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RCoN Patho Chapter 3 > Mechanisms of Cell Injury > Flashcards

Mechanisms of Cell Injury Flashcards

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1
Q

what are 5 categories of causes of cell injury’s

A 
injury from:
physical agent
radiation injury
chemical injury
biological agent
nutritional imbalances
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2
Q

first indication of cell injury is

A

biochemical lesion @ point of injury -:>lesion changes chemistry of metabolic reactions with in the cell

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3
Q

types of physical agents that cause cell injury

A

mechanical forces, extremes of temp,

electrical forces

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4
Q

mechanical injury forces occur (physical injury)

A

when body impacts with another object

tissue or bone tear, fracture, blood vessels can be injured to disrupt blood flow

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5
Q

extreme temp (physical injury)

A

causes damage to the cell, its organelles, and enzyme systems

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6
Q

low intensity heat causes (physical damage)

A

causes partial thickness burn or sever heat stroke
causes cell injury by causing vascular injury->accelerates cell metabolism, inactivates temp sensitive enzymes and disrupts cell membrane

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7
Q

more intense heat (physical damage)

A

coagulation of blood vessels and tissue proteins occur

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8
Q

cold exposure temp (physical damage)

A

increase blood viscosity, induces vasoconstriction as a reflex of sympathetic nervous system-> decreased blood flow may lead to hypoxic tissue injury

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9
Q

cold exposure temp can lead to (physical damage)

A

hypoxic injury due to capillary stasis and thrombosis

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10
Q

hypoxic means

A

deprived of adequate oxygen supply at tissue level

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11
Q

freezing (physical injury)

A

may result from a combo of ice crystal formation and vasoconstriction leads to edema

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12
Q

electrical forces (physical injury)

A

can affect body through ext. tissue injury and disruption of neural and cardiac impulses

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13
Q

much of damage caused by electrical injury is caused by

A

heat production in tissue that have highest electrical resistance

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14
Q

radiation injury types

A

ionizing radiation

UV and non-ionizing

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15
Q

ionizing radiation injury

A

causes release of free radicals that destroy cells->can kill cells or interrupt cell replication or cause variety of genetic mutations

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16
Q

example of ionizing radiation

A

cancer treatment

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17
Q

UV radiation

A

causes sunburns, increase risk of skin cancer

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18
Q

uv radiation damage caused

A

from reactive oxygen species (ROS) (free radicals) and damage to melanin producing processing the skin to damage DNA

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19
Q

non-ionizing radiation examples

A

infrared light, ultrasounds, microwaves, laser energy

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20
Q

non-ionizing radiation causes

A

direct break of chemical bonds caused by vibrations and rotation of atoms and molecules, energy converted into thermal energy, can burn skin and cause thermal injury to dermal subcut, and deeper tissue

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21
Q

types of chemical injury

A

drugs, lead toxicity, mercury toxicity,

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22
Q

examples of chemicals that can damage cells

A

carbon tetrachloride when ingested, tobacco when inhaled, preservatives, carbon monixde

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23
Q

drugs (chemical injury)

A

affects cells/tissue based on chemical nature of drug and how it is metabolized can impact cells, tissues, and organs

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24
Q

how does alcohol cause damage

A

can harm gastric mucosa, live developing fetus, can directly or indirectly damage tissue

