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RUSVM Pathology I > Pigments and Tissue Deposits > Flashcards

Pigments and Tissue Deposits Flashcards

1
Q

Heart Failure Cells

A

Hemosiderin-laden macrophages

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2
Q

Histological appearance of lipofuscin

A

Golden-brown, fine granular cytoplasmic pigment

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3
Q

Local hemoglobin catabolism results in

A

Chronic congestion

Hemorrhage

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4
Q

A beta amyloid is commonly associated with

A

Cerebral lesion of Alzheimer disease

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5
Q

Common causes of hepatic hyperbilirubinemia

A

Hepatic Insufficiency

Hepatitis

Hepatocellular Degeneration

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6
Q

Microscopic appearance of hemosiderin

A

Dark-yellow-brown, coarse granular cytoplasmic pigment

Stains blue-black with prussian blue/Perls stain

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7
Q

When bilirubinemia is how much mg/dL you get jaundice

A

2mg/dL

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8
Q

Erythropoietic Porphyria

A

Developmental anomaly of calves, cats and pigs due to inherited deficiency of Uroporphyrinogen III Cosynthetase

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9
Q

Pathogenesis of Erythropoietic porphyria

A
  1. Deficiency of uroporphyrinogen III cosynthetase
  2. Defect in heme synthesis
  3. Porphyrins accumulate in dentin and bone
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10
Q

Common cause of Prehepatic hyperbilirubinemia

A

Hemolysis

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11
Q

Posthepatic Hyperbilirubinemia

A

Reflux of conjugated bilirubin into blood

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12
Q

General etiologies of intravascular hemolysis

A

Oxidative Damage

Erythrocyte metabolic deficiency

Infectious

Immune mediated

Direct membrane damage

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13
Q

Amyloid A deposition associated with

A

chronic inflammatory conditions; certain breeds predisposed

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14
Q

Widespread hemoglobin catabolism results in

A

Hemolysis

Inherited disorders of Fe storage

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15
Q

Pathogenesis of Reactive Systemic Amyloidosis

A
  1. Chronic inflammation
  2. Liver produces Saa in response to IL-4 and IL-6
  3. Spontaneous conversion of SAA to AA
  4. Formation of Amyloid fibrils
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16
Q

