Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens during hypoxia?

A
  • Area/body is deprived of Oxygen

- Decreases the rate of aerobic respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the four types of hypoxia?

A
  • Hypoxaemic Hypoxia
  • Anaemic Hypoxia
  • Ischaemic Hypoxia
  • Histiocytic Hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe hypoxaemic hypoxia

A

Low arterial oxygen content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe anaemic hypoxia

A

Compromise in ability of haemoglobin to transport Oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe ischaemic hypoxia

A

Interruption of blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe histiocytic hypoxia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe Ischaemia

A
  • Loss of blood supply

- More serious as substrate as well as oxygen is lacking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the effects of an increase in cellular Ca2+

A

Activates enzymes such as:

  • ATPase
  • Phospholipase
  • Proteases
  • Endonucleases

(Irreversible effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can cause non-ischaemic injury?

A
  • Extreme cold therefore leading to frostbite

- Free radicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the fenton reaction?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the Haber-Weiss Reaction?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Describe coagulative necrosis

A
  • Protein denaturation is greater than active protease release
  • Forms a ‘ghost outline’ of cells
26
Q

Describe liquefactive necrosis

A
  • Enzyme release is greater than protein denaturation
  • Enzymatic digestion of tissues
  • Proteins lyse and dissolve
27
Q

Where is liquefactive necrosis common and why?

A
  • In the brain

- Lacks coagulative factors

28
Q

Describe caseous necrosis

A
  • Forms a structureless debris (no ghost outline)
  • Looks like cottage cheese
  • Closely associated with TB
29
Q

Describe fat necrosis. Where is it most likely to happen?

A
  • 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
Q

What is gangrene? What are the types?

A
  • 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
Q

What are the two types of infarction that cause necrosis?

A
  • White

- Red

32
Q

Describe the features of white infarction (3)

A
  • No blood
  • No haemorrhage
  • Single blood supply
33
Q

Describe the features of red infarction (3)

A
  • Extensive haemorrhage
  • Venous insufficiency or reperfusion
  • Dual blood supply
34
Q

What is the consequence of infarction and what does this depend on?

A 
- Death
Depends on:
- Blood supply
- Speed of ischaemia
- Tissue involved
- Oxygen content
35
Q

Name 3 molecules released by injured/dying cells and give their effects

A
  • Potassium (Can cause heart to stop)
  • Enzymes (time dependent i.e. small enzymes are first)
  • Myoglobin (indicator of renal failure)
36
Q

Give the two types of apoptosis

A
  • Intrinsic

- Extrinsic

37
Q

Describe intrinsic apoptosis

A
  • Mitochondria plays the central role
  • Increases permeability of membranes
  • Leads to cytochrome C leakage
38
Q

Describe extrinsic apoptosis

A
  • Death ligands bind to receptors on CSM

- Directly activates caspases

39
Q

Give 5 examples of abnormal intracellular accumulations

A
  • Water and electrolytes
  • Lipids e.g. cholesterol
  • Carbohyrdates
  • Proteins
  • ‘Pigments’ e.g. tattoos, bruising
40
Q

What are the mechanisms for abnormal accumulations? (4)

A
  • Abnormal metabolism
  • Changes in protein folding/transport
  • Enzyme deficiencies
  • Can’t degrade phagocytosed particles

ESA 2 (63 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions