced arterial blood flow (infarction) which leads to necrosis

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36
Q

What is an infarct?

A

Area of necrotic tissue

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37
Q

What is dry gangrene?

A

Coagulative necrosis modified by exposure to air

38
Q

What is wet gangrene?

A

Liquefactive necrosis modified by infection

39
Q

What is gas gangrene?

A

Wet gangrene where the infection is with anaerobic bacteria that produce gas

40
Q

What are the causes of infarction?

A
  1. Thrombosis
  2. Embolism
  3. External pressure on vessels
41
Q

When are infarcts white?

A
  • Mostly in coagulative necrosis
  • solid organs
  • occlusion of an end-artery
42
Q

When are infarcts red?

A
  • mainly in loose tissue
  • dual blood supply
  • anastomoses
  • prior congestion
  • raised venous pressure
  • reperfusion
43
Q

What is ischaemia-reperfusion injury?

A

Blood flow returned to damaged tissue results in worse damage than if blood flow wasn’t returned

44
Q

What are the causes of ischaemia-reperfusion injury?

A
  1. Increased production of free radicals
  2. Increased number of neutrophils - inflammation
  3. Delivery of complement proteins
45
Q

Which important substances leak out of cells? (3)

A
  1. Potassium
  2. Enzymes
  3. Myoglobin
46
Q

What is apoptosis?

A

Programmed cell death with shrinkage, induced by regulated intracellular program where a cell activates enzymes that degrade it’s own nuclear DNA and proteins

47
Q

List the characteristics of apoptosis. (4)

A
  1. Equal and opposite force to mitosis
  2. Enzymes activated that degrade nuclear DNA and protein
  3. Membrane integrity is maintained
  4. Lysosomal enzymes not involved
  5. Can be pathological or physiological
48
Q

When does apoptosis occur physiologically? (2)

A
  1. Hormone-controlled involution - ovaries smaller in menopausal women
  2. Embryogenesis - cells between fingers-to-be undergo apoptosis
49
Q

When does apoptosis occur pathologically? (3)

A
  1. Cytotoxic T cell killing of virus infected or neoplastic cells
  2. Damaged cells (particularly DNA damage)
  3. Graft vs host disease (eg bone marrow transplant)
50
Q

Describe the process of apoptosis visually. (4)

A
  1. Normal cell
  2. Condensation (shrinking)
  3. Fragmentation
  4. Apoptotic bodies - budding (equal sized fragments)
51
Q

What are the 3 phases of apoptosis?

A
  1. Initiation
  2. Execution
  3. Degradation and phagocytosis
52
Q

How do initiation and execution of apoptosis occur?

A

Intrinsic and extrinsic mechanisms
Activation of caspases
- control and mediate apoptosis
- cause cleavage of DNA and proteins of cytoskeleton

53
Q

What triggers the intrinsic pathway (apoptosis)?

A
  • irreparable damage

- withdrawal of growth factors (eg ovaries in menopause)

54
Q

What happens in the apoptosis intrinsic pathway? (4)

A
  1. Triggered p53 activation
  2. outer mitochondrial membrane becomes leaky
  3. Mitochondria releases cytochrome C 4. activation of caspases
55
Q

What triggers the apoptosis extrinsic pathway?

How do they trigger this process?

A
  • Cells that are a danger - tumour cells, virus-infected cells
  • Display proteins on membrane detected by immune cells
56
Q

Why apoptotic bodies express proteins phagocytosed?

A
  • Apoptotic bodies express proteins on their surface

- Recognition by phagocytes or neighbouring cells

57
Q

What are the differences between apoptosis and oncosis? (3)

A
  1. Shrinkage and chromatin condensation (A) vs swelling (O)
  2. Budding (A) vs blebbing with disruption of cell membrane (O)
  3. No inflammation (A) vs inflammation (O)
  4. Single cells (A) vs Contiguous group of cells (O)
58
Q

What happens to a cell’s membrane in oncosis and apoptosis?

A

Oncosis - disrupted, early lysis

Apoptosis - intact

59
Q

When does fluid accumulate in cells?

A

Energy supplies cut off (eg hydroxia) - Hydropic swelling

60
Q

How does fluid accumulate in cells?

A

Na+ and water flood into cell

61
Q

Why is fluid accumulation a particular problem in the brain (cerebral oedema)?

A

Fluid sits in the skull which is a solid ‘cage’ - limited volume to expand into
Blood supply is compromised - increased pressure

62
Q

When do lipids accumulate in cells?

A
  1. Reduced function of liver (major organ of fat metabolism)
  2. Cholesterol not able to be broken down and is insoluble - excess stored in vesicles
    - steatosis (accumulation of triglycerides
63
Q

What are the causes of lipid accumulation in cells?

