Cell Injury Flashcards

1
Q

reversible functional and structural responses to changes in physiological and some pathological stimuli to maintain homeostasis

A

adaptation

ex: hyperplasia/hypertrophy, atrophy/ metaplasia

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2
Q

hypertrophy vs hyperplasia

A

hypertrophy: cells increase in size (occurs in tissue whose cells have limited capacity to divide - muscle)

hyperplasia: cells increase in number

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3
Q

T/F: hyperplasia is controlled and the body has a mechanism to stop further profileration

A

TRUE: hyperplasia is controlled - remove stimulus (hormones, other signaling molecules) and proliferation ceases

*may progress to neoplasia if it becomes uncontrolled

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4
Q

atrophy causes decrease in:
a. cell number
b. cell size

A

BOTH, due to apoptosis (decrease cell number) and decreased protein synthesis and increased degradation (decrease cell size)

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5
Q

metaplasia

A

reversible change whereby one adult cell type is replaced by another

cell type vulnerable to particular stress is replaced by a less vulnerable cell type

change results from altering the maturation of stem cells

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6
Q

reversible change whereby one adult cell type vulnerable to a type of stress is replaced by another which is less vulnerable

A

metaplasia - change resulting from alteration of maturation of stem cells

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7
Q

drawback of metaplasia

A

reversible change - one adult cell type is replaced by another that is better equipped to handle a stress

for example, if someone has Barrett’s esophagus (gastric acid reflux), cells of the esophagus that are contacted by acid will become mucus-secreting columnar (rather than squamous) for better protection

drawback: loss of specialized function, growth deregulation

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8
Q

in smoker’s bronchi, ciliated columnar cells transform into tougher squamous cells

what is this process called and what is the risk of this physiological adaptation?

A

metaplasia - replacing cells with others better equipped for a stress

drawback: loss of specialized function and growth deregulation

as stress continues, malignant transformation can occur

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9
Q

which of these represent irreversible cell injury:
a. decreased ATP
b. cell swelling
c. severe mitochondrial damage
d. increased [Ca2+]
e. DNA damage

explain your choice(s)

A

irreversible:
c. severe mitochondrial damage —> leakage of apoptotic proteins, reduced ATP
d. increased [Ca2+] —> catabolic enzymes, increased mitochondrial permeability

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10
Q

is cell swelling reversible or irreversible cell injury?

A

it CAN be reversible, but can also lead to formation of membrane blebs —> necrosis

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11
Q

what does increased eosinophilia seen in a cell indicate

A

irreversible cell injury (necrosis)

lysosome rupture, mitochondrial damage, myelin figures

*eosin is anionic, acts as acidic dye (binds positively charged proteins)

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12
Q

how will cells with hypoxic injury appear?

A

more eosinophilic (pink) - acidic dye, binds positively charged molecules

hypoxia —> decreased ATP —> increase in anaerobic glycolysis and lowered pH (acidic)

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13
Q

____ is a passive, irreversible, unregulated response to injury - no energy required

A

necrosis -
lysosomal enzymes enter cytoplasm, leakage of cell contents through damaged plasma membrane into ECS causes inflammation, denaturation of cellular proteins

always pathological

appears eosinophilic

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14
Q

coagulative necrosis

A

underlying tissue architecture is preserved

example: cardiac infarction

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15
Q

liquefactive necrosis

A

underlying tissue architecture is lost, viscous/liquid

example: cerebral infarction

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16
Q

coagulative vs liquefactive necrosis

A

coagulative: underlying tissue architecture is preserved (ex - cardiac infarction)

liquefactive: underlying tissue architecture is lost, viscous/liquid (ex - cerebral infarction)

17
Q

what type of necrosis follows cardiac infarction, and cerebral infarction, respectively? explain

A

cardiac infarction - coagulative necrosis (tissue architecture preserved) - muscle tissue is strong

cerebral infarction - liquefactive necrosis (tissue architecture lost) - brain tissue is soft, does not have strong ECM

18
Q

gangrenous necrosis

A

clinically, and ischemic limb with coagulative necrosis (underlying tissue architecture preserved)

“wet” if bacterial superinfection —> then becomes liquefactive necrosis

19
Q

fat necrosis typically result from release of…

A

activated pancreatic lipases

(such as in acute pancreatitis)

20
Q

caseous necrosis

A

tissue architecture and cell outlines obliterated

surrounded by granuloma inflammation (walled off)

mainly seen in tuberculosis

21
Q

match to apoptosis or necrosis:
a. consumes energy
b. passive response (no energy)
c. cell shrinking
d. cell swelling

A

apoptosis: consumes energy, cell shrinking (blebs —> apoptotic body)

necrosis: passive (no energy), cell swelling (—> disruption of PM)