Robbins: Cell injury and Cell death Flashcards

book based (63 cards)

1
Q

study of the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease

A

pathology

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2
Q

concerned in the common reactions of cells and tissues to injurious stimuli.

A

general pathology

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3
Q

examines the alterations and underlying mechanisms in diseases of particular organ systems

A

systemic pathology

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4
Q

initiating cause of disease

A

etiology

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5
Q

sequence of molecular, bio-chemical, and cellular events that lead to the development of disease

A

pathogenesis

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6
Q

predict disease progression and therapeutic responses

A

biomarkers

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7
Q

structural alterations in cells or tissues that are
characteristic of a disease and hence diagnostic of an etiologic process

A

morphologic changes

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8
Q

end results of genetic, biochemical, and structural changes inn cell and tissues.

A

clinical manifestation

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9
Q

four aspects of a disease process

A

etiology
pathogenesis
morphologic changes
clinical manifestation

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10
Q

father of modern
pathology

A

rudolf virchow

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11
Q

healthy steady state

A

homeostasis

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12
Q

reversible functional and
structural responses to changes in physiologic
states.

A

adaptations

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13
Q

increase in size

A

hypertrophy

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14
Q

increase in cell number

A

hyperplasia

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14
Q

decrease in size and cell number

A

atrophy

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14
Q

change in phenotype of cells

A

metaplasia

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14
Q

normal and essential process in embryogenesis

A

cell death

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15
Q

reduced blood flow

A

ischemia

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16
Q
A
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17
Q

accidental cell death; consequence of severe injury

A

necrosis

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18
Q

regulated cell death; induced by a tightly regulated suicide program

A

apoptosis

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19
Q

nutrient deprivation triggers an adaptive cellular response; cell eats its own contents

A

autophagy

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20
Q

calcium deposited at
sites of cell death

A

pathologic calcification

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21
Q

deficiency of oxygen

A

hypoxia

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22
mechanical trauma, extremes of temperature, etc.
physical agents
23
submicroscopic viruses to tapeworms several feet in length.
infectious agents
24
defense against infectious pathogens
immunologic reactions
25
cause cell injury because of deficient protein function.
genetic abnormalities
26
major causes of cell injury
nutritional imbalances
27
Functional and structural alterations in early stages or mild forms of injury
reversible injury
28
earliest manifestation of almost all forms of injury to cells.
cellular swelling
29
some forms of necrosis are genetically controlled through a defined molecular pathway.
necroptosis
30
show increased eosinophilia in H&E stains.
necrotic cells
31
dead cells replaced by large whorled phospholipid precipitates.
myelin figures
32
nuclear shrinkage and increased basophilia
pyknosis
33
loss of DNA because of enzymatic degradation by endonucleases.
karyolysis
34
pyknotic nucleus undergoues fragmentation
karyorrhexis
35
form of necrosis in which the architecture of dead tissue is preserved for a span of at least some days.
coagulative necrosis
36
localized area of coagulative necrosis
infarct
37
digestion of dead cells, resulting in transformation of the tissue into a viscous fluid.
liquefactive necrosis
38
focal areas of fat destruction
fat necrosis
38
necrotic material is frequently creamy yellow because of the presence of leukocytes.
pus
39
focus of inflammation
granuloma
40
not a specific pattern of cell death; giving rise to wet gangrene
gangrenous necrosis
40
derived from the friable white appearance of the area of necrosis
caseous necrosis
41
special form of vascular damage usually seen in immune reactions involving blood vessels.
fibrinoid necrosis
41
controlled by the action of a small number of genes and is required for normal embryogenesis.
programmed cell death
41
activation of enzymes as a result of apoptosis
caspases
41
caspases become catalytically active and unleash a cascade of other caspases
initiation phase
42
terminal caspases trigger cellular fragmentation
execution phase
43
responsible for apoptosis in most physiologic and pathologic situations
mitochondrial pathway
44
gene that is frequently overexpressed due to chromosomal translocations and other aberrations in certain B cell lymphomas
BCL2
44
binds to caspase-9, the critical initiator caspase of the mitochondrial pathway
apoptosome
44
contain a cytoplasmic domain involved in protein-protein interactions.
Tumor necrosis factor (TNF)
44
essential for delivering apoptotic signals; their function is to activate inflammatory cascades.
death domain
45
best known receptor, its related protein is Fas (CD95)
Type 1 TNF receptor (TNFR1)
46
expressed on T cells that recognize self antigens and functions to eliminate selfreactive lymphocytes
Fas ligand (FasL)
47
kill virus-infected and tumor cells
CTLs
47
cytoplasmic death domains form a binding site for an adaptor protein
Fas-associated death domain (FADD)
47
activates the initiator caspase-9
Intrinsic mitochondrial pathway
48
activates caspase-8 and caspase-10
Extrinsic death receptor pathway
48
what are the two execution phase of apoptosis?
Intrinsic mitochondrial pathway Extrinsic death receptor pathway
49
dead cells disappear, often within minutes, without leaving a trace
Efferocytosis