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25
acetaminophen damages (drug/chemical injury)
detoxed in liver- converted to toxic metabolite->detoxed by pathway that uses sub-> but when in large amounts, pathway is overwhelmed and toxic metabolite accumulates causing liver necrosis
26
lead toxicity (chemical)
one of most serious forms of chemical injury
27
lead is absorbed
in gastro tract and lungs then into blood stream
28
lead is eliminated
in kidneys
29
lead half life
hours->days but done deposits may maintain blood lead levels for months to years
30
major targets of lead toxicity
RBCs (decrease RBC lifespans), gastro tract, kidney damage
31
cardinal sign of lead toxicity
anemia
32
lead in nervous system
causes peripheral demyelinating neuropathy in adults and demyelinating of cerebral ad cerebrum white matter (breakdown of myelin sheath) and death of corticol cells
33
lead poisoning can also cause
acute encephalopathy, lead colic in adults, diffuse kidney damage, lead line
34
mercury toxicity (chemical injury)
can affect CNS and kidneys
35
main source of mercury exposure
is consumption of long-lives fish like tuna and swordfish recommended that pregnant women and children do not eat due to susceptible damage to brain
36
biological injury
biological injury agents differ from other injurious agents b/c they are able to replicate and can cont to produce their injurious effects
37
how do biological agents injure cell
by diverse mechanisms, and b/c (bacteria, viruses, fungi, etc.) can cont to replicate and continue to injure cell
38
injury from nutritional imbalances
excess and deficiencies predispose cells to injury obesity->atherosclerosis starvation->iron def anemia, scurvy, etc.
39
3 mechanisms where injurious agents exert their effects
free radical formation hypoxia impaired calcium homeostasis
40
free radical injury can lead to
can lead to production of free radicals
41
what are free radicals
unstable (extra electron) and highly reactive in that they react with molecules in the vicinity w/out purpose
42
free radicals react with
proteins, lipids, carbs
43
what do free radicals do
damage cells membranes, inactivate enzymes, and damage nucleic acids that make up DNA- can lead to mutations in cell structure and lead to premature cell death cause ischemia->injury->cell death
44
free radicals derived from
oxygen and are known as superoxide and hydroxl radical
45
ROS=
oxygen containing molecules that include free radical
46
oxidative stress simple
and reperfusion injury to oxygen-> created oxygen free radicals (ROS)-> oxidative stress
47
oxidative stress book
occurs when gen. of ROS exceeds the ability of the body to neutralize and eliminate ROS-> oxidation of cell components-> activation of signal transduction pathways -> changes in gene and protein expression-> DNA mod and damage
48
oxidative stress associated with what disease/conditions
inflammation, ALS, cancer development
49
oxidative stress in inflammation or profusion (mycardial infarction, stroke, sepsis, shock)
free radicals are produced in response to inflammations= WBCs convert oxygen to free radicals b/c thinks it is fighting bacteria-> oxidative stress-> tissue damage
50
antioxidants
can decrease tissue damage from free radicals but replacing the missing electron on free radicals-> less free radicals
51
hypoxic cell injury mechanism
cell is deprived of oxygen->interrupts oxidative metabolism and generation of ATP
52
loss of oxygen in brain
with in 4-6 min causes perm damage
53
list causes of hypoxia
inadequate oxygen in air, resp. disease, ischemia, anemia, edema, inability of cells to use oxygen
54
ischemia
impaired oxygen delivery and impaired removal of metabolic end products creating lactic acid-> affects blood vessels an produces local tissue injury
55
simply put hypoxia
cause power failure in the cells-> effects cells structure and function
56
hypoxia- as oxygen falls
oxidative metabolism ceases and cell averts to aerobic metabolism-> using limited glycogen stores to maintain vital cell functions, lactic acid accumulated causing PH to FALL
57
hypoxia- > reduced ATP->
-> acute ccell swelling caused by failure of energy dependent NA+/K+ATPase membrane pump-> intracellular K+ decreased and NA+ AND water Increase
58
impaired calcium homeostasis cell injury mechanism
ischemia and certain toxins lead to increase in cytosolic calcium due to influx leading to release of CA+ from intracellular stores-> activates enzymes which can be damaging
59
CA+ levels in call are normally
extremely low compare to extracellular
60
2 patterns of reversible cell injury
cellular swelling and fatty changes
61
reversible cell injury- cellular swelling
occurs w/ impairment of ATP dependent NA+/K+ATPase membrane pump; usually a result of hypoxic cell injury
62
reversible cell injury- fatty changes
linked to intracellular accumulations of fat;;
63
what happens with reversible cell injury- fatty changes
small vacuoles of fat are dispersed through out cytoplasm and usually indicate sever injury
64
fatty changes may occur
b/c normal cells are presented with increased fat load or injured cells are unable to metabolize the fat properly
65
key diff. between reversible cell dealt and cell death
is removing the stimuli that is causing the injury before too much damage is done

RCoN Patho Chapter 3 (5 decks)

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