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Pathology 1 > cell injury, cell death, and adaptations > Flashcards

cell injury, cell death, and adaptations Flashcards

1
Q

4 adaptation responses

A

hypertrophy
hyperplasia
atrophy
metaplasia

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2
Q

hypertrophy

A

increase cell SIZE

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3
Q

hyperplasia

A

increase NUMBER of cells

*uterus during pregancy

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4
Q

metaplasia

A

transfer one cell group to another cell type

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5
Q

atrophy

A

cell shrinks

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6
Q

vitamin A deficiency may induce squamous metaplasia in ____ epithelium

A

respiratory

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7
Q

define reversible cell injury

A

in early stages or mild forms of injuries, functional and morphological changes are reversible IF the damaging stimulus is removed

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8
Q

define irreversible cell injury

A

as stimulus continues, the injury persists and cellular damage become irreversible

  • *inability to reverse mitochondrial dysfuntion
  • *development of profound disturbances in membrane function and integrety resulting in necrosis
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9
Q

necrosis is pathologic or physiologic?

A

pathologic only

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10
Q

apoptosis is pathologic or physiologic?

A

can be either pathologic or physiologic

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11
Q

necrosis

A
  • need ATP
  • cells SWELL
  • affects larger areas of cells/tissues
  • has immune rxn
  • not regulated
  • only pathologic
  • leakage of enzymes/cell contents ocurs
  • not a normal regulation method
  • many cells affected
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12
Q

apoptosis

A
  • NO ATP
  • cell itself is degraded
  • minimal disruption of surrounding tissues
  • inner leaflet flips out causing BLEBING
  • regulated, organized, programmed
  • normal mechanism to regulate organs
  • patho and physiologic
  • single cell affected and SHRINK
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13
Q

pyknosis

A

shrink

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14
Q

karyorrhexis

A

fragment

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15
Q

karyolysis

A

disintegrate

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16
Q

inability to reverse mitochondrial dysfunction causes irreversible injury how?

A

results in lack of oxidative phosphorylation and ATP generation

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17
Q

4 major factorss required for maintaining the ion permeability of the cell

A

1) considerable amounts of ATP
2) structural integrity of phospholipid bilayer/cell membrane
3) intact ion channel proteins
4) normal association of membrane with cytoskeletal elements

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18
Q

what color are necrotic cells?

A

pale pink. Bc eosin binds to denatured proteins

blue=DNA/RNA=H

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19
Q

signs of reersible cell injury

A

1) cellular swelling
- -ion pumps fail causing altered homeostatsis
- failure of ATP generation= failed sodium pump

2) fatty change (steatosis)
- -hypoxic, toxic, metabolic injury
- liver affected commonly
- increase eosin staining
- alcohol COMMON cause

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20
Q

patterns of tissue necrosis

A 
coagulative
liquefactive
gangrenous
caseous
fat
fibrinoid
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21
Q

coagulative necrosis

A
  • structure maintained, cells dead
  • in solids organs EXCEPT the brain
  • phago removes
  • persists for days/weeks
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22
Q

liquefactive necrosis

A
  • bacterial or fungal infections
  • function and structure lost
  • hypoxic death of cells within CNS evokes liquefactive necrosis known as BRAIN INFARCTS
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23
Q

gangrenous necrosis

A
  • in limbs!

- usually due to small or large artery occlusion

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24
Q

wet gangrene

A

when a bacterial infection is superimposed then coagulative necrosis is modified by liquefactive pattern known as ‘wet’

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25
Q

caseous necrosis

A
  • CHEESE LIKE
  • associated with tuberculosis
  • rements become GANULAR (not solid like coagulase or liquid like liqufactive)
  • often enclosed by a granuloma
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26
Q

fat necrosis

A
  • white color
  • pancreus
  • FA bind to Ca+
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27
Q

fibrinoid necrosis

A
  • immune reactions involving BV= Polyarteritis nodosa
  • antigen/antibody complexes depositied within the walls of arteries
  • Ag-Ab immune complexes together with fibrin
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28
Q

early vs late lesions of arteries with fibrinoid necrosis

A

early= PMNs and eosinophils

late= lymphocytes, plasma cells, GRANULOMATOUS INFLAMMATION does NOT occur

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29
Q

what happens id Ag-Ab immune complexes together with fibrin are not removed from artery walls

A

they attract Ca+ and cause blockages

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30
Q

what are 4 subcellular responses to injury?

