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ESA 2 MoD > Session 1 - Cell Injury 1 > Flashcards

Session 1 - Cell Injury 1 Flashcards

Cell Injury 1

1
Q

Define disease

A

A consequence of failed homeostasis with morphological and functional disturbances

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2
Q

Define cell injury

A

When a cell reach or exceed their limits of adaptive response showing reversible injury or irreversible injury and death

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3
Q

What does the degree of injury depend on?

A

The type, duration and severity of injury and type of tissue

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4
Q

Causes of cell injury? (7)

A
  • Hypoxia
  • Physical agents e.g. trauma, temperature, pressure, electricity, radiation
  • Chemical agents and drugs
  • Micro-organisms
  • Immune (hypersensitivity e.g. uticaria or autoimmune e.g. Grave’s)
  • Dietary insufficiency and excess
  • Genetic abnormalities
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5
Q

What is hypoxia and how is it damaging?

A

Oxygen deprivation. Decreased aerobic oxidative respiration results in atrophy, injury or death.

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6
Q

Causes of hypoxia? (4)

A
  • Hypoxaemic hypoxia - arterial content of oxygen is low
  • Anaemic hypoxia - decreased ability of haemoglobin
  • Ischaemic hypoxia - interuption to blood supply
  • Histotoxic hypoxia - cells cannot use oxygen, disabled oxidative phosphorylation enzymes (cyanide)
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7
Q

Targets of cell injury? (4)

A
  • Membranes
  • Nucleus
  • Proteins (cytoskeleton + enzymes)
  • Mitochondria
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8
Q

Mechanism of reversible hypoxic injury?

A

Decreased ATP ( Na+ K+ pump fails)

  • -> increase in intracellular Na+ (swelling) -> Increased Ca2+ -> damage
  • -> anaeobic glycolysis -> lactic acid -> lower pH (affects enzymes + chromatin clumping)
  • -> Ribosomes detach from ER -> less protein synthesis -> contributes to intracellular accumulations
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9
Q

Mechanism of irreversible hypoxic injury?

A
  • Disturbances of membrane integrity and high Ca2+ accumulation (damaged plasma & lysosomal membrane + release from ER and Mitochondria)
  • Ca2+ causes: activation of enzymes (ATPases, Phospholipases, proteases, endonucleases)
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10
Q

How do we test for cell injury?

A

When membranes are damaged, intracellular substances leak into circulation -> detected in blood

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11
Q

What is ischaemia-reperfusion injury?

A
  • When blood flow is returned to a tissue that has been ischaemic but not necrotic, injury can be worse.

This is due to:

  • More ROS
  • More neutrophils
  • Complement pathway
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12
Q

When are free radicals produced? (4)

A
  • Chemical and radiation injury
  • ischaemia-reprefusion injury
  • cellular aging
  • high oxygen concentrations
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13
Q

How are free radicals damaging?

A

Attack lipids (lipid peroxidation) and damage proteins and nucleic acids, mutagenic

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14
Q

Name (3) free radicals

A
  • OH• (most dangerous),
  • H202 (Hydrogen peroxide),
  • O2- (superoxide)
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15
Q

How can OH• be formed?

A
  • Radiation of water
  • Fenton and Haber-Weiss reactions (SEE NOTES)
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16
Q

What antioxidants exist?

A
  • SOD (superoxide dismutase)
  • Catalase and peroxidases (H2O2)
  • Vitamins ACE, GSH, NADPH
  • Transferrin and ceruloplasmin sequester transition metals
17
Q

What are heat shock proteins?

A

These proteins upkeep cellular proteins (ensure proteins are refolded correctly)

18
Q

Cell morphology (light microscopy) - Describe cytoplasmic changes

A
  • reduced pinks staining (increased water) followed by increased pink staining (accumulation of proteins)
19
Q

Cell morphology (light microscopy) - Describe nuclear changes

A
  • Chromatin clumped (reversible)
  • Pyknosis (shrinkage), Karyorrhexis (fragmentation), Karyolysis (dissolution)(Irreversible)
  • Abnormal intracellular accumulations
20
Q

Cell morphology (electron microscopy) - Describe reversible changes

A
  • Swelling (Na+ K+ pump failure)
  • Cytoplasmic blebs (swelling)
  • Clumped chromatin (reduced pH)
  • Ribosome separation from ER
21
Q

Cell morphology (electron microscopy) - Describe irreversible changes

A
  • Further cell swelling
  • Nuclear (Pyknosis, karyorrhexis, karyolysis)
  • Swelling and rupture of lysosomes
  • Membrane defects
  • Myelin figures (on membrane)
  • ER lysis
  • Amorphous densities in swollen mitochondria
22
Q

How long can a neurone tolerate hypoxia?

A

A few minutes

23
Q

How long can a dermal fibroblast tolerate hypoxia?

A

A number of hours

24
Q

How do ROS damage cells?

A

cross-linking proteins

oxidising membrane lipids

ESA 2 MoD (5 decks)

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