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Pathology I > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

necrosis is ___ injury

A

unselective
irreversible

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2
Q

apoptosis is ___ injury

A

selective
irreversible

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3
Q

hepatic lipidosis is ___ injury

A

reversible

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4
Q

what are the 4 main categories of cell injury causes?

A

deficiency of critical material
lack of cellular energy production
accumulation of abnormal substances
physical injury

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5
Q

define ischemia

A

inadequate blood supply to an organ or part of body

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6
Q

describe the pathogenesis of the irreversible ischemic cell injury

A

MEMBRANE INJURY (phospholipid loss, cytoskeleton issue) -> Ca influx, enzyme leakage

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7
Q

describe the pathogenesis of reversible ischemic cell injury

A

MITOCHONDRIA DAMAGE -> decrease oxidative phosphorylation -> decrease ATP -> decrease Na pump -> influx Na/water/Ca -> cell swell, blebs, ER swell

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8
Q

list the physical signs of reversible cell injury

A

cell swell
ER swell
loss of microvilli
membrane blebs
clumped chromatin
lipid accumulation
myelin figures

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9
Q

list the physical signs of irreversible cell injury

A

cell membrane damage, rupture

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10
Q

list the physical signs of cell death

A

pyknosis
karyorrhexis
karyolysis
absence of nuclei
cytoplasmic eosinophilia

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11
Q

describe the pathogenesis of cell injury due to oxygen deprivation.
what if no oxygen appears to reverse the injury?

A

hypoxia -> aerobic cell metabolism stops -> decreased ATP production

switch to anaerobic metabolism -> intracellular acidosis -> lose ribosomes due to swollen ER -> lysosome rupture -> release RNA/DNA -> membrane rupture -> cell death

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12
Q

what happens if there’s a LARGE number of cell deaths?

A

gap is replaced with fibrous CT

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13
Q

what pathology is shown in this image?

A

renal infarct

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14
Q

define infarct

A

small area of dead tissue due to failure of blood supply

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15
Q

define hydropic degeneration

A

water movement into cells (swelling)
reversible

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16
Q

describe the pathogenesis of hydropic degeneration

A

injury/HYPOXIA
decreased mitochondria activity
damage cell membrane
interfere ion channels of membranes
decreased Na/K activity
increased Na in cytoplasm
water accumulation
mitochondria/ER swell
hydropic degeneration

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17
Q

what type of hydropic degeneration is caused by parapoxvirus?

A

bovine papular stomatitis

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18
Q

what type of cell injury is caused in this image of mucosa?

A

hydropic degeneration

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19
Q

what is this an example of in the mucosa of a cow tongue? (black circles and arrow)

A

circles - ballooning degeneration
arrow - viral inclusion bodies

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20
Q

define hepatic lipidosis

A

“fatty change”
intracellular accumulation of fatty acids within cytoplasm of hepatocytes

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21
Q

what are the possible mechanisms that can result in hepatic lipidosis?

A

*** only one of these needs to occur for lipidosis

free fatty acids excessively delivered from fat stores
decreased oxidation/use of FFA
impaired apoprotein synthesis
impaired lipoprotein formation
impaired release of lipoproteins from hepatocytes

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22
Q

what organ is this? describe the abnormality

A

liver
pale/yellow, swollen, friable, greasy

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23
Q

what cell injury does this liver have?

A

hepatic lipidosis
note nucleus pushed to side unlike hydropic degeneration

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24
Q

SLIDE 32 - rewatch

A
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25
Q

what diseases are associated with hepatic lipidosis?

A

ketosis and pregnancy toxemia
anorexia
high fat diets, obesity
hepatotoxins
hypoxia
hypothyroidism

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26
Q

difference between gross texture/color of lipid vs glycogen hepatocyte accumulation

A

lipid - pale yellow, friable
glycogen - pale tan/white, firm

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27
Q

list some disorders associated with lipid hepatocyte accumulation

A

ketosis
pregnancy toxemia
high fat diet
obesity
hepatotoxins
hypoxia
diabetes mellitus
hypothyroidism

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28
Q

list some disorders associated with glycogen hepatocyte accumulation

A

excess glucocorticoids
diabetes mellitus
young animals

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29
Q

describe positioning of nuclei in lipid hepatocyte accumulation histology

A

nuclei pushed to periphery

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30
Q

describe vacuole shape/border in lipid hepatocyyte accumulation

A

distinct borders

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31
Q

describe positioning of nuclei in glycogen hepatocyte accumulation histology

A

nuclei stay central

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32
Q

describe vacuole shape/border in glycogen hepatocyte accumulation

A

margins are irregular or indistinct

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33
Q

ID the liver accumulation circled in this image

A

glycogen

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34
Q

SLIDE 38

A
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35
Q

ID the organ and pathology

A

liver
glycogen accumulation - hepatocellular vacuolation

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36
Q

ID the organ and the pathology

A

liver
fat accumulation - since nuclei are off-center

37
Q

what disease is shown in this image of a dog brain?