A
  1. Alcohol (reversible in about 10 days)
  2. Diabetes mellitus
  3. Obesity
  4. Toxins (eg carbon tetrachloride)
64
Q

Where is excess cholesterol accumulated and in which conditions?

A
  • atherosclerotic plaques: smooth muscle cells and macrophages
  • hereditary hyperlipidaemias: macrophages in skin and tendons (xanthomas)
65
Q

What do accumulated proteins in cells look like?

A

Eosinophilic droplets or aggregations in the cytoplasm

66
Q

In which conditions do proteins accumulate in cells?

A
  1. Alcoholic liver disease - damaged keratin filaments (Mallory’s hyaline)
  2. a1-antitrypsin deficiency
67
Q

When do (non-endogenous) pigments accumulate in cells?

A
  • Urban air pollutants - carbon/coal/dust/soot

- tattooing

68
Q

What happens as a result of accumulation of carbon/coal/dust/soot in the lungs? (Explanation + conditions) (4)

A
  • alveolar macrophages phagocytose the particles
    1. anthracosis (carbon in lungs)
    2. blackened peribronchial lymph nodes (macrophages migrate from alveoli to peribronchial lymph nodes
    3. Fibrosis - if in large amounts
    4. Emphysema (coal worker’s pneumoconiosis)
69
Q

What happens to tattoo pigments that are pricked into the skin?

A

Phagocytosed by macrophages in dermis and remains there

- some pigment reaches draining lymph nodes

70
Q

Name an endogenous pigment that can be accumulated.

A

Haemosiderin

71
Q

What is haemosiderin?

A

Iron storage molecule

- derived from haemoglobin, yellow/brown

72
Q

What can lead to haemosiderin being accumulated?

A

Systemic or local excess of iron - eg BRUISES

73
Q

In which clinical can haemosiderin be accumulated? (4)

A
  1. Haemosiderosis - systemic overload of iron
  2. Haemolytic anaemias
  3. Blood transfusion
  4. Hereditary haemochromatosis
74
Q

What is hereditary haemochromatosis?

A
  • genetically inherited disorder
  • results in increased intestinal absorption of dietary iron
  • iron deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas
  • ‘bronze’ diabetes
75
Q

What are the symptoms and treatment of/for hereditary haemochromatosis?

A
  • liver damage
  • heart dysfunction
  • multiple endocrine failures - especially of the pancreas
  • treatment: repeated bleeding
76
Q

What does hereditary haemochromatosis look like to the naked eye?

A

Very tanned skin

77
Q

What accumulates in jaundice?

A

Bilirubin

78
Q

What is bilirubin?

A

Breakdown product of heme, stacks of broken porphyrin rings

79
Q

Where is bilirubin produced?

A

Bilirubin is formed in all cells of the body because all cells contain cytochromes which contain heme

80
Q

Which carrier protein transports bilirubin in the body? Where is bilirubin transported to?

A

Albumin transports bilirubin from tissues to liver

81
Q

How does jaundice arise?

A

When bile flow is obstructed or overwhelmed, bilirubin in blood rises and results in jaundice

82
Q

Where is excess bilirubin deposited? (2)

A
  1. In tissues extracellularly

2. Macrophages

83
Q

What are the different mechanisms of intracellular accumulations? (4)

A
  1. Abnormal metabolism
  2. Alterations in protein folding and transport
  3. Substrate build-up - deficiency of critical enzymes
  4. Inability to degrade phagocytosed particles
84
Q

Where does dystrophic (local) calcification occur? (4)

A
  1. Area of dying tissue
  2. Atherosclerotic plaques
  3. Aging or damaged heart valves
  4. Tuberculous lymph nodes
85
Q

Why does dystrophic calcification occur?

A

A local change or disturbance in the tissue favours the nucleation of hydroxyapatite crystals

86
Q

Which type of calcification occurs due to abnormality in calcium metabolism or serum calcium or potassium concentrations?

A

Metastatic

87
Q

Why does metastatic calcification occur?

A

Due to hypercalcemia secondary to disturbances in calcium metabolism
- increased secretion of parathyroid hormone or
destruction of bone

88
Q

What causes hypercalcaemia?

A
  1. Increased secretion of parathyroid hormone (PTH) resulting in bone resorption
  2. Destruction of bone tissue
89
Q

Which cells can replicate indefinitely?

A

Germ cells

90
Q

Why can germ cells replicate indefinitely?

A

They contain telomerase - maintains the original length of telomeres

ESA 2 - Pathological Processes (4 decks)

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