A

1) autophagy
2) induction (hypertrophy) of smooth ER
3) mitochondrial alterations most important
4) cytoskeletal abnormalities

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31
Q

autophagy

**subcellular responses to injury

A

process of self survival in nutrient deprivation

  • preserves heath of cells by replacing damaged ones with fresh cells
  • starved cells lives by eating its own contents
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32
Q

cancer and autophagy

A

autophagy has a downside bc cancer cells exploit it to survive in nutrient-poor tumors

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33
Q

autophagicavuoles vs autophagolysosomes

A

autophagicavuoles= form from the ribosome free region of the ER

autophagolysosomes= upon fusion with lysosome itself

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34
Q

heterophagy

A

process of cell consuming material from its environment. the mechanisms that takes place in the macrophages to destruct ingested substances

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35
Q

residual bodies

A

when some lysosomes with undigested debris persist within a cell after autophagy

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36
Q

induction (hypertrophy) of smooth ER

**subcellular responses to injury

A
  • smooth ER involved
  • response to chemicals causing ER hypertrophy
  • BARBITURATES are metabolized in liver and its tolerance is due to in INcrease of
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37
Q

P-450 enzyme

A

detoxifiers of chemicals, process may also render more injurious (CCl4) by resulting in reactive oxygen species (ROS ) that can injure cell

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38
Q

mitochondrial alterations

**subcellular responses to injury

A

-alterations in #, size, shape, and function

39
Q

cellular hypertrophy vs cellular atrophy

A
  • cellular hypertrophy= increased # of mito
  • cellular atrophy= decreased # of mito

**mitochondrial alterations– subcellular responses to injury

40
Q

mitochondrial myopathies

A

defect in mito metabolism associated with increased # unusually large mitochondria, containing abnormal cristae

**mitochondrial alterations– subcellular responses to injury

41
Q

cytoskeletal abnormalities

**subcellular responses to injury

A

interfere with assembly and function of cytoskeletal filaments, may results in abnormal accumulations of filaments, aberrent movement or organelles

42
Q

vinca alakaloids

A

bind to MT and decrease tototic spindles during replication (cytoskeleton abnomality)

43
Q

cardiac or skeletal muscle take longer to die after ischemia?

A 
skeletal= 2-3 hours
cardiac= 20-30 minutes
44
Q

major causes of ATP depletion?

A

1) decreased oxygen and nutrients
2) mitochondrial damage
3) toxins (cyanide)

45
Q

depletion of ATP to ____% of normal has widespread effects on critical cellular systems

A

<5-10%

46
Q

glycolytic pathway can generate?

A

ATP in the absense of oxygen using glucose!

*Liver can survive longer than other organs with limited glycolysis, like the brain

47
Q

Na+/K+ pump… how many in and out?

A

3 Na+ OUT
2 K+ IN
*uses ATP to get Na+ out, becomes ADP allowing the pump to open letting K+ in, once K+ is in the pump ditches ADP and restarts with ATP

48
Q

damage to mitochondria

A
  • mito needed to ATP production, and cell energy/death
  • damaged by increased INtracellular Ca++, ROS and O2 deprivation (hypoxia/toxins)
  • damage causes MPTP formation and pH changes
  • Either ATP depletion leading to necrosis OR apoptosis due to leakages (like cytochrome c)
49
Q

increased Ca++ in a cell can cause?

A

apoptosis (activates caspases and mito permeability)

*activation of phopholipase, protease, endonuclease, ATPase

50
Q

Reactive Oxygen Species (ROS) is produced and removed where?

A

produced in mito and removed by degradation

51
Q

what is oxidative stress?

