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General Pathology > Lecture 1: Cell Injury > Flashcards

Lecture 1: Cell Injury Flashcards

1
Q

__ is an abnormal body process with a characteristic set of signs or symptoms and lesions that may affect the whole body or any of its parts.

A

Disease

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2
Q

The fundamental disease process begins with injury at the __ level

A

molecular and cellular

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3
Q

__ refers to damage or pathologic alterations in cell molecules or structure

A

cell injury

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4
Q

__ are cell alterations that are associated with disease

A

lesions

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5
Q

What are the 8 causes of cell injury

A
  1. hypoxia/hypoxemia
  2. physical agents
  3. chemicals/drugs
  4. infectious agents
  5. immunologic reactions
  6. Genetic defects
  7. nutritional imbalances
  8. aging
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6
Q

What are the responses to cell injury

A
  1. adaptation (hypertrophy)
  2. reversible cell injury
  3. irreversible cell injury and death (necrosis and apoptosis)
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7
Q

Necrosis (oncotic necrosis) is a pattern of cell death that often follows hypoxic, toxic and microbial injury and is characterized by __

A

Cell swelling with nuclear changes

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8
Q

__ is cell death induced by tightly regulated intracellular program where enzymes degrade the cell’s nuclear DNA and proteins leading to nuclear framentation w/o loss of plasma membrane integrity

A

Apoptosis

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9
Q

3 microscopically visible changes in reversible cell injury

A
  1. cell swelling
  2. chromatin clumping
  3. lipidosis
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10
Q

7 ultrastructural changes in reversible cell injury

A
  1. dilation of ER
  2. ribosomal detach from RER
  3. Loss of microvilli and cilia
  4. mitochondrial swelling
  5. chromatin clumping
  6. membrane blebs
  7. lipid accumulation
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11
Q

Many things that cause swelling are due to

A

mitochondrial damage

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12
Q

Ischemia causes a decrease in oxidative phosphorylation by the mitochondria which causes a decrease in __

A

ATP

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13
Q

Decrease in ATP due to ischemia causes what 3 things

A
  1. decrease Na pump (ER, cellular swell, loss of microvilli, blebs)
  2. increase anaerobic glycolysis
  3. decreased protein synthesis
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14
Q

What happens when ischemia causes decreased ATP leading to decreased Na pump activity

A

Ca, water, and Na flow into the cell and K flows out causing swelling

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15
Q

What happens when ischemia causes decreased ATP leading to an increase in anaerobic glycolysis

A

cell uses up glycogen (decreases) and pH decreases (acidic) causing chromatin clumping

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16
Q

When ischemia causes decreased ATP and protein synthesis what can be seen

A

lipid deposition

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17
Q

Irreversible cell injury (necrosis) has 2 microscopically visible changes

A
  1. nuclear changes (pyknosis, karyorrhexis, chromatolysis)

2. increased eosinophilia of cytoplasm

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18
Q

Irreversible cell injury (necrosis) has 4 ultrastructural changes

A
  1. high mitochondrial swelling
  2. membrane defects
  3. lysosomal membrane rupture
  4. nuclear condensation, fragmentation, dissolution
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19
Q

Necrotic tissue has what gross changes

A

pale/dull coloration

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20
Q

what are the 6 forms of necrosis discussed

A
  1. coagulation necrosis (simplest)
  2. liquefactive necrosis
  3. caseous necrosis
  4. gangrenous necrosis
  5. fat necrosis
  6. fibrinoid necrosis
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21
Q

What are 3 microscopic features seen in coagulative necrosis

A
  1. nuclear changes
  2. increased eosinophilia of cytoplasm
  3. cell borders STILL VISIBLE
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22
Q

__ necrosis pathogenesis is due to high influx of neutrophils (protease destruction) in tissue with high fat content (brain, lung)

