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MFM > Cell Injury, Apoptosis, Necrosis > Flashcards

Cell Injury, Apoptosis, Necrosis Flashcards

1
Q

cellular response to stress

A

reversible modifications to structure or function to allow cells to survive

  1. hypertrophy
  2. hyperplasia
  3. atrophy
  4. metaplasia
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2
Q

what is hypertrophy

A

increase in the size of nondividing cells due to increased production of cellular proteins

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3
Q

what is hyperplasia

A

increase in number of dividing cells

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4
Q

what is an example of pathologic hypertrophy?

A

increase in left ventricle in hypertension

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5
Q

what is example of hormone induced hypertrophy

A

increase in size of uterus during pregnancy

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6
Q

example of pathologic hyperplasia

A

excess hormones or growth factors, viral infection

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7
Q

examples of physiologic hyperplasia

A

hormonal hyperplasia and compensatory hyperplasia

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8
Q

examples of hormonal hyperplasia

A

(increased functional capacity of tissue when needed, can regress) endometrial hyperplasia during pregnancy, breast hyperplasia during puberty

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9
Q

example of compensatory hyperplasia

A

(increased tissue mass after damage/resection) regeneration of liver after portion is removed, elargement of remaining kidney post unilateral nephrectomy

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10
Q

what is atrophy

A

reduced size in organ resulting from decreased in cell size AND number, due to decrease in protein synthesis and increase in protein degradation
CAN BE ASSOCIATED WITH AUTOPHAGY IN RESPONSE TO DEFECIENT NUTRIENTS

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11
Q

example of physiological atrophy

A

loss of endocrine stimulation, endometrial atrophy after menopause

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12
Q

causes of pathologic atrophy

A
  1. decreased workload - like skeletal muscle atrophy after immobile
  2. loss of innervation - damage to nerves
  3. diminished blood supply
  4. inadequate nutrition - seen in cancer patients, cachexia (muscle wasting)
  5. pressure - tumor pressure on surrounding tissue
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13
Q

what is metaplasia

A

reversible change where one differentiated cell type is replaced by a different cell type

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14
Q

what is metaplasia caused by

A

chronic irritation, cells adapt to cells that are more resistant to stress/adverse environment

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15
Q

what is an example of epithelial metaplasia?

A

chronic smoking causes irritation in respiratory tract, causing the columnar cells (ciliated pseudostratified columnar) to transform into more rugged squamous cells

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16
Q

pathology of barrett esophagus

A

acid reflux causes increased acidity in cells, so the squamous cells in the esophagus (nonkeratinized) transform into columnar cells which can tolerate the acidity better

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17
Q

7 causes of cellular injury

A
  1. hypoxia
  2. physical agents
  3. chemical agents
  4. infectious agents
  5. immunologic reactions
  6. genetic derangements
  7. nutritional imbalances
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18
Q

how does hypoxia damage cells?

A

decreased oxygen transport caused by ischemia, CR failure, anemia, severe blood loss - causes decreased ATP

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19
Q

ex of physical agents that can harm cells

A

trauma, temp extremes, radiation, electrical shock

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20
Q

ex of chemical agents that can harm cells

A

hypertonic/hypotonic solutions, poisons, pesticides, alcohol, drugs, oxygen in high concentrations - causes decreased ATP

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21
Q

ex of infectious agents causing harm to cells

A

virus, bacteria, fungi, parasites

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22
Q

ex of immunological reactions to harm cells

A

anaphylaxis, autoimmune diseases

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23
Q

ex of genetic derangements to harm cells

A

chromosomal abnormalities, enzyme defects

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24
Q

6 mechanisms of cell injury

A
  1. decreased ATP
  2. mitochondrial damage
  3. entry of calcium
  4. increased ROS
  5. membrane damage
  6. protein misfolding/DNA damage
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25
Q

causes of ATP depletion?

A

hypoxia, chemical agents (toxins), reduced nutrients, mitochondrial damage

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26
Q

what systems could be affected by reducing ATP by even 5-10%

A
  1. loss of Na/K ATPase
  2. altered metabolism
  3. detachment of ribosomes
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27
Q

how does Na/K ATPase affect the cell?

A

increased efflux of K via leak channels, increased Ca, H2O and Na into the cell – leading to ER swelling, cellular swelling and loss of microvilli

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28
Q

how does the cell’s metabolism alter from decreased ATP?