A

lysosomal storage disease

lysosome can’t digest proteins

38
Q

define necrosis

A

hypoxia, ischemia, direct cell membrane injury
SWELLING (onco-)
pathologic cell death/murder
inflammation
release cell content
disrupt cell membrane
messy looking

39
Q

define apoptosis

A

programmed cell death/suicide
SHRINKAGE
physiologic cell death
NO inflammation
cell membrane stays intact
organized, clean

40
Q

define pyknosis

A

irreversible condensation of chromatin in nucleus of cell

41
Q

define karyorrhexis

A

fragmentation of nucleus

42
Q

define karyolysis

A

nucleus is pale

43
Q

define absence of nucleus

A

later stage of karyolysis

44
Q

Name the cell stage of cellular necrosis and describe the nucleus

A
45
Q

Match each number to its terms
terms - pyknosis, karyorrhexis, and karyolysis

A

1 - pyknosis
2 - karyorrhexis
3 - karyolysis

46
Q

describe the mitochondrial/intrinsic path of apoptosis

A

cell injury
BCL2 family sensor
BCL2 effectors (BAX, BAK)
mitochondria
cytochrome c (pro-apoptosis)
initiator capase 9
executioner capase 3, 7, 9, 12
endonuclease activation and breakdown of cytoskeleton
bleb
apoptotic body

47
Q

describe the death receptor/extrinsic pathway of apoptosis

A

receptor ligand interaction (Fas, TNF)
adaptor protein
initiator capases
executioner capases
endonuclease activation and breakdown cytoskeleton
bleb
apoptotic body

48
Q

list the pro-apoptotic BCL2

A

BAX
BAK

49
Q

list the anti-apoptotic BCL2

A

BCL2
BCL-XL

50
Q

list the initiator capases for intrinsic and extrinsic pathways

A

intrinsic - capase 9
extrinsic - capase 8

51
Q

list the executioner capases

A

capase 3, 6, 7, 12

52
Q

list the key morphologic features of apoptosis

A

cell shrinkage
chromatin condensation
cytoplasmic blebs and apoptotic bodies
phagocytosis of apoptotic bodies

53
Q

apoptosis or necrosis? explain why

A

apoptosis
since fragmentation but no inflammation

54
Q

apoptosis or necrosis? explain why

A

apoptosis
since fragmentation but no inflammation

55
Q

what does hematoxylin stain in H&E?

A

stains purple
nuclei, bacteria, calcium

56
Q

what does eosin stain in H&E?

A

stains pink
cytoplasm, collagen, fibrin, RBC
*protein is pink

57
Q

which is basophilic vs eosinophilic?

A
58
Q

define basophilic

A

purple
basic

59
Q

define eosinophilic

A

pink
acidic

60
Q

define amphophilic

A

both basophilic and eosinophilic

61
Q

what is this from H&E

A

amphophilic

62
Q

list key features of necrosis on H&E stain

A

increased eosinophilia (RNA degrade)
glassy appearance (glycogen is lost)
cytoplasm vacuolation
karyorrhexis become karyolysis
ghost cells
necrotic cells induce leukocyte migration to dissolve cell

63
Q

what are ghost cells?

A

pale eosionophilic outlines of residual cell cytoplasm

64
Q

what does the red indicate?

A

hypereosinophilia
indicates cell death/necrosis

65
Q

what does the arrow show? (in nucleus)

A

viral inclusion body

66
Q

if the right image is normal, what can you say is likely occurring in the left image?

A

necrosis
* tissue has become unrecognizable

67
Q

define coagulative necrosis

A

denaturation with dense/rigid texture to dead cells

68
Q

define liquefactive necrosis

A

process of complete enzymatic digestion of cells
usually in the brain

69
Q

caseous necrosis define

A

cheesy, coagulative, granulomatous reaction

70
Q

define fat necrosis

A

saponification
fatty acids mixed with calcium
chalky white

71
Q

define gangrenous necrosis

A

necrosis due to ischemia of distal extremities

72
Q

what type of necrosis is occurring?

A

coagulative - since the myocardial cells appear dry with a loss of nuclei, fragmented

73
Q

why are leukocytes present?

A

clear up sarcoplasmic debris from the necrosis

74
Q

what type of necrosis is renal papillary necrosis?

A

coagulative necrosis - due to ischemia after NSAID use

75
Q

pathogenesis of renal papillary necrosis

A

inhibition of PG synthesis via NSAID blocking COX-1 and COX-2 -> renal hypoperfusion > ischemia -> papillary necrosis

76
Q

what are the primary vasodilators of kidney?

A

renal PGs

77
Q

what’s wrong with the kidney?

A

renal infarct aka hypoxic injury

78
Q

which portion is abnormal/normal (R/L)?

A

L side of kidney - abnormal, dead tissue
middle - hemorrhage where cells are dying
R side - inflamed

79
Q

suppurative necrosis is a type of ___ necrosis

A

liquefactive

80
Q

ID the type of necrosis

A

liquefactive - uterus

81
Q

ID the type of necrosis in this brain sample

A

liquefactive - R side vacuolated, excess lipid
* L side normal

82
Q

ID the type of necrosis

A

caseous - lung
cheesy appearance

83
Q

caseous necrosis is a combination of which necrosis types?

A

coagulative and liquefactive

84
Q

caseous necrosis is most characteristic of ___ inflammation

A

granulomatous

85
Q

where does fat necrosis most commonly occur?

A

next to pancreas

86
Q

ID the necrosis type

A

fat necrosis - pancreas

87
Q

ID the necrosis type

A

gangrene

88
Q

define “wet” gangrene necrosis

A

combination of coagulative (loss of blood supply) and liquefactive (superimposed infection)

Pathology I (17 decks)

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