Cell Injury (Part 2) Flashcards

1
Q

What are ways a cell can have intracellular accumulations?

A

excessive production
can’t get rid of a substance
cell lacks machinery to break down material - example carbon

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2
Q

What are intracellular accumulations?

A

endogenous
exogenous
pigments

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3
Q

What does endogenous mean?

A

cell itself makes it & accumulates

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4
Q

What does exogenous mean?

A

comes from outside the cell (viral inclusions)

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5
Q

How do pathologists determine glycogen vs. lipid on H&E?

A

lipids: will displace nuclei peripherally
glycogen: will not displace anything

both look like empty spaces

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6
Q

What are some stains used to identify lipid and glycogen? What happens?

A

PAS stain - glycogen stains magenta; diastase stain will remove this

lipids don’t stain with PAS

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7
Q

What are diagnostics for pale, swollen livers?

A

lipid (hepatic lipidosis)

glycogen

hepatic amyloidosis

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8
Q

What does hepatic lipidosis look like pathology-wise?

A

enlarged, yellow, soft, friable, rounded borders, bulge on cut surface, greasy texture

hepatocytes contain lipid vacuoles

adding lipids to hepatocytes - get bigger

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9
Q

What does a glycogen disorder look like pathology-wise?

A

(steroid induced hepatopathy, diabetes, glycogen storage diseases)

enlarged, rounded borders, pale beige to tan white, NONGREASY

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10
Q

What does a hepatic amyloidosis disorder look like pathology-wise?

A

enlarged yellow to orange, bulge on cut surface

Spaces of Disse

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11
Q

What do spaces of disse contain?

A

amyloid (also basement membranes of other organs)

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12
Q

What is the purpose of amyloid in the body?

A

made in times of inflammation (serum amyloid A)

irregular protein conformation - starts to accumulate

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13
Q

Which liver diagnosis could this be? Why?

A

hepatic lipidosis - greasy, enlarged with round borders

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14
Q

Which liver diagnosis could this be?

A

hepatic lipidosis - yellow to orange tinged

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15
Q

What liver disease could this be? Why?

A

glycogen disorder: enlarged, rounded borders, pale beige to tan white

NON-GREASY

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16
Q

A liver can have a reticular pattern and can be diffuse. What does this indicate?

A

excessive fat production and uneven distribution

whatever is happening in one lobule is happening to another at another location

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17
Q

What are some extracellular accumulations?

A

amyloid
cholesterol clefts (acicular clefts)
sodium urate crystals (or urates) = gout

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18
Q

What are the types of amyloidosis?

A

AL amyloid
AA amyloid
B-amyloid

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19
Q

What is AL amyloid?

A

secreted in B cell proliferative disorders -

B cells replicate like crazy —> AL

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20
Q

What is AA amyloid?

A

liver secretes SAA during inflammation

beta-pleated sheet

Hereditary amyloidosis - Shar Pei, Abyssinian

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21
Q

What is a beta-pleated sheet?

A

saw-tooth conformation and is folding up incorrectly; deposits in blood vessels, basement membranes, spaces of disse, spleen

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22
Q

What are the types of stains?

A

iodine
special

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23
Q

What is an iodine stain for?

A

fresh tissue - not 100% diagnostic

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24
Q

What is a special stain? What are the specific parts?

A

formalin-fixed tissue

  • congo red - NAVLE question
  • apple green perfringence under polarized light
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25
Q

What stain?

A

iodine stain

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26
Q

What stain?

A

special stain - congo red

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27
Q

What stain?

A

special stain - apple green perfringence under polarized light

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28
Q

What stain?

a. iodine
b. H & E
c. apple green perfringence
d. congo red

A

d. congo red

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29
Q

What is the problem with amyloidosis?

A

deposition of material that cannot be broken down (formation of beta-pleated sheet)

compression, occlusion of spaces (spaces of disse)

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30
Q

What are the organs most affected with amyloidosis?

