Cell Injury Flashcards

1
Q

common causes of cell injury

A
  • hypoxia and anoxia (primary cause)
  • free radicals
  • toxins
  • infection
  • immunologic or inflammatory responses
  • genetic and metabolic disturbances
  • traumatic injury
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2
Q

time course of cell injury:

1) homeostasis
2) cell injury
3) reversible changes:
- _____
- _____
- _____
4) cell death
5) irreversible changes:
- _____
- _____
- _____

A

ATP depletion;
biochemical dysfunction;
early ultrastructural changes: cytoplasmic swelling, vacuolation;

late ultrastructural changes;
early light microscopic changes: pyknosis;
late light microscopic changes: karyorrhexis, karyolysis

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3
Q

hypoxic injury and cellular swelling

A

reduces oxygen delivery to the cell –> inhibits cell’s ability to create adequate ATP –> water moves into cell (bc pumps aren’t working w/o ATP) –> swelling and vacuolation; can be reversible if oxygen delivery is restored

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4
Q

ischemic hypoxia

A

decreased blood flow therefore decreased oxygen (ex: pinched blood vessel); most common

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5
Q

ischemic anoxia

A

no blood flow (ex: blocked blood vessel)

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6
Q

anemic hypoxia

A

red blood cells can’t deliver sufficient oxygen to cells (ex: sickle cell anemia, carbon monoxide poisoning)

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7
Q

reactive oxygen species:

____ and _____ generated

A

internally; externally

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8
Q

normal metabolic processes (e.g., mitochondrial electron transport chain) and immune responses generate ___

A

free radicals

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9
Q

free radicals can cause damage to molecules by ____ through oxidation (called oxidative damage)

A

stealing their electrons

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10
Q

a free radical is an atom or group of atoms that have ____, making them extremely ___

A

1 or more unpaired electrons; reactive

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11
Q

___ and ___ forms of reactive oxygen species

A

radical; non-radical

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12
Q

ROS’s are typically neutralized by ____

A

internally produced anti-oxidants

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13
Q

ROS’s are produced in larger amounts with ____

A

injury and aging (oxidative stress)

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14
Q

ROS’s can break ____

A

covalent bonds in molecules

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15
Q

radical forms have an ____

A

unpaired electron- donates to or acquires electron from cellular molecules

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16
Q

ROS associated injury

A
  • lipid peroxidation
  • protein degradation
  • DNA damage
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17
Q

ROS sources

A
  • mitochondria
  • inflammation
  • exercise
  • cigarette smoke
  • pollution
  • certain drugs, pesticides
  • solvents
  • reperfusion
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18
Q

direct toxic injury and examples

A

disrupt cellular function;
lead: CNS toxicity;
mercury: CNS toxicity;
carbon monoxide: anemic hypoxia

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19
Q

indirect toxic injury and examples

A

toxic after metabolism;
ethanol: CNS and liver toxicity (can also have direct toxicity);
ethambutol (TB drug): toxic optic neuropathy;
cyclosporine: renal toxicity

20
Q

infectious injury direct cellular damage

A

ex: virus targets cell and causes cell to rupture; bacteria releases toxin that damages the cell

21
Q

infectious injury indirect cellular damage via immune response

A

collateral damage that comes along with the immune response to an infection; typically normal

22
Q

genetic and metabolic injury can be ___ or ____; they disrupt normal cell function; examples?

A

acquired; congenital;

sickle cell anemia, fatty liver disease, hepatolenticular degeneration, type 2 diabetes mellitus

23
Q

traumatic injury examples in the eye

A
  • blunt force trauma
  • sharp force trauma
  • penetrating trauma
  • ionizing radiation
24
Q

____ is a response to stress

A

adaptation

25
adaptation attempts to restore ____; result of altered ____; type depends on cell and stressor
homeostasis; gene expression
26
atrophy
decreased cell size; can be result of injury/decreased use
27
hypertrophy
increased cell size; can be result of exercise, pregnancy; left ventricular hypertrophy caused by obesity/hypertension
28
hyperplasia
increased cell number; ex: calluses form due to mechanical irritation, pregnancy
29
metaplasia
conversion of one cell type to another; in ectropion the exposed conj. may begin to keratinize due to exposure to external environment
30
dysplasia
disorderly growth; not an adaptation but rather damage; a precursor to cancer
31
intracellular and extracellular accumulations as adaptation
- water - lipids - cholesterol - calcium - pigments - ex: bilirubin, lipofuscin
32
primary theories of aging
- accumulation of injurious events - genetically controlled program - likely a combination of both
33
as we age, our cells produce less ____ and more ____, which further reduces the ability to produce ____
ATP; free radicals; ATP
34
necrosis
initiated by (external) cell injury, leads to inflammation; group of cells; type of necrosis that occurs depends on the type of tissue in which it occurs
35
apoptosis
programmed cell death; initiated by suicide gene activation; single cell; orderly and non-inflammatory; body can recycle materials; developmentally necessary; ordered cell turnover; can also result from injury
36
coagulative necrosis
- kidneys, heart, adrenal glands | - begins with ischemia, leads to protein denaturation, cellular lysis, and clotting
37
liquefactive necrosis
- neurons and glial cells of the brain - cells release hydrolytic enzymes which digest tissues into a wet/runny wound - may form abscess or cysts
38
caseous necrosis
- cheese-like - tuberculosis pulmonary infection - combination of coagulative and liquefactive necrosis
39
gangrenous necrosis
clinical term; large area of affected tissue
40
dry gangrene
large area with coagulative necrosis
41
wet gangrene
large area with liquefactive necrosis
42
gas gangrene
associated with anaerobic bacteria that produce gas
43
fat necrosis
- breast, pancreas, and other abdominal organs | - action of lipases may cause saponification (changing of tissue into soapy texture)
44
somatic death
sufficient death of cells/tissues of vital organs: heart, brain, kidneys; occurs when the death of the tissue exceeds the body's ability for normal life processes
45
postmortem changes; useful for investigating unobserved deaths
- algor mortis: cooling of the body - livor mortis: pooling of the blood - rigor mortis: muscle contraction - postmortem autolysis (endogenous) and putrefaction (exogenous)