Pigments/Tissue Deposits (Ex3)

Question 1

What 3 components is hemoglobin broken down into?

Answer 1

Fe
Globin
Heme

Question 2

What happens to the Fe portion of hemoglobin?

Answer 2

• stored intracellularly as ferritin

- converted to hemosiderin

Question 3

What happens to the globin portion of hemoglobin?

Answer 3

broken down into amino acids

Question 4

What happens to the heme portion of hemoglobin?

Answer 4

• converted by heme oxygenase to biliverdin
• bv reductase converts it to bilirubin
• unconjugated bilirubin put back into blood
• picked up by hepatocytes, conjugated, and excreted in bile

Question 5

Describe Jaundice/Icterus

Answer 5

• increase bilirubin in the tissues
• yellow-green discoloration
• most prominent in mucus membranes
• do not use fat to assess

Question 6

What is hyperbilirubinemia?

Answer 6

to much bilirubin in the blood

Question 7

What are the pre-hepatic causes of hyperbilirubinemia?

Answer 7

• excessive red blood cell breakdown
• bilirubin exceeds hepatocellular uptake
• caused by hemolysis

Question 8

What are the hepatic causes of hyperbilirubinemia?

Answer 8

• hepatocellular dystfunction: decreased bilirubin uptake, conjugation, or secretion into bile
• caused by hepatic insufficiency

Question 9

What are the post-hepatic causes of bilirubinemia?

Answer 9

• reflux of conjugated bilirubin into blood

- caused by biliary obstruction or rupture

Question 10

Describe the gross and microscopic appearance of hemoglobinuria

Answer 10

G: red-brown coloration of kidney and urine
- pink serum
M: homogenous red-orange material in renal tubules

Question 11

Explain extravascular hemolysis

Answer 11

• macrophage breaks RBCs down into hemoglobin
• no hemoglobin is free in the blood to be filtered by the kidney
• all is turned into bilirubin

Question 12

Explain intravascular hemolysis

Answer 12

• RBC breaks down in the blood stream, hemoglobin is released and bound to haptoglobin
• excess hemoglobin is filtered by the kidney
• kidney appears red/brown, urine is tinged red

Question 13

Explain the pathogenesis of acute copper toxicosis

Answer 13

• insufficient metallothionein for safe copper storage
• high copper diet
• chronic hepatic copper accumulation
• acute copper release
• oxidative RBC damage
• intravascular hemolytic anemia
• hemoglobinuria

Question 14

Microscopic appearance of hemosiderin

Answer 14

• dark yellow-brown, coarse granular cytoplasmic pigment

- stains blue-black with prussian blue

Question 15

What are causes for hemosiderin accumulation?

Local and widespread

Answer 15

Local:
- chronic congestion
- hemorrhage
Widespread:
- hemolysis
- inherited disorders of Fe storage

Question 16

What are “heart-failure” cells?

Answer 16

hemosiderin-laden macrophages within alveoli

Question 17

What is Erythropoietic porphyria?

- include pathogenesis and gross appearance

Answer 17

• developmental anomally of calves, cats, and pigs
• inherited deficiency of uroporphyrinogen III cosynthetase > defect in heme synthesis > porphyrins accumulate in dentin and bone
• pink-red discoloration of teeth and bones
• fluoresces with UV light

Question 18

Gross and Histo appearance of melanin

Answer 18

G: black/brown tissue color
H: fine black/brown cytoplasmic granules

Question 19

What is melanosis?

Answer 19

• developing melanocytes develop in sites where they should not be
• no functional consequences

Question 20

Lipofuscin

• where does it come from
• what does it contain
• where is it found

Answer 20

• derived from the breakdown of lipids
• composed of lipid complexed with protein
• commonly found in aged cells and injured cells (post-mitotic cells)

Question 21

Describe the gross and histo appearance of Lipfuscin

Answer 21

G: usually nothing
- tissue turns brownish after large amount of accumulation
H: golden brown, fine granular cytoplasmic pigment

Question 22

What is omental carotenoid pigmentation?

Answer 22

• exogenous pigment

- vitamin A accumulates in fatty tissues and causes yellow-orange discoloration

Question 23

What is pulmonary anthracosis?

Answer 23

• exogenous pigment
• inhaled carbon deposits in macrophage aggregates
• black color, amorphous

Question 24

Describe the gross and histo appearance of calcification

Answer 24

G: white, gritty granules/plaques
- hard
H: basophilic amorphous granules of inconsistent size/shape
- stains black with vonKossa

Question 25

Explain dystrophic type of calcification

Answer 25

• local deposition of calcium in areas of injury

- especially necrotic fat

Question 26

Explain metastatic type of calcification

Answer 26

• widespread deposition of calcium in otherwise normal tissues
• caused by hypercalcemia

Question 27

What are possible causes of hypercalcemia?

Answer 27

Excess PTH
- renal secondary hyperparathyroidism
- nutritional secondary hyperparathyroidism
- paraneoplastic syndromes
- parathyroid tumor
Excess vitamin D
- vitamin D toxicity (rodenitcides)
- granulomatous disease

Question 28

What is calcinosis cutis?

Answer 28

• widespread mineralization of the dermal collagen and epidermal basement membranes (skin is calcified)
• not really dystrophic or metastatic
• in dogs with hyperadrenocorticism or Cushing’s disease

Question 29

What is Amyloid?

Answer 29

• fibrils made of stacked beta-pleated sheets

- deposited and accumulates in extracellular space, compressing adjacent tissues and causing atrophy

Question 30

Describe the gross and histo appearance of amyloid

Answer 30

G: enlarged, firm organs with waxy appearance
- stains blue violet with iodine + sulfuric acid
H: amorphous homogenous eosinophilic extracellular material
- stains pink and has green with congo red stain

Question 31

Describe Amyloid Light Chain

Answer 31

• derived from immunoglobin light chain

- deposition in tumors of monoclonal B-cell proliferation

Question 32

Describe Amyloid A

Answer 32

• made from serum amyloid A protein synthesized by liver in response to inflammation
• deposited in reactive systemic amyloidosis

Question 33

Describe Endocrine Amyloid

Answer 33

• derived from islet amyloid polypeptide produced by the islet cells
• deposition in islets associated with diabetes

Question 34

What is gout?

Answer 34

accumulation of uric acid in tissues

Question 35

Uric acid in birds and reptiles

• end product
• causes of gout

Answer 35

• no uricase, end product is uric acid

- get gout from decreased renal function, dehydration

Question 36

Uric acid in mammals

• end product
• causes of gout

Answer 36

• urea is end product

- get gout from diet, genetic disorders, chemotherapy

Question 37

What is the gross appearance of uric acid accumulation?

Answer 37

• chalky, white foci on surface of visceral organs and serous membranes
• my involve soft tissues around joints
• soft, not gritty/hard

Question 38

What is the histological appearance of uric acid accumulation?

Answer 38

• needle-like clear spaces

- “tophi” = granulomatous inflammation surrounding deposit