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VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND …people.upei.ca/hanna/CELL PATH GROSS...

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VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND OTHER TISSUE DEPOSITS Dr. Scott McBurney Department of Pathology and Microbiology Office 3333N January 30, 2015
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Page 1: VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND …people.upei.ca/hanna/CELL PATH GROSS LABS/SMcB-gross3-2015.pdf · VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND OTHER TISSUE DEPOSITS

VPM 152 GENERAL PATHOLOGY LAB 3

PIGMENTS AND OTHER TISSUE DEPOSITS

Dr. Scott McBurney

Department of Pathology and Microbiology

Office 3333N

January 30, 2015

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A. Type of necrosis? B. Type of necrosis?

C. Type of necrosis?

D. Morphological

Diagnosis?

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E. Type of necrosis?

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http://research.vet.upenn.edu/GeneralandSystemicPathology/tabid/3600/Default.aspx

Contralateral testis

Canine testicle with a sertoli cell tumor

(produces estrogen – feminization syndrome)

F. Cellular Adaptation in Contralateral Testis?

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http://research.vet.upenn.edu/GeneralandSystemicPathology/tabid/3600/Default.aspx

G. Cellular Adaptation in Brain with Hydrocephalus?

Hydrocephalus

Normal Brain

Photo courtesy of Dr. Daoust

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PIGMENTS AND OTHER TISSUE DEPOSITS

• Many pathologic processes are accompanied by

accumulations of material either within the cell

(intracellular) or within the matrix (extracellular).

1) Amyloid - extracellular hyaline substance.

2) Endogenous pigments – melanin and bilirubin.

3) Exogenous pigments – parasite pigments.

4) Pathologic mineralization – dystrophic and

metastatic.

5) Crystals – urate.

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1. Amyloid

• A pathologic extracellular proteinaceous substance (95% amyloid fibrils) that is

deposited between cells in many tissues and is resistant to proteolysis. It

compresses adjacent cells, causing atrophy and death from ischemia/compression.

• Amyloid fibrils are insoluble aggregates that result from the self-assembly of

abnormally folded proteins. Typically the abnormal folded protein has excess β

sheet conformational change. Misfolded proteins are normally degraded

intracellularly (proteosomes) or extracellularly (macrophages) but when too much

and/or certain types of misfolded protein produced, amyloid can form.

• Amyloid is deposited by several different pathogenetic mechanisms, and thus

AMYLOIDOSIS should not be considered a single disease; rather, a group of

diseases that share in common the deposition of similar appearing proteins.

• The most common in veterinary medicine is serum amyloid-associated protein

(SAA) an acute phase protein secondary to chronic inflammatory conditions

(REACTIVE SYSTEMIC AMYLOIDOSIS). Reactive systemic amyloidosis is

common in birds, particularly waterfowl, and is frequently associated with chronic

bacterial infections (eg. Tuberculosis).

• Grossly, affected organs (eg. kidneys, liver, spleen and lymph nodes) are often

swollen, enlarged, firm and waxy. Lugol’s iodine can stain the amyloid black in

fresh tissue.

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RENAL AMYLOIDOSIS

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RENAL AMYLOIDOSIS

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HEPATIC AMYLOIDOSIS

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HEPATIC AMYLOIDOSIS

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2.Endogenous Pigments

a) Melanin

• Insoluble, intracellular brown-black pigment derived from tyrosine.

• Normal in certain tissues (eg. eye and skin-melanocytes) and occurs incidentally at

other sites (MELANOSIS) - aorta, leptomeninges, etc.

• Grossly, dark pigmented area in otherwise normal tissue.

http://research.vet.upenn.edu/systemicpathology/exam4/commonlargeanimallesions/tabid/3648/albumid/6008-41/default.aspx

EOSOPHAGUS TONGUE AND LARYNX

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2. Endogenous Pigments

b) Bilirubin

• Bilirubin is the end product of heme degradation by macrophages and most is derived

from the breakdown of senescent erythrocytes.

