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cell injury Flashcards

1
Q

structures and processes that maintain cell viability include:

A
  • plasma membrane
  • mitochondria
  • macromolecular synthesis (RNA rep, RNA transcription, translation, cell wall (peptidoglycan) synthesis, fatty acid (lipid) biosynthesis
  • nucleus
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2
Q

mechanisms of cell injury

A
  • ATP depletion
  • generation of ROS (oxidative stress)
  • loss of Ca homeostasis
  • altered plasma membrane perm
  • mitochondrial/DNA/protein damage
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3
Q

decreased oxygen (hypoxia) or no oxygen (anoxia) is due to:

A
  • impaired absorption of oxygen
  • decreased blood flow (ischemia)
  • disease of blood or BVs
  • inadequate oxygenation of the blood
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4
Q

decreased oxygen due to ischemia impairs ____ in the mitochondria, which leads to a decrease in ____

A

oxidative phosphorylation; ATP

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5
Q

reduced ATP reduces the ability of the plasma membrane to _____; there is impaired function of the _____ which leads to _____

A

maintain homeostasis; plasma membrane ATP-dependent Na pump; increased influx of Na, Ca, and water and increased efflux of K (net gain of solute and isoosmotic gain in cytoplasmic water)

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6
Q

gain in isoosmotic water leads to:

A
  • cell swelling with formation of cell surface blebs
  • mitochondria swelling
  • swelling of ER
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7
Q

swelling of the ER leads to:

A

detachment of ribosomes/dissociation of polysomes and a decrease in protein synthesis (which can lead to increased lipid deposition)

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8
Q

reduced oxidative phosphorylation leads to increased _____ which produces ____

A

anaerobic glycolysis; lactic acid and inorganic phosphates

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9
Q

an increase in lactic acid decreases ____ leading to ____

A

intracellular pH; chromatin clumping

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10
Q

_____ (a mechanism of cell damage by ROS) affects the ____ which plays a role in maintaining homeostasis

A

lipid peroxidation (oxidative degradation of lipids); cell membrane (disrupted membrane makes it more permeable)

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11
Q

_____ is a final common pathway of cell injury

A

increase cytoplasmic Ca

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12
Q

high levels of Ca will activate various _____ such as:

A

degradative enzymes; phospholipases, proteases, endonucleases, ATPase

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13
Q

degree of cell injury is determined in part by:

A
  • cell type/physiologic state of cell
  • intensity/duration of insult
  • number of exposures to etiologic agent
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14
Q

common etiologies of reversible (sub-lethal) cell injury include:

A

toxins, infectious agents, hypoxia, and thermal injury

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15
Q

reversible cell injury includes ____ and ____ morphology changes

A

hydropic ; fatty

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16
Q

morphologic changes in necrosis include: cell ____, ____ yielding a glassy homogenous pink staining cytoplasm, ____ breakdown which may result in a _____ cytoplasm, ____ changes, and ______

A
  • cell swelling
  • protein denaturation
  • organelle breakdown- vacuolated cytoplasm
  • nuclei changes (karyolysis/pyknosis/karyorrhexis/total loss)
  • inflammation (acute or granulomatous)
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17
Q

morphologic types of necrosis

A
  • coagulative
  • liquefactive
  • caseous
  • enzymatic (fat)
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18
Q

the type of necrosis is dependent upon patterns of _____ of cells and ECM, the type of ____, and by _____ when present

A

enzymatic degradation; necrotic debris; bacterial products

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19
Q

in coagulative necrosis (most common form), _____ are coagulated; the ____ is lost, but the _____ of the cell is retained for a short time prior to being removed by the inflammatory response

A

cytoplasmic proteins; nucleus; eosinophilic outline

20
Q

in liquefactive necrosis, the tissue is totally digested by the release of _____ during the ______

A

lysosomal enzymes; acute inflammatory response

21
Q

liq necrosis often assoc with ____ or _____ (abscesses and wet gangrene), also seen in the _____

A

focal bacterial; fungal infections; central nervous system (brain)

22
Q

caseous necrosis assoc with _____ infection; the tissue has a ____ and ____ appearance on gross examination