A

liquefactive

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23
Q

Liquefactive necrosis has 3 microscopic features

A
  1. LOSS of cell borders (unlike in coagulative necrosis)
  2. granular basophilic and eosinophilic debris with nuclear fragments
  3. tissue structure is obliterated
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24
Q

__ necrosis involves recruitment of macrophages with persistence of stimulus and inflammatory cell component breakdown and is commonly seen in mycrobacterial infections

A

caseous

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25
Q

caseous necrosis is seen with __ infections

A

mycrobacterial (bovis, tuberculosis), corynebacterium ovis, fusobacterium necrophorum

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26
Q

Caseous necrosis has 3 microscopic features

A
  1. LOSS of cell borders (like liquefactive)
  2. center of lesions homogenously eosinophilic with scattered nuclear basophilia
  3. tissue structure is obliterated (like liquefactive)
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27
Q

__ necrosis is characterized by the loss of blood supply to distal extremities (toes, feet, ear) and hypoxia induced necrosis

A

gangrenous necrosis

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28
Q

___ necrosis can be seen in pancreatitis and vitamin E deficiency

A

fat necrosis

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29
Q

__ is characterized by enzymes cleaving triglycerides and making free FA wich form soaps of yellow-white areas in the fat

A

fat necrosis

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30
Q

little to no inflammation is seen with: necrosis or apoptosis

A

apoptosis (cell buds off keeping damaging enzymes contained)

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31
Q

__ is a process of cell death that occurs both physiologically and pathologically

A

apoptosis

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32
Q

DNA damage (UV, chemo, carcinogens), misfolded protein accumulation, drug/cytokine induced (glucocorticoid,TNF), viral induced (lentivirus), atrophy of organs after duct obstruction are examples of __ induced apoptosis

A

pathologic

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33
Q

embryogenesis, hormones, tissue repair, deleting autroreactive t cells in thymus, virus infected cells induced by cytotoxic t-cells are examples of __ induced apoptosis

A

physiologic

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34
Q

2 things that inhibit apoptosis

A
  1. neoplastic dz (P53 mutations)

2. viral-induced proliferative dz (Epstein Bar virus has protein homologe)

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35
Q

list intrinsic (changes in the mitochondrial) that initiate apoptosis

A
  1. withdraw of growth factors or

2. injury (radiation, toxins, free radicals)

36
Q

list extrinsic (death receptor-initiated pathways) that initiate apoptosis

A
  1. receptor-ligand interations (FAS, TNF) or

2. Cytotoxic T lymphocytes

37
Q

after apoptosis in initiated (intrisic or extrinsically) what happens

A

caspases are initiated

38
Q

Caspases initiated

A

cytoskeleton breakdown (proteases) and DNA/nuclear fragmentation (endonucleases), apoptotic body formation

39
Q

Apoptotic bodies express __ for phygocytic cell receptors

A

ligands (phophatidylserine or thrombospondin)

40
Q

Apoptotic bodies contain cell material and allow apoptosis to occur without __ and __

A

swelling and minimal inflammation (unless they are lysed)

41
Q

6 steps of the extrinsic apoptosis pathway

A
  1. stimulation of receptor by ligand
  2. alteration in second signals
  3. activation of caspases
  4. activation of endonucleases and cytoskeleton breakdown
  5. nuclear and cytoplasmic fragmentation
  6. phagocytosis of apoptotic bodies
42
Q

Loss of stimuli, injury, or positive stimulus increases decreases ATP production and allows mitochondrial permeability which releases __ and other activators of the caspase system to initiate the intrinsic/mitochondrial pathway to apoptosis

A

cytochrome c

43
Q

the extrinsic (death receptor-initiated) apoptotic pathway is initiated by __ which activates caspase system

A

FAS-FAS Ligand

TNF-TNF receptor

44
Q

Apoptosis is detectable microscopically but there is rarely __

A

gross changes

45
Q

__ is characterized by cell swellign and nuclear changes, is pathologic, grossly visible (coagulation, liquefactive, caseous), ussualy causes inflammation

