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Pathology I > 2: Cell Injury > Flashcards

2: Cell Injury Flashcards

1
Q

cells are stressed so severely that they are no longer able to adapt when exposed to damaging agents or abnormal changes within

A

cell injury

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2
Q

a cell that is constantly replicating

A

labile

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3
Q

a cell that needs a signal to replicate

A

stable

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4
Q

MPD

A

membranes (cell and organelle)
protein
DNA

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5
Q

mitochondrial damage —>

A

1) decrease in ATP: multiple downstream effects

2) increase in ROS: damage to lipids, proteins and DNA

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6
Q

entry of Ca2+ —>

A

1) increase in mitochondrial permeability

2) activation of multiple cellular enzymes

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7
Q

membrane damage —>

A

1) PM: loss of cellular components

2) lysosomal membrane: enzymatic digestion of cellular components

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8
Q

protein misfolding, DNA damage —->

A

activation of pro-apoptotic proteins

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9
Q

5 major biochemical mechanisms of cell injury

A
  • influx of calcium into the cell and loss of calcium homeostasis
  • mitochondrial damage
  • depletion of ATP
  • accumulation of ROS
  • defects in membrane permeability
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10
Q

what is the downstream effect of increased mitochondrial permeability due to increased cytosolic Ca2+

A

decreased ATP

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11
Q

what cellular enzymes are activated by an increased cytosolic Ca2+

A
  • phospholipase, protease –> membrane damage
  • endonuclease —> nuclear damage
  • ATPase –> decreased ATP
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12
Q

3 things that cause damage to the mitochondria

A
  • increased calcium in cytosol
  • ROS
  • breakdown of phospholiipids
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13
Q

breakdown of phospholipids….

A

phospholipase A2 and sphingomyelin pathways may break down lipids.
- the breakdown products (FFA and ceramide) also damage mitochondria

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14
Q

How does H+ move in the CAC?

A

H+ is pumped out into the intermembrane space by ETC
H+ is taken in by the ATP synthase
( creation of energy ATP is dependent of H+ gradient in the mitochondria)

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15
Q

How is O2 important in the mitochondria?

A

it is the final electron acceptor

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16
Q

what mitochondrial attacks lead to necrosis v. apoptosis?

A

necrosis: decrease O2 supply, toxins, radiation
apoptosis: decrease survival signals, DNA or prtn damage

17
Q

necrotic mitochondrial changes

A

decreased ATP production

increased ROS production

18
Q

apoptotic mitochondrial changes

A

leakage of mitochondrial proteins

19
Q

What are the three specific changes in the cell caused by a decrease in ATP production?

A

1) decreased Na pump
2) increased anaerobic glycolysis
3) detachment of ribosomes

20
Q

decreased Na+ pump —>

A

increased influx of Ca2+, H2O, and Na+, increased efflux of K+ ——> swelling (ER, cell, loss of microvilli, blebs)

21
Q

increased anaerobic glycolysis —>

A

decreased glycogen, increased lactic acid —> decreased pH —-> clumping of nuclear chromatin

22
Q

detachment of ribosomes –>

A

decreased protein synthesis

23
Q

mechanism of lipid peroxidation of membranes

A

double bond of unsaturated FA are attacked by oxygen-derived ROS–> peroxides formed —> peroxides react with membrane lipids —> damage and form more peroxides

24
Q

how is the self-sustaining peroxidation of membranes stopped

A

free radicals are captured by free radical scavengers

25
Q

examples of free radical scavengers

A

vitamin E (in membrane)
Vitamin C and A
Beta carotene

26
Q

what changes does oxidation cause in proteins

A
  • oxidation of side chains changes function/structure of proteins
  • formation of disulfide bonds leads to cross-linking
  • oxidation of some enzymes leads to inactivation
27
Q

how do ROS cause ss breaks in DNA?

A

ROS interacts with thymine to cause ss breaks in DNA

28
Q

SOD superoxide dismutase

A
  • in mitochondria

- converts O2 –> H2O2

29
Q

glutathione peroxidase

A
  • in mitochondria

- converts OH–> H2O2

30
Q

catalase

A
  • in peroxisomes

- converts H2O2 —> H2O and O2

31
Q

describe how PMNs use a respiratory burst of ROS to phagocytize bacteria

A
  • O2 to O2- with NADPH oxidase
  • O2- to H2O2 with SOD
  • H2O2 activates PMN granules, is converted to HOCl by myeloperoxidase, is converted to OH radical by Fe2+ (fenton rxn)
32
Q

________ prevents reacylationof phospholipids and diminishes synthesis so that the cell membrane can’t repair itself

A

lack of ATP

33
Q

what activates phoshpolipases in cytosol

A

damage to membrane permeability

34
Q

Observe:

  • swelling of ER and mitochondria
  • membrane blebs
  • clumping of chromatin
A

reversible cell injury

35
Q

Observe:

  • swelling of ER and loss of ribosomes
  • lysosome rupture
  • myelin figures
  • nuclear condensation
  • swollen mitochondria w/ amorphous densities
A

irreversible injury

Pathology I (12 decks)

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