7: Mechanisms of Cell Death and Tissue Repair Flashcards

1
Q

homeostasis is when a cell is at

A

optimal function, meeting physiological demands

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2
Q

reversible changes in response to cell’s environment/ stressors

A

adaptation

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3
Q

_____ happens when cells can not adapt or are at the max adaptive response to stimuli

A

cell injury

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4
Q

factors affecting cell injury include

A

nature/ duration/ severity + cell type/ adaptation + activation of multiple mechanisms

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5
Q

list the 6 mechanisms of cell injury

A

mitochondrial damage
abnormal calcium homeostasis
DNA damage
membrane damage
ER stress
oxidative stress

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6
Q

describe why mitochondrial damage causes cell injury

A

essential for survival by producing ATP, but is also a major source of reactive oxygen species production + activates cell death pathways (apoptosis, autophagy, etc)

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7
Q

describe why abnormal calcium homeostasis causes cell injury

A

increased Ca activates Ca dependent enzyme degradation

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8
Q

describe how ER stress causes cell injury

A

releases Ca stores, misfolded proteins

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9
Q

chemical injury directly targets

A

organelles

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10
Q

chemical injury requires __________ activation and often trigger an _____ response

A

metabolic activation
inflammatory response

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11
Q

chemical injury is
1. selective, not based on kinetics
2. nonselective, not based on kinetics
3. nonselective, based on kinetics
4. selective, based on kinetics

A

4

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12
Q

cellular damage occurs when __________are overwhelmed = damage to membrane, mitochondria, ER, DNA, proteins

A

antioxidant systems

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13
Q

hypoxia

A

tissues are starved of oxygen- 1-2% oxygen

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14
Q

ischemia

A

blood flow is cut off to tissues (no blood/ oxygen delivered but also no removal of metabolic wastes)

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15
Q

mild ischemic/ hypoxic injury is reversible if

A

tissue oxygen supply is restored

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16
Q

anoxia is

A

0% oxygen left

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17
Q

reversible cell injury is _______ insult or ______ duration

A

milder
shorter

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18
Q

describethe hibdernating myocardium

A

Delayed return to function once regional flow reestablished because muscle was hibernating to try to survive longer

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19
Q

loss of blood flow and oxygen results in (series after ATP drops)

A

↓ ATP results in
↓ ion pumps (no ATP to drive pumps Na/K levels change = cell swelling
↑ glycolysis (from ↓ oxphos)
↓pH (lactic acid production), disruption of synthesis/ storage

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20
Q

loss of blood flow and oxygen for too long =

A

membrane injury, calcium influx activates enzymes to break down cell = lysosomal breakdown of organelles/ proteins = autodigestion = protein markers released

21
Q

the point at which the cell becomes unable to recover its normal morphology and function even if all processes leading to its dissolution stopped

A

cell death

22
Q

what is programmed cell death

A

a active process that depends on the execution of a defined sequence of signaling events
Dependent on genetic encoded signals or activities
Not the same as apoptosis

23
Q

what are the 3 distinct routes of cellular catabolism

A

apoptosis
autophagy
necrosis

24
Q

accidental necrosis is a _________ process

A

passive
energy independent

25
give 4 characteristics of accidental necrosis
Pathological (following noxious stimuli) Occurs synchronously in multiple cells of a tissue region Early loss of membrane integrity Generalized cell and nuclear swelling Nuclear chromatin disintegration Inflammatory reactions (triggered as membrane dies) Energy independent (dramatic irreversible drop in ATP) Historically regarded as unregulated cell death
26
4 morphological descriptions of necrosis
coagulative/ infarct liquefactive fatty caseous
27
describe coagulative/ infarct necrosis
Infarction- necrosis caused by ischemia or anoxia (heart attack/ stroke) Tissue shows red staining indicating clot proteins (Ex- fibrin), anoxic injury Loss of blood supply
28
describe liquefactive necrosis
Death of tissue releases many lytic enzymes = degrades surrounding tissues Fluid remains following digestion of necrotic tissue
29
describe fatty necrosis
Pancreas release of enzymes = lipase digests fat = produces soaps microscopically(saponification) Loss of cellular membrane Necrotic fat cells Release of fatty acids combined with minerals
30
describe caseous necrosis
Combination of coagulative and liquefactive necrosis Granulomas (cluster of WBCs) as a result of immune response
31
apoptosis is critical in the
maintenace of normal organ and tissue homeostasis sculpting development and maintaining normal function
32
apoptosis is a ______ process
active
33
apoptosis is _____ controlled
geneticallly
34
which evokes less inflammatory response, necrosis or apoptosis
apoptosis
35
autophay is
Self digestive process to remove damaged proteins/ organelles by fusing with lysosomes for digestion
36
which does not display chromatin condensation 1. ncrosis 2. apoptosis 3. autophagy
3
37
autophagy is caspase ____ (dep/ indep)
independent
38
3 major categories of autophagy
macroautophagy microautophagy chaperone mediated autophagy
39
macroautophay is the
fusion of autophagosome with lysosome → degradation in lysosome → efflux of metabolites
40
microautophay is
specific type of organelle (may be damaged) is sequestered into lysosome for degradation
41
chaperone mediated autophagy is
uses specific proteins (LAMP-2A, Hsp70 chaperone) to target specific motif on proteins → translocates to lysosome → degradation → efflux
42
autophahy is often associated with
cell survival
43
autophagy is triggered by
nutrient deprivation- enables cells to restore sufficient energy levels + promotes viability
44
in early stages after cell death, debris is cleaned up by __________ that accumulate over ______. this process begins within ______
cleaned up by phagocytes that accumulate over few days starts within minutes
45
in early tissue repair, tissue ____ begins to repair, there is new _______ to provide ________ , also known as
tissue scaffold new blood supply granulation tissue
46
when does early tissue repair start happening
several days post injury
47
in late tissue repair, ____ proliferate and synthesize collagen
fibroblasts
48
3 responses to abnormal physiologic stress
tissue adaptations metabolic responses growth responses