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Foundations II > cell injury & death > Flashcards

cell injury & death Flashcards

1
Q

mitochondrial damage following cell injury

A

mitochondrial damage => formation of mitochondrial transition pore => loss of mitochondrial membrane potential and function

apoptotic pathway = leakage of apoptotic proteins from mitochondria

necrotic pathway = decreased ATP production and increased ROS

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2
Q

what kinds of molecular and biochemical changes occur as a result of cell injury?

A
  • decreased ATP generation
  • mitochondrial damage
  • Ca2+ influx
  • ROS accumulation
  • membrane permeability
  • DNA damage
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3
Q

increased membrane permeability following cell injury

A

damage to cell/lysosomal/mitochondrial membranes from:

  • ROS => lipid peroxidation
  • hypoxia => decreased phospholipid synthesis
  • increased cytosolic Ca => protease and phospholipase activation
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4
Q

morphological changes in reversible cell injury visible (via light microscope and EM)

A

light:

  • cell swelling
  • eosinophilia
  • cytoplasmic vacuoles

EM:

  • cytoplasmic blebbing
  • microvilli loss
  • nuclear condensation
  • mild mitochondrial swelling
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5
Q

calcium influx following cell injury

A

increased cytosolic calcium from:

1) release from intracellular stores
2) influx across membranes

mitochondrial transition pore opens and enzymes (like ATPase) activate => less ATP

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6
Q

when does cell injury occur?

A

when a cell’s ability to adapt to a stress is exceeded; can be reversible or irreversible

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7
Q

gangrenous necrosis: cause and characteristics

A

cause: hypoxia/ischemia of the soft tissues of the lower limbs
characteristics: similar to coagulation necrosis

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8
Q

abnormal intracellular depositions and calcifications in cell injury/death

A
  • deposition of lipids (fatty liver)
  • deposition of abnormal proteins
  • lysosomal storage disease (endogenous materials)
  • accumulation of indigestible (exogenous) materials
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9
Q

fat necrosis: cause and characteristics

A

cause: alcohol/gall stones => hypersecretion => activated lipases generate FFA => saponification of FFA + Ca
characteristics: seen in pancreas, white chalky deposits

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10
Q

cellular changes in necrosis

A
  • cell swelling
  • eosinophilia (due to RNA loss)
  • glassy homogeneous pattern due to protein degradation
  • loss of nuclear material: karyolysis (loss of basophilia with DNase activity), pyknosis (nuclear shrinkage), karyorrhexis (fragmentation)
  • ghost like appearance
  • inflammatory response to clean up
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11
Q

morphological changes in irreversible cell injury visible (via light microscope and EM)

A

light:

  • absent nuclei
  • membrane disruption

EM:

  • disrupted cell membranes
  • swollen mitochondria
  • electron dense deposits
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12
Q

reperfusion injury

A

severe tissue damage following re-oxygenation after transient ischemia….burst of ROS => necrosis

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13
Q

characteristics of irreversible cell injury

A
  • mitochondrial swelling
  • accumulations of dense inclusions in mitochondria
  • nuclear changes
  • rupture of lysosomes and membranes
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14
Q

what kind of changes follow cell injury

A

molecular/biochemical => => => morphological

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15
Q

intrinsic apoptotic pathway

A

aka mitochondrial pathway

  1. cell injury
  2. BCL2 signalling
  3. mitochondrial destruction and release of pro-apoptotic proteins
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16
Q

liquefactive necrosis: cause and characteristics

A

cause: brain ischemia
characteristics: liquefaction - cell outlines not intact and no nuclei visible

17
Q

accumulation of ROS following cell injury

A

produced by injurious stimuli and lead to:

  • DNA damage/mutations
  • lipid peroxidation and membrane damage
  • protein modifications and misfolding
18
Q

fibrinoid necrosis: cause and characteristics

A

cause: immune reactions in blood vessels
characteristics: bright pink, amorphous appearance of vessel

19
Q

coagulative necrosis: cause and characteristics

A

cause: ischemia or exposure to toxic agents
characteristics: ghost cells - absent nuclei but outlines and cytoplasm still there

20
Q

what are some causes of cell injury?

A
  • oxygen deprivation
  • physical agents (trauma)
  • chemical agents (toxins, drugs)
  • infectious agents
  • immune system
  • genetic disease (polymorphism causing a different response to injury)
  • nutritional abnormalities
21
Q

DNA damage following cell injury

A

DNA damage => triggering of death pathways

22
Q

extrinsic apoptotic pathway

A

aka death receptor pathway

  1. receptor-ligand interactions
  2. signalling pathway activates caspases
23
Q

how does hypoxia impact pH?

A

pH decrease due to:

  • increased anaerobic glycolysis
  • reduced glycogen
  • increased lactic acid
24
Q

caseous necrosis: cause and characteristics

A

cause: tb
characteristics: granuloma forms with surrounding inflammatory cells

25
Q

characteristics of reversible cell injury

A
  • ATP depletion
  • inhibited protein synthesis
  • loss of glycogen
  • subtle membrane failure => cell swelling
26
Q

key differences of necrosis vs apoptosis

A

necrosis:
- death of groups of cells
- always pathologic
- causes inflammation
- no energy required
- random DNA degradation

apoptosis:
- death of single cells
- physiologic or pathologic
- no unregulated inflammation
- requires energy (protein synthesis + de novo transcription)
- nonrandom DNA fragmentation

27
Q

what happens when a cell does not have sufficient oxygen?

A
  1. decreased generation of ATP by the ETC
  2. failure of the Na+/K+ ATPase to maintain the membrane electrochemical gradient
  3. increased intracellular Na+ leads to fluid entry and cell swelling

separately, hypoxia => membrane damage

28
Q

cellular changes in apoptosis

A
  • cell shrinkage
  • cytoplasmic blebbing
  • chromatin condensation
  • fragmentation of nucleus
  • caspase degradation of DNA into ladder
  • phagocytosis

Foundations II (17 decks)

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