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Pathology > Cell Injury & Death > Flashcards

Cell Injury & Death Flashcards

1
Q

Can cell injury be either reversible or irreversible?

A

yes

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2
Q

What is the first morphologic change in reversible injury?

A

cellular swelling

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3
Q

In reversible injury, what is derived from damaged ER?

A
  • blebs (distorted plasma membrane)
  • early chromatin clumping
  • cytoplasmic vacuoles
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4
Q

What can reversible injury be noted as?

A

increased turgor, pallor, and weight

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5
Q

What can lead to dysfunctional cell membrane transport in reversible injury?

A

decrease in ATP

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6
Q

Reversible injury results in an influx of what?

A

water and Na+ that appear as cell swelling

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7
Q

In reversible injury, decreased oxidative phosphorylation promotes what?

A

glycolysis

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8
Q

Anaerobic respiration leads to what?

A

lactic acid accumulation and reduced intracellular pH

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9
Q

What are the consequences of the glycolytic pathway?

A
  • altered enzyme function
  • decreased protein synthesis
  • protein structure and folding
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10
Q

Reduced protein synthesis is refleted in what from the RER?

A

detachment of ribosomes

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11
Q

The time scale of injury vaties upon what?

A

the metabolic status of cells

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12
Q

In irreversible injury, why are the membranes weaker?

A

rupture of lysosomes and autolysis

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13
Q

What is the main difference between reversible and irreversible injury?

A

lysosomes are damaged in irreversible injury and intact in reversible

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14
Q

What are the 3 nuclear changes in irreversible injury?

A

karyolysis, pyknosis, and karyorrhexis

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15
Q

What is karyolysis?

A

progressive disruption and random digestion of nucleus fades away

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16
Q

What is pyknosis?

A

chromatin becomes densely clumped appearing hard, dark, and shrunken

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17
Q

What is karyorrhexis?

A

when pyknotic nuclei break up into smaller, dense structures

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18
Q

What are the clinical diagnoses of irreversible injury??

A
  1. AST & ALT
  2. CK & troponin from myocardial cells
  3. lipase and amylase from pancreas
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19
Q

What are the 2 major forms of cell death?

A

necrosis and apoptosis

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20
Q

What is necrosis characterized by?

A
  • cell swelling
  • protein denaturation
  • organelle breakdown
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21
Q

When does necrosis occur?

A

after loss of blood/oxygen supply or exposure to noxious chemical toxin

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22
Q

What is apoptosis?

A

programmed cell death

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23
Q

What is apoptosis characterized by?

A

cell shrinkage, but intact organelles

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24
Q

When does the formaton of DNA fragmentation ladder occur?

A

during apoptosis

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25
Q

What type of cell injury has intrinsic and extrinsic pathways with no inflammation?

A

apoptosis

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26
Q

What are the normal physiological processes?

A
  • embryogenesis
  • hormone-dependent involution in adult organs
  • hoemstasis
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27
Q

What are the pathological processes?

A
  • injury
  • viral diseases
  • pathologic atrophy in organs after duct obstruction
  • immunologic reactions
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28
Q

What is the process of intrinsic apoptosis?

A
  1. release of cytochrome-c initiates formation of apoptosome
  2. Apaf-1 binds cytochrome-c and recruits pro-caspase-9 to apoptosome
  3. caspase 9 is activated and cleaves other caspases -> apoptosis
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29
Q

What is the difference between intrinsic and extrinsic apoptosis?

A
  • intrinsic= damage to cell
  • extrinsic= involves ligand
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30
Q

What are the anti-apoptotic proteins?

A

BCI-2 and livin

31
Q

What are the inhibitor/propoptotic proteins?

A
  • XIAP
  • c-IAP-1
  • c-IAP-2
  • survivin
  • bax, bid, bad
32
Q

What is Fas?

A

membrane spanning protein

33
Q

What does microscopically apoptosis appear as?

A

apoptotic bodies

34
Q

Biochemically/molecularly apoptosis appears as what?

A

DNA fragmentation ladder

35
Q

How does intact DNA, apoptotic DNA, and necrotic DNA appear?

A
  • intact: sits at the top
  • apoptotic: ladder
  • necrotic: big mush
36
Q

What are the morphologic changes of apoptosis?