A

necrosis

46
Q

list 4 things that are pathogenetic mechanisms to necrosis

A
  1. ATP depletion
  2. membrane damage
  3. free radical injury
  4. calcium influx
47
Q

__ is characterized by nuclear and cytoplasmic fragmentation (endonuclease/protease activation by caspases), NO CELL SWELLING, can be pathologic or physiologic, little/no inflammation, not usually detected grossly

A

apoptosis

48
Q

2 pathogenic mechanisms of apoptosis

A
  1. intrinsic/mitochondrial permeability and cytochrome c release
  2. extrinsic (death receptors FAS, TNF, granzyme)
49
Q

__ is a form of programmed cell death similar mechanically to apoptosis but morphologically appears like necrosis

A

necroptosis “programed necrosis”

50
Q

4 features of necroptosis

A
  1. caspase 8 independent
  2. RIP signaling
  3. mitochondrial alterations and decreased ATP
  4. cell damage = inflammation

overall, not apoptotic bodies, looks like necrosis (swelling and nuclear changes) but is programmed

51
Q

How does TNF cause apoptosis vs necroptosis

A

apoptosis - TNF activates caspase 8

necroptosis - TNF fails to activate capsase 8

52
Q

___ caused when microbial products interact with NOD like receptors to induce activation of inflammasome and apoptotic like mechanisms

A

pyroptosis

53
Q

during __ animal gets fevers and becomes leukopenic (IL 1), there is severe swelling and inflammation, cell death looks like necrosis (capsase 1 and 11)

A

pyroptosis

54
Q

both apoptosis and necroptosis can be

A

regulated/programmed

55
Q

__ is the oldest recognized programmed cell death where __ is the newest recognized programmed cell death

A

apoptosis, necroptosis

56
Q

__ is programmed cell death via caspase 8 independent mechanisms involving mitochondrial permeability and “necrosis”

A

necroptosis

57
Q

How can you the difference between necrosis and post-mortem autolysis?

A

diffuse change throughout body/organs
NO INFLAMMATORY reaction/no tissue response
microscopically tissue appears pale/washed out

58
Q

ischeima/hypoxemia injury causes Increase in cytoplasmic __ from outside the cell, the mitochondria, and ER cause membrane damage via decreased ATP and phospholipids, nuclear changes, and disruption of cytoskeleton

A

Ca

59
Q

__ is a chemical species that has a single unpaired electron in an outer orbital (highly reactive with proteins and nucleic acids)

A

free radical

60
Q

list 2 common free radicals

A

superoxide radicals (O2-) and hydoxyl radical (OH-)

61
Q

3 ways free radical damage occurs

A
  1. absorb radiant E (UV)
  2. reduction-oxidation rxn during normal physiologic processes
  3. exposure to toxins (oxygen, carbon tetrachloride, drugs)
62
Q

What are some normal physiological process (redox rxns) that create free radicals

A
  1. respiratory enzymes and o2
  2. xanthine oxidase (purine metabolism)
  3. cytochrome P450 monooxygenase activity
  4. NADPH oxidase
  5. fenton reaction
63
Q

radicals are trasferred to many different substrates via __ reactions forming free radical intermediates

A

autocatalytic

64
Q

4 substrates most at risk for free radical propagation

A
  1. proteins - especially sulfur containing AA
  2. nucleic acids
  3. membrane lipids-unsaturated bond (lipid peroxidation)
  4. cytosolic molecules - Hemoglobin
65
Q

when lipid peroxidation occurs at high levels it can become __ causing complete lipid hydroperoxide formation which leads to membrane dysfunction and permeability.