A

kidney (mesangium, BM)
liver
spleen
etc

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31
Q

What part of the kidney is affected with amyloidosis, and what disease does it cause?

A

mesangium, BM

glomerulonephropathy = protein loss

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32
Q

What part of the liver is affected with amyloidosis, and who does it affect?

A

liver - space of disse

birds

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33
Q

What part of the spleen is affected with amyloidosis?

A

red pulp, PAL sheaths

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34
Q

What is the cause of gout?

A

dehydration, renal failure, excess protein intake

hyperuricemia —> visceral and articular deposition of uric acid crystals

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35
Q

Which species are generally affected with gout?

A

birds, reptiles

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36
Q

With gout, what blood changes do you expect to see?

A

elevated uric acid levels in the blood - because of visceral and articular deposition of uric acid crystals (urates)

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37
Q

What does this image show?

A

articular deposition of uric acid crystals - gout

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38
Q

What is this?

A

visceral gout (in a laying hen)

deposition of uric acid crystals

39
Q

What are the types of pathologic calcification?

A

dystrophic
metastatic

40
Q

What is dystrophic in the context of pathologic calcification?

A

results from dying cells (necrosis)

high precipitation of calcium in tissues

41
Q

What is metastatic in the context of pathologic calcification?

A

resulting from hypercalcemia

high Ca2+ in blood

42
Q

What are the causes of hypercalcemia?

A

GOSH DARN IT (or HARD IONS)

43
Q

Why does high calcium lead to myocyte degeneration, necrosis, and mineralization?

A

muscle fibers have lots of calcium

dying and are released - cut into it would feel gritty

44
Q

What are these arrows pointing to?

A

myocardial necrosis with mineralization and fibrosis

45
Q

What is melanin?

A

an endogenous pigment - formed by oxidation of tyrosine (which needs copper containing enzyme tyrosinase)

can occur as a result of chronic inflammation (corneal pigmentation)

46
Q

What is albinism?

A

lack of tyrosinase

47
Q

What is congenital melanosis? Is it pathologic?

A

abnormal deposits of melanin where it is not normally found

non-pathologic

48
Q

What is lipofuscin?

A

an endogenous pigment - “wear and tear” pigment

intracellular - non-pathologic

parts of cells don’t get broken down = end result of auto phagocytosis - undegradable material accumulation

49
Q

What are ceroids?

A

an endogenous pigment - looks similar to lipofuscin - pathologic

results from malnutrition (vitamin E deficiency) or inherited

  • brown gut

intracellular or extracellular

50
Q

What is the difference between lipofuscin and ceroids?

A

lipofuscin - normally non-pathologic

ceroids: pathologic

51
Q

What are the exogenous pigments?

A

carotenoids
carbon

52
Q

What are carotenoids?

A

fat soluble pigments from plants

precursors of vitamin A (B carotene)

can be confused with icterus

53
Q

Is this icterus or carotenoids?

A

carotenoids - yellows the skin, sclera and mucous membranes unaffected

54
Q

What is carbon as an exogenous pigment?

A

tattoos

pneumoconiosis (dust, including carbon) = anthracosis

55
Q

What are the hematogenous pigments?

A

hemoglobin
hemosiderin
hematoiden
bilirubin
porphyria

56
Q

What is hemosiderin?

A

along with ferritin, stores iron

formed from aggregates of ferritin

golden yellow to brown globules

57
Q

This is [hemoglobin/hemosiderin]

A

hemosiderin

58
Q

What is hematoiden?

A

contains NO iron; resembles bilirubin

yellow brown to orange-red

59
Q

What is bilirubin?

A

results from rbc degradation in macrophages

pre-hepatic, hepatic, post-hepatic processes when excess bilirubin in blood

60
Q

What is pre-hepatic?

A

unconjugated bilirubin - from hemolysis

61
Q

What is hepatic?

A

elevated levels of both conjugated and unconjugated bilirubin due to liver disease.

62
Q

What is post-hepatic?