A
  • organelles remain intact
  • cell shrinks
  • blebs form on cell surface
  • nuclear fragmentation
  • little or no infllamatory reaction
  • single cell
37
Q

Does apoptosis have inflammation?

38
Q

What is the mitochondrial (intrinsic) pathway?

A
  • growth factor withdrawal
  • DNA damage
  • protein misfolding
39
Q

What is the death receptor (extrinsic) pathway?

A

includes receptor-ligand interactions (Fas and TNF receptor)

40
Q

What is the most common form of cell death?

41
Q

What is necrosis?

A
  • hypoxia, toxins
  • involves areas of tissue
42
Q

What are the morphologic changes that happen to the cell during necrosis?

A
  • cell swells
  • organelles are disrupted
  • multiple cells
43
Q

What are the nuclear changes in necrosis?

A

karyolysis, pyknosis, karyorrhexis

44
Q

Is there inflammation in necrosis?

45
Q

What are the 2 types of necrosis?

A

coagulative and liquefactive

46
Q

What is coagulative necrosis?

A

protein denaturation

47
Q

What is liquefactive necrosis?

A

enzymatic digestion

48
Q

What is the most common form of necrosis?

A

coagulative

49
Q

Denaturation of cellular proteins causes what?

A

inhibition of proteolytic enzymes

50
Q

In what type of necrosis is the architecture reserved?

A

coagulative

51
Q

What is the characteristic of hypoxic death?

A

myocardial infarction

52
Q

How is proteolysis blocked?

A

denaturation of proteins and enzymatic proteins

53
Q

What is gangrene?

A

type of coagulation necrosis that is the gradual ischemia of distal extremities (foot, leg)

54
Q

When can gangrene occur?

A

with diabetes or frostbite

55
Q

What is the difference between “wet” and “dry” gangrene?

A
  • wet: bacterial superinfection of necrotic material
  • dry: black-brown, mummified appearance
56
Q

What is the difference between coagulative and liquefactive necrosis?

A
  • coagulative: inhibition of indogenous protease enzymes
  • liquefactive: enzymes that destroy tissue
57
Q

What is liquefactive necrosis?

A

digetsion of cells and tissue due to proteolytic activity with loss of structure

58
Q

What are the subtypes of liquefactive necrosis?

A

caseous and fat

59
Q

What is caseous necrosis?

A

necrosis due to myobacterial and fungal infections

60
Q

What is the appearance of caseous necrosis?

A

cheesy, white

61
Q

When does fat necrosis occur?

A

following pancreatic injury and realease of pancreatic enzymes

62
Q

Lipase digests triglycerides of adjacent what?

A

adipocytes release of fatty acids

63
Q

What do fatty acids combine with to form soaps?

A

extracellular Ca+

64
Q

What is the appearance of fat necrosis?

A

chalky white

65
Q

What are the stimuli resulting in cell injury?

A
  • oxygen deprivation
  • chemical and physical agents
  • infectious agents
  • immunologic reactions
  • genetic defects
  • nutritional imbalances
  • aging
66
Q

What are the biochemical mechanisms affected in injury?

A
  1. depletion of ATP
  2. generation of reactive O2 species
  3. defects in membrane permeability
  4. increased intracellular/loss of Ca
  5. mitochondrial damage
67
Q

Proteolysis during ischemia produces what oxidase?

68
Q

Xanthine oxidase can act on purines to produce what?

A

uric acid & superoxide anion

69
Q

How is the CCl3 radical formed?

A

when CCl4 is acted upon by P450 oxidases

70
Q

How is a free radical injury prevented?

A
  • cellular antioxidant (vitamins E&A)
  • sequestration of molecules
  • intracellular enzymes
71
Q

What is Carpal tunnel syndrome?

A

compression of median nerve

72
Q

What is Tarsal tunnel syndrome?

A

compression of tibial nerve

73
Q

What is Variant tarsal tunnel syndrome?

A

compression of deep peroneal nerve

74
Q

In the case study, what was wrong with the ballet dancer?

A
  • bilateral anterior tarsal tunnel syndrome variant
  • extensor hallucis bervis muscle hypertrophy

Pathology (7 decks)

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