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Path > Test 3- Pigments and Tissue Deposits > Flashcards

Test 3- Pigments and Tissue Deposits Flashcards

1
Q

Jaundice or Icterus

A
  • Jaundice or Icterus = increased bilirubin in tissues
  • Gross

– Yellow‐green discoloration of tissue or fluid

– Most prominent in mucous membranes, adventicial surfaces

– Do not use fat to assess, especially in livestock!

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2
Q
A

Dog MDx: generalized jaundice

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3
Q
  1. Prehepatic hyperbilirubinemia
A

Bilirubin production exceeds hepatocellular uptake

  1. conjugated bilirubin
  2. unconjugated bilirubin

Cause: hemolysis (intravascular or extravascular)- accerated breakdown of RBC

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4
Q
  1. Hepatic hyperbilirubinemia
A

Hepatocellular dysfunction

  1. Decreased bilirubin conjugated bilirubin uptake
  2. Decreased conjugation
  3. Decreased secretion in bile

Causes: hepatic insufficiency, hepatitis, hepatocellular degeneration, etc…- SOMETHING IS WRONG WITH HEPATOCYTES

seen in severe liver disease

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5
Q
  1. Posthepatic hyperbilirubinemia
A

Reflux of conjugated bilirubin into blood

Cause: biliary obstruction (cholestasis) or rupture

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6
Q
  • JaundiceorIcterus= increased bilirubin in tissues
  • Microscopic
A

• Microscopic

– Do not see pigment in jaundiced tissues!

– Exception = cholestatic(some process obstructing bile flow) liver

– Yellow‐brown intracellular (hepatocytes, kupffer cells) or extracellular pigment (bile canalliculi)

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7
Q
A

JaundiceorIcterus

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8
Q
A

jaudice

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9
Q

Hemoglobinuria

A

• Gross
– Red‐brown coloration of kidney and urine

– Pink serum

• Microscopic

– Homogenous re‐orange material in renal tubules

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10
Q
A

Sheep kidney with hemoglobinuria

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11
Q

You only see hemogloburia with…

A

vascular hemolysis because hemoglobin is free in the blood

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12
Q

You are called out to a sheep farm…..

Clinical signs

  • 6/500 unexpected death
  • Several ewes now weak
  • Pale yellow mucous membranes
  • Urinated red urine
A
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13
Q

What is the term for yellow discoloration of a tissue?

A

Jaundice or Icterus( NOT BILE INHIBITION)

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14
Q

Hemoglobin catabolism

A

Heme gets through broken down into billirubin

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15
Q

Hemoglobin catabolism with the enzymes

A
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16
Q

Bilirubin Processing

A

conjugated bilirubin gets secreted into bile

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17
Q

Hyperbilirubinemia

A

Too much billrubin the blood

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18
Q

When do you get jaundice?

A

when the billrubinemia is greater than 2mg/dL

HAS TO BE QUITE INCREASED TO GET JAUDICE

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19
Q

MDx ?

A

Dog MDx: generalized jaundice

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20
Q

Jaundice or Icterus

A
  • Jaundice or Icterus = increased bilirubin in tissues
  • Gross

– Yellow‐green discoloration of tissue or fluid

– Most prominent in mucous membranes, adventicial surfaces

– Do not use fat to assess, especially in livestock

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21
Q

Which mechanism of jaundice is to blame with this sheep?

A

PRE- HEPATIC- because the mucus membrances are pale

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22
Q

How do you tell the difference between hemoglobin or myoglobin since they both have the same redish tint?

A

SERUM

hemoglobin has the pink serum

myoglobin has clear serum

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23
Q

Extravascular hemolysis

A

macrophages take abnormla RBC out of the blood

NO HEMOGLOBURIA

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24
Q

Do you have jaudice with intra or extra vascular hemolysis?

A

BOTH!

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25
Q

Etiology of Intravascular hemolysis

A

Oxidative, immune mediated,

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26
Q

What was the Edx for the sheep on the farm?

A

Etiology = acute copper toxicosis

Pathogenesis: Insufficient metallothionein for safe copper storagehigh copper diet (copper‐storing plants)chronic hepatic copper accumulation acute copper release (i.e. from hepatic damage)oxidative RBC damage intravascular hemolytic anemiahemoglobinuria

—–sheep eat plants that have high copper from the soil

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27
Q
A

HEMOGLOBIN INHIBTION- POST MORTEM CHANGE

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28
Q

Is pre, hepatic, or post-hepatic the most severe?

slowest onset?

A

post-hepatic; no billirubin getting out of the body; has the fastest onset

hepatic- onset is the slowest

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29
Q
A

Pre- Hepatic

immune mediated hemolytic anemia

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30
Q
A

Puppy

Hepatic- infectious canine hepatits

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31
Q
A

hepatic- hepatic lipidosis

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32
Q
A

Posthepatic

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33
Q

Sick foal….
What would you do with the live animal to determine the cause of jaundice in this case?

