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Miscellaneous > MCB Lecture 56 Changes to Cells > Flashcards

MCB Lecture 56 Changes to Cells Flashcards

0
Q

What are the features of physiological adaptations?

A

This is a cellular response to a normal stimulus in the body

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1
Q

What are the two types of adaptation?

A

Physiological and Pathological

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2
Q

What are two examples of physiological adaptation?

A 
Hormonal
Endogenous chemical (proteins)
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3
Q

What are the features of pathological adaptation?

A

This is a stress response in the cells to avoid injury

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4
Q

What are the reversible changes that cells undergo?

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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5
Q

What is hyperplasia?

A

This is the increase in number of cells

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6
Q

What is hypertrophy?

A

This is an increase in the size of cells

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7
Q

Which types of cells undergo hyperplasia? Compare with hypertrophy

A

Hyperplasia: labile or stable cells; ie able to enter the cell cycle and replicate
Hypertrophy: cells that cannot re-enter the cell cycle, Permanent cells

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8
Q

By what mechanism do cells undergo hypertrophy?

A

They increase in size by increasing the amount of stuff inside the cells (protein, organelles)

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9
Q

By what mechanism do cells undergo hyperplasia?

A

Growth factors acting on:

a. Mature cells
b. Stem cells

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10
Q

What is an example of hypertrophy?

A

Increase in the size of muscles in response to lifting weights

Increase in the size of the heart due to hypertension (pathological)

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11
Q

What is the stimulus for hypertrophy and hyperplasia?

A

Increased workload of the cells

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12
Q

What is atrophy?

A

Shrinking of the cells

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13
Q

Give some examples of how physiological and pathological adaptations result in hyperplasia

A

Physiological:

  • puberty
  • liver hepatocytes compensating
  • RBCs at high altitude

Pathological:

  • chronic injury eg. Callouses
  • hormonal: endometriosis
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14
Q

What is the mechanism that cells undergo for atrophy?

A

Decrease in amount of stuff in the cell (proteins, organelles)
Decrease in protein synthesis
Increase in protein degradation

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15
Q

What is the stimulus resulting in atrophy?

A

Decreased workload

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16
Q

Give some examples of stimuli that result in atrophy

A 
Immobilisation
Loss of innervation --> immobilisation
Loss of blood supply
Loss of endocrine stimulation
Inadequate nutrition
Ageing
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17
Q

What is metaplasia?

A

Replacement of one cell type with another that is supposedly more able to handle the stress

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18
Q

What is the mechanism for cells undergoing metaplasia?

A

The stem cell is reprogrammed to produce a different type of cell

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19
Q

Give some examples of cells undergoing metaplasia

A

Smoking, ciliated columnar cells are replaced with stratified squamous. These cannot beat up mucus and catch all the gross stuff

Chronic gastric reflux: stratified squamous replaced with columnar epithelial

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20
Q

What are the consequences of cell injury?

A

Recovery or death

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21
Q

What does failure to adapt cause?

A

Injury

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22
Q

What factors does irreversibility of injury rely on?

A

The features of the cell and the stimulus:
Cell:
- type: eg. Brain, skeletal, heart
- state: eg. Glycogen store
- adaptability
- genetics: eg. What sort of toxin metaboliser does the cell produce? (Cytochrome P450)

Stress: duration, severity, type

23
Q

Describe what happens to function in reversible cell injury

A

There is a decrease in cell function

24
Q

Describe the time scale of loss of function and seeing morphological changes in irreversible cell damage

A

Loss of function ->
Death of cell ->
Morphological changes are only seen a while after the cell has died

25
Q

What are the ways we can see irreversible damage on a macroscopic scale?

A

Staining

The healthy tissue takes up the stain and the dead tissue doesn’t

26
Q

What are the ways we can see damage on a microscopic scale?

A

Haematoxylin and Eosin stain

27
Q

Describe the different staining of the haematoxylin and eosin stain

A

Haematoxylin:
Basic stain, nucleic acid takes up the stain, purple colour

Eosin:
Acidic stain, protein and cytoplasm takes up the stain, pink colour

28
Q

What things happen to the cell in reversible injury?

ER
mitochondria
Cell membrane
Nucleus

A

ER: swells
Mitochondria: swells
Cell membrane: blebs form
Nucleus: chromatin clumping

29
Q

What are the things that happen to a cell in irreversible injury?
Organelles
Nucleus
Membrane

A 
Mitochondria: severely swollen and dysfunctional, cytochrome c released into cytoplasm
ER: swollen, ribosome detach
Lysosomes: burst
Nucleus: fragmentation
Cell membrane: fragmentation
30
Q

What is the hallmark of irreversible cell injury?

