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ESA 2 > MOD 1.1 - Cell Injury > Flashcards

MOD 1.1 - Cell Injury Flashcards

1
Q

What can cause cell injury/death? (7)

A
  • Hypoxia
  • Toxins
  • Physical agents e.g. temperature extremes
  • Radiation
  • Micro-organisms
  • Immune mechanisms e.g. allergic responses
  • Dietary deficiencies
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2
Q

What happens during hypoxia?

A
  • Area/body is deprived of Oxygen

- Decreases the rate of aerobic respiration

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3
Q

What are the four types of hypoxia?

A
  • Hypoxaemic Hypoxia
  • Anaemic Hypoxia
  • Ischaemic Hypoxia
  • Histiocytic Hypoxia
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4
Q

Describe hypoxaemic hypoxia

A

Low arterial oxygen content

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5
Q

Describe anaemic hypoxia

A

Compromise in ability of haemoglobin to transport Oxygen

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6
Q

Describe ischaemic hypoxia

A

Interruption of blood supply

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7
Q

Describe histiocytic hypoxia

A

Oxygen can’t be used due to disabled oxidative phosphorylation enzymes

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8
Q

Describe Ischaemia

A
  • Loss of blood supply

- More serious as substrate as well as oxygen is lacking

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9
Q

What are the two immune mechanisms for cell injury? Describe them

A
  • Hypersensitivity = Host tissue is injured after an over vigorous immune reaction
  • Autoimmune = Immune system can’t distinguish self from non-self
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10
Q

Give 3 effects of the decrease in oxidative phosphorylation and therefore decrease in ATP as a result of ischaemic hypoxia

A
  • Activity of Na+-K+ pump decreases therefore more Na+ and H20 in the cell which causes swelling, blebbing and oncosis
  • Increases amount of Ca2+ in the cell
  • Increases rate of Glycolysis which decreases pH and Glycogen therefore causing nuclear chromatin clumps
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11
Q

Describe the effects of an increase in cellular Ca2+

A

Activates enzymes such as:

  • ATPase
  • Phospholipase
  • Proteases
  • Endonucleases

(Irreversible effects)

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12
Q

What can cause non-ischaemic injury?

A
  • Extreme cold therefore leading to frostbite

- Free radicals

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13
Q

What is the fenton reaction?

A

Fe2+ + H2O2 ==== Fe3+ + OH- + OH. (free radical)

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14
Q

What is the Haber-Weiss Reaction?

A

O2- + H+ + H2O2 === O2 + H2O + OH. (free radical)

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15
Q

Give four mechanisms of protection against cell injury

A
  • Enzymes e.g. Catalase, Superoxide Dismutase
  • Free radical scavengers
  • Storage proteins e.g. transferrin
  • Heat shock proteins e.g. Ubiquitin
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16
Q

What are the reversible changes of cell oncosis that can be seen with electron microscopy? (4)

A
  • Blebbing
  • Swelling
  • Clumping of nuclear chromatin
  • Dispersion of ribosomes
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17
Q

What are the irreversible changes of cell injury that can be seen with electron microscopy? (4)

A
  • Myelin figures
  • Cell membrane defects
  • Rupturing of lysosomes
  • Pyknosis, karyorrhexis, karyolysis
18
Q

What are the reversible changes of oncosis that can be seen with light microscopy?

A

Decrease in pink cytoplasmic staining

19
Q

What are the irreversible changes of oncosis that can be seen with light microscopy?

A
  • Pyknosis (nuclear shrinkage)
  • Karyolysis (lack of nucleus)
  • Karyorrhexis (nuclear fragmentation)
20
Q

Define oncosis

A

Cell death with swelling, changes occur in injured cells prior to death

21
Q

Define necrosis

A

Cell death in living organisms where the morphological changes occur after a cell has been dead for some time. Leads to leakage of cell contents

22
Q

Define apoptosis

A

Cell death with shrinkage, happens due to a regulated intracellular program where the cell activates enzymes for its own nuclear DNA and protein degradation. Forms apoptotic bodies

23
Q

Which is ATP dependent/independent, necrosis or apoptosis?

A
  • Necrosis = ATP independent

- Apoptosis = ATP dependent

24
Q

What are the 4 types of necrosis?

A
  • Coagulative necrosis
  • Liquefactive necrosis
  • Caseous necrosis
  • Fat necrosis
25
Describe coagulative necrosis
- Protein denaturation is greater than active protease release - Forms a 'ghost outline' of cells
26
Describe liquefactive necrosis
- Enzyme release is greater than protein denaturation - Enzymatic digestion of tissues - Proteins lyse and dissolve
27
Where is liquefactive necrosis common and why?
- In the brain | - Lacks coagulative factors
28
Describe caseous necrosis
- Forms a structureless debris (no ghost outline) - Looks like cottage cheese - Closely associated with TB
29
Describe fat necrosis. Where is it most likely to happen?
- Destruction of adipose tissue - Increases lipase therefore increasing lipolysis - Fatty acids are released which react with Ca2+ therefore forming calcium salts - Happens in pancreas
30
What is gangrene? What are the types?
- Clinical term for necrosis that is visible to the naked eye - Dry necrosis = air exposure e.g. umbilical cord - Wet necrosis = infection e.g. septicaemia - Gas necrosis
31
What are the two types of infarction that cause necrosis?
- White | - Red
32
Describe the features of white infarction (3)
- No blood - No haemorrhage - Single blood supply
33
Describe the features of red infarction (3)
- Extensive haemorrhage - Venous insufficiency or reperfusion - Dual blood supply
34
What is the consequence of infarction and what does this depend on?
``` - Death Depends on: - Blood supply - Speed of ischaemia - Tissue involved - Oxygen content ```
35
Name 3 molecules released by injured/dying cells and give their effects
- Potassium (Can cause heart to stop) - Enzymes (time dependent i.e. small enzymes are first) - Myoglobin (indicator of renal failure)
36
Give the two types of apoptosis
- Intrinsic | - Extrinsic
37
Describe intrinsic apoptosis
- Mitochondria plays the central role - Increases permeability of membranes - Leads to cytochrome C leakage
38
Describe extrinsic apoptosis
- Death ligands bind to receptors on CSM | - Directly activates caspases
39
Give 5 examples of abnormal intracellular accumulations
- Water and electrolytes - Lipids e.g. cholesterol - Carbohyrdates - Proteins - 'Pigments' e.g. tattoos, bruising
40
What are the mechanisms for abnormal accumulations? (4)
- Abnormal metabolism - Changes in protein folding/transport - Enzyme deficiencies - Can't degrade phagocytosed particles

ESA 2 (63 decks)

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