T/F: Amyloid looks the same no matter what it is made out of

A

True

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17
Q

Causes of hypercalcemia

A

Excess PTH

Excess Vitamin D

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18
Q

Calcitonin

A

Decreases Ca and Decreases P

Synthesized in response to increased Ca

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19
Q

Vitamin D effect on Ca and P

A

Increase Ca, incease P

Synthesized in response to decreased Ca and decreased P

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20
Q

Hemosiderin

A

Iron stored intracellurly as ferritin- bound to apoferitin

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21
Q

Metastatic Calcification

A

Widespread deposition of calcium in otherwise normal tissues

Caused by hypercalcemia

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22
Q

Microscopic appearance of jaundice/icterus

A

Do not see pigment in jaundiced tissues - unless cholestatic liver

Yellow-brown intracellular or extracellular pigment

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23
Q

Amyloid light chain (AL) deposition associated with

A

Monoclonal B-lymphocyte proliferation

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24
Q

Lipofuscin

A

Derived from the breakdown of lipids

Composed of lipid complexed with protein

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25
Gout
Accumulation of uric acid in tissues
26
Microscopic appearance of hemoglobinuria
Homogenous re-orange material in renal tubules
27
Common causes of excess PTH
Renal secondary hyperparathyroidism Nutritional secondary hyperparathyroidism Paraneoplasmic syndrome
28
Type types of calcification
Dystrophic Metastatic
29
Important pigments
Hematogenous pigments Melanin Lipofuscin Exogenous pigments
30
Type of amyloid tissue deposits
Amyloid Light Chail (AL) Amyloid A Endocrine Amyloid A beta Amyloid
31
Dystrophic Calcification
Local deposition of calcium in areas of injury Especially necrotic fat Muscle, granulomas, parasites
32
Gross appearance of calcification
White gritty granules/ plaques Hard
33
Ways in which hyperbilirubinemia occurs
Prehepatic Hyperbilirubinemia Hepatic Hyperbilirubinemia Posthepatic Hyperbilirubinemia
34
Amyloid as is made from SAA protein synthesized by the liver in response to
Inflammation
35
Pigments responsible for coloration of bruises
Bilirubin - yellow Hemoglobin - red/blue Hemosiderin - brown
36
Amyloid Light Chain (AL) is derived from
Immunoglobulin light chain
37
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
38
Common clinical tests to perform when presented with an animal with jaundice
CBC, PCV Chemistry Urine Ultrasound
39
Histologic experience of calcification
Basophilic amorphous granules of inconsistent size/shape Stain black with vonKossa
40
Amyloid
Fibrils of stacked beta-pleated sheets Deposited and accumulates in extracellular space - compress adjacent tissues causing atrophy
41
Uric Acid is the end product of
Birds and reptiles
42
Calcinosis circumscripta
Widespread mineralization of the dermal collagen and epidermal basement membranes
43
Birds and reptiles get gout from
Decreased renal function Dehydration
44
Bilirubin is conjugated where
within the hepatocyte by diglucuronide
45
Common cause of posthepatic hyperbilirubinemia
Biliary obstruction (cholestasis) or rupture
46
Important hematogenous pigments
Hemoglobin Hemosiderin Bilirubin Porphyrins
47
Extravascular Hemolysis
Red blood cell → Hemoglobin by Erythrophagocytosis in macrophage Hb not free in blood to be filtered by kidney
48
Gross appearance of amyloid tissue deposits
Enlarged, firm organs with waxy appearance Stains blue violet when treated with iodne + sulfuric acid
49
Terms used for yellow discoloration of the tissue
Icterus Jaundice
50
Prehepatic Hyperbilirubinemia
Bilirubin production exceeds hepatocellular uptake
51
Histological appearance of melanin
Fine brown/black cytoplasmic granules
52
Pathogenesis of Neonatal Isoerythrolysis
1. A/Q negative mare bred A/Q positive stallion 2. Fetus develops A/Q blood type 3. Fetal cells passed to mares during gestation 4. Mare sensitized 5. Mare bred **again** to A/Q stallion 6. **2nd foal** ingests colostrum packed with antibodies against its blood type 7. Intravascular hemolysis
53
Saponification
Calcium ions interact with fatty acids, producing insoluble calcium soaps
54
Which hyperbilirubinemia is most severe?
Posthepatic hyperbilirubinemia
55
Gross appearance of Lipofuscin
Usually nothing Tissue obtains a brownish color after a large amound of accumulation
56
Gross appearance of Erythropoietic porphyria
Pink-red discolored bones and teeth Fluoresces with UV light
57
Hepatic Hyperbilirubinemia
Hepatic dysfunction: - Decreased bilirubin uptake - Decreased conjugation - Decreased secretion in bile
58
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
59
Both intra and extra-vascular hemolysis can result in
Hyperbilirubinemia
60
Parathyroid Hormone
Increases Ca, decreases P Synthesized in response to decreased Ca
61
Mechanism of Uric Acid/ Urea Production
1. Nucelic acid catabolism 2. Purine → Xanthinie 3. Xanthinine → Uric acid by Xanthine Oxidase 4. Uric Acid → Allantoin by Uricase 5. Allantoin → Urea 6. Renal excretion
62
Calcinosis cirucumscripta is seen in dogs with
Hyperadrenocorticism
63
Gross appearance of hemoglobinuria
Red-brown coloration of kidney and urine Pink serum
64
Jaundice - Icterus
Increased bilirubin in tissues
65
Hemoglobin catabolism can be distributed
Local or widespread
66
Hyperbilirubinemia
Too much bilirubin in the blood
67
Mechanism of melanin synthesis
Tyrosine → Tyrosinase Cu → Dihydroxyphenylalanine → Melanin → Packaged melanosomes → transferred to epithelial cells or melanophages \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Occurs within melanocyte
68
Gross appearance of melanin
Black/brown tissue color
69
Describe the process that the heme undergoes within the macrophage to become bilirubin
Heme → Hemeoxygenase → Biliverdin → BV Reductase → Bilirubin
70
Mammals get gout from
Diet Genetic disorders Chemotherapy
71
Lipofuscin is commonly found in
Aged Cells Injured Cells \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ "Wear and Tear" Pigment
72
Urea is the endproduct of
Mammals
73
In the blood, bilirubin is (conjugated/unconjugated)
Unconjugated
74
Histologic appearance of amyloid tissue deposits
Amorphous homogenous eosinophilic extracellular material "hyaline" Stains pink and has green birefringence with polarized light
75
In the macrophage hemoglobin is broken down into
Fe → Stored as hemoseriden Globin → Broken down into amino acids Heme → Bilirubin
76
Endocrine amyloid deposition associated with
Diabetes
77
Gross appearance of hemosiderin
Must have a lot to impart gross brown color
78
Gross appearance of jaundice/icterus
Yellow-green discoloration of tissue or fluid Most prominant in mucous membranes or adventicial surfaces
79
Endocrine amyloid tissue deposits are derived from
Islet amyloid polypeptide produced by islet cells
80
How does hemoglobinuria occur?
Extravascular hemolysis Intravascular hemolysis
81
Important tissue deposits
Calcification Amyloid Uric Acid
82
Tophi
Granulomatous inflammation surrounding deposit
83
Which hyperbilirubinemia has the slowest onset?
Hepatic Hyperbilirubinemia
84
Intravascular Hemolysis
Red Blood Cell → Lysis into haptoglobin+hemoglobin Some hemoglobin is taken up by the macrophage Remainder of hemoglobin is filtered by kidney
85
Histologic appearance of uric acid
Needle like clear spaces - crystals dissolve out in processing "Tophi"
86
Bilirubin is (conjugated/unconjugated) in bile
Conjugated
87
Common causes of excess vitamin D
Vitamin D toxicity Granulomatous disease
88
Pathogenesis of hypercalcemia
Vitamin D deficiency and hyperphosphatemia → PTH production → hypercalcemia

RUSVM Pathology I (18 decks)

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