Robbins: Cell injury and Cell death Flashcards
book based
study of the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease
pathology
concerned in the common reactions of cells and tissues to injurious stimuli.
general pathology
examines the alterations and underlying mechanisms in diseases of particular organ systems
systemic pathology
initiating cause of disease
etiology
sequence of molecular, bio-chemical, and cellular events that lead to the development of disease
pathogenesis
predict disease progression and therapeutic responses
biomarkers
structural alterations in cells or tissues that are
characteristic of a disease and hence diagnostic of an etiologic process
morphologic changes
end results of genetic, biochemical, and structural changes inn cell and tissues.
clinical manifestation
four aspects of a disease process
etiology
pathogenesis
morphologic changes
clinical manifestation
father of modern
pathology
rudolf virchow
healthy steady state
homeostasis
reversible functional and
structural responses to changes in physiologic
states.
adaptations
increase in size
hypertrophy
increase in cell number
hyperplasia
decrease in size and cell number
atrophy
change in phenotype of cells
metaplasia
normal and essential process in embryogenesis
cell death
reduced blood flow
ischemia
accidental cell death; consequence of severe injury
necrosis
regulated cell death; induced by a tightly regulated suicide program
apoptosis
nutrient deprivation triggers an adaptive cellular response; cell eats its own contents
autophagy
calcium deposited at
sites of cell death
pathologic calcification
deficiency of oxygen
hypoxia
mechanical trauma,
extremes of temperature, etc.
physical agents
submicroscopic viruses to tapeworms several feet in
length.
infectious agents
defense against infectious pathogens
immunologic reactions
cause cell injury because of deficient protein function.
genetic abnormalities
major causes of cell injury
nutritional imbalances
Functional and structural alterations in early stages or mild forms of injury
reversible injury
earliest manifestation of
almost all forms of injury to cells.
cellular swelling
some forms of necrosis are genetically controlled through a defined
molecular pathway.
necroptosis
show increased eosinophilia in
H&E stains.
necrotic cells
dead cells replaced by large whorled phospholipid precipitates.
myelin figures
nuclear shrinkage and increased basophilia
pyknosis
loss of DNA because of enzymatic degradation by endonucleases.
karyolysis
pyknotic nucleus undergoues fragmentation
karyorrhexis
form of necrosis in which the architecture of
dead tissue is preserved for a span of at least some days.
coagulative necrosis
localized area of coagulative necrosis
infarct
digestion of dead cells, resulting in transformation of the tissue into a viscous fluid.
liquefactive necrosis
focal areas of fat destruction
fat necrosis
necrotic material is frequently creamy yellow because of the presence of leukocytes.
pus
focus of inflammation
granuloma
not a specific pattern of cell death; giving rise to wet gangrene
gangrenous necrosis
derived from the friable white appearance of the area of
necrosis
caseous necrosis
special form of vascular damage usually seen in immune reactions involving blood vessels.
fibrinoid necrosis
controlled by the action of a small number of genes and is required
for normal embryogenesis.
programmed cell death
activation of enzymes as a result of
apoptosis
caspases
caspases become catalytically active and unleash a cascade of other caspases
initiation phase
terminal caspases trigger
cellular fragmentation
execution phase
responsible for apoptosis in most physiologic and pathologic
situations
mitochondrial pathway
gene that is frequently overexpressed due to chromosomal translocations and other aberrations in certain B cell lymphomas
BCL2
binds to caspase-9, the critical
initiator caspase of the mitochondrial pathway
apoptosome
contain a cytoplasmic domain
involved in protein-protein
interactions.
Tumor necrosis factor (TNF)
essential for delivering apoptotic signals; their function is to activate inflammatory cascades.
death domain
best known receptor, its related
protein is Fas (CD95)
Type 1 TNF receptor (TNFR1)
expressed on T cells that recognize self antigens and functions to eliminate selfreactive lymphocytes
Fas ligand (FasL)
kill virus-infected and tumor cells
CTLs
cytoplasmic death domains form a binding site for an adaptor protein
Fas-associated death domain
(FADD)
activates the initiator caspase-9
Intrinsic mitochondrial pathway
activates caspase-8 and caspase-10
Extrinsic death receptor pathway
what are the two execution phase of apoptosis?
Intrinsic mitochondrial pathway
Extrinsic death receptor pathway
dead cells disappear, often
within minutes, without leaving a trace
Efferocytosis
