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Pathophysiology I > 1 - Cell Injury & Death > Flashcards

1 - Cell Injury & Death Flashcards

1
Q

Define pathophysiology

A

study of disordered physiological processes associated with disease or injury

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2
Q

Define Etiology

A

why = cause of disease

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3
Q

Define pathogenesis

A

how = mechanisms of disease

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4
Q

What are 8 causes of cell injury

A
  • hypoxia (can lead to ischemia)
  • ischemia
  • toxins
  • infectious microbes
  • genetic abnormalities
  • abnormal immune reactions
  • nutritional imbalance
  • physical agents
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5
Q

What is ischemia?

A

absence/suppression of blood flow

decreased nutrients/O2 delivery

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6
Q

What are the 2 most common cause of cell injury?

A

hypoxia and ischemia

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7
Q

What are 3 causes of hypoxia?

A
  • decreased blood supply
  • decreased O2 carrying capacity of blood
  • decreased ATP production via oxidative phosphorylation
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8
Q

What is ischemia due to?

A

arterial blockage

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9
Q

What does Cytochrome P450 do?

A

detoxifies the exogenous chemicals or converts them into active metabolites

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10
Q

Where is Cytochrome P450 most active in?

A

endoplasmic reticulum of liver

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11
Q

What are 5 examples of physical agents that can cause cell injury?

A
  • mechanical trauma
  • temperature extremes
  • radiation
  • electric shock
  • sudden changes in atmospheric pressure
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12
Q

What is the sequence of events in cell injury?

A

healthy cell @ homeostasis&raquo_space; injurious stimulus&raquo_space; REversible injury&raquo_space; severe/progressive&raquo_space;» IRREversible injury&raquo_space;> cell death via necrosis or apoptosis

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13
Q

During the mechanism of cell injury, what does the cellular response depend on?

A
  • Injury = type, duration and severity
  • Cell = type, metabolic state, adaptability, and genetic makeup
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14
Q

What are 8 cell characteristics of reversible cell injury?

A
  • increased cell size
  • chromatin clumping
  • ER & mitochondria swelling
  • small amorphous deposits in mitochondria
  • membrane blebbing
  • myelin figures
  • pinched off ER segments (intracytoplasmic vacuoles)
  • detachment of ER ribosomes
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15
Q

What is hydropic change/vacuolar degeneration?

A

distended and pinched-off segments of the endoplasmic reticulum (ER)

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16
Q

What is the fatty change in reversible cell injury?

A

appearance of lipid vacuoles in cytoplasm (common in organs involved in lipid metabolism)

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17
Q

What are the 4 characteristics of IRReversible cell injury?

A
  • breakdown of plasma membrane, organelles, and nucleus
  • large amorphous deposits in mitochondria
  • content leakage
  • inflammation
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18
Q

When does irreversible cell injury occur?

A
  • inability to restore mitochondrial function = lose ability to store/make ATP
  • altered structure + loss of function of plasma and intracellular membranes
  • loss of structural integrity of DNA and chromatin
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19
Q

What are the 6 mechanisms of cell injury?

A
  • mitochondrial dysfunction
  • oxidative stress
  • membrane damage
  • disturbance in calcium homeostasis
  • ER stress
  • DNA damage
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20
Q

What are the 2 mechanisms of mitochondrial dysfunction?

A
  • decreased ATP generation and depletion
  • lack of ATP
21
Q

What is the mechanism of mitochondrial dysfunction via decreased ATP generation and depletion of ATP?

A

1) decreased ATP generation & ATP depletion&raquo_space;>
2) reduced activity of ATP-dependent plasma Na+ pumps&raquo_space;>
3) Na+ accumulates inside cell&raquo_space;>
4) osmotic gain of H2O&raquo_space;>
5) cell swells and dilates

22
Q

What is the mechanism of mitochondrial dysfunction via lack of ATP?

A

lack of ATP = increased anaerobic glycolysis&raquo_space;»> lactic acid build-up&raquo_space;» acidic inside cell&raquo_space;» decreased activity of cellular enzymes&raquo_space;» protein-synthesis apparatus disrupted&raquo_space;> Ca2+ influx = activates unwanted enzymes

23
Q

What is a reactive oxygen species (ROS)?

A

type of free radical = unstable chemical species w/ a single unpaired electron on outer shell

24
Q

How is a chain of free radicals produced?

A

when the “attacked” molecules converts into other types of free radicals

25
Q

What are the 2 types of oxidative stress mechanisms?

A
  • physiological production
  • pathological production
26
Q

Mechanism of oxidative stress via physiological production?

A

redox reactions during cellular respiration

27
Q

5 mechanisms of oxidative stress via pathological production.

A
  • phagocytic leukocytes when killing pathogens = release free radicals
  • ionizing radiation
  • chemical metabolism
  • metal accumulation
  • reperfusion
28
Q

What are the 3 things that oxidative stress can lead into?

A
  • lipid peroxidation
  • protein modification = crosslinking
  • DNA mutation/breaks
29
Q

What is lipid perioxidation?

A

double-bonds in membranes = vulnerable&raquo_space;» membrane damage

lipid-radical interation = peroxides = unstable and reactive = autocatalytic chain reaction

30
Q

How do free radicals induce protein modification?

A

radicals promote protein cross-linking enhanced degradation or loss of functional activity

31
Q

What are the 4 causes of membrane damage in cell injury?

A
  • reactive oxygen species
  • decreased phospholipid biosynthesis
  • increased membrane degradation
  • cytoskeletal abnormalities
32
Q

How can reactive oxygen species cause membrane damage?

A

radical-lipid interaction = peroxide = autocatalytic chain reaction

33
Q

How can decreased phospholipid biosynthesis cause membrane damage in cell injury? What is it due to?

A

hypoxia/nutrient deprivation = decrease phospholipid biosynthesis = breakdown of membrane

34
Q

What causes the increase degradation of the membrane in cell injury?

A

increase phospholipase activity due to increase Ca2+ levels

35
Q

How do cytoskeletal abnormalities cause membrane damage?

A

disrupt anchors for plasma membrane = weakens integrity of membrane

36
Q

What can an excess of intracellular Ca2+ lead to?

A

activation of unwanted enzymatic activity

37
Q

What can result from an increased mitochondrial Ca2+?

A

increased permeability = release Cytochrome C into cytoplasm = not good

38
Q

What does endoplasmic reticulum stress cause?

A

misfolded proteins

39
Q

What happens when there is an abundance of misfolded proteins?

A

initiates/triggers apoptosis

40
Q

How does an accululation of misfolded proteins happen?

A

decreased degradation OR increased production

41
Q

How does protein misfolding cause disease?

A

creating deficiency of an essential protein or induces apoptosis

42
Q

How can DNA damage trigger apoptosis?

A

if too damage and no repairs worked

43
Q

What are the 2 types of cell death?

A

apoptosis and necrosis

44
Q

Why is necrosis considered an “accidental” cell death?

A

rapid/uncontrolled cell death

45
Q

What are 5 factors that necrosis is often due to?

A
  • loss of O2/nutrients
  • ischemia
  • toxins
  • infections
  • trauma
46
Q

In necrosis, how is leakage of intracellular proteins beneficial?

A

allows for detection of tissue-specific necrosis

47
Q

How can hypoxia cause necrosis?

A

No O2 = anaerobic glycolysis = lactic acid build-up = acidic intracellular = decreased enzyme activity = ATP depletion = decreased ATP-Na+ pump activity = Na+ build-up inside cell = draws water inside cell = cell swells/dilates = bursts

48
Q

What are the 5 kinds of necrosis?

A
  • coagulative
  • gangrenous
  • liquefactive
  • caseous
  • fat
49
Q
A

Pathophysiology I (1 decks)

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