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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
what are pathologic causes of apoptosis
eliminate injured cells that cannot be repaired
26
in which situations do cells go through physiologic apoptosis
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)
27
what type of cells will go through pathologic apoptosis
cells injured beyond repair damaged DNA misfolded proteins virally infected cells
28
what are the two phases of apoptosis
initiation and execution phase
29
describe the initiation phase of apoptosis
caspases are activated which unleashes cascade of other caspases
30
describe the execution phase of apoptosis
terminal caspases trigger cellular fragmentation
31
what is the family type of the mitochondrial pathway
BCL2 family
32
what are the anti-apoptotic proteins of the mitochondrial pathways and what do they do
BCL2 and BCL-X decrease membrane permeability
33
what are the pro-apoptotic proteins of the mitochondrial pathways and what do they do
BAX and BAK enhance membrane permeability
34
what are apoptosis initiator proteins and what do they do
BAD, BIM, and BID when upregulated and activated, they initiate apoptosis by activating pro-apoptotic proteins and inhibiting anti-apoptotic proteins
35
what are the four ways cells can die (not including necrosis and apoptosis)
necroptosis pyroptosis ferroptosis autophagy
36
what is necroptosis (programmed necrosis)
mixture of apoptosis and necrosis cell death that does not include caspases cell lysis which leads to inflammation
37
what is pyroptosis
form of apoptosis release of cytokine IL-1 which causes fever and inflammation
38
what is ferroptosis
intracellular iron dependent lipid peroxide accumulation that disrupts plasma membrane
39
what is autophagy
self destructive process that helps balance sources at critical times
40
what are the 6 types of abnormalities that cause cell injury
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
what are some features of free radicals
single, unpaired electrons in the outer shell very unstable and autocatalytic (can self react with others)
42
what are some features of reactive oxygen species (ROS)
produced during oxidative phosphorylation and used in many physiological processes ex. superoxide, hydrogen peroxide, and hydroxyl radical
43
how do antioxidants remove free radicals
block or inactivate them
44
what are two storage and transport proteins with which free radicals can bind to
transferrin and ferritin
45
what are the 3 enzymes that can help remove free radicals
catalase superoxide dismutase (SOD) glutathione peroxidase
46
define oxidative stress
a condition in which increased production or decreased scavenging of ROS may lead to an excess of free radicals eventually leads to damage
47
what are 7 things that generate oxidative stress
normal metabolic processes ionizing and UV radiation transition metals (Cooper and iron) chronic inflammation chemical or drug toxicity ischemia-reprefusion injury nitric oxide
48
what are two disorders caused by misfolded proteins
cystic fibrosis and Alzheimer's disease
49
define hypertrophy
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
define pathologic hypertrophy
chronic increase in workload causes enlarged tissue
51
what is the stimuli that causes pathological cardiac hypertrophy
disease such as pressure or volume overload
52
what is the stimuli which causes physiological cardiac hypertrophy
aerobic exercise training
53
does apoptosis occur in pathological cardiac hypertrophy
yes
54
does apoptosis occur in physiological cardiac hypertrophy
no
55
is pathological cardiac hypertrophy reversible
no
56
is physiological cardiac hypertrophy reversible
yes
57
define hyperplasia
increase in number of cells which leads to a larger organ
58
what is the physiological reasoning behind hyperplasia
tissue has an increase in need for functional capacity
59
what is the pathological reasoning behind hyperplasia
excessive or inappropriate actions of growth factor/hormones acting on target cells
60
what is an example of physiologic atrophy
thyroglossal duct
61
what are 6 examples of pathological atrophy
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
what is marasmus
severe undernourishment due to low caloric intake, especially protein
63
what does senile atrophy of the brain lead to
can be caused by atherosclerosis and can lead to decrease in blood getting to the brain
64
what are the two main mechanisms of atrophy
reduced trophic signals from growth factors leads to **decreased protein synthesis** **increased protein degradation** due to the activation of the ubiquitin-proteasome pathway
65
define metaplasia
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
explain the mechanism of metaplasia
cytokines, growth factors, or extracellular matrix components cause reprogramming of stem cells or colonizaiton from adjacent sites
67
define dyplasia
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
what are the three processes that affect cells and tissues
intracellular accumulations pathologic calcification cellular aging
69
explain inadequate removal of intracellular accumulation
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
explain the accumulation of endogenous substances of intracellular accumulations
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
explain the failure to degrade a metabolite of intracellular accumulation
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
explain deposition and accumulation of an abnormal exogenous substance of intracellular accumulation
cell lacks enzymatic machinery to degrade and/or transport a substance which leads to its accumulation ex. carbon of silica from work sites
73
what is dystrophic calcification
when calcifications occur in necrotising tissue patients have normal blood calcium levels despite this
74
what is metastatic calcification
calcification occuring in normal tissue due to hypercalcemia (excess calcium in the blood)
75
define cellular aging
result of a progressive decline in the life span and functional activity of cells
76
how do carcinogen exposure, sporadic errors, and ROS lead to cellular aging
they damage DMA which leads to mutations and therefore cellular again
77
how does cellular senescence lead to cellular aging
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
how does defective protein homeostasis lead to cellular aging
as the number of damaged proteins exceeds the number of normal proteins, we get decreased cell function this can lead to cell aging
79
what happens to the lifespan of a cell as there is a decrease in caloric intake
the lifespan of a cell goes up as caloric increase goes down
80
which cells do and do not have telomerase
expressed in: germ, stem, and cancerous cells not expressed in: somatic cells (unless they become cancerous)

Disease Mechanisms (19 decks)

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