A

Loss of mitochondrial function

31
Q

Describe the changes in ATP concentration in damaged cells

A

ATP concentration decreases because

  • mitochondria no longer make it
  • reduced blood flow (nutrients and O2)
32
Q

What causes acidosis?

What does acidosis lead to?

A

Acidosis is caused by a build up of lactic acid in the cell
This is caused by
- increased anaerobic respiration

33
Q

What causes ribosomes to detach?

What does this result in?

A

The swelling of ER due to increased ion influx into the cell

Results in a halt in protein synthesis

34
Q

What causes ion pumps to fail?

What does this result in?

A

Ion pumps require ATP
When this stops being produced, they can no longer pump ions
There is a net influx of ions (including calcium) into the cell

35
Q

What changes occur to mitochondria in cell injury?

A

Swell and lose their function
Cause: increase in calcium, ROS, lipid per oxidation

Cytochrome c is lost to the cytosol
Aerobic respiration can’t occur

36
Q

What happens to cytochrome c?

What does this then cause?

A

An influx of calcium to the cell causes cytochrome c to be lost from the mitochondria

This then causes the cell to undergo apoptosis

37
Q

What happens to calcium in cell injury?

A

Influx of calcium into the cytosol from outside the cell, the ER and the mitochondria

This

  • activates many proteins that start to degrade molecules in the cell
  • membrane damage
  • activates caspases
38
Q

What causes calcium concentration in the cell to rise?

A

Failure of the ion pumps which normally pump it out of the cell

39
Q

Describe how enzymes in the cell become activated, and what this then leads to

A

Enzymes become activated due to the influx of calcium the cell

This leads to degradation of many macromolecules

  • phospholipids of membrane degraded
  • membrane and cytoskeletal proteins degraded
40
Q

What causes membrane damage?

A
  • Action by phospholipases
  • action by proteases
  • lipid per oxidation by ROS
  • decrease in phospholipid recycling (no ATP)
41
Q

What does caspase activation lead to?

How is caspase activated?

A

Apoptosis

It is activated by increased cytosolic calcium

Cytochrome c release by the mitochondria

42
Q

What happens to reactive oxygen species during cell injury?

A

Normally they are neutralised by scavengers, but in cell injury, there is a decrease in scavenging, or an increase in ROS production

43
Q

What is the normal function of ROS?

A

Killing intracellular pathogens

Byproduct from respiration

44
Q

Which membranes are affected during cell injury?

A

Nuclear membrane
Plasma membrane
Lysosome
Mitochrondrial

45
Q

Hypoxia is an example of …

A

Irreversible cell injury

46
Q

What are the causes of hypoxia?

A 
Ischemia
Pneumonia
Anaemia
CO poisoning
Occlusion
47
Q

What are the direct consequences of hypoxia?

A

Decrease in aerobic respiration

Increase in anaerobic respiration

48
Q

What does decreased aerobic respiration lead to?

A

Decrease in ATP production

Decreased synthesis of macromolecules

49
Q

How can damage be characterised (ie either reversible or irreversible) during myocardial infarction?

A

Monitor the levels of proteins in the serum that should normally only be found inside the cell

50
Q

Which enzymes are released by my oxygen during MI?

A

Creating kinase

Contractile troponin

51
Q

Why is cytochrome P450 important?

A

Different individuals have different versions that are better able to metabolise toxins.

This is an example of genetics determining your susceptibility to cell injury

52
Q

Describe what happens in transient ischemia of the heart

A

Reversible

However, some loss of function

Due to the transiently non-contractile myocytes

53
Q

In hypoxia of the heart, decreased synthesis and increased digestion of macromolecules leads to …

A
  • Cell membrane damage

- Cytoskeleton damage

54
Q

Describe what damage ROS can do

When are ROS released? And from where?

A

ROS are released from the mitochondria
During pathological injury to cells, they aren’t scavenged, so they cause damage to cells

  1. Lipid peroxidation - disrupt cell membrane
  2. DNA oxidation - mutation and breaks
  3. Protein oxidation - loss of function
55
Q

Describe the appearance of heart cells after hypoxia damage

A

Eosinophilia: Increased eosin staining of the proteins in the cytoplasm

Oedema

Reduced nuclei (reduced haematoxylin staining)

Inflammatory cells

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