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Tissues > T23 - Cell Injury II > Flashcards

T23 - Cell Injury II Flashcards

1
Q

What are the eight common causes of cellular injury?

A

radiation

infections/toxins

chemicals

immune-mediated damage

oxygen

genetic defects

aging

physical agents

[RICIOGAP]

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2
Q

What are the six most common effects of cellular injury?

A

mitochondrial damage

depletion of ATP

disturbance in calcium homeostatis

damage to cell membranes

damage to DNA

misfolding of proteins

[MACCDP]

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3
Q

What are the four effects of ATP depletion?

A

(1) decrease in ATP-dependent proton pumps → retention of Na+ → efflux of K+ → cell swelling
(2) increase in anaerobic glycolysis → lactic acid buildup → pH increase → decreased enzyme activity
(3) failure of ATP-dependent Ca2+ pumps → influx of Ca2+
(4) disruption of protein synthesis → detached of ribosomes from RER → decreased protein synthesis

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4
Q

What are the four mitochondrial responses to mediate cell injury?

A

(1) failure in OxPhos → ATP depletion → necrosis
(2) abnormal OxPhos → ROS production
(3) formation of mitochondrial permeability transition pores
(4) release of internal proteins that initiate apoptosis

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5
Q

Compare intracellular and extracellular calcium concentrations.

A

intracellular calcium is 10,000x lower than extracellular calcium

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6
Q

List the five enzymes that are activated as a consequence of calcium homeostasis disturbance.

A

(1) phospholipases: membrane damage
(2) proteases: breakdown of membrane/cytoskeletal proteins
(3) endonucleases: DNA/chromatin fragmentation
(4) ATPases: hasten ATP depletion
(5) caspases: initiate apoptosis

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7
Q

What are the four pathways by which ROS are generated?

A

normal metabolism

inflammation

radiant energy

toxic chemical metabolism (of CCl4, for example)

[NIRT]

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8
Q

How are ROS removed? (3)

A

spontaneous decay

antioxidant scavengers

enzymatic removal

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9
Q

Give four examples of antioxidant ROS scavengers.

A

vitamin A

vitamin E

vitamin C

beta-carotene

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10
Q

Give three examples of enzymes that remove ROS.

A

superoxide dismutases

catalases (peroxidases)

gluthiatione peroxidase

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11
Q

What are the three ROS effects on cells?

A

lipid peroxidation

cross-linking proteins

DNA fragmentation

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12
Q

Describe the effects of ROS on lipid peroxidation.

A

free radicals break double bonds of membrane polyunsaturated lipids, yielding peroxides

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13
Q

Describe the effects of ROS on cross-linking proteins.

A

free radicals promote sulfhydryl-mediated protein cross-linking, leading to loss of enzyme activity

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14
Q

Describe the effects of ROS on DNA fragmentation.

A

free radicals interact with thymine and produce single-stranded breaks

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15
Q

What are the five pathways that give rise to membrane damage?

A

(1) decreased phospholipid synthesis because of lower ATP
(2) phospholipase breakdown of membranes
(3) ROS damage
(4) protease breakdown of cytoskeletal proteins
(5) liberated lipids (like free fatty acids) that act as detergents

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16
Q

What kinds of damage lead to apoptosis? (3)

A

damage by:

ROS

calcium-activating proteases

DNAses

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17
Q

What kinds of damage lead to necrosis?

A

membrane damage

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18
Q

Differentiate between apoptosis and necrosis.

A

apoptosis = programmed cell death

necrosis = unprogrammed cell death

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19
Q
A
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20
Q

What is physiologic apoptosis?

A

normal apoptotic phenomenon that eliminates cells no longer needed

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21
Q

Give an example of physiological apoptosis.

A

embryogenesis: apoptosis of cells between fingers

22
Q

What is pathologic apoptosis?

A

elimination of cells genetically altered or injured beyond repair, without eliciting a severe host reaction to keep tissue damage to a minimum

23
Q

Give three examples of pathologic apoptosis.

A

apoptosis in response to DNA damage

apoptosis in response to misfolded proteins

apoptosis due to viral infection

24
Q

What are the two pathways of apoptosis?

A

extrinsic = death receptor pathway

intrinsic = mitochondrial pathway

25
Q

What are caspases?

