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Disease Mechanisms > Ch 2: Cell Injury, Cell Death, And Adaptations > Flashcards

Ch 2: Cell Injury, Cell Death, And Adaptations Flashcards

1
Q

what are compensatory mechanisms

A

things that happen within a cell to keep it intact

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2
Q

what are pathophysiologic mechanisms

A

lead to loss of cell integrity

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3
Q

what leads cell injury to being irreversible

A

mitochondrial damage - cannot restart oxidative phosphorylation
widespread membrane damage - compromised lysosomes and massive calcium influx

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4
Q

define hypoxia

A

oxygen deficiency

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5
Q

what are the three main causes of hypoxia

A

ischemia - reduced blood flow
inadequate oxygenation of blood
decreased oxygen carrying capacity of blood

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6
Q

what are the 7 main causes of cell injury

A

hypoxia
physical agents (electric shock)
chemical agents and drugs (poison)
infectious agents (bacteria)
immunologic reactions (autoimmune reactions)
genetic abnormalities (DNA mutations)
nutritional imbalances (vitamin deficiency)

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7
Q

what two features are seen with reversible cell injury

A

swelling of cells and organelles
fatty change

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8
Q

what causes swelling of cell and it’s organelles

A

failure of sodium/potassium ATPase pumps causes water influx
leads to blebbing of plasma membrane, detaching of ribosomes from ER, and clumping of nuclear chromatin

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9
Q

what causes fatty change of a cell

A

deposits of intracellular triglyceride

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10
Q

what are the two main ways cell “die”

A

necrosis and apoptosis

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11
Q

what is necrosis

A

cell membrane damage due to cell swelling
enzymes can enter the cytoplasm and digest cell
plasma membrane and cellular contents disrupted
inflammation

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12
Q

what is apoptosis

A

activation of internally controlled suicide program which leads to pieces of cell being phagocytosed
cell shrinks
nucleus fragments
plasma membrane and cellular contents remain intact
no inflammation

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13
Q

what is pyknosis

A

when the nucleus shrinks

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14
Q

what is kharyorrhexis

A

fragmentation of the nucleus

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15
Q

what is karyolysis

A

fading of basophilia of the chromatin due to the digestion of the DNA within the nucleus

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16
Q

what are the 6 types of necrosis

A

coagulation
liquefactive
caseous
fat
gangrenous
fibrinoid

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17
Q

what is coagulative necrosis

A

proteins become denatured
leaves architecture of dead tissue intact (infarct)
in all organs but the brain

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18
Q

what is liquefactive necrosis

A

enzyme digestion causes digestion of dead cell leaving a liquid, viscous mass with pus
in the brain, it’s caused by ischemic injury to neurons and glial
seen often in focal bacterial or fungal infection

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19
Q

what is caseous necrosis

A

caused by pulmonary tuberculosis infection
dead cells disintegrates which causes a granulomatous inflammation response
leads to soft and granular tissue formation

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20
Q

what is fat necrosis

A

lipases from pancreas cause the breakdown of triglycerides
free fatty acids combine with calcium and cause chalky, white areas (fat saponification)

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21
Q

what is fibrinoid necrosis

A

complexes of antigens and antibodies are deposited in called of arteries
seen mostly in immune reactions involving blood vessels

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22
Q

what is gangrenous necrosis

A

severe hypoxia injury leads to bacterial invasion
wet: bacteria and liquefactive necrosis cause swelling, blistering, and wet appearance
limb becomes cold, swollen, and black
dry: results from coagulative necrosis due to ischemia
skin becomes dry and shriveled, brown or black

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23
Q

how does apoptosis work

A

cell breaks up into plasma membrane bound fragments (apoptotic bodies)
plasma membrane puts out signals for phagocytes to take up the apoptotic bodies

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24
Q

why do cells undergo apoptosis physiologically

A

cells that are not needed are deprived of necessary signals to survive
they are eliminated to maintain a constant number of various cell populations in a time

