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HISTOPATHOLOGY > Robbins: Cell injury and Cell death > Flashcards

Robbins: Cell injury and Cell death Flashcards

book based

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
Q

mechanical trauma,
extremes of temperature, etc.

A

physical agents

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23
Q

submicroscopic viruses to tapeworms several feet in
length.

A

infectious agents

24
Q

defense against infectious pathogens

A

immunologic reactions

25
Q

cause cell injury because of deficient protein function.

A

genetic abnormalities

26
Q

major causes of cell injury

A

nutritional imbalances

27
Q

Functional and structural alterations in early stages or mild forms of injury

A

reversible injury

28
Q

earliest manifestation of
almost all forms of injury to cells.

A

cellular swelling

29
Q

some forms of necrosis are genetically controlled through a defined
molecular pathway.

A

necroptosis

30
Q

show increased eosinophilia in
H&E stains.

A

necrotic cells

31
Q

dead cells replaced by large whorled phospholipid precipitates.

A

myelin figures

32
Q

nuclear shrinkage and increased basophilia

A

pyknosis

33
Q

loss of DNA because of enzymatic degradation by endonucleases.

A

karyolysis

34
Q

pyknotic nucleus undergoues fragmentation

A

karyorrhexis

35
Q

form of necrosis in which the architecture of
dead tissue is preserved for a span of at least some days.

A

coagulative necrosis

36
Q

localized area of coagulative necrosis

A

infarct

37
Q

digestion of dead cells, resulting in transformation of the tissue into a viscous fluid.

A

liquefactive necrosis

38
Q

focal areas of fat destruction

A

fat necrosis

38
Q

necrotic material is frequently creamy yellow because of the presence of leukocytes.

A

pus

39
Q

focus of inflammation

A

granuloma

40
Q

not a specific pattern of cell death; giving rise to wet gangrene

A

gangrenous necrosis

40
Q

derived from the friable white appearance of the area of
necrosis

A

caseous necrosis

41
Q

special form of vascular damage usually seen in immune reactions involving blood vessels.

A

fibrinoid necrosis

41
Q

controlled by the action of a small number of genes and is required
for normal embryogenesis.

A

programmed cell death

41
Q

activation of enzymes as a result of
apoptosis

A

caspases

41
Q

caspases become catalytically active and unleash a cascade of other caspases

A

initiation phase

42
Q

terminal caspases trigger
cellular fragmentation

A

execution phase

43
Q

responsible for apoptosis in most physiologic and pathologic
situations

A

mitochondrial pathway

44
Q

gene that is frequently overexpressed due to chromosomal translocations and other aberrations in certain B cell lymphomas

A

BCL2

44
Q

binds to caspase-9, the critical
initiator caspase of the mitochondrial pathway

A

apoptosome

44
Q

contain a cytoplasmic domain
involved in protein-protein
interactions.

A

Tumor necrosis factor (TNF)

44
Q

essential for delivering apoptotic signals; their function is to activate inflammatory cascades.

A

death domain

45
Q

best known receptor, its related
protein is Fas (CD95)

A

Type 1 TNF receptor (TNFR1)

46
Q

expressed on T cells that recognize self antigens and functions to eliminate selfreactive lymphocytes

A

Fas ligand (FasL)

47
Q

kill virus-infected and tumor cells

A

CTLs

47
Q

cytoplasmic death domains form a binding site for an adaptor protein

A

Fas-associated death domain
(FADD)

47
Q

activates the initiator caspase-9

A

Intrinsic mitochondrial pathway

48
Q

activates caspase-8 and caspase-10

A

Extrinsic death receptor pathway

48
Q

what are the two execution phase of apoptosis?

A

Intrinsic mitochondrial pathway
Extrinsic death receptor pathway

49
Q

dead cells disappear, often
within minutes, without leaving a trace

A

Efferocytosis

HISTOPATHOLOGY (16 decks)

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