Pigments and Tissue Deposits Flashcards
Heart Failure Cells
Hemosiderin-laden macrophages
Histological appearance of lipofuscin
Golden-brown, fine granular cytoplasmic pigment
Local hemoglobin catabolism results in
Chronic congestion
Hemorrhage
A beta amyloid is commonly associated with
Cerebral lesion of Alzheimer disease
Common causes of hepatic hyperbilirubinemia
Hepatic Insufficiency
Hepatitis
Hepatocellular Degeneration
Microscopic appearance of hemosiderin
Dark-yellow-brown, coarse granular cytoplasmic pigment
Stains blue-black with prussian blue/Perls stain
When bilirubinemia is how much mg/dL you get jaundice
2mg/dL
Erythropoietic Porphyria
Developmental anomaly of calves, cats and pigs due to inherited deficiency of Uroporphyrinogen III Cosynthetase
Pathogenesis of Erythropoietic porphyria
- Deficiency of uroporphyrinogen III cosynthetase
- Defect in heme synthesis
- Porphyrins accumulate in dentin and bone
Common cause of Prehepatic hyperbilirubinemia
Hemolysis
Posthepatic Hyperbilirubinemia
Reflux of conjugated bilirubin into blood
General etiologies of intravascular hemolysis
Oxidative Damage
Erythrocyte metabolic deficiency
Infectious
Immune mediated
Direct membrane damage
Amyloid A deposition associated with
chronic inflammatory conditions; certain breeds predisposed
Widespread hemoglobin catabolism results in
Hemolysis
Inherited disorders of Fe storage
Pathogenesis of Reactive Systemic Amyloidosis
- Chronic inflammation
- Liver produces Saa in response to IL-4 and IL-6
- Spontaneous conversion of SAA to AA
- Formation of Amyloid fibrils
T/F: Amyloid looks the same no matter what it is made out of
True
Causes of hypercalcemia
Excess PTH
Excess Vitamin D
Calcitonin
Decreases Ca and Decreases P
Synthesized in response to increased Ca
Vitamin D effect on Ca and P
Increase Ca, incease P
Synthesized in response to decreased Ca and decreased P
Hemosiderin
Iron stored intracellurly as ferritin- bound to apoferitin
Metastatic Calcification
Widespread deposition of calcium in otherwise normal tissues
Caused by hypercalcemia
Microscopic appearance of jaundice/icterus
Do not see pigment in jaundiced tissues - unless cholestatic liver
Yellow-brown intracellular or extracellular pigment
Amyloid light chain (AL) deposition associated with
Monoclonal B-lymphocyte proliferation
Lipofuscin
Derived from the breakdown of lipids
Composed of lipid complexed with protein
Gout
Accumulation of uric acid in tissues
Microscopic appearance of hemoglobinuria
Homogenous re-orange material in renal tubules
Common causes of excess PTH
Renal secondary hyperparathyroidism
Nutritional secondary hyperparathyroidism
Paraneoplasmic syndrome
Type types of calcification
Dystrophic
Metastatic
Important pigments
Hematogenous pigments
Melanin
Lipofuscin
Exogenous pigments
Type of amyloid tissue deposits
Amyloid Light Chail (AL)
Amyloid A
Endocrine Amyloid
A beta Amyloid
Dystrophic Calcification
Local deposition of calcium in areas of injury
Especially necrotic fat
Muscle, granulomas, parasites
Gross appearance of calcification
White gritty granules/ plaques
Hard
Ways in which hyperbilirubinemia occurs
Prehepatic Hyperbilirubinemia
Hepatic Hyperbilirubinemia
Posthepatic Hyperbilirubinemia
Amyloid as is made from SAA protein synthesized by the liver in response to
Inflammation
Pigments responsible for coloration of bruises
Bilirubin - yellow
Hemoglobin - red/blue
Hemosiderin - brown
Amyloid Light Chain (AL) is derived from
Immunoglobulin light chain
Gross appearance of uric acid tissue deposits
Chalky white foci on surface of visceral organs and serous membranes
May involve soft tissues around joints - visceral gout
Common clinical tests to perform when presented with an animal with jaundice
CBC, PCV
Chemistry
Urine
Ultrasound
Histologic experience of calcification
Basophilic amorphous granules of inconsistent size/shape
Stain black with vonKossa
Amyloid
Fibrils of stacked beta-pleated sheets
Deposited and accumulates in extracellular space - compress adjacent tissues causing atrophy
Uric Acid is the end product of
Birds and reptiles
Calcinosis circumscripta
Widespread mineralization of the dermal collagen and epidermal basement membranes
Birds and reptiles get gout from
Decreased renal function
Dehydration
Bilirubin is conjugated where
within the hepatocyte by diglucuronide
Common cause of posthepatic hyperbilirubinemia
Biliary obstruction (cholestasis) or rupture
Important hematogenous pigments
Hemoglobin
Hemosiderin
Bilirubin
Porphyrins
Extravascular Hemolysis
Red blood cell → Hemoglobin by Erythrophagocytosis in macrophage
Hb not free in blood to be filtered by kidney
Gross appearance of amyloid tissue deposits
Enlarged, firm organs with waxy appearance
Stains blue violet when treated with iodne + sulfuric acid
Terms used for yellow discoloration of the tissue
Icterus
Jaundice
Prehepatic Hyperbilirubinemia
Bilirubin production exceeds hepatocellular uptake
Histological appearance of melanin
Fine brown/black cytoplasmic granules
Pathogenesis of Neonatal Isoerythrolysis
- A/Q negative mare bred A/Q positive stallion
- Fetus develops A/Q blood type
- Fetal cells passed to mares during gestation
- Mare sensitized
- Mare bred again to A/Q stallion
- 2nd foal ingests colostrum packed with antibodies against its blood type
- Intravascular hemolysis
Saponification
Calcium ions interact with fatty acids, producing insoluble calcium soaps
Which hyperbilirubinemia is most severe?