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25
Q

what are pathologic causes of apoptosis

A

eliminate injured cells that cannot be repaired

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26
Q

in which situations do cells go through physiologic apoptosis

A

removal of supernumerary cells during development (removing skin between fingers)
involution of hormone-dependent tissues on hormone withdrawal (shedding of uterus)
cell turnover in proliferating cell populations (T cells in thymus replenish)
elimination of potentially harmful self-reactive lymphocytes (prevents autoimmune reactions)
death of host cells that served purpose (killing neutrophils after an immune response)

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27
Q

what type of cells will go through pathologic apoptosis

A

cells injured beyond repair
damaged DNA
misfolded proteins
virally infected cells

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28
Q

what are the two phases of apoptosis

A

initiation and execution phase

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29
Q

describe the initiation phase of apoptosis

A

caspases are activated which unleashes cascade of other caspases

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30
Q

describe the execution phase of apoptosis

A

terminal caspases trigger cellular fragmentation

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31
Q

what is the family type of the mitochondrial pathway

A

BCL2 family

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32
Q

what are the anti-apoptotic proteins of the mitochondrial pathways and what do they do

A

BCL2 and BCL-X
decrease membrane permeability

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33
Q

what are the pro-apoptotic proteins of the mitochondrial pathways and what do they do

A

BAX and BAK
enhance membrane permeability

34
Q

what are apoptosis initiator proteins and what do they do

A

BAD, BIM, and BID
when upregulated and activated, they initiate apoptosis by activating pro-apoptotic proteins and inhibiting anti-apoptotic proteins

35
Q

what are the four ways cells can die (not including necrosis and apoptosis)

A

necroptosis
pyroptosis
ferroptosis
autophagy

36
Q

what is necroptosis (programmed necrosis)

A

mixture of apoptosis and necrosis
cell death that does not include caspases
cell lysis which leads to inflammation

37
Q

what is pyroptosis

A

form of apoptosis
release of cytokine IL-1 which causes fever and inflammation

38
Q

what is ferroptosis

A

intracellular iron dependent lipid peroxide accumulation that disrupts plasma membrane

39
Q

what is autophagy

A

self destructive process that helps balance sources at critical times

40
Q

what are the 6 types of abnormalities that cause cell injury

A

mitochondrial damage
membrane damage
DNA damage
disturbance in calcium homeostasis
oxidative stress (excess free radicals can trigger apoptosis)
endoplasmic reticulum stress (too many misfolded proteins)

41
Q

what are some features of free radicals

A

single, unpaired electrons in the outer shell
very unstable and autocatalytic (can self react with others)

42
Q

what are some features of reactive oxygen species (ROS)

A

produced during oxidative phosphorylation and used in many physiological processes
ex. superoxide, hydrogen peroxide, and hydroxyl radical

43
Q

how do antioxidants remove free radicals

A

block or inactivate them

44
Q

what are two storage and transport proteins with which free radicals can bind to

A

transferrin and ferritin

45
Q

what are the 3 enzymes that can help remove free radicals

A

catalase
superoxide dismutase (SOD)
glutathione peroxidase

46
Q

define oxidative stress

A

a condition in which increased production or decreased scavenging of ROS may lead to an excess of free radicals
eventually leads to damage

47
Q

what are 7 things that generate oxidative stress

A

normal metabolic processes
ionizing and UV radiation
transition metals (Cooper and iron)
chronic inflammation
chemical or drug toxicity
ischemia-reprefusion injury
nitric oxide

48
Q

what are two disorders caused by misfolded proteins

A

cystic fibrosis and Alzheimer’s disease

49
Q

define hypertrophy

A

an increase in the size of cells which causes the organ or tissue to become enlarged
caused by an increase in functional demand or stimulation from hormonal/growth factors

