40 - Cell Injury Flashcards

1
Q

do you know

A

review

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

What are some common causes of cell injury?

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

What is important in identifying cell injury?

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

How can cell injury be determined morphologically stage-by-stage?

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

How can reversible cell injury be identified morphologically?

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

What is ultrastructural morphology and how can it be identified? What are the functional consequences of the cell injury that results in ultrastructural morphology?

A

Ultrastructural morphology refers to the detailed examination of cellular structures at the electron microscope level. When cells are injured, either by physical, chemical, or biological factors, these alterations in ultrastructural morphology can provide important insights into the nature and extent of the injury.
* Cell membrane (blebs, loss of microvilli)
* Myelin figures (membrane-derived)
* Swelling of mitochondria and endoplasmic reticulum
* Detachment of ribosomes
* Nuclear chromatin clumping

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

What are the differences between necrosis and apoptosis?

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

What is the morphology of necrosis?

A
  • Increased eosinophilia (decreased RNA, protein
    denaturation)
  • Homogenization (glycogen depletion)
  • Dystrophic calcification
  • Nuclear changes (pyknosis, karyorrhexis, karyolysis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the types of necrosis? aka patterns of necrosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the features of coagulative necrosis?

A
  • Individual cell architecture preserved
  • Firm consistency (no significant tissue digestion)
  • Most commonly due to ischemia
  • Infarction
  • Gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the feature of liquefactive necrosis?

A
  • Individual cell architecture not preserved
  • Soft consistency (more extensive tissue digestion,
    many neutrophils)
  • May be purulent (abscess)
  • Bacterial infections
  • Brain involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the features of caseous necrosis? (think casein)

A
  • Individual cell architecture not preserved
  • White, friable (cheese-like) appearance
  • Central amorphous eosinophilic material with
    peripheral chronic inflammation (macrophages)
  • Granuloma
  • Most commonly due to tuberculosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the features of fat necrosis?

A
  • Occurs in adipose tissue (peripancreatic, soft tissues)
  • Activation of lipases (breakdown of fat)
  • Secondary calcification
  • Common causes include pancreatitis and trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the features of fibrinoid necrosis?

A
  • Occurs in blood vessel walls
  • Leakage of plasma proteins (fibrinogen) due to
    vascular injury
  • Zone of eosinophilic necrosis in vessel wall with
    surrounding inflammation
  • Commonly seen with vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are free radicals (ROS)? What are the most common ones? How do they cause cell injury?

A
  • Highly reactive oxygen-containing molecules (unpaired electrons)
    Most common: Superoxide, Hydrogen peroxide, Hydroxyl radicals, Peroxynitrite
  • Normal products of cell metabolism
  • Normal systems to neutralize free radicals
  • Injury causes increased ROS (oxidative stress)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does cell injury result in generally depending on the type of injury?

A
17
Q

What are some common ROS? How are they made? How are they inactivated? What are their effects?

A
18
Q

How are free radicals neutralized?

A
  • Superoxide dismutase (superoxide)
  • Glutathione peroxidase (hydroxyl radicals)
  • Catalase (hydrogen peroxide)
  • Other anti-oxidants (vitamins)
19
Q

What is reperfusion injury?

A