A

metabolism changes to anaerobic metabolism, leading to decreased glycogen, increased lactic acid, decrease in pH and clumping of nuclear chromatin (no transcription, no making proteins)

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29
Q

how does detachment of ribosomes affect the cell

A

decrease in protein synthesis, leading to lipid deposition and irreversible damage to mitochondria and lysosomal membranes

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30
Q

how is the mitochondria damaged?

A

an increase in cytosolic Ca, depletion of oxygen, and increase in ROS

31
Q

consequences of mitochondria damage?

A

forms mitochondrial permeability transition pore, that 1. creates the loss of membrane potential, oxidative phosphorylation fails due to loss of potential, and ATP is depleted and 2. allows leakage of apoptosis-activating proteins into cytoplasm, leading to activation of apoptosis

32
Q

how does influx of Ca into the cytoplasm affect the cell?

A

activation of enzymes such as phospholipase C (membrane damage), proteases (membrane damage), and endonucleases (nuclear damage), and caspases (to cause apoptosis)

33
Q

what are ROS

A

free radicals with unpaired electron, extremely reactive and unstable

34
Q

how do free radicals accumulate?

A
  1. redox reactions
  2. absorption of radiant energy
  3. inflammation
  4. enzymatic metabolism of exogenous chemicals or drugs
  5. transition metals,
  6. NO
35
Q

3 effects of free radicals

A
  1. lipid peroxidation in membranes (disrupts cell membranes)
  2. oxidative modification of proteins (loss of enzymatic activity and abnormal folding)
  3. lesions in the DNA (due to oxidation, mutations and breaks occur)
36
Q

how can the membrane be damaged?

A
  1. ROS
  2. decreased phospholipid synthesis
  3. increased phospholipid breakdown
  4. cytoskeletal abnormalities
37
Q

consequences of membrane damage

A
  1. mitochondrial membrane damage (pore stops membrane potential, apoptosis-activating proteins)
  2. plasma membrane damage (loss of osmotic balance and loss of cellular contents)
  3. injury to lysosomal membranes (leakage of enzymes into cytoplasm leading to digestions of proteins, RNA, DNA, glycogen)
38
Q

examples of reversible injury:

A
  1. cellular swelling
  2. plasma membrane alterations (blebbing)
  3. mitochondrial changes (swelling, amorphous densities)
  4. dilation of ER
  5. minor nuclear alterations
39
Q

examples of traumatic injury that has to lead to cell death

A
  1. electric shock
  2. poison
  3. physical injury
  4. lack of oxygen
40
Q

examples of natural injury leading to cell death

A
  1. DNA damage
  2. normal development
  3. cell turnover
41
Q

what is necrosis

A

passive and pathological process induced by acute injury or disease - cells undergo apoptosis at the same time

42
Q

3 cellular characteristics of necrosis

A
  1. denaturation of intracellular proteins and enzymatic digestion of injured cell (lysosome contents are released)
  2. plasma membrane is compromised (water rushes in and cell lyses)
  3. formation of myelin figures
43
Q

what are myelin figures

A

large, whorled damaged phospholipids in the cytoplasm that are derived from damaged cell membranes

44
Q

what is unique about necrosis versus apoptosis?

A

necrosis elicits inflammatory response, swells, and plasma membrane is damaged, and apoptosis is tightly controlled, cell shrinks, and plasma membrane is intact

45
Q

characteristics of apoptosis

A
  1. no cell swelling due to plasma membrane staying intact
  2. activation of self-degrading enzymes
  3. shrinkage of cell
  4. formation of apoptotic bodies
  5. phagocytosed without inducing inflammatory response
46
Q

steps of apoptosis

A
  1. microvilli contract, intercellular junctions break, chromatin condenses
  2. cell shrinks, chromatin condenses around nuclear periphery
  3. cell blebs violently, chromatin condensation continues
  4. cell fragments into membrane-enclosed apoptotic bodies
  5. apoptotic bodies phagocytosed by neighboring cells and roving macrophages
47
Q

steps of necrosis

A
  1. trauma
  2. cells and organelles swell, chromatin condenses, membrane compromised and fluid rushes in
  3. dissolution of cellular structures
  4. cell lysis, invasion of phagocytic cells, inflammation
48
Q

when would a cell be condemned to apoptosis in pathological conditions?

A
  1. dna damage
  2. misfolded proteins
  3. infections
49
Q

how is apoptosis used in normal development?