A

when there is an increased ROS production or the scavenger system fails to remove them which results in increased free radicals
*ROS production is greater than body’s ability to remove

52
Q

what are some triggers that cause excess ROS production?

A

UV light exposure, pollution, smoking, eating an unhealthy diet, excessive exercise, certain medications and/or treatments

53
Q

Vitamins A, C, E, and B-carotene are all examples of?

A

antioxidents that block the formation o f free radicals or scavenge them

54
Q

3 main reactions that are particularly relevant to cell injury mediated by free radicals?

A

1) lipid peroxidation of cell membranes
2) cross-linking of proteins (increases protein degradation)
3) DNA fragmentation (single strand breaks)

55
Q

examples of cell injury and necrosis

A

1) ischemic and hypotoxic injury
2) ischemica-reperfusion injury
3) chemical (toxic) injury)

56
Q

root word of apoptosis?

A

“falling away from”

57
Q

In regards to the cellular membrane, how does necrosis and apoptosis differ?

A
  • apoptotic cell membrane remains intact (except for blebing) and becomes a target for phago so there is no leakage or inflammation
  • necrosis has loss of membrane integrity, enzymatic digestion of cells and leakage of cellular contents frequently causing inflammation or host reaction
58
Q

the fundamental event in apoptosis is the activation of enzyme called?

A

caspase

Cysteine proteases that cleave protein after ASPartic residues

59
Q

activation of caspases causes activation of?

A

nucleases that degrade DNA and other enzymes that destroy nucleoproteins and cytoskelatal proteins
**activation of apoptosis depends on a balance between pro and anti apoptotic molecules

60
Q

what are the 2 distinct pathways that activate appoptosis that do interact?

A

1) mitochondrial/intrinsic pathway

2) death receptor/extrinsic pathway

61
Q

anti-apoptotic molecules?

A 
BCL-2
BCL-XL
BCLW
MCL
BCLB
\+viral homologs
62
Q

BCL-2 vs BCL-2 superfamily

A

BCL-2 protein is ANTI ONLY

*BCL-2 superfamily is both pro and anti

63
Q

executioner caspases cause (caspase 3)?

A

1) endonucleases activation

2) breakdown of fcytoskeleton

64
Q

phagocytic clearance of apoptotic cells may be considered to consist of 4 distinct steps

A

1) accumulationof phagocytes
2) recognition of dying cells- bridge molecules and receptors
3) engulfment
4) processing

65
Q

what molecule is in both apoptosis and necrosis (coexist)?

A

poly-ADP polymerase
*DNA damage, during apoptosis, activates poly-ADP polymerase, which depletes nicotinamide adenine, leading to fall of ATP, resulting in necrosis

66
Q

p53

A

causes BOTH a helt in the cell cycle and repair of damaged DNA!! If unsuccessful, activates Bax and Bak for apoptosis

67
Q

growth hormones, lymphocytes and nerves, typically activate what pathway for apoptosis?

A

mitochondrial

68
Q

accumulation of misfolded proteins causes ___ stress

A

ER stress; resulting in apatosis

*common in neurodegenerative diseases

69
Q

cytotoxic T lymphocytes (CTL) granule protease called ______ cleaves proteins at aspartate residues and can activates?
*may induce what?

A

called Granzymes

  • activate caspases, effector phase of apoptosis, without involving tradittional pathways (death receptor or mitochondria)
  • may also induce apoptosis by ligation of Fas receptors on target cells
70
Q

describe autophagy

A

self eating
*intracellular stuff is first sequestered in autophagic vacuole, and THEN fuses with lysosomes to form an autophagolysosomes for digestion

71
Q

5 common intracellular accumulations?

A

1) fat
2) cholesterol and cholesteryal esters
3) proteins
4) glycogen
5) pigments

72
Q

fatty change (intracellular accumulation)

A
  • accomulation fo triglycerides within parenchymal cells
  • cause FATTY LIVER
  • apoproteins form lipoprotein complex
73
Q

most common causes of fatty liver?