Four things you can do clinically:

A
  1. urine- look for intravascular hemolysis
  2. blood- serum chem and look at billirubin; you can look at liver enzymes
  3. X-ray- of the liver; look for obstruction
  4. CBC- look for anemia(no ameia; then not pre-hepatic!)
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34
Q

pathogeneiss

A

Pathogenesis of neonatal isoerythrolysis:

A/Q negative mare bred to A/Q positive stallionfetus develops A/Q blood type fetal cells passed to mares blood during gestationmare sensitizedmare bred again to A/Q stallion2nd foal ingests colostrum packed with antibodies against its blood typeintravascular hemolysis

What other lesions would this foal have?? janudice, and hemogloburia(BAD INJURIES THE KIDNEY)

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35
Q

What pigments are responsible for the color of this bruise?

A

red- hemoglobin

yellow- billirubin

brown- hemosideron

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36
Q

Hemosiderin

A

• Iron stored intracellularly as ferritin (bound to apoferritin)

• Gross
– Must have a lot to impart

gross brown color

• Microscopic

– Dark‐yellow‐brown, coarse granular cytoplasmic pigment

– Stains blue‐black with prussian blue / Perls

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37
Q
A

Hemosiderin

38
Q

How do we get accumulation of hemosiderin?

A

2 types: local or widespread

usually has to do hemoglobin breakdown

39
Q
A

Dog

Lung
Localized hemosiderosis due to chronic congestion

“Heart failure cells” – hemosiderin‐laden macrophages within alveoli

40
Q
A

lungs have hemosideron acummulation- VERY HARD TO SEE

41
Q
A

Mynah bird
Liver
Generalized hemosiderosis due to hemolysis

42
Q

Stain to test for iron to see if the pigment is hemosideron

A

Prussian blue stain for iron

43
Q

Erythropoietic porphyria

A
  • A developmental anomaly of calves, cats, pigs
  • Inherited deficiency of uroporphyrinogen III cosynthetasedefect in heme synthesis  porphyrins accumulate in dentin and bone

• Gross
– Pink‐red discolored bones and teeth - PATHONUEMOTIC LESION

– Fluoresces with uv light

44
Q
A

Cow Bone MDx: porphyria

45
Q

Melanin

A

Gross:

– Black/brown tissue color

Histo:

– Fine brown/black cytoplasmic granules

46
Q

Melanin synthesis

A
47
Q
A

Dog, skin MDx: Cutaneous hyperpigmentation (hypermelanosis)

Disease: Flea allergy dermatitis

48
Q
A

Sheep brain MDx: meningeal melanosis

Pathogenesis: Developmental anomaly

49
Q
A

Sheep uterus
MDx: endometrial melanosis

Pathogenesis: Developmental anomaly

50
Q
A

Cow lungs
MDx: pleural melanosis
Pathogenesis: Developmental anomaly

51
Q

had intestines smashed up against it

A

pseduo-melnosis- PORT MORTEM CHANGE

52
Q
A

Pig
lungs, liver

53
Q

Lipofuscin

A

Lipofuscin

• Derived from the breakdown of lipids

‐ an un‐degradable remnant of breakdown of organelles

  • Composed of lipid complexed with protein
  • Commonly in found in aged cells and injured cells (“wear and tear” pigment)
  • Especially accumulates in post‐ mitotic cells

NEURONS AND MUSCLE CELLS

Gross:
– Usually nothing

– Tissue obtains a brownish color after large amount of accumulation

• Histo:
– Golden‐brown, fine granular

cytoplasmic pigment

54
Q
A

Lipofusin

55
Q
A

Elephant heart MDx: Myocardial lipofuscinosis

56
Q
A

usually can’t see grossly- LIPOFUSCIN

57
Q

How can you tell hemosideron from lipofusion?

A

special stain for iron!

58
Q

What type of pigment is in this lesion from a young cat?

A. Endogenous

B. Exogenous

A

This could be a melanoma- endogenous

exogenous pigments that produces melanin- Neutorphils, macrophages

PIGMENTED ORGANISM CAN CAUSE THIS!

59
Q
A

Pony lesser omentum
MDx: omental carotenoid pigmentation
Pathogenesis: vitamin A accumulates in fatty tissues and causes yellow‐orange discoloration

EXOGENOUS PIGMENT

60
Q
A

Dog lung
MDx: pulmonary anthracosis
Pathogenesis: inhaled carbon deposits in peribronchiolar macrophage aggregates
“Pneumoconiosis” = inhaled dust, anthracosis is a subtype of this

Fig. 1‐56 Anthracosis, lung, aged dog. B, Carbon (black) inhaled into the alveoli has been phagocytosed by macrophages and transported to the peribronchial region. H&E stain.

61
Q
A

Sheep liver
MDx: chronic cholangitis & biliary parasitic hematin

pigment is from liver flukes- around parasties or lesions that they have caused

62
Q
A

Macaque lung
MDx: chronic bronchiolitis and parasitic hematin & lung mites

63
Q

A young dog has died unexpectedly….. PM findings…..

