Pathology 4: Cell injury 2 Flashcards

1
Q

What are mechanisms of cell injury?

A

ATP Depletion
Membrane damage
Metabolic disturbance
Genetic damage

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2
Q

What does mitochondrial damage lead to?

A
  • Leakage of proapoptotic proteins (point of no return)
  • Decrease of ATP with multiple downstream effects
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3
Q

Effects of Ca2+ entry from damage of ions pumps

A
  • Increase of mitochondrial permeability
  • Activation of multiple cellular enzymes
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4
Q

Increased in ROS (Reactive oxygen species)

A

ROS: Metabolites lead to
Damage to lipids, proteins, DNA

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5
Q

Damage to membrane

A

Plasma membrane damage:
- Loss of cellular components
Lysosomal membrane damage:
- Enzymatic digestion of cellular components

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6
Q

Effects of protein misfolding and DNA damage

A

Activation of proapoptotic proteins

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7
Q

9 causes of cell injury

A
  • Oxygen deficiency
  • Physical damage
  • Infectious agents
  • Nutrition imbalance
  • Genetic damage
  • workload imbalance
  • Toxic damage
  • Immune dysfunction
  • Aging
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8
Q

What is ischemia?

A

Impairment in blood supply to the tissue.
- Physical or mechanical barrier of bloody supply to tissue.
- No O2 or glucose delivered and no water removed.

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9
Q

Infarction

A

Death of tissue related to ischemia

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10
Q

Oxygen deficiency leads to

A

Hypoxia
Ischemia

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11
Q

Types of physical damage

A

Trauma
temp extremes
radiation/electricity

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12
Q

Workload imbalance can lead to

A

Hypertrophy
Hyperplasia
Atrophy

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13
Q

What is hypoxia? Example?

A

Lack of oxygen (anemia)

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14
Q

Causes of toxic damage

A

Chemicals: drugs, toxins

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15
Q

Name of reversible cellular injury- morphologic features

A

Hydropic degeneration

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16
Q

Hydropic degeneration

A
  • Increased cell size/volume
    -Cytoplasmic vacuolation (swollen mitochondria, ER, and Golgi)
17
Q

What happens when reversible cell injury is becoming irreversible

A

Acute cell swelling can lead to death

18
Q

What is necrosis

A

Cell death of injury by hypoxia, ischemia, cell membrane damage

19
Q

Acute swelling effects

A

Swelling can lead to necrosis and point of no return is unclear.
- Restoring O2 supply can lead to free radical creation.

20
Q

Cell membrane damage due to

A

Chemical injury
Free radical injury

21
Q

Anti-oxidant protective mechanisms to avoid free radical injury

A
  • Superoxide dismutase (SOD)
  • Glutathione peroxidase
  • Vitamins E,C
22
Q

What is Ischemia-reperfusion injury

A
  • continued damge to tissue following restoration of blood supply to ischemic tissue
  • Generation of ROS
  • Ca2+ influx, impaired ion pumps
23
Q

Histologic changes for necrosis

A
  • Cytoplasmic hypereosinophilia
  • Nuclear changes: Pykonsis, Karyorrhexis, karyolysis
24
Q

What is pyknosis?

A

Nucleus: shrunken, dark, round

25
Q

What is karyorrhexis?

A

Nuclear fragments

26
Q

What is karyolysis?

A

Pale nucleus (dissolution of chromatin)

27
Q

Necrosis: morphologic types- gross appearance

A
  • Coagulation necrosis
  • Caseous necrosis
  • Liquefactive necrosis
  • Gangrenous necrosis
  • Fat necrosis
28
Q

What is Coagulation necrosis?

A

The tissue is dead but the outline of the architecture remains in place

29
Q

What is Caseous necrosis?

A

Cheese-like fibrous decay. A lot of leukocytes/WBC fo inflammation response

30
Q

What is Liquefactive necrosis?

A

Often in brain, Softening of brain = Malacia

31
Q

What is Gangrenous necrosis?

A
  • Occurs in the extremities or skin from loss of blood supply
    Wet: heavy, wet, full of blood and edema
    Dry: usually distal limbs becoming leather-like
32
Q

What is Fat necrosis?

A

Will Saponify- Chalky white development of fat.