Test 3- Pigments and Tissue Deposits Flashcards Preview

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Flashcards in Test 3- Pigments and Tissue Deposits Deck (92):
1

Jaundice or Icterus

• 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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Dog MDx: generalized jaundice

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1. Prehepatic hyperbilirubinemia

Bilirubin production exceeds hepatocellular uptake

1. conjugated bilirubin

2. unconjugated bilirubin

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

 

 

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2. Hepatic hyperbilirubinemia

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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3. Posthepatic hyperbilirubinemia

Reflux of conjugated bilirubin into blood

Cause: biliary obstruction (cholestasis) or rupture

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• JaundiceorIcterus= increased bilirubin in tissues

• Microscopic

• 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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JaundiceorIcterus

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jaudice

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Hemoglobinuria

• Gross
– Red‐brown coloration of kidney and urine

– Pink serum

• Microscopic

– Homogenous re‐orange material in renal tubules

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Sheep kidney with hemoglobinuria

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You only see hemogloburia with...

vascular hemolysis because hemoglobin is free in the blood

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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

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What is the term for yellow discoloration of a tissue?

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Jaundice or Icterus( NOT BILE INHIBITION)

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Hemoglobin catabolism

Heme gets through broken down into billirubin

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Hemoglobin catabolism with the enzymes

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Bilirubin Processing

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conjugated bilirubin gets secreted into bile

 

 

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Hyperbilirubinemia

Too much billrubin the blood

 

 

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When do you get jaundice?

when the billrubinemia is greater than 2mg/dL

 

HAS TO BE QUITE INCREASED TO GET JAUDICE

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MDx ?

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Dog MDx: generalized jaundice

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Jaundice or Icterus

• 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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Which mechanism of jaundice is to blame with this sheep?

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PRE- HEPATIC- because the mucus membrances are pale

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

SERUM

hemoglobin has the pink serum

myoglobin has clear serum

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Extravascular hemolysis

macrophages take abnormla RBC out of the blood

 

NO HEMOGLOBURIA

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Do you have jaudice with intra or extra vascular hemolysis?

BOTH!

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Etiology of Intravascular hemolysis

Oxidative, immune mediated,

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What was the Edx for the sheep on the farm?

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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HEMOGLOBIN INHIBTION- POST MORTEM CHANGE

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

 

slowest onset?

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

 

hepatic- onset is the slowest

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Pre- Hepatic

immune mediated hemolytic anemia

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Puppy

Hepatic- infectious canine hepatits

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hepatic- hepatic lipidosis

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Posthepatic

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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:

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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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pathogeneiss

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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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What pigments are responsible for the color of this bruise?

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red- hemoglobin

yellow- billirubin

brown- hemosideron

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Hemosiderin

• 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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Hemosiderin

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How do we get accumulation of hemosiderin?

2 types: local or widespread

 

usually has to do hemoglobin breakdown

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Dog

Lung
Localized hemosiderosis due to chronic congestion

 

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

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lungs have hemosideron acummulation- VERY HARD TO SEE

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Mynah bird
Liver
Generalized hemosiderosis due to hemolysis

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

Prussian blue stain for iron

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Erythropoietic porphyria

• 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

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Cow Bone MDx: porphyria

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Melanin

 

Gross:

– Black/brown tissue color

Histo:

– Fine brown/black cytoplasmic granules

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Melanin synthesis

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Dog, skin MDx: Cutaneous hyperpigmentation (hypermelanosis)

 

 

Disease: Flea allergy dermatitis

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Sheep brain MDx: meningeal melanosis

Pathogenesis: Developmental anomaly

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Sheep uterus
MDx: endometrial melanosis

Pathogenesis: Developmental anomaly

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Cow lungs
MDx: pleural melanosis
Pathogenesis: Developmental anomaly

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had intestines smashed up against it

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pseduo-melnosis- PORT MORTEM CHANGE

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Pig
lungs, liver

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Lipofuscin

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

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Lipofusin

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Elephant heart MDx: Myocardial lipofuscinosis

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usually can't see grossly- LIPOFUSCIN

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How can you tell hemosideron from lipofusion?

special stain for iron!

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

A. Endogenous

B. Exogenous

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This could be a melanoma- endogenous

exogenous pigments that produces melanin- Neutorphils, macrophages

 

PIGMENTED ORGANISM CAN CAUSE THIS!

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

 

EXOGENOUS PIGMENT

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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.

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Sheep liver
MDx: chronic cholangitis & biliary parasitic hematin

 

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

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

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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

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These are classic changes of calcification!

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Calcification

• Gross
– White gritty granules/plaques – Hard

• Histo
– Basophilic amorphous granules

of inconsistent size/shape – Stain black with vonKossa

• Two types:
– Dystrophic

– Metastatic

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calcification of the heart

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Dystrophic Calicification

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

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Metastatic

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

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What is the best morphological diagnosis for our dog case?

Metastatic Calification

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Calicum Homeostasis

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What are the two main causes for hypercalcemia ?

1. Excess PTH

2. Excess Vit. D

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Dog Pancreas and mesentry

Dystrophic- necrotic fat; pancreas is leaking out fat;

pancreatistic

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Cow liver

Granuloma- TB

Dystropic

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Metastatic

Cow heart

Cestrum diurnum toxicitiy

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Young dog sq mass

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Calcinosis circumscripta

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

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Calcinosis cutis

Not really metastatic or dystrophic

Dogs with hyperadrenocorticism

Pathogenesis not understood

• Widespread mineralization of the dermal collagen and epidermal basement membranes

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Calcinosis cutis

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Amyloid

• 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

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Macaque liver

MDx: hepatic amyloidosis

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Amyloid- special stain CONGO RED

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Types of Amyloid

AMYLOID A- most common

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

 

protein being lost in kidneys/urine

kidneys tan and waxy

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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”

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

Amyloid light chain

Endocrine amyloid

Amyloid of alzheimer’s disease

Amyloid A

Amyloid A- formed by chronic inflammation

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Pathogenesis of ‘reactive systemic amyloidosis’:

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

Uric Acid

• 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

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Gross and Histo of Uric Acid

• 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

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Uric Acid in a macaw

 

USUALLY IN THE KIDNEYS- THIS CAUSES AN INFLAMMATION RESPONSE

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Snake lung and kidney MDx: visceral gout

 

white chalky material on the surface

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How do we differeniate between gout from ca?

Gout is soft

Ca+ is very hard

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gout in a macaw

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Swan heart
MDx: visceral gout

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What pigment is this?

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Vertebral Melanosis in a cow

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Hilar lymph node of a cow

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