A

apoptosis-associated enzymes that are cystine proteases which cleave substrates after an aspartyl residue

26
Q

Describe the steps of the extrinsic pathway of apoptosis. (3)

A

Death signals (FasL, TRAIL, TNF-alpha) bind to Death Receptors (TNFR1)

formation of Death Inducing Signaling Complex (DISC), which contains FADD adaptor protein + pro-initiator caspase 8

DISC converts procaspase 8 into active caspase 8, which cleaves effector caspases to induce apoptosis

27
Q

Describe the steps of the intrinsic pathway of apoptosis. (3)

A

stimuli (growth factor withdrawal, DNA damage, etc.) cause release of cytochrome c from mitochondria

CytC binds Apaf-1 + pro-caspase caspase-9 = forms apoptosome

apoptosome cleaves pro-caspase 9 into caspase 9, which cleaves effector caspases

28
Q

Which protein family mediates the extrinsic pathway of apoptosis?

A

TNF-superfamily

29
Q

Which protein family mediates the intrinsic pathway of apoptosis?

A

BCL2 family

30
Q

Describe the roles of the BCL2, BAX, BAK, and BH3 proteins in the intrinsic/mitochondrial pathway of apoptosis.

A

BCL2: anti-apoptotic

BAX/BAK: pro-apoptotic

BH3: inhibit BCL2 and therefore pro-apoptotic

31
Q

How do BAX and BAK serve as proapoptotic proteins in the intrinsic pathway of apoptosis? (2)

A

increase permeability of mitochondrial membrane

release cytochrome c

32
Q

What is autophagy?

A

lysosomal digestion of cell’s own components

33
Q

Why would autophagy be useful?

A

survival mechanism in times of nutrient deprivation

34
Q

Describe how autophagy and apoptosis are related. (3)

A

autophagic vacuoles form w/ intracellular organelles and cytosolic contents

vacuole fuses w/ lysosomes to form autophagolysosome

starved cell can no longer survive by eating itself, so apoptosis is initiated

35
Q

Describe the relationship between autophagy and neurodegenerative disease.

A

defective autophagy means misfolded proteins aren’t properly cleared, leading to neurodegenerative disease

36
Q

What are intracellular inclusions?

A

aggregates of nuclear or cytosolic material due to inadequate removal of the substance, secondary to defects in transport or packaging

37
Q

What are four pathways to intracellular inclusions?

A

packaging/transport defects

accumulation of abnormal endogenous substance

failure to degrade metabolite due to inherited deficiences

deposition/accumulation of abnormal exogenous substance

38
Q

What is anthracitic pigment? (2)

A

carbon dust

air pollutant that aggregates in lymph nodes and pulmonary parenchyma as black pigment

39
Q

What is lipofuscin? (3)

A

pigment that accumulates as a result of “wear and tear”

function of age or atrophy

appears as granular brown-yellow intracellular pigment

40
Q

What is melanin? (2)

A

endogenous brown-black pigment synthesized by melanocytes

found in basal keratinocytes (freckles) or in dermal macrophages

41
Q

What is hemosiderin? (3)

A

hemoglobin-derived granular pigment

golden yellow-brown color

accumulates in tissue with excess iron

42
Q

What are four pigments that commonly accumulate in cells?

A

anthracitic pigment

lipofuscin

melanin

hemosiderin

43
Q

Differentiate between striated and cardiac muscle in terms of how they can tolerate ischemia.

A

striated muscle can tolerate ischemia for 2-3 hours

cardiac muscle can tolerate ischemia for 30 minutes

44
Q

(T/F) Morphological changes in cells precede loss of function.

A

False. It’s the other way around — loss of function precedes morphological changes.

45
Q

In terms of damage to cellular membranes, which organelle membranes are the most critical?

A

mitochondrial (decreases ATP)

plasma membrane (loss of osmotic balance)

lysosomes (leakage of contents)

46
Q

What is hepatic steatosis?

A

accumulation of TGs in liver parenchymal cells (i.e. hepatocytes)

47
Q

What are two causes of hepatic steatosis?

A

alcohol abuse

diabetes associated with obesity

48
Q

In a hemorrhage, RBCs are observed outside vessels. Describe how RBCs are then degraded.

A

RBC → hemoglobin → bilirubin → biliverdin

49
Q

(T/F) Lipofuscins are dangerous to cells.

A

False. Lipofuscin is not dangerous to cells.

50
Q

The presence of lipofuscin in a cell indicates

A

oxidative damage

51
Q

What is hemosiderosis? (4)

A

increased iron presence in cells, due to:

increased absorption of dietary iron

impaired utilization

hemolytic disease

red blood cell transfusion

52
Q

Give an example of an antioxidant scavenger.

A

glutathione

Tissues (23 decks)

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