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Cell Injury Flashcards

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1
Q

Draw/describe cell injury/adaptation/death pathway

A 
HOMEOSTATIC CHANGE:
cell adapts to changed environment
- metaplasia
- hyperplasia
- atrophy
- hypertrophy

If cell can’t adapt to homeostatic change/if cell is injured:
CELL INJURY:
- cell membrane damage
- DNA damage/misfolded proteins
- increased ROS
- decreased ATP production/mitochondrial damage
- increased cytosolic calcium

REVERSIBLE INJURY:

  • cellular and organelle swelling (hydropic change/vacuolar degeneration)
  • fatty change

IRREVERSIBLE INJURY:

  • loss of ATP production
  • loss of membrane function
  • irreparable DNA/protein damage

CELL DEATH:

APOPTOSIS

  • physiological or pathological
  • programmed cell death
  • no leakage of intracellular material
  • no tissue reaction

NECROSIS

  • always pathological
  • leakage of intracellular material
  • tissue reaction
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2
Q

Cell injury

  • definition (3 general causes)
  • Factors affecting severity of cell injury (4); reasons some are reversible and irreversible (3 each)
A

Definition:

  • homeostatic change causes damage because:
    1) adaptational failure
    2) change causes inherent damage to cell
    3) abnormality??

Factors affecting severity:

  • nature of stimulus/abnormality
  • target of stimulus/abnormality
  • severity/duration of exposure
  • capacity for cellular adaptation

Reversible:

  • Minor damage to DNA/proteins/membrane
  • short duration of exposure
  • general target; no specific pathway damaged

Irreversible:

  • major damage to DNA/proteins/membrane
  • long exposure duration
  • specific pathway targeted
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3
Q

Mechanisms of Cellular Injury

  • what does the response to injury depend on?
  • what do consequences of injury depend on?
A
  • Cell response depends on nature, severity, and duration of exposure to stimuli
  • cell type, state, and adaptability
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4
Q

Cell injury timeline

  • point of no return?
  • irreversible injury features
A
  • no clear, consistent, singular molecular event. This is point at which homeostasis is lost
  • features of irreversible injury:
    1) loss of cell membrane function
    2) irreparable damage to DNA
    3) incapacity to produce ATP
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5
Q

Cell injury mechanism of injury (5)

A

1) mitochondrial damage: loss of ATP production; leakage of pro-apoptotic proteins
2) membrane damage: plasma membrane –> loss of cellular components; lysosomal membrane –> enzymatic digestion of cellular components
3) increased intracellular calcium: increase mitochondrial permeability; activation of enzymes
4) Protein misfolding and DNA damage: not enough cellular components; release of pro-apoptotic proteins
5) ROS: damage to lipids, DNA, and proteins

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6
Q

Reversible injury

- 2 components: list and describe

A

1) Swelling of cell
- First reaction to almost all cell injury
- Results in damage to cell membrane, pallor, distention (turgor), increased weight of organ
- Structural changes: Cell membrane changes, ER dilation, and nuclear alterations, mitochondrial changes

2) Steatosis
- Accumulation of triglycerides in parenchymal cells (the functional cells)
- causes: toxins, protein malnutrition, diabetes, obesity, anoxia
- Liver (alcohol and non alcohol fatty liver disease), heart, kidney, muscle

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7
Q

Reversible vs. Irreversible Injury

A
  • point of no return is not defined
  • no reliable morphologic or biochemical correlates of irreversibility
  • Irreversibility: inability to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATP generation); profound disturbances in membrane function (leaky membrane)
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8
Q

Necrosis

  • definition
  • stimuli
  • cause
A
  • pathological irreversible process and unregulated form of cell death resulting from damage to cell membranes and leak of cellular content eliciting inflammatory reaction
  • ischemia, toxins, infection, trauma
  • denaturation of intracellular proteins and enzymatic digestion of lethally injured cell
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9
Q

Necrosis Morphology

A
  • increased eosinophilia on stain due to destruction of cytoplasmic RNA
  • loss of glycogen particles
  • dilation of mitochondria, amorphous debris and aggregates of denatured protein
  • nuclear changes: karyolysis (loss of DNA); pyknosis (shrinkage of nucleus); karyorrhexis (nuclear fragmentation)
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10
Q 
Necrosis Patterns
List types (6)
A
  • Coagulative necrosis
  • Liquefactive necrosis
  • Gangrenous necrosis
  • Caseous necrosis
  • Fat necrosis
  • Fibrinoid necrosis
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11
Q

Coagulative necrosis

A
  • denaturing and coagulation of proteins within cytoplasm
  • preserved architecture of dead tissue, but loss of the nucleus
  • affected tissue is firm
  • localized area is called an infarct
  • e.g. myocardial infarction, renal infarction
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12
Q

Liquefactive necrosis

A
  • cellular destruction by hydrolytic enzymes
  • digestion of dead cells
  • transformation of tissue into liquid mass
  • pus (acute inflammatory cells)
  • e.g. hypoxic death of CNS
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13
Q

Gangrenous necrosis

A
  • combination of coagulative and liquefactive necrosis
  • soft
  • lost blood supply and necrosis
  • superimposed bacterial infection results in wet gangrene
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14
Q