Posthepatic hyperbilirubinemia
Gross appearance of Lipofuscin
Usually nothing
Tissue obtains a brownish color after a large amound of accumulation
Gross appearance of Erythropoietic porphyria
Pink-red discolored bones and teeth
Fluoresces with UV light
Hepatic Hyperbilirubinemia
Hepatic dysfunction:
- Decreased bilirubin uptake
- Decreased conjugation
- Decreased secretion in bile
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
Both intra and extra-vascular hemolysis can result in
Hyperbilirubinemia
Parathyroid Hormone
Increases Ca, decreases P
Synthesized in response to decreased Ca
Mechanism of Uric Acid/ Urea Production
- Nucelic acid catabolism
- Purine → Xanthinie
- Xanthinine → Uric acid by Xanthine Oxidase
- Uric Acid → Allantoin by Uricase
- Allantoin → Urea
- Renal excretion
Calcinosis cirucumscripta is seen in dogs with
Hyperadrenocorticism
Gross appearance of hemoglobinuria
Red-brown coloration of kidney and urine
Pink serum
Jaundice - Icterus
Increased bilirubin in tissues
Hemoglobin catabolism can be distributed
Local or widespread
Hyperbilirubinemia
Too much bilirubin in the blood
Mechanism of melanin synthesis
Tyrosine → Tyrosinase Cu → Dihydroxyphenylalanine → Melanin → Packaged melanosomes → transferred to epithelial cells or melanophages
_________________________
Occurs within melanocyte
Gross appearance of melanin
Black/brown tissue color
Describe the process that the heme undergoes within the macrophage to become bilirubin
Heme → Hemeoxygenase → Biliverdin → BV Reductase → Bilirubin
Mammals get gout from
Diet
Genetic disorders
Chemotherapy
Lipofuscin is commonly found in
Aged Cells
Injured Cells
________________________
“Wear and Tear” Pigment
Urea is the endproduct of
Mammals
In the blood, bilirubin is (conjugated/unconjugated)
Unconjugated
Histologic appearance of amyloid tissue deposits
Amorphous homogenous eosinophilic extracellular material “hyaline”
Stains pink and has green birefringence with polarized light
In the macrophage hemoglobin is broken down into
Fe → Stored as hemoseriden
Globin → Broken down into amino acids
Heme → Bilirubin
Endocrine amyloid deposition associated with
Diabetes
Gross appearance of hemosiderin
Must have a lot to impart gross brown color
Gross appearance of jaundice/icterus
Yellow-green discoloration of tissue or fluid
Most prominant in mucous membranes or adventicial surfaces
Endocrine amyloid tissue deposits are derived from
Islet amyloid polypeptide produced by islet cells
How does hemoglobinuria occur?
Extravascular hemolysis
Intravascular hemolysis
Important tissue deposits
Calcification
Amyloid
Uric Acid
Tophi
Granulomatous inflammation surrounding deposit
Which hyperbilirubinemia has the slowest onset?
Hepatic Hyperbilirubinemia
Intravascular Hemolysis
Red Blood Cell → Lysis into haptoglobin+hemoglobin
Some hemoglobin is taken up by the macrophage
Remainder of hemoglobin is filtered by kidney
Histologic appearance of uric acid
Needle like clear spaces - crystals dissolve out in processing
“Tophi”
Bilirubin is (conjugated/unconjugated) in bile
Conjugated
Common causes of excess vitamin D
Vitamin D toxicity
Granulomatous disease
Pathogenesis of hypercalcemia
Vitamin D deficiency and hyperphosphatemia → PTH production → hypercalcemia
