Pigments/Tissue Deposits (Ex3) Flashcards
What 3 components is hemoglobin broken down into?
Fe
Globin
Heme
What happens to the Fe portion of hemoglobin?
- stored intracellularly as ferritin
- converted to hemosiderin
What happens to the globin portion of hemoglobin?
broken down into amino acids
What happens to the heme portion of hemoglobin?
- 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
Describe Jaundice/Icterus
- increase bilirubin in the tissues
- yellow-green discoloration
- most prominent in mucus membranes
- do not use fat to assess
What is hyperbilirubinemia?
to much bilirubin in the blood
What are the pre-hepatic causes of hyperbilirubinemia?
- excessive red blood cell breakdown
- bilirubin exceeds hepatocellular uptake
- caused by hemolysis
What are the hepatic causes of hyperbilirubinemia?
- hepatocellular dystfunction: decreased bilirubin uptake, conjugation, or secretion into bile
- caused by hepatic insufficiency
What are the post-hepatic causes of bilirubinemia?
- reflux of conjugated bilirubin into blood
- caused by biliary obstruction or rupture
Describe the gross and microscopic appearance of hemoglobinuria
G: red-brown coloration of kidney and urine
- pink serum
M: homogenous red-orange material in renal tubules
Explain extravascular hemolysis
- macrophage breaks RBCs down into hemoglobin
- no hemoglobin is free in the blood to be filtered by the kidney
- all is turned into bilirubin
Explain intravascular hemolysis
- 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
Explain the pathogenesis of acute copper toxicosis
- insufficient metallothionein for safe copper storage
- high copper diet
- chronic hepatic copper accumulation
- acute copper release
- oxidative RBC damage
- intravascular hemolytic anemia
- hemoglobinuria
Microscopic appearance of hemosiderin
- dark yellow-brown, coarse granular cytoplasmic pigment
- stains blue-black with prussian blue
What are causes for hemosiderin accumulation?
Local and widespread
Local: - chronic congestion - hemorrhage Widespread: - hemolysis - inherited disorders of Fe storage
What are “heart-failure” cells?
hemosiderin-laden macrophages within alveoli
What is Erythropoietic porphyria?
- include pathogenesis and gross appearance
- 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
Gross and Histo appearance of melanin
G: black/brown tissue color
H: fine black/brown cytoplasmic granules
What is melanosis?
- developing melanocytes develop in sites where they should not be
- no functional consequences
Lipofuscin
- where does it come from
- what does it contain
- where is it found
- derived from the breakdown of lipids
- composed of lipid complexed with protein
- commonly found in aged cells and injured cells (post-mitotic cells)
Describe the gross and histo appearance of Lipfuscin
G: usually nothing
- tissue turns brownish after large amount of accumulation
H: golden brown, fine granular cytoplasmic pigment
What is omental carotenoid pigmentation?
- exogenous pigment
- vitamin A accumulates in fatty tissues and causes yellow-orange discoloration
What is pulmonary anthracosis?
- exogenous pigment
- inhaled carbon deposits in macrophage aggregates
- black color, amorphous
Describe the gross and histo appearance of calcification
G: white, gritty granules/plaques
- hard
H: basophilic amorphous granules of inconsistent size/shape
- stains black with vonKossa
Explain dystrophic type of calcification
- local deposition of calcium in areas of injury
- especially necrotic fat
Explain metastatic type of calcification
- widespread deposition of calcium in otherwise normal tissues
- caused by hypercalcemia
What are possible causes of hypercalcemia?
Excess PTH - renal secondary hyperparathyroidism - nutritional secondary hyperparathyroidism - paraneoplastic syndromes - parathyroid tumor Excess vitamin D - vitamin D toxicity (rodenitcides) - granulomatous disease
What is calcinosis cutis?
- 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
What is Amyloid?
- fibrils made of stacked beta-pleated sheets
- deposited and accumulates in extracellular space, compressing adjacent tissues and causing atrophy
Describe the gross and histo appearance of amyloid
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
Describe Amyloid Light Chain
- derived from immunoglobin light chain
- deposition in tumors of monoclonal B-cell proliferation
Describe Amyloid A
- made from serum amyloid A protein synthesized by liver in response to inflammation
- deposited in reactive systemic amyloidosis
Describe Endocrine Amyloid
- derived from islet amyloid polypeptide produced by the islet cells
- deposition in islets associated with diabetes
What is gout?
accumulation of uric acid in tissues
Uric acid in birds and reptiles
- end product
- causes of gout
- no uricase, end product is uric acid
- get gout from decreased renal function, dehydration
Uric acid in mammals
- end product
- causes of gout
- urea is end product
- get gout from diet, genetic disorders, chemotherapy
What is the gross appearance of uric acid accumulation?
- chalky, white foci on surface of visceral organs and serous membranes
- my involve soft tissues around joints
- soft, not gritty/hard
What is the histological appearance of uric acid accumulation?
- needle-like clear spaces
- “tophi” = granulomatous inflammation surrounding deposit