Parietal pleura – white chalky plaques

Gastric mucosa – dry, white streaks

Lungs – dry, fail to collapse

Lungs – Basophilic intracellular and extracellular pleomorphic granular material

Stains black with vonKossa stain

A

These are classic changes of calcification!

64
Q

Calcification

A

• Gross
– White gritty granules/plaques – Hard

• Histo
– Basophilic amorphous granules

of inconsistent size/shape – Stain black with vonKossa

• Two types:
– Dystrophic

– Metastatic

65
Q
A

calcification of the heart

66
Q

Dystrophic Calicification

A

Dystrophic

Local deposition of calcium in areas of injury

Especially necrotic fat – calcium ions interact with fatty acids, producing

insoluble calcium soaps (“saponification”)

• Also muscle, granulomas, dead parasites

67
Q

Metastatic

A

Metastatic- Type of Calcification

Widespread deposition of calcium in otherwise normal tissues

Caused by hypercalcemia

Favorite sites

– vascular intima/adventicia

– gastric mucosa

– renal tubular epithelium

– pulmonary interstitium, pleura

– basement membranes

68
Q

What is the best morphological diagnosis for our dog case?

A

Metastatic Calification

69
Q

Calicum Homeostasis

A
70
Q

What are the two main causes for hypercalcemia ?

A
  1. Excess PTH
  2. Excess Vit. D
71
Q
A

Dog Pancreas and mesentry

Dystrophic- necrotic fat; pancreas is leaking out fat;

pancreatistic

72
Q
A

Cow liver

Granuloma- TB

Dystropic

73
Q
A

Metastatic

Cow heart

Cestrum diurnum toxicitiy

74
Q

Young dog sq mass

A

Calcinosis circumscripta

Dystropic; usally in large breed dogs at a site of previous injury

75
Q

Calcinosis cutis

A

Not really metastatic or dystrophic

Dogs with hyperadrenocorticism

Pathogenesis not understood

• Widespread mineralization of the dermal collagen and epidermal basement membranes

76
Q
A

Calcinosis cutis

77
Q

Amyloid

A
  • Fibrils made of stacked β ‐pleated sheets
  • Can be formed by lots of different protein monomers
  • Deposited and accumulates in extracellular space – compresses adjacent tissues causing atrophy- BAD

• Gross
– Enlarged, firm organs with

waxy appearance

– Stains blue violet when treated with iodine + sulfuric acid

• Histo

– Amorphous homogenous eosinophilic extracellular material (“hyaline”)

– Stains pink and has green birefringence with polarized light

78
Q
A

Macaque liver

MDx: hepatic amyloidosis

79
Q
A

Amyloid- special stain CONGO RED

80
Q

Types of Amyloid

A

AMYLOID A- most common

81
Q

A dog that you treated for protein losing nephropathy…..

protein being lost in kidneys/urine

kidneys tan and waxy

A

kidney have amyloid being deposited into the glomeruli; proteins will be let out from the kidney

MDx: Glomerular amyloidosis
Pathologist comment: consistent with “reactive systemic amyloidosis”

82
Q

What type of amyloid is deposited in ‘reactive systemic amyloidosis’?

Amyloid light chain

Endocrine amyloid

Amyloid of alzheimer’s disease

Amyloid A

A

Amyloid A- formed by chronic inflammation

83
Q

Pathogenesis of ‘reactive systemic amyloidosis’:

A

Pathogenesis of ‘reactive systemic amyloidosis’:

Chronic inflammationliver produces SAA in response to IL‐4 & IL‐6 spontaneous conversion of SAA to AAformation of amyloid fibrils

Most common form in animals Hereditary in sharpeis and abyssinians Kidney, liver, spleen, lymph nodes- DIE FROM RENAL FAILURE

84
Q

Uric Acid

A

• Gout = accumulation of uric acid in tissues

• Birds and reptiles

– No uricase; uric acid is the end product(instead of urea)

– Get gout from decreased renal function, dehydration

• Mammals

– Urea is the end product

– Get gout from diet, genetic disorders, chemotherapy

85
Q

Gross and Histo of Uric Acid

A

• Gross

– Chalky white foci on surface of visceral organs and serous membranes (liver, myocardium, spleen, pleura, air sacs, etc…)

• Histo

– Needle‐like clear spaces (crystals dissolve out in processing)

– “Tophi” ‐ granulomatous inflammation surrounding deposit

86
Q
A

Uric Acid in a macaw

USUALLY IN THE KIDNEYS- THIS CAUSES AN INFLAMMATION RESPONSE

87
Q
A

Snake lung and kidney MDx: visceral gout

white chalky material on the surface

88
Q

How do we differeniate between gout from ca?

A

Gout is soft

Ca+ is very hard

89
Q
A

gout in a macaw

90
Q
A

Swan heart
MDx: visceral gout

91
Q

What pigment is this?

A

Vertebral Melanosis in a cow

92
Q

Hilar lymph node of a cow

A

exogenous- anthrocosis- in the airways, but it can also go to the lymphnodes

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