• Heme → biliverdin (by heme oxygenase in MØ) → uncongugated bilirubin (by

biliverdin reductase in MØ) → binds albumin & transported to the liver → conjugated to

its glucuronide (water soluble) → excreted in bile.

• Abnormal accumulation called ICTERUS or JAUNDICE. Can be:

o Prehepatic – excess production of bilirubin - increased breakdown of

eryrthrocytes (hemolytic diseases).

o Hepatic – failure of uptke, conjugation or excretion of bilirubin – liver diseases

causing hepatocellular damage.

o Post-hepatic – obstruction of bile flow – can be intrahepatic (hepatic bile ducts)

or extrahepatic (common bile duct).

• Grossly, in blood and tissues produces a yellow discoloration.

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Diseases and Disorders of the Horse, Saunders, 2003

ICTERUS OR JAUNDICE

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Diseases and Disorders of the Horse, Saunders, 2003

ICTERUS OR JAUNDICE

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ICTERUS OR JAUNDICE

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ICTERUS OR JAUNDICE

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ICTERUS OR JAUNDICE

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ICTERUS OR JAUNDICE

Photo courtesy of Dr. Andrea Bourque

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3. Exogenous

Pigments

a) Parasite Pigments

Fascioloides magna (giant liver

fluke) - black discoloration of tissue

around bile ducts due to “fluke puke”

(iron-porphyrin pigment or parasite

hematin). http://cal.vet.upenn.edu/projects/paraav/labs/lab6.htm

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4. Pathologic Calcification (Mineralization) a) Dystrophic Calcification

• Calcification of injured or Damaged/Dying cells.

• Occurs in areas of necrosis or in cells injured from other processes (toxic, vascular,

inflammation or metabolic).

• Grossly, white, irregular areas in tissue that can be dry or gritty (eg. white muscle

disease and fat necrosis).

Photos courtesy of Dr. Martinson

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4. Pathologic Calcification (Mineralization) a) Metastatic Calcification

• Calcification of normal cells/tissues due to hypercalcemia/altered Ca2+ Metabolism.

• Causes include: - primary hyperparathyroidism, renal failure / secondary

hyperparathyroidism, vitamin D toxicosis (iatrogenic, rodenticide or plant analogues),

and paraneoplastic syndrome with certain neoplastic diseases (eg. canine apocrine

gland adenocarcinoma of the anal sac and canine lymphosarcoma).

• Grossly, white plaques or streaks in tissues (i.e., particularly gastric and intestinal

mucosa, interstitium of blood vessel walls and basement membranes of many tissues,

especially lung and kidney).

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DYSTROPHIC METASTATIC

Vitality of affected

tissue

Necrotic/Degenerate Normal/Viable

Serum calcium level Normal High

Where calcification

begins

Intracellular Extracellular

PATHOLOGIC CALCIFICATION

(MINERALIZATION)

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5.Crystals

a) Urates and Uric Acid

• Birds, reptiles and primates lack the enzyme uricase that promotes the oxidation of uric

acid to allantoin. Therefore, in these species, uric acid is the end product of nitrogen

metabolism, so any significant renal dysfunction (including dehydration) can lead to

abnormal extracellular accumulations/deposits of urates which is called GOUT.

• Can be found in and around joints (articular gout) and on serosal surfaces or in tissues

(visceral gout).

• Grossly, chalky white deposits in tissues (tophi) or frosting of crystals on serosal

surfaces.

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VISCERAL GOUT

Page 26: VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND …people.upei.ca/hanna/CELL PATH GROSS LABS/SMcB-gross3-2015.pdf · VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND OTHER TISSUE DEPOSITS

VISCERAL GOUT

Page 27: VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND …people.upei.ca/hanna/CELL PATH GROSS LABS/SMcB-gross3-2015.pdf · VPM 152 GENERAL PATHOLOGY LAB 3 PIGMENTS AND OTHER TISSUE DEPOSITS

VISCERAL GOUT

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VISCERAL GOUT

NORMAL

Photo courtesy of Dr. Forzán

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VISCERAL GOUT

Photo courtesy of Dr. Forzán


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