A

M. tuberculosis; white; cheesy

23
Q

caseous necrosis microscopically characterized by ______ material within a ring of _____ and loss of _____

A

amorphous pink granular; granulomatous inflammation; tissue architecture

24
Q

fat necrosis common in ____ to the breast or in cases of _____; adipose tissue has a _____ gross appearance; dead adipocytes give a _____ histologic appearance

A

trauma; pancreatitis; chalky white-yellow; “soap bubble”

25
Q

diseases of excessive apoptosis

A 
AIDS
ischemia
neurodegenerative diseases
myelodysplasia
toxin induced liver injury
26
Q

diseases of inhibition of apoptosis

A 
cancer (follicular lymphoma, carincinomas of the breast, prostate, ovaries)
autoimmune disease (SLE)
viral diseases (HSV, poxvirus, adenovirus)
27
Q

morphologic features of apoptosis include: cell ____, ____ condensation followed by _____, _____ formation, and _____

A

shrinkage; chromatin condensation followed by fragmentation; apoptotic bodies formation; phagocytosis of apoptosis bodies without sig inflammatory response

28
Q

signaling involved in mechanisms of apoptosis

A
  1. intrinsic system (mitochondrial pathway)
  2. “death signals”- Fas ligand binding to Pas receptor
  3. removal of a trophic signal (hormones)
  4. ROS, radiation, toxins
  5. effect of cytotoxic T cells
29
Q

_____ family serve as on and off switches that regulate the _____ of the mitochondria

A

Bcl-2 gene family; membrane permeability

30
Q

____ and ____ gene products inhibit apoptosis

A

Bcl-2; Bcl-x

31
Q

____ and ____ gene products stimulate apoptosis

A

Bax; Bak

32
Q

_____ released from outer mitochondria membrane serves to disrupt the _____ function of bcl-2, _____ apoptosis

A

cytochrome-c; inhibitory; favoring

33
Q

cellular adaptations include:

A

alterations in cell size (hypertrophy/atrophy)
alterations in cell number (hyperplasia)
alterations in cell differentiation (metaplasia)
intracellular accumulations

34
Q

one adult cell type is replaced by another adult cell type in response to chronic stress

A

metaplasia

35
Q

mechanisms of intracellular accumulations

A
  1. abnormal metabolism (fatty liver)
  2. lack of an enzyme (lysosomal storage disease: accumulation of endogenous materials)
  3. abnormal protein folding or transport (accumulation of abnormal proteins)
  4. ingestion of indigestible material (accumulation of exogenous materials)
36
Q

an abnormal accumulation of triglycerides within parenchymal cells of the liver, heart, kidney, and skeletal muscle

A

steatosis (fatty liver)

37
Q

cholesterol accumulates primarily in _____

A

macrophages (foam cells)

38
Q

3 examples of protein accumulation

A

alpha1 anti-trypsin deficiency
mallory bodies
neurofibrillary tangles in alzheimer’s disease

39
Q

in glycogen storage diseases, there is abnormal glycogen metabolism due to _____; ____ accumulates within cytoplasm of cells

A

enzyme deficiency; substrate

40
Q

“wear-and-tear” brown-yellow granular pigment”, a lipoprotein complex due to ROS peroxidation of membranes

A

lipofuscin (endogenous pigment)

41
Q

black-brown pigment - produced by melanocytes but accumulated in adjacent epidermal cells and in macrophages.

A

melanotic macule (endogenous pigment)

42
Q

A yellow-brown pigment represents aggregates of ferritin micelles;Its accumulation arises from excess iron locally due to hemorrhage and can lead to hemosiderosis

A

hemosiderin (endogenous pigment)

43
Q

genetic disease assoc with cell death due to uncompensated hemosiderin accumulation

A

hemochromatosis

44
Q

a yellow-brown pigment; end product of heme metabolism

A

bilirubin

45
Q

bilirubin accumulates in hepatocytes and bile ducts due to ____, _____, and/or _____

A

hemolysis; obstructed bile flow; hepatocellular disease

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