Caseous necrosis

A
  • in foci of tuberculosis infection
  • microscopically: granulomatous inflammation - lysed cells and amorphous debris with collection of activated histiocytes (phagocytes) and inflammatory cells
  • soft, cheesy in appearance
  • *histiocytes at periphery (what make it a granuloma)
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15
Q

Fat necrosis

A
  • local areas of fat destruction
  • acute pancreatitis with release of activated lipase with split of triglyceride esters
  • free fatty acids combine with calcium (saponification)
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16
Q

Fibrinoid necrosis

A
  • immune reaction involving blood vessels

- antibody-antigen complex deposits in the wall of arteries (bright pink amorphous appearance on histology)

17
Q

Apoptosis

A
  • tightly regulated form of cell death through the degradation of nuclear DNA, nuclear and cytoplasmic proteins, with preservation of plasma membrane integrity and without eliciting an inflammatory response (unless it is pathologic and associated with tissue necrosis)
18
Q

Physiologic vs Pathologic apoptosis

A

Physiologic:
- eliminate cells that are no longer needed
- to maintain a steady number of various cell populations in tissues
- examples:
Embryogenesis: involution of hormone-dependent tissues due to hormone withdrawal
Cell loss in proliferating cells
Elimination of potentially harmful self-reactive lymphocytes
Death of host cells that finished their purpose (cells needed for damage repair; now done and don’t need; breast gets smaller after pregnancy)

Pathologic:
- Elimination of cells beyond repair limiting collateral tissue damage
- examples:
DNA damage
Accumulation of misfolded proteins
Cell death in certain infections
Pathologic atrophy in parenchymal organs after duct obstruction

19
Q

Morphologic changes in apoptosis

A
  • cell shrinkage
  • chromatin condensation - most characteristic feature of apoptosis
  • formation of cytoplasmic blebs and apoptotic bodies
  • phagocytosis of apoptotic cells or cell bodies (no inflammation)

Summary: reduced cell size, fragmentation of nucleus, cytoskeleton breakdown, preservation of cell membrane with packaging of cellular content, no inflammatory response

20
Q

Mechanisms of apoptosis

  • list 2 types
  • describe each
A

1) Intrinsic (mitochondrial) pathway
- the major mechanism of apoptosis in mitochondrial cells
- initiated by survival signals, mis-folded protein accumulation, and DNA damage
- increased permeability of the outer mitochondrial membrane with release of pro-apoptotic molecules in the cytoplasm, where they activate caspases (anti-apoptotic: bcl-2, mcl; pro-apoptotic: bax)
NORMAL: survival signal (growth factor) binds onto membrane receptor, anti-apoptotic signals like bcl made, bcl binds to mitochondrial membrane receptor, no leaking of cytochrome c
ABNORMAL: lack of survival signals, and cellular damage (ROS), production of sensors that antagonize bcl receptors, activation of bax/bak channel, leakage of cytochrome c, activation of caspases –> apoptosis

2) Extrinsic (death receptor initiated) pathway
- initiated by engagement of plasma membrane death receptors (TNF family) on a variety of cells
- responsible for elimination of self reactive lymphocytes (death receptors TNFR1 and a related protein Fas (CD95)
- the two pathways converge to a cascade of caspase (8 and 9) activation, which mediates the final phase of apoptosis

21
Q

Features of apoptosis vs. necrosis

  • cell size
  • nucleus
  • plasma membrane
  • cellular contents
  • adjacent inflammation
  • physiologic or pathologic role
A

Apoptosis:

  • shrinks
  • fragmentation into nucleosome-size fragments
  • stays intact; altered orientation
  • intact, may be released in apoptotic bodies
  • none
  • often physiologic, sometimes pathologic, especially for DNA damage

Necrosis:

  • enlarged (swelling)
  • shrinks and destroyed (pyknosis, karyorrhexis, karyolysis)
  • destroyed
  • enzymatic digestion, may leak out of cell
  • yes
  • always pathologic
22
Q

General describe process of necrosis and apoptosis

A

Necrosis:

  • cell swelling
  • membrane blebs
  • breakdown of membrane, organelles and nucleus, leakage of contents
  • inflammation

Apoptosis:

  • chromatin condensation
  • cell shrinkage
  • membrane blebs
  • cellular fragmentation into apoptotic bodies
  • phagocytosis of apoptotic cells and fragments
23
Q

Necroptosis

A
  • hybrid of necrosis and apoptosis
  • necrosis morphologically, and apoptosis mechanistically as a form of programmed cell death
  • triggered by litigation of TNFR1
  • caspase independent but dependent on signalling of RIP1 and RIP3
  • release of cellular contents evokes an inflammatory reaction as in necrosis
  • e.g. steatohepatitis, acute pancreatitis, reperfusion injury, etc
24
Q

Pyroptosis

A
  • occurs in cells infected by microbes
  • similar to apoptosis
  • activation of caspases 1/4/5 and 11 with activation of pyrogenic cytokine
  • cell death of infected cell
  • gasdermin is activated, and leads to the activation of caspases
  • gasdermin also creates pores in the cell membrane (leading to swelling and release of inflammatory factors)
  • the excessive release of inflammatory mediators (often in release to microbial infection) can lead to sepsis and septic shock
  • Therefore, gasdermin blocking may be new therapy for septic shock
  • gasdermin mutations are associated with genetic diseases suggests broad function of gasdermin

Cell Biology (7 decks)

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