A

elevated conjugated bilirubin due to bile duct obstruction

63
Q

What is porphyria?

A

inherited metabolic defect in heme synthesis

deficiency of uroporphyringen III cosynthetase

64
Q

What enzyme is deficient in porphyria? What happens?

A

uroporphyrinogen III cosynthetase

doesn’t have the ability to complete heme synthesis —> results in excess porphyrins being produced - gets deposited in tissues

65
Q

What is this an example of?

A

porphyria - deficiency in uroporphyrinogen III cosynthetase

66
Q

What is this an example of?

A

porphyria - deficiency in uroporphyrinogen III cosynthetase

67
Q

T/F: Hyperbilirubinemia = icterus

A

FALSE - you can have hyperbilirubinemia without icterus

color takes a while to accumulate

68
Q

A 2 day old foal presents with icterus and lethargy. What is a possible differential?

A

neonatal isoerythrolysis: hyperbilirubinemia due to hemolysis

69
Q

Necropsy revealed this on the right side. Is it a post-mortem or ante-mortem lesion and why?

A

post-mortem - would have seen cardinal signs of inflammation

is congestion in which there was gravitational pooling of blood, pig died on right side

white is from pressure points

70
Q

What is this an example of?

A

autolysis (tissue breakdown), post-mortem

71
Q

Post-mortem or antemortem and why?

A

post-mortem - would’ve seen cardinal signs of inflammation; also is bilateral and cows usually have unilateral eye lesions

72
Q

Post-mortem or antemortem and why?

A

antemortem: caused a blood product

hemomelasma ilei

73
Q

What is hemomelasma ilei?

A

characterized by the presence of dark, raised, pigmented plaques or nodules on the serosal surface (outer layer) of the small intestine, specifically the ileum

lesions are composed of hemosiderin, a pigment derived from hemoglobin, indicating previous bleeding or hemorrhage within the intestinal wall

74
Q

What is/are diagnostic(s) of postmortem lesions?

A

psuedomelanosis
sometimes bile imbibition

75
Q

What is pseudomelanosis? Antemortem or postmortem?

A

false black color - bacteria break down blood —> hydrogen sulfide

postmortem

76
Q

What is/are diagnostic(s) of antemortem lesions?

A

bile imbibition
melanosis
hemoglobinuric/myoglobinuric nephrosis

77
Q

What is bile imbibition? Antemortem or postmortem?

A

staining of tissue with bile

can be both

78
Q

What is melanosis? Antemortem or postmortem?

A

“black gums” not normal but not pathologic

antemortem

79
Q

What is hemoglobinuric nephrosis? Antemortem or postmortem?

A

peeing out Hb (hemolysis) —> Hb stains urine

antemortem

80
Q

What is myoglobinuric nephrosis? Antemortem or postmortem?

A

muscle pigment being peed out in kidney

muscle fibers are damaged

ex: dog hit by car

antemortem

81
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

postmortem - pseudomelanosis

82
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

postmortem - bile imbibition

no cardinal signs of inflammation

83
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

hemoglobin inbibition - post mortem

uniform discoloration of the intestines and the absence of signs indicating an antemortem process, such as localized hemorrhage with an inflammatory response

84
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

hemoglobin imbibition - postmortem

85
Q

Why is this antemortem?

A

vein is distended and filled with blood (vein could be contracted by twisting)

  • congestion: packing of veins
86
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

antemortem - intusseption

87
Q

What is intusseption?

A

telescoping of a tubular organ to another tubular organ

88
Q

Is this a postmortem or antemortem change?

A

postmortem - bloated from gas - push liver towards thorax and squeeze blood out where ribs are

89
Q

Lesion or postmortem change?

A

lesion - color isn’t affecting the entire organ

90
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

postmortem - autolysis and bile imbibition

91
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

postmortem - autolysis

92
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

postmortem - rectal prolapse

93
Q

Is this a postmortem or antemortem change? What differential diagnosis specifically?

A

postmortem - chicken fat clot