Lecture 58 - Gen Path Pigments Flashcards

1
Q

what are the 4 pathways of abnormal intracellular accumulations

A
  1. defect in metabolism
  2. defect in protein folding
  3. lack of enzyme (lysosomal storage disease)
  4. ingestion/inhalation of indigestible materials
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2
Q

Describe the intracellular accumulation of:

lipids

A
  • best seen in the liver
  • common in protein malnutrition, diabetes, obesity, etc.
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3
Q

what are the mechanisms of lipidosis/steatosis

A
  1. negative energy balance
  2. decreased oxidation of FFA
  3. decreased apoprotein synthesis
  4. ineffective lipoprotein synthesis
  5. ineffective lipoprotein transport
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4
Q

T/F: negative energy balance is the most common mechanism of lipidosis

A

TRUE

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5
Q

describe the gross and microscopic appearance of hepatic lipidosis

A

gross: enlarged liver, diffuse pallor, rounded edges, greasy

microscopic: large, discrete clear vacuoles that displace the nucleus

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6
Q

T/F: hepatic lipidosis occurs focally or regionally

A

TRUE

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7
Q

Atherosclerosis

A

cholesterol accumulation in arteries resulting from hypothyroidism or diabetes

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8
Q

what are the gross and microscopic appearance of atherosclerosis

A

gross: medium-sized arteries are firm and white

microscopic: foamy macrophages

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9
Q

describe the intracellular accumulation of:

glycogen

A

irregular borders of clear vacuoles
acquired causes = diabetes, Cushing’s, glucocorticoid admin.

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10
Q

what 5 pigment accumulations are seen

A
  1. red
  2. green
  3. yellow
  4. brown
  5. black
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11
Q

what causes red discoloration of tissue

A
  • vasodilation, hemorrhage, hemoglobin imbibition
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12
Q

hemoglobin imbibition

A

post-mortem change
tissues uptake hemoglobin

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13
Q

what causes green discoloration of tissue

A
  • old hemorrhage (biliverdin) or eosinophilic infiltrate
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14
Q

why is it uncommon to see green discoloration in mammalian species after hemorrhage

A

hemoglobin breaks down into hemosiderin rather than biliverdin

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15
Q

What causes brown discoloration of tissue

A
  • hemosiderin, ceroid-lipofuscin, and melanin
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16
Q

when do we see hemosiderin accumulation?

A
  1. hemolytic anemias - filtering organs turn brown
  2. local excess - bruise, heart disease
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17
Q

L-sided heart disease will cause what organ to have hemosiderin build-up

A

Lungs

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18
Q

R-sided heart disease will cause what organ to have hemosiderin build-up

19
Q

why are heart failure cells present in the lungs

A

increased pressure in pulmonary vessels from backed up blood causes erythrocytes to be consumed by alveolar macrophages

20
Q

Lipofuscin

A
  • wear and tear
  • oxidative damage and age indicator
  • heart and liver cells
21
Q

Ceroid

A
  • pathological pigment
  • oxidative injury, nutritional panniculitis, lysosomal storage disorder
22
Q

lipofuscin is commonly seen in what organ

23
Q

ceroid is commonly seen in what organ

A

intestines (“brown dog gut”)

24
Q

what causes yellow discoloration in tissues

A

Bilirubin and carotenoid build up

25
write the steps of erythrocyte breakdown
1. heme 2. biliverdin 3. bilirubin 4. conjugation in liver 5. urobilinogen in GIT
26
what causes icterus
hyperbilirubinemia
27
what are the causes of hyperbilirubinemia
1. pre-hepatic (hemolysis) 2. hepatic (liver disease; unconjugated form) 3. post-hepatic (obstruction of bile flow; conjugated form)
28
what is the only endogenous black-brown pigment
melanin
29
what locations are melanin pathologic
melanocytic neoplasms hyperpigmentation in skin
30
what causes black pigment in tissues
pesudomelanosis (hydrogen sulfide producing bacteria) anthracosis (carbon dust accumulation)
31
amyloidosis
- protein-folding disorder resulting in insoluble amyloid - predominantly extracellular - local or systemic
32
what forms of amyloid are there
1. AA (amyloid A) 2. AL (amyloid light chain) 3. IAPP (Islet associated polypeptide) 4. AB (amyloid beta)
33
describe AA
- serum amyloid A (positive acute phase protein) - hereditary to share pei, Abyssinian, and Siamese
34
describe AL
- derived from light chains of antibodies - B-cell neoplasms or blood disorders
35
Describe IAPP
- associated with diabetes in humans
36
describe AB
- found in neural plaques of Alzheimer's
37
describe the gross anatomy of amyloid
enlarged, waxy, pale organs dark brown with iodine
38
describe the histomorphology of amyloid
pink color present at space of disse in liver = pressure atrophy of hepatic cords lymphoid follicles in spleen glomeruli of kidneys = protein loss
39
what are the two kinds of mineralization?
1. dystrophic calcification 2. metastatic calcification
40
describe dystrophic calcification
within mitochondria or membrane-bound matrix vesicles gross: fine, white granules or clumps histology: basophilic, granular
41
describe metastatic mineralization
systemic Ca:P imbalance where the product is elevated (intercostal pleura, kidney, stomach, lungs, etc.)
42
what are the causes of metastatic mineralization
renal disease (↑ P) hypervitaminosis D bone turnover (↑ Ca) hyperparathyroidism PTH related protein (↑ Ca)
43
T/F: a functional tumor produces a hormone
TRUE
44
T/F: primary hyperparathyroidism is concurrent with renal disease
FALSE - secondary