50
Q

define pathologic hypertrophy

A

chronic increase in workload causes enlarged tissue

51
Q

what is the stimuli that causes pathological cardiac hypertrophy

A

disease such as pressure or volume overload

52
Q

what is the stimuli which causes physiological cardiac hypertrophy

A

aerobic exercise training

53
Q

does apoptosis occur in pathological cardiac hypertrophy

A

yes

54
Q

does apoptosis occur in physiological cardiac hypertrophy

A

no

55
Q

is pathological cardiac hypertrophy reversible

A

no

56
Q

is physiological cardiac hypertrophy reversible

A

yes

57
Q

define hyperplasia

A

increase in number of cells which leads to a larger organ

58
Q

what is the physiological reasoning behind hyperplasia

A

tissue has an increase in need for functional capacity

59
Q

what is the pathological reasoning behind hyperplasia

A

excessive or inappropriate actions of growth factor/hormones acting on target cells

60
Q

what is an example of physiologic atrophy

A

thyroglossal duct

61
Q

what are 6 examples of pathological atrophy

A

decreased workload (disuse atrophy) due to a cast
denervation atrophy (loss of innervation)
pressure over a length of time (tumor compression)
diminished blood supply (chronic ischemia)
inadequate nutrition (muscle wasting)
loss of endocrine stimulation (menopause)

62
Q

what is marasmus

A

severe undernourishment due to low caloric intake, especially protein

63
Q

what does senile atrophy of the brain lead to

A

can be caused by atherosclerosis and can lead to decrease in blood getting to the brain

64
Q

what are the two main mechanisms of atrophy

A

reduced trophic signals from growth factors leads to decreased protein synthesis
increased protein degradation due to the activation of the ubiquitin-proteasome pathway

65
Q

define metaplasia

A

when one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type - can lead to malignancy
ex. columnar changing to squamous due to chronic irritation due to acid reflux

66
Q

explain the mechanism of metaplasia

A

cytokines, growth factors, or extracellular matrix components cause reprogramming of stem cells or colonizaiton from adjacent sites

67
Q

define dyplasia

A

disordered growth, usually of epithelial cells
change in shape, size, and organization of differentiated cells
have a larger, hyperchromatic nucleus (darker in color)
can become malignant

68
Q

what are the three processes that affect cells and tissues

A

intracellular accumulations
pathologic calcification
cellular aging

69
Q

explain inadequate removal of intracellular accumulation

A

accumulation is caused by the inability to remove a substance from a cell, typically due to defects in packaging and transport
ex. triglyceride buildup in the liver (steatosis)

70
Q

explain the accumulation of endogenous substances of intracellular accumulations

A

accumulation is caused by a defect in the cell’s folding, packaging, transport, or secretory machinary
ex. mutation in alpha1-antitrypsin which leads to emphysema

71
Q

explain the failure to degrade a metabolite of intracellular accumulation

A

cell lacks certain enzymes, usually lysosomal
it is unable to degrade a certain metabolite because of this which leads to storage of things broken down by lysozymes
ex. pompe disease

72
Q

explain deposition and accumulation of an abnormal exogenous substance of intracellular accumulation

A

cell lacks enzymatic machinery to degrade and/or transport a substance which leads to its accumulation
ex. carbon of silica from work sites

73
Q

what is dystrophic calcification

A

when calcifications occur in necrotising tissue
patients have normal blood calcium levels despite this

74
Q

what is metastatic calcification

A

calcification occuring in normal tissue due to hypercalcemia (excess calcium in the blood)

75
Q

define cellular aging

A

result of a progressive decline in the life span and functional activity of cells

76
Q

how do carcinogen exposure, sporadic errors, and ROS lead to cellular aging

A

they damage DMA which leads to mutations and therefore cellular again

77
Q

how does cellular senescence lead to cellular aging

A

the telomeres in a cell shorten as they divide
as cells become old, they divide less or stop dividing at all which leads to cell loss and aging
in cancer cells specifically, they activate telomerase which allows them to replicate indefinitely

78
Q

how does defective protein homeostasis lead to cellular aging

A

as the number of damaged proteins exceeds the number of normal proteins, we get decreased cell function
this can lead to cell aging

79
Q

what happens to the lifespan of a cell as there is a decrease in caloric intake

A

the lifespan of a cell goes up as caloric increase goes down

80
Q

which cells do and do not have telomerase

A

expressed in: germ, stem, and cancerous cells
not expressed in: somatic cells (unless they become cancerous)

Disease Mechanisms (19 decks)

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