A

autocatylitic (chain reaction)

66
Q

3 ways free radicals are terminated

A
  1. scavengers (vitamin E)
  2. Enzymatic degradation/adaptation ( SOD, catalase, glutathione)
  3. spontaneous decay
67
Q

What enzymes degrade free radicals

A
  1. SOD (O2- to O2 and H2O2)
  2. Glutathione (OH- to water and O2)
  3. Catalase (H2O2 to water and O2)
68
Q

3 antioxidant defense scavengers for free radicals

A
  1. sulfhydryl rich molecules (glutathione, cystine)
  2. vitamin E and C
  3. Ceruloplasmin and transferrin
69
Q

How does Vitamin E and C scavenge free radicals

A

terminantes lipid peroxidation

70
Q

how do ceruloplasmin and transferrin scavenge free radicals

A

apoproteins bind copper and Fe (stops fenton rxn?)

71
Q

4 common pathways in cell death

A
  1. ischemia and hypoxic injury
  2. free radical injury
  3. chemical injury
  4. infectious agent injury
72
Q

reperfusion injury is combined __ and __ damage

A

hypoxic (ischemia) AND free radical (O2 and inflammatory cells)

73
Q

during reperfusion injury: reduced blood flow causes hypoxic damage through __. Ca activated proteases causing increased __. When blood flow is reestablished it brings __, __, and __. Oxygen and inflammatory cells create __ further damaging the membrane and causing __.

A 
decreased ATP
xanthine oxidase (makes free rads later)
oxygen, Ca, inflammatory cells 
free radical 
increased intracellular Ca/cell death
74
Q

__ causes CCl4 (carbon tetracholoride) to be converted into CCL3- (free radical). CCl3- radical damages hepatocytes via __. The enzymes that activate this toxin leads to centrilobular ___ . Toxin uses local generation of free rads by the cell to cause injury.

A

Cytochrome P450.
lipid peroxidation.
hepatocellular coagulation necrosis

75
Q

exotoxin released by __ causes phospholipase induced membrane damage and immediately induce cell necrosis.

A

Clostridia bacteria (clostridium perfringens type C)

76
Q

3 ways Endotoxin released by bacteria induce cell injury/death

A
  1. direct membrane damage
  2. endotoxin directly initiating apoptosis
  3. TNF alpha induced in macs and binds to TNF receptors to induce apoptosis in lymphocytes.
77
Q

What is most likely the main mechanism of endotoxins to cause cell death

A

high levels of TNF and other cytokines inducing apoptosis via extrinsic mechanism

78
Q

Cellular adaptation to injury in 4 ways (ie exposed to low levels of free radicals over time)

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

hyperplasia and mataplasia are important events leading to neoplasias

79
Q

__ is reduciton in size of an organ/tissue/cell due to decrease in cell size and number

A

atrophy (physiologic/development or pathologic)

pathologic response: immobilization, deinnervation, decrease blood/nutrition/hormones, increased pressure,

80
Q

mechanisms of atrophy

A

protein degradation and autophagy (lysosomeal digestion of cell’s own components)

81
Q

__ is increase in cell size that results in an increase in the affected organ size

A

hypertrophy (physiologic or pathologic)

physio = increase muscle size for increased workload
path = increased liver size due to drug or toxin metabolism
82
Q

mechanism of hypertrophy

A

increased and/or altered protein production

83
Q

mechanism of hypertrophy

A

increased and/or altered protein production

84
Q

what cell organelle proliferates during hypertrophy

A

SER (increase protein production)

85
Q

__is an increase in the number of cells in an organ/tissue in response to stimulus and often occurs with __

A

hyperplasia (path or physiologic), hypertrophy

path = excess/inappropriate hormone/growth factors, chronic injury, viral infections

86
Q

__ is a REVERSIBLE change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type.

A

metaplasia (path, i.e. heavy smoker gets squamous metaplasia in trachea)

87
Q

mechanism of metaplasia

A

chronic injury (infection/toxin) causes reprogramming of tissue stem cells to a different type (columnar epi to stratified squamous metaplasia)

General Pathology (14 decks)

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