A
  1. forms digits during embryogenesis
  2. establishment of neuronal connections
  3. lymphocyte maturation in thymus
50
Q

what are caspases

A

cysteine proteases, containing a cysteine in the active site, which cleaves after the aspartic acid residues in substrate
without apoptotic signal, are held inactivated called procaspase (prodomain must be cleaved)

51
Q

biochemical features of apoptosis

A
  1. activation of caspase (prodomain cleaved off procaspase)
  2. dna and protein are broken down (DNA fragmented and cleavage between nucleosomal subunits)
  3. membrane alteration (promotes recognition by phagocytes)
52
Q

what occurs when caspases are activated?

A

once procaspase is cleaved, active caspase results in amplification cascade that activates many molecules of the down stream caspase

53
Q

what are initiator caspases

A

first type of caspase activated, cleaves and activates executioner caspases
CASPASE 2,8,9,10

54
Q

what are executioner caspases

A

activated by initiator caspases, activate protease and nuclease downstream
CASPASE 3,6,7

55
Q

difference between plasma membrane in healthy vs apoptotic cells

A

phosphatidylserine (PS) is only found in the inner leaflet of the PM in healthy cells, in apoptotic cells PS flips to outer leaflet and the exposure services as ligand for PS receptor on surface of phagocytic cells

56
Q

what causes intrinsic apoptosis

A

internal damage or physiologically normal elimination of cells - deprivation of nutrients, DNA damage, misfolded proteins

57
Q

what causes extrinsic apoptosis

A

external signal initiation

58
Q

what are the components of intrinsic pathway

A

Bcl family of proteins

59
Q

what are the pro-apoptotic proteins of the Bcl family

A 
BH3only: Bim, Bid, Bad
Channel forming (associated with mitochondrial membrane): Bax, Bak
60
Q

what are the anti-apoptotic proteins of the Bcl family

A

Bcl-2, Bcl-X, Mcl-1

61
Q

what is the main pathway of intrinsic pathway of apoptosis

A

increase in mitochondrial permeability and repease of pro-apoptotic proteins

62
Q

what are Bax and Bak

A

transmembrane proteins located in outer mitochondrial membrane, the oligomerize to form pores in the mitochondrial membrane when signaled by apoptotic signaling

63
Q

pathway of activation of Bax and Bak

A

pore is formed in the outer mitochondrial membrane, allowing release of intermembrane sequestered proteins, including cytochrome C

64
Q

what is cytochrome C

A

sequestered intermembrane protein that is directly responsible for initiating apoptotic signaling cascade - once cytochrome C leaves, the cell dies

65
Q

what occurs in the presence of survival factors?

A

anti-apoptotic proteins Bcl-X, Bcl-2, and Mcl-1 produced, and bind to Bax and Bak to prevent oligomerization, maintains mitochondrial membrane integrity and prevents cytochrome C from exiting the mitochondrial intermembrane space

66
Q

what is induced by stress signaling through the intrinsic pathway

A

BH3 only proteins Bim, Bad, Bid inhibit the anti-apoptotic proteins (Mcl-1, Bcl-2, and Bcl-X), and Bax and Bak are allowed to oligomerize and create channels in the mitochondrial outer membrane, cytochrome C is released, cell dies

67
Q

what is the apoptosome

A

a large complex created by the cytochrome C that combined with adaptor proteins Apaf-1

68
Q

what does the apoptosome do

A

recruits procaspase-9, which is cleaved to produce caspase-9, and caspase-9 activates executioner caspases (initator–>executioner–>proteases, nucleases)

69
Q

example of extrinsic pathway

A

the death receptor pathway: Fas signaling, FasL binds to FasR, when bound FasR containing cell dies

70
Q

details of death receptor pathway

A
  1. FasL binds to FasR
  2. 3 FasR molecules cluster and bind the adaptor protein FADD (Fas-Associated Death Domain) through their intracellular tails
  3. FADD recruits procaspase-8 molecules
  4. FADD and procaspase-8 form complex alled Death-Inducing Signaling Complex (DISC)
  5. procaspase-8 cleaves each other, making caspase-8
  6. caspase-8 cleaves procaspases 3,6,7 to produce active executioner caspases 3,6,7
71
Q

what do caspases do?

A

degrade nuclear laminins and activate DNAses that cleave genomic dna between adjacent nucelosome coils

72
Q

what does cleaving adjacent nucelosome coils by caspases result in

A

fragments of DNA that are mulitples of 180bp in length - creates a laddering pattern unique to cells undergoing apoptosis

73
Q

difference between intrinsic and extrinsic pathways

A

intrinsic pathway requires mitochondrial involvement, but activation of extrinsic pathway could lead to activation of intrinsic pathway, resulting in amplification of cellular response

MFM (39 decks)

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