A

alcohol consumption and diabetes mellitus

74
Q

cholesterol and cholesteryal esters (intracellular accumulation)

A
  • cholesterol metabolism is tightly regulated but may become overloaded with lipids
  • macrophages become “FOAMY macrophages” upon contact
  • artherosclerosis
  • hyperlipidemic syndrome
75
Q

artherosclerosis

A

smooth muscle cells and macrophages filled with lipid vacuoles giving the plaque their characteristic yellow appearance

76
Q

hyperlipidemic syndrome

A

hereditary or acquired

*forming of masses of foamy macrophages celled xanthomas

77
Q

protein (intracellular accumulation)

A
  • less common than lipid accumulation
  • due to excess synthesis
  • pinocytic vesicle containing proteins fuse with lysosomes resulting in PINK hyaline cytoplasmic droplets
  • Nephrotic syndrome
  • Russell bodies
  • Mallory body (alcoholic hyalin)
  • neurofibrillary tangle
78
Q

Nephrotic syndrome

A

when heavy protein (albumin) leaks, there is an increased reacsorption of albumin by pinocytosis in the proximal convoluted tubules

79
Q

Russell bodies

A

accumulation of immunoglobulins in the RER of some plasma cells

80
Q

Mallory body (alcoholic hyalin)

A

eosinophilic cytoplasmic inclusion in the liver cells composed of aggregated intermediate filaments that presumably resist degradation
*seen in alcoholic liver disease

81
Q

neurofibrillary tangle

A

seen in brain of Alzheimers patient

*aggregation of microtubule-associated proteins and neurofilaments that disrupt neuronal cytoskeleton

82
Q

glycogen (intracellular accumulation)

A

indiabetes, glycogen may accumulate in renal tubular epithelium, hepatocytes and cardiac myocytes and B cells of Islets of Langerahnds
*enzyme myophosphorylase is needed

83
Q

B cells in liver produce?

A

insulin

84
Q

myophosphorylase

A

enzyme needed for breakdown of glycogen into sugar in muscles
*in hereditary glycogen storgae disease you LACK this enzyme

85
Q

pigments (intracellular accumulation) of CARBON

A

exogenous or endogenous

  • Carbon most common exogenous; causes black streaking in lungs called ANTHRACOSIS
  • not harmful unless it accumulates which would induce emphysema and coal workers pneumonocniosis
86
Q

lipofusion

A

an endogenous pigment for “wear and tear”

*in large amounts cause ‘brown atrophy’ which is PERINUCLEAR and accumulate in many tissues (heart, lung)

87
Q

melanin

A

brown-black endogenous pigment that protects against UV radiation
*causes freckles, benign moles and melonoma

88
Q

Hemosiderin

A

hemoglobin-derived pigment from breakdown of erythocytes, golden to brown.. CAUSES BRUISES
*is the iron complex to apoferrin forming ferritin micelles

89
Q

SIR2 proteins

A

activated by calorie restriction

  • activate DNA repair mechanisms
  • gets worse with aging
90
Q

p16

A

inhibits cell cycle

*reduced regeneration capacity of tissue in stem cells

91
Q

telomeric DNA is composed of ____ repeats

A

tandem repeats of guanine rich sequence TTAGGG in a single stranded overhang at the 3’ end

92
Q

telomerase and its proteins

A

enzyme that replicates telomer

**exclusive proteins are TRF1, TRF2, POT1

93
Q

senescence

A

a potent anti-carcinogenic regulatory program that is important for telomerase and telomers; will disappear with cell age

94
Q

1) superoxide dismutases (SODs)
2) glutathione peroxidase
3) catalase (in peroxisomes)
4) vitamine A, C, E and B-carotene
5) transferrin, ferritin, lactoferrin, and ceruloplasmin

A

1) spontaneousy decay superoxide
2) catalyze free radicals
3) degenerate hydrogen peroxide
4) antioxidants that block formation of free radicals
5) bind iron and copper to catalyze formation of ROS

Pathology 1 (21 decks)

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