Growth Adaptations, Cell Injury and Cell Death Flashcards

1
Q

describe the mechanisms of cell injury and how it affects the organelles

A
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2
Q

describe why hypoxia causes cellular injury

A
  • low O2 delivery to tissue; important cause of cellular injury
    • O2 is the final electron acceptor in the ETC of oxidative phosphorylation
    • decreased O2 impairs oxidative phosphorylation, resulting in decreased ATP production
    • lack of ATP (essential energy source) leads to cellular injury
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3
Q

low ___ disrupts key cellular functions, including: ____

A

low ATP disrupts key cellular functions, including:

  • Na/K pump, resulting in sodium and water buildup in the cell
  • Ca2+ pump, resulting in Ca2+ buildup in the cytosol of the cell
  • switch to anaerobic glycolysis
    • lactic acid buildup results in low pH which denatures proteins and precipitates DNA
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4
Q

the initial phase of injury is ____; the hallmark of ____ injury is ____

explain this concept

A

the initial phase of injury is reversible; the hallmark of reversible injury is cellular swelling

  • cytosol swelling results in loss of microvilli and membrane blebbing
  • swelling of the rER results in dissociation of ribosomes and decreased protein synthesis
  • blebs, myelin figures (cell memb.), mt swelling
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5
Q

the hallmark of irreversible injury is _____

explain examples of this in the cell

A

the hallmark of irreversible injury is membrane damage

  • plasma membrane damage results in:
    • cytosolic enzymes leaking into the serum (cardiac troponin)
    • additional Ca2+ entering into the cell
  • mitochondrial membrane damage results in:
    • loss of the ETC (inner mt membrane)
    • cytochrome c leaking into cytosol (activates apoptosis)
  • lysosome membrane damage results in hydrolytic enzymes leaking into the cytosol, which, in turn, are activated by the high intracellular Ca2+
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6
Q

describe what is seen in the image

A
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7
Q

describe what is seen in the image

A
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8
Q

describe injury to the nucleus

A
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9
Q

describe injury to the lysosomes

A
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10
Q

describe injury to mitochondria

A
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11
Q

list reversible ischemic injury events

A
  • impaired aerobic respiration (mt)
  • decreased ATP (energy)
  • anaerobic glycolysis
  • glycogen depletion
  • lactic acidosis and nuclear chromatin clumping
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12
Q

list the sequence of events in reversible injury

A
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13
Q

the critical point of cellular injury is the inability of ___ to recover

A

the critical point of cellular injury is the inability of mitochondria to recover

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14
Q

list the sequence of events for an irreversible injury

A
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15
Q

describe injury by free radicals and explain what most free radicals do

A

most affect cell membranes producing energy loss

  • the most common = activated oxygen radicals (aging, chemical, x-rays, infxns, inflammation, tumors, etc.)
  • free radicals affect cell membranes by lipid peroxidation and affect nucleic acids with mutations
  • protective mechanisms (antioxidants) = catalase, glutathione
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16
Q

give an example of direct effect of chemicals on cells

A
  • direct = Hg (mercury) binds to proteins and cell membranes
17
Q

describe coagulative necrosis

A

most common type of necrosis

  • necrotic tissue that remains firm
  • cell shape and organ structure are preserved by coagulation of cellular proteins
  • nucleus disappears
    • acidophilic mass (since nucleus no longer stains basophilic)
  • characteristic of ischemic infarction of any organ except brain
18
Q

describe liquefactive necrosis and name the 3 situations it is seen in

A
  • necrotic tissue becomes liquified
  • enzymatic lysis by hydrolytic enzymes of cells and proteins results in liquefaction
  • characteristic of:
    • brain infarction
    • abscess (bacterial infxns)
    • pancreatitis
19
Q

describe fat necrosis

A
  • necrotic adipose tissue with chalky-white appearance due to deposition of calcium
  • in fat, release of lipases from dead pancreatic cells –> FFA + Ca2+ = saponification
    • example of dystrophic calcification
20
Q

describe gangrenous necrosis

A
  • coagulative necrosis that resembles mummified tissue (dry gangrene)
  • characteristic of ischemia of lower limb and GI tract
  • if superimposed infection occurs, then liquefactive necrosis ensues (wet gangrene)
21
Q

describe caseous necrosis

A
  • soft, friable necrotic tissue with “cottage cheese-like” appearance
  • eosinophilic
  • combination of coagulative + liquefactive necrosis
  • characteristic of granulomatous inflammation due to TB or fungal infection
22
Q

describe fibrinoid necrosis

A
  • necrotic damage to blood vessel wall
  • leaking of proteins into vessel wall results in bright pink staining
  • characteristic of malignant hypertension or vasculitis
23
Q

describe intracellular accumulations

A
  • fatty change = accumulation of lipids
  • accumulation of proteins = Ig (Russell bodies)
  • accumulation of glycogen = storage disorders, diabetes
  • mixtures of lipids and carbohydrates = mucopolysaccharides
24
Q

describe how free radicals cause damage

A
  • peroxidation of lipids
  • oxidation of DNA and proteins
    • DNA damage is implicated in aging and oncogenesis
25
name the enzymes that eliminate free radicals
* **superoxide dismutase** (in mt) + superoxide (O2-) = H2O * **glutathione peroxidase** (in mt): 2GSH + free radical = GS-SG and H2O * **catalase** (in peroxisomes): H2O2 --\> O2 and H2O
26
describe chemical injury due to carbon tetrachloride (CCl4)
* **converted to CCl3** free radical by P450 system of hepatocytes * **results in cell injury with swelling of rER**; consequently, ribosomes detach, impairing protein synthesis * **decreased apolipoproteins** cause accumulation of lipid in cells (ER) because apolipoproteins are necessary for triglycerides to leave the cell * **lead to** **fatty** **change in the liver**
27
describe what is seen in this image
